As We See It

Dietary Supplements Under Attack

William Faloon — Wed, 15 Jul 2009 13:48:00 GMT

Life Extension Magazine April 2009
Original Article: Dietary Supplements Under Attack

Dietary Supplements Under Attack

By William Faloon

Near the end of 2008, the media ran headline news stories claiming that vitamins C, D, and E do not prevent heart attack, stroke, or breast cancer. Within five days, we posted a rebuttal on the home page of our website.

When these biased stories are launched, the media never gives us prior notice to prepare a response. That means the public only hears conventional medicine’s distorted side of the story.

What follows is a slightly modified version of how we responded to these unfounded attacks:

In the early 1990s, several large population studies showed significant reductions in cardiovascular disease in those who consumed vitamin C or vitamin E.1-6

The most widely reported study emanated from UCLA, where it was announced that men who took 800 mg a day of vitamin C lived six years longer than those who consumed the recommended daily allowance of 60 mg a day. The study, which evaluated 11,348 participants over a 10-year period of time, showed that higher vitamin C intake reduced cardiovascular disease mortality by 42%.7

These kinds of findings did not go unnoticed by the federal government, who subsequently invested hundreds of millions of dollars in an attempt to ascertain if relatively modest vitamin doses could prevent common age-related diseases.

In a recent study used by the media to attack dietary supplements, four groups of male doctors were given various combinations of vitamin C and/or vitamin E or placebo. After eight years, there was no reported difference in heart attack or stroke incidence among the groups.8 This led the media to state that consumers should not buy these supplements.

As you will read, there were so many flaws in this study that the findings are rendered meaningless. Regrettably, consumers who trust their lives to the mainstream media may fall victim to this latest charade to discredit validated methods to reduce cardiovascular disease risk.

Do You Take Your Vitamins Every Other Day?

In the study involving four groups of male doctors, subjects in the vitamin E groups were told to take one 400 IU capsule of synthetic alpha tocopherol every other day.8 This design flaw raises several issues that are rather obvious to serious supplement takers.

First of all, we don’t take our vitamins every other day. Free radicals are constantly being generated in our bodies, and supplement users today seek to take their antioxidants with most meals, as oxidative damage is generally the greatest after eating.9,10

It is ludicrous to think that these study subjects would reduce their vascular risk by taking a modest dose, every other day, of a form of vitamin E with inferior antioxidant capacity.

If one were to rely only on synthetic alpha tocopherol, the minimum daily dose needed has been shown to exceed 800 IU,11,12 far greater than the 400 IU ingested every other day by the subjects in this poorly designed study.

Serious supplement users normally take 400 IU every day of natural vitamin E along with a plethora of complementary nutrients. We would not expect 400 IU of synthetic vitamin E taken every other day to produce much of an effect. Yet that is the dose given to these study subjects with the expectation that this would produce a reduction in cardiovascular disease. This is not the only flaw of this study.

Natural Versus Synthetic Vitamin E

There was a longstanding debate as to whether natural or synthetic vitamin E is better. For most vitamins, there is no difference between natural and synthetic. In fact, for most vitamins, the only forms available are synthetic. With vitamin E, however, the natural form has proven to be far superior.4,13-16

Natural vitamin E is distributed through the body much better than the synthetic form.12,17-21 The reason is that specific carrier proteins in the liver selectively bind to natural vitamin E and transport it through the blood to our cells. These carrier proteins only recognize a portion of synthetic vitamin E and ignore the remainder.22-25

Japanese researchers gave natural or synthetic vitamin E to young women to measure how much vitamin E actually made it into their blood. It took only 100 mg (149 IU) of natural vitamin E to produce blood levels that required 300 mg (448 IU) of synthetic vitamin E to achieve.12

How to Check Vitamin E Labels

When checking vitamin labels, natural vitamin E is usually stated as the “d” form or RRR- [for example d-alpha tocopheryl acetate or RRR-alpha-tocopheryl acetate, d-alpha tocopherol, and d-alpha tocopheryl succinate]. Synthetic vitamin E will have an “l” after the “d” or all-rac- [for example, dl-alpha tocopheryl acetate or all-rac-alpha-tocopheryl acetate, dl-alpha tocopheryl succinate, and dl-alpha tocopherol]. Remember – “dl” or “all rac-” signifies synthetic vitamin E, whereas “d” or “RRR-” signifies natural vitamin E. If you are getting 400 IU of natural d-alpha tocopherol (d-alpha tocopheryl succinate or acetate), it is equal to about 800 IU of synthetic dl-tocopherol (dl-alpha tocopheryl succinate or acetate).

Most studies show that synthetic vitamin E is only half as active in the body as the natural form.17 As it relates to the flawed study claiming that vitamin E does not prevent heart attack, the 400 IU of synthetic alpha tocopherol given every other day equates to only 100 IU a day of the natural form.

We would not expect 100 IU of natural vitamin E a day by itself to reduce vascular disease risk. As you will continue to read, however, there are many other flaws in this study that render its conclusions useless.

Vitamin C Potencies Too Low

If all you are going to take to protect against free radical damage is vitamin E and/or vitamin C, then you will need far greater potencies than were given to the study subjects in this flawed study.

Published studies that document vascular benefits in response to vitamin C typically use doses of 1,000-6,000 mg each day.26-31 The authors of the flawed study alluded8 to this when they stated:

“In a pooled analysis of nine cohorts, vitamin C supplement use exceeding 700 mg/day was significantly associated with a 25% reduction in coronary heart disease risk.”8,32

Since the doctors who designed this flawed study knew that vitamin C intakes exceeding 700 mg a day significantly reduce heart attack rates,32 we cannot figure out why they limited their subject’s daily dose to only 500 mg.8

Two-time Nobel Prize laureate Linus Pauling and his associates advocated daily doses of vitamin C ranging from 10,000 to 20,000 mg to protect against heart attack. Linus Pauling’s theory was that atherosclerosis is primarily caused by insufficient vitamin C intake.33 Dr. Pauling compared the high amount of vitamin C naturally synthesized in the bodies of animals that don’t typically die of heart attacks.34 A 150-pound goat, for example will maintain an ascorbate blood concentration equivalent to ingesting 13,000 mg of vitamin C.34

Unlike most animals, humans lack an internal enzyme needed to manufacture vitamin C in their body. If humans don’t obtain enough vitamin C from external sources, they die acutely from scurvy, or according to Linus Pauling…slowly suffer atherosclerotic occlusion. Dr. Pauling crusaded to educate humans about the need to take mega-doses of vitamin C.

Dr. Pauling and his associates published papers stating that when vitamin C levels are insufficient, the body uses cholesterol to repair the inner lining of arteries. Dr. Pauling believed that cholesterol’s involvement in atherosclerosis was a direct result of insufficient vitamin C.34-36

Life Extension has long recommended that its members take at least 2,000 mg a day of vitamin C, along with potent plant extracts to enhance the biological benefits of ascorbate inside the body. The 500 mg daily dose of vitamin C given to the subjects of this flawed study8 was clearly inadequate. This did not stop the headline-hungry media and many conventional doctors from recommending that aging humans avoid these supplements altogether.

Alpha Tocopherol Users Need CoQ10

A number of studies document the ability of ubiquinol CoQ10 to protect against LDL oxidation better than alpha tocopherol (and other lipid-soluble antioxidants).79-83

Some of these studies show that alpha tocopherol vitamin E can turn into an LDL pro-oxidant unless ubiquinol is also present.84,85 These studies help explain the inability of the alpha form of vitamin E by itself to significantly reduce heart attack rates in certain populations.

The good news is that most members have been taking CoQ10 supplements since around 1983 (when Life Extension introduced it to the American public) and have thus protected their alpha tocopherol from converting into a pro-oxidant.

The subjects given synthetic alpha tocopherol in this flawed study were not given CoQ10 supplements, which further explains why there were no reductions in heart attack and stroke risk.

As we noted already, the dose of vitamin E used in this study was also too low to expect a reduction in vascular disease events. While alpha tocopherol vitamin E is a classic antioxidant, its free radical-quenching efficacy pales in comparison to polyphenol extracts37 from green tea, pomegranate, grape seed, and blueberry.

Based on the superior anti-oxidant properties of plant extracts such as pomegranate, health-conscious people today are able to obtain greater protection against free radicals and enhance the efficacy of the vitamin C without necessarily having to take the mega-doses recommended by Linus Pauling. On the flip side, to attack the value of vitamin C based on a group of doctors who took only 500 mg a day does not make sense, since this amount does not correspond to the doses that scientific studies show are needed to prevent heart attack.

Alpha Tocopherol Displaces Gamma Tocopherol

An increasing number of scientists are questioning the wisdom of administering alpha tocopherol vitamin E by itself.38-42 The reason is that alpha tocopherol displaces critically important gamma tocopherol in the body.43 The authors of the flawed study admitted that the failure to include gamma tocopherol may have been a reason that no effect was seen in the alpha tocopherol groups.8 Here is a quote directly from the flawed study:

“Moreover, PHS II and other prevention trials have used alpha-tocopherol, whereas the gamma-tocopherol isomer also may have a role in cardiovascular disease prevention because it has greater efficacy than alpha-tocopherol to inhibit lipid peroxidation and it may be suppressed in the presence of alpha-tocopherol.”8

The above admission understates the critical importance that gamma tocopherol plays in maintaining arterial health. While alpha tocopherol helps protect against lipid peroxidation, gamma tocopherol is required to neutralize the dangerous peroxynitrite free radical.44

Peroxynitrite damages arteries because:

1. Peroxynitrite promotes the degradation of alpha tocopherol, thereby depleting the body of the vitamin E needed to protect the lipid (fat) part of LDL against oxidation.45 LDL is composed of both lipid and protein parts (moieties), and oxidation associated with both moieties has been implicated in atherosclerosis.46,47 In a fascinating paradox, when alpha tocopherol is given without gamma tocopherol, the result is that alpha tocopherol itself can be neutralized in the body by the peroxynitrite free radical. This in turn promotes oxidation of the lipid moiety of LDL, a major step on the path towards atherosclerosis.

2. Peroxynitrite promotes LDL protein oxidation.48-51 While alpha tocopherol inhibits LDL lipid peroxidation, gamma tocopherol is needed to protect against oxidation of the protein moiety of LDL.42,52,53

In the absence of gamma tocopherol, which can occur when alpha tocopherol is given without gamma tocopherol, both LDL lipid and protein oxidation is increased, which reveals the egregious mistake of trying to prevent vascular disease by administering only alpha tocopherol. Health-conscious individuals should be assured that other nutrients such as lipoic acid and polyphenol plant extracts also block protein and lipid LDL oxidation.9,54-62

Some studies suggest that only gamma tocopherol prevents heart attacks.6 As it relates to atherosclerosis, gamma tocopherol blood concentrations have been reported to be significantly lower in coronary heart disease patients than in healthy control subjects. While alpha and gamma tocopherols each perform life-sustaining functions, only gamma tocopherol increases endothelial nitric oxide protein expression.52,53,63 As I will describe next, a deficit of nitric oxide in the endothelium is a primary cause of arterial disease.

Vitamin E Basics

Alpha tocopherol and gamma tocopherol are the two major forms of vitamin E in human plasma. The dietary intake of gamma toco-pherol is generally two- to four-fold higher than that of alpha tocopherol. Alpha tocopherol plasma levels, however, are about four-fold higher than those of gamma tocopherol.64 One reason is that there is a preferential cellular uptake of gamma tocopherol over alpha tocopherol, meaning that more gamma tocopherol is removed from the blood and assimilated into cells.65

Scientific studies consistently show that gamma tocopherol plays a significant role in modulating intracellular antioxidant defense mechanisms.39,42,66 Interestingly, the presence of gamma tocopherol dramatically increases the cellular accumulation of alpha tocopherol.67

A Hidden Cause of Heart Attack and Stroke

Even when all conventional risk factors are controlled, the progressive decline of nitric oxide in the arterial wall (the endothelium) too often leads to coronary heart attack and stroke.68-75

Seven years ago, Life Extension researchers identified a critical compound (tetrahydrobiopterin) that is an essential cofactor for the enzyme that synthesizes nitric oxide in the endothelium.76 We spent several hundred thousand dollars trying to develop an affordable way to manufacture this compound as it offered tremendous promise for eradicating atherosclerosis.

We failed to find an affordable way to make tetrahydrobiopterin. The good news is that nutrients that suppress peroxynitrite (like gamma tocopherol and pomegranate) increase endothelial nitric oxide by blocking the oxidation of tetrahydrobiopterin.77,78

Indeed, clinical studies show that supplemental gamma tocopherol enhances platelet endothelial nitric oxide synthase activity.52,53 Furthermore, a diet high in gamma tocopherol-rich walnuts improves endothelium-dependent vasodilation in those with high cholesterol.63

By administering only alpha tocopherol as was done in the flawed study, one would expect gamma tocopherol to be suppressed, peroxynitrite levels to increase, and precious tetrahydrobiopterin to be oxidized, thus depriving the endothelium of the nitric oxide it needs to protect against heart attack and stroke. Is it any wonder that this study failed to show vascular disease reduction in those given only alpha (but not gamma) tocopherol?

Failing to Account For All Vascular Risk Factors

Numerous independent risk factors are associated with the development of atherosclerosis and subsequent heart attack and stroke risk. A major flaw in this study was expecting low-dose vitamin C and/or E to somehow overcome all of these underlying causes of artery disease.

We know it is impossible for vitamins C and E to overcome these many risk factors, but this did not stop the media from recommending that Americans discard their supplements.

The following represents a succinct list of documented vascular disease risk factors:

Low testosterone (in men)
Excess fibrinogen
Low HDL
Excess LDL and total cholesterol
Excess glucose
Excess C-reactive protein
Excess homocysteine
Hypertension
Low blood EPA/DHA
Excess triglycerides
Excess insulin
Excess estrogen (in men)
Oxidized LDL
Excess platelet activity
Nitric oxide deficit (endothelial dysfunction)
Insufficient vitamin D
Insufficient vitamin K2

The basis for doing this study, as outlined by the study’s authors, was to use vitamins C and/or E to:

Trap organic free radicals… deactivate excited oxygen molecules… inhibit LDL oxidation
Modify vascular reactivity… prevent tissue damage
Modify platelet activity and thus reduce thrombotic potential.

As one can clearly see on the previous page, there are 17 documented cardiovascular risk factors. Yet only three of these risk factors are what formed the basis for conducting this low-dose vitamin C and/or E clinical trial. The three most important risk factors the authors of the flawed study expected to favorably influence with vitamins C and E were:

LDL oxidation
Platelet activity and thrombotic potential
Vascular reactivity (another term for endothelial dysfunction).

For every one mechanism the study’s authors proposed might enable low-dose vitamin C and/or synthetic vitamin E to work, there are five additional risk factors that would not be corrected. For instance, vitamins C and E in these low doses are not going to reduce C-reactive protein,86 homocysteine, fibrinogen, or glucose.87 Vitamins C and E in any dose are not going to increase testosterone, decrease estrogen, or provide cardioprotective EPA/DHA and vitamin D.

On the contrary, as we have already shown, by giving only alpha but not gamma tocopherol, one might expect increased LDL oxidation and impaired endothelial function. That’s because alpha tocopherol displaces gamma tocopherol in the body. Gamma tocopherol suppresses the peroxynitrite radical that oxidizes both LDL protein and the tetrahydrobiopterin that is needed to produce endothelial nitric oxide.

As far as platelet activity and thrombotic potential (abnormal clotting inside a blood vessel) are concerned, gamma tocopherol is significantly more potent than alpha tocopherol in inhibiting platelet aggregation that can lead to a heart attack or stroke.52,53 By displacing gamma tocopherol, the alpha tocopherol used alone in this study may have increased abnormal platelet aggregation risk.

From everything we know today, this study was designed to fail. Not only did it not correct for the major causes of vascular disease, but it may have exacerbated some of the more dangerous ones.

None of What I Wrote So Far May Really Matter

You have just learned why low-dose vitamin C and/or E supplementation would not be expected to reduce heart attack and stroke risk.

I have saved the biggest shocker for last. It turns out that a significant number of the study subjects (who were all medical doctors) who were supposed to take the vitamin C and/or E supplements did not take their pills. Yet when the calculations for heart attack or stroke incidence were made, those who took as little as 66% of their low-dose vitamin C and/or E supplements were counted as having taken the entire dose.

At the end of the study, 28% of the study subjects admitted they had not even taken 66% of their low-dose vitamin C and/or E supplements.

Even more troubling is the method used to track who was really taking their supplements. Participants were asked to remember and track supplement usage for over eight years’ time without any verification of actual pill counts, compliance by plasma antioxidant analysis, or in vivo surrogate markers of oxidative stress. Relying upon participants’ memory and recollection over a lengthy time period of many years is a rather pathetic way of ensuring adherence, and renders the authors’ so-called “sensitivity analysis” meaningless.

The lack of adherence, i.e., the fact that a significant percentage of the study participants were not even taking their vitamins, may be the most significant flaw to this study. No one in the mainstream media bothered to report this, or any of the other flaws that jumped out at us.

Instead, the media’s message was don’t waste your money on vitamin C or E pills. Many supplement users who are taking the right form and dose of their vitamin C and E nutrients may believe the media’s biased reporting.

Shocking Deficiencies of Vitamin E

The media used this horrific-ally flawed study as a basis to steer Americans away from vitamin C and E supplements. It’s as if all of the previous positive published studies disappeared overnight.

What was omitted is the fact that 92% of American men and 98% of American women do not consume the recommended dietary allowance of vitamin E in their diet. The federal government says Americans need 15 milligrams per day of vitamin E, yet even this minute amount is not found in the diets of the vast majority of people.88

This means that most Americans require a vitamin E supplement to avoid a chronic deficiency, but this important fact was conveniently left out of the news stories.

Conventional medicine says that severe vitamin E deficiency results mainly in neurological symptoms such as impaired balance and coordination and muscle weakness. These neurological symptoms do not develop for 10-20 years, as it takes time for free radicals to inflict nerve damage in the absence of sufficient vitamin E. The reality is that chronic vitamin E deficiency adversely impacts virtually every cell of the body.89-94

Does Drug Money Influence How Medical Journals Report on Dietary Supplements?

A group of statistical researchers investigated the relationship between pharmaceutical advertising and articles regarding dietary supplements in medical journals.99 The analysis revealed that:

Journals with the most pharmaceutical ads published significantly fewer major articles about dietary supplements per issue than journals with the fewest pharmaceutical ads (P < 0.001).
The percentage of major articles concluding that dietary supplements were unsafe was 4% in journals with the fewest pharmaceutical ads and 67% among those with the most pharmaceutical ads (P < 0.005).
The percentage of articles concluding that dietary supplements were ineffective was almost twice as high (50%) among journals with more pharmaceutical ads than among those with fewer pharmaceutical ads (27%).

The researchers concluded that increased pharmaceutical advertising is associated with the publication of fewer articles about dietary supplements and more articles with conclusions that dietary supplements are unsafe.99

A major reason why many conventional doctors are biased against dietary supplements is that the journals they read seldom publish the favorable studies. Dietary supplements compete directly against prescription drugs in many disease categories. When dietary supplements are properly used to prevent disease, demand for expensive pharmaceutical agents is diminished. It is thus in the financial interest of pharmaceutical companies to encourage negative studies to be published in influential medical journals.

It seems more than a coincidence that mainstream medical journals publish negative editorials against dietary supplements at times of the year that garner the most media coverage. Life Extension has long argued that the billions of advertising dollars spent by pharmaceutical companies influences media bias against dietary supplements. This latest study reveals that drug money may also be corrupting medical journals that have a significant impact on professional and public opinion.

A Media Coup for Pharmaceutical Companies

The optimal moment of the year to get your message to the masses is the second week of November. This is a time in between holidays, when winter is setting in, and few people are on vacation. The television networks consider this their most important “sweeps week” as it provides the most accurate measurement of their ratings.

The timing of the release of this horrendously flawed vitamin C and E study could not have been more perfect for pharmaceutical interests. It came out less than one week after the November elections, when the media was primed to sensationalize any story that would attract viewers for their all important “sweeps week.”

On the very same day the media launched its attack on vitamins C and E, the same news sources reported that very high doses of the statin drug Crestor® reduced heart attack rates by 54% in healthy people who had high C-reactive protein levels.95 Just think, uneducated consumers read on the same day that vitamins C and E are worthless and an expensive statin drug performs miracles.

Financial analysts predict a windfall for the makers of Crestor® based on this widely distributed report. In retrospect, conducting a study only on people with high C-reactive protein (but not particularly high LDL) was a brilliant marketing strategy. It had a high probability of a successful outcome, and if the study failed, Crestor® was never approved to lower C-reactive protein or be used in this population group, so the pharmaceutical company had nothing to lose.

We at Life Extension have long warned about the vascular dangers of elevated C-reactive protein and even recommended statin drugs if natural approaches fail to reduce C-reactive protein. We don’t believe most people have to purchase expensive brand name drugs like Crestor®, as generic simvastatin (name brand Zocor®) or pravastatin (name brand Pravachol®) can provide similar benefit at a fraction of the price.

Media Also Attacks Vitamin D

Not content to bash only vitamins C and E, the media the very next day in November 2008 ran a headline story stating that “Supplements don’t reduce breast cancer risk.” This story was based on a study of women who received only 400 IU a day of supplemental vitamin D.96

As has been reported for years in this and other health publications, 400 IU a day of vitamin D is clearly inadequate.97 To reduce breast cancer risk by around 50%, a daily dose of 1,000 IU and higher is required. The major flaw in this study is that participants in the active and placebo group were allowed to take vitamin D outside the study, which rendered the findings meaningless even if the proper dose had been given.

The fact that the media made this study headline news is regrettable because only about 20% of the study population achieved a 25-hydroxyvitamin D blood result at the minimum level required to prevent breast cancer (approximately 30 ng/mL or higher). In other words, most participants in the active or placebo group failed to achieve even the minimal blood concentrations of vitamin D that other studies document are needed to protect against breast cancer.98 So all this study did was help confirm what vitamin D experts have been saying for over five years now, i.e., a minimum of 800 IU to 1,000 IU of vitamin D a day is required… not the 400 IU used in this study.

Don’t Be a Victim of This Flawed Propaganda

It is in the economic interests of drug companies to steer Americans away from healthier lifestyles and dietary supplements. As more Americans fall ill to degenerative disease, drug company profits increase exponentially.

Enormous amounts of pharmaceutical dollars are spent influencing Congress, the FDA, and other federal agencies. The result is the promulgation of policies that cause Americans to be deprived of effective, low-cost means of protecting themselves against age-related disease.

As a member of the Life Extension Foundation, you gain access to scientific information that is interpreted in the context of what health-conscious people are really doing to protect themselves against age-related diseases. You also learn how this information is distorted by the government, drug companies, and the media to discourage the public from following healthier lifestyles.

Click Here for References

Ending The Atrocities

William Faloon — Fri, 17 Apr 2009 21:04:00 GMT

Life Extension Magazine March 2009
Original Article: Ending the Atrocities

Ending the Atrocities

By William Faloon

Today’s population lives on a railroad track. Everything may be fine for the moment—until a freight train comes along and wipes us out.

We at Life Extension have pled for 29 years to get off the track before the train comes.

A startling number of reports reveal the FDA is in far worse shape than originally thought. Few people comprehend that they are likely to suffer and die prematurely as a result of FDA’s failures.

The media does a decent job reporting on FDA disasters. The apathetic public, however, often forgets what they read the next day. That is, until they are diagnosed with a serious illness. Then they go into a panic mode to find an effective treatment. All too often, however, the cure does not exist because of FDA bureaucratic roadblocks. In other cases, the FDA-approved drugs available induce horrific side effects.

It is our mission to memorialize these tragedies to demonstrate the urgent need to radically reform the FDA. This “state-sponsored” carnage of the American citizenry must be stopped!

FDA Disseminates Fraudulent Safety Data

Ketek® (telithromycin) is a drug the FDA approved to treat mild-to-moderate pneumonia. Ketek® can also cause sudden and serious liver damage. In some cases, complete liver failure develops necessitating the need for a liver transplant. Some patients die before a liver transplant can be performed.1-5

The risks of liver failure (and other toxic side effects) were known before the FDA approved Ketek®. In order to convince an outside scientific advisory committee to recommend that Ketek® be approved, the FDA knowingly allowed a fraudulent safety study to be presented. Here is what the Senate Investigative Committee uncovered:6

FDA accepted the resubmission of a new drug application, which included safety data that were fraudulent, in whole or in part.
FDA employees presented the fraudulent study data to the advisory committee that was tasked with recommending Ketek®’s approval or disapproval.
FDA instructed its employees preparing to appear before the advisory committee that they should present these fraudulent safety data.
FDA approved a pediatric clinical trial of Ketek®, involving infants as young as six months old, despite concerns related to known toxicities affecting the heart, eyes, liver, and vascular system.
FDA continued to knowingly cite the fraudulent study data in publically released safety information on Ketek®.

How fraudulent were these data? While the FDA was presenting these fake data, a criminal investigation was simultaneously being conducted that found the clinic where the “safety” study allegedly occurred was closed during the time the study was supposed to have taken place. It was also determined that documents relating to the safety study had date modifications and signature inconsistencies.

Shortly after the advisory committee meeting where the fake safety data were presented by FDA employees, the person who conducted the study was criminally indicted, pled guilty, and was sentenced to almost five years in jail.

It is even more shocking that the FDA continued to cite this safety study long after the principal investigator admitted it was fraudulent. While the perpetrator of this “safety” study was in prison for falsifying the data, the FDA used the very same study to issue a Public Health Announcement stating:

“Based on the pre-marketing clinical data it appeared that the risk of liver injury with telithromycin [Ketek®] was similar to that of other marketed antibiotics.”7

The “pre-marketing clinical data” FDA cited to mislead the public about Ketek® was the fraudulent study, a study that may never have actually occurred. According to the Senate Investigative Committee report, “it defies explanation why the FDA would continue to cite” this fraudulent study to the American public to imply that Ketek® is safe.8

The Senate Committee report concluded by stating that, “Retaliation against these individuals, or any other FDA employees who communicate with the committee with reference to Ketek® will not be tolerated.”8

Based on the tone of the Senate investigative report, it would appear that the FDA functioned as a continuous criminal enterprise in this instance.8,9

The Revolving Door

You may wonder why certain officials in the FDA would go to such extreme lengths to get a lethal drug like Ketek® approved.

Look no further than the gargantuan economic benefits drug companies reap when a patented compound like Ketek® receives the FDA seal of approval.

When we first exposed the revolving door of FDA employees going to work for companies they regulate, virtually no one believed us. Back in the 1980s, most Americans were deceived by FDA propaganda stating that the agency “is responsible for protecting the public health by assuring the safety…of human drugs.”12

The harsh reality is that the FDA functions primarily to protect the financial interests of the pharmaceutical industry, not the public’s health. If anyone ever questioned this, look no further than the FDA’s attempts last year to ban the safest form of estrogen (estriol). The FDA has no qualms about publically stating that its ban on estriol was based on a petition filed by Wyeth, the maker of dangerous estrogen drugs like Premarin® and Prempro®.

There are a number of estrogen drugs that have not been shown to increase stroke or breast cancer risk.13 The FDA, however, has done nothing to remove Premarin® or Prempro®. Instead, the FDA openly seeks to protect Wyeth’s market share by denying American women access to natural estriol.

According to the FDA, “bioidentical hormone products are unsupported by medical evidence and are considered false and misleading by the agency.”14 The truth is that bioidentical hormones are far less expensive and pose a major competitive threat to Wyeth, ergo the FDA’s aggressive attempts to disallow them.

In a report issued by the Associated Press just last year, it was revealed that a record number of FDA employees are leaving the agency to go to work for pharmaceutical companies. According to the Associated Press, these FDA staffers are resigning in order to go into “the more lucrative side of the business…”15

The FDA’s Brain Drain

As experienced FDA scientists leave the agency to work for Big Pharma, the remaining staff is leaner and less competent to approve new life-saving medications. As reported by the Associated Press, a consequence of FDA employees going to work for pharmaceutical companies is a clogging of the drug approval pipeline.

As long time Life Extension members know, the FDA drug approval process has always been a bureaucratic quagmire, where life-saving medications languish for years, decades, and sometimes forever. The drug pipeline has been “clogged” for almost 50 years. We are deeply disturbed that it is now taking even longer for life-saving medications to become available to those in need.

The Wall Street Journal continues to support our position with blistering exposés describing human beings who suffer horrendously and die while potential life-saving therapies languish at the FDA. An article published last year titled “Sick Patients Need Cutting-Edge Drugs” disclosed heart-wrenching reports of young cancer patients who were denied compassionate-use access to experimental drugs. The Wall Street Journal article raised the logical questions:

“Why do terminally ill patients have to wait so long to get access to the only treatments that hold any promise of saving their lives? And why is it not their right to decide?”16

These very issues have been discussed in Life Extension’s publications for nearly 30 years. We have analogized in previous articles how it is perfectly legal to engage in all kinds of risky activities, such as parachuting from high bridges, but it is illegal to make experimental medications available to terminally ill people without the FDA’s permission.

According to the Wall Street Journal, the drug delay problem is getting much worse. The problem has been magnified in recent years as the number of new drug approvals has fallen dramatically. The FDA approved just 16 new drugs in 2007 and 24 in 2008.17,18 That’s down from 139 in 1996.

With the approval of life-saving drugs grinding to a snail’s pace, the moronic cruelty of denying experimental drugs to terminal patients must stop. Each day a life-saving drug is delayed, human beings perish. The case for radical reform of the Food, Drug, and Cosmetic Act and the FDA itself has never been stronger.

How Many Drug-Induced Suicides?

The same Senate committee investigating the Ketek® scandal uncovered another study with falsified data. These fake data were used to support the approval of a popular antidepressant drug used by millions of human beings.

According to a report authored by a Harvard medical doctor, when the Paxil® application was submitted to an FDA advisory committee in 1991, the drug company improperly put people who had previously attempted suicide into the placebo group, so that it would appear that the Paxil® group would have the same rate or an even lower rate of suicide than the placebo recipients. This was done to make it appear that there was no increased risk of suicidal behavior in those taking Paxil® compared with placebo.

It took until 2006 for the manufacturer to send a letter to doctors admitting that the risk of suicidal behavior was 6.7 times higher in study subjects taking Paxil® compared with placebo.10

Suicide is the 11th leading cause of death in the United States.11 It killed over 32,000 people in the United States in 2004. The number of suicides attributed to drugs like Paxil® (selective serotonin-reuptake inhibitors) could be in the hundreds of thousands during the 13 years it was fraudulently marketed.8,9

FDA Bungles New System to Track Side Effects

Even when data used to approve a new drug are not fraudulent, there are inherent limitations in assessing toxic side effects in the clinical study setting. Reasons for this include the relatively short time period the drugs are evaluated in a clinical study compared with how long patients use them in the real world. Another problem is that clinical studies are often tightly controlled by doctors with specialized expertise in the particular drug they are evaluating. Practicing physicians, on the other hand, see dozens of patients a day and may not be familiar with the proper way to prescribe drugs that have a narrow safety window. Still another issue is the relatively small number of patients taking the drugs in a clinical study compared with the millions who may eventually be prescribed them.

Due to these serious limitations, post-approval surveillance is critical to identifying lethal side effects of prescription drugs that were not detected in the clinical trials.

According to a report by an independent auditing institute, the FDA squandered $25 million on a bungled computer system to track side effects of approved drugs.19,20 As a result, the FDA will have to rely on a dysfunctional system to track what are record-breaking numbers of adverse reports being made about drugs the agency previously approved as safe.

After this report showing that FDA errors and mismanagement caused this computer system to not be available, the FDA asked that most of the findings of the report be deleted. The independent institute who put the report together refused to capitulate to the FDA’s attempts to obstruct the report’s findings.20,21

Drug Prices Surge

In today’s upside-down regulatory system, Americans are prescribed drugs whose approval may be based on fraudulent or insufficient research data. Experimental therapies that could save their lives are routinely denied. The cost of existing medications meanwhile is skyrocketing.

Drug price increases often exceed the inflation rate. The average cost increase for the top 50 best-selling drugs was 7.82% in 2007, 6.73% in 2006, and 6.22% in 2005.22

Some very popular drugs are increasing at astronomical rates. The cost of the antidepressant Wellbutrin XL® went up by 44.5% from 2005 to 2007. The cost of the attention-deficit drug Adderall XR® went up by 33.5%. The price of the sleep aid drug Ambien® shot up 70.1% during this period.22

On less popular drugs, the price surges are worse than obscene. A drug used to treat heart problems in premature babies went from $136.10 to $1,875 in one year. A drug used to treat a certain cancer (Cosmegen®) increased from $16.79 to $593.75 in one year. A drug used to treat spasms in babies (Acthar®) was increased from about $1,650 to more than $23,000 in one year. Just imagine your baby suffering spasms and being asked to fork over $23,000 for one drug!23

Whether you use these drugs or not, you still suffer. The thoroughly corrupt Medicare Prescription Drug Act passed at the behest of pharmaceutical lobbyists mandates that taxpayers pay full retail prices for these drugs.24 Taxpayers will fork over $600 billion for these egregiously overpriced drugs in the first 10 years.25

Where consumers are really hurting is in their ever-increasing health insurance premiums. If you are fortunate enough to have someone else paying your premiums, you cannot help but note the higher deductibles and greater exclusions.

The FDA enables drug companies to financially rape the American consumer by stifling competition. There are so many regulatory hurdles to getting FDA approval for even a competitive generic drug that consumers often pay eight times more than they need to.

Under the guise of “consumer protection,” the FDA has been manipulated by pharmaceutical interests to restrict free market forces that would drive down drug costs.

FDA Botches Public Relations Campaign

The FDA has been pummeled by Congress and the media about its many scandals, including poor inspections of tainted foods, drugs, and other products it regulates.

Needless to say, this has created a severe image problem. So FDA officials decided to hire a public relations agency that would “create and foster a lasting positive public image of the agency for the American public,” according to agency documents.26

When taxpayer dollars are involved, the law mandates that a bidding process is used to ensure that the contract goes to the lowest cost contractor. According to an exposé published by the Washington Post, the propaganda contract went instead to a public relations firm with ties to the FDA official who arranged the deal. A loophole was used to avoid putting the contract up for bid.27

After being made aware of this apparent corrupt act, an FDA deputy commissioner suspended the public relations contract and ordered an independent investigation.

Congress responded by launching still another investigation into the FDA. According to the chairman of the House committee that oversees the FDA, “The agency chose to use its limited resources to save face instead of saving the public health.”27

The FDA retains the power to make life and death decisions that affect all of us. When it comes to analyzing new therapies to extend human longevity, this involves the scientific and common sense ability to understand complex biochemical interactions that occur within living organisms. The FDA’s botched attempt to launch a misinformation campaign to cover up its inadequacies further calls into question its competency and moral legitimacy.

Do Drug Companies Have Any Decency?

It is beyond my comprehension to understand how pharmaceutical companies can look themselves in the mirror when they know they are selling drugs proven to kill.

Back in 1994, our best-selling product was shark cartilage. The problem we uncovered was that it was not curing cancer patients. We immediately notified our customers that a survey we conducted of those who bought shark cartilage showed it to be ineffective. We urged these people to seek other therapies.

The supplement industry was shocked at our findings, but most stopped promoting shark cartilage as an anticancer therapy. Our findings about shark cartilage’s lack of efficacy were confirmed several years later in a controlled study.

We were a relatively small organization in 1994 and losing our best-selling product was financially challenging. In no way, however, could we continue telling cancer patients that shark cartilage might help them when our own findings showed it did not work.

The fact the multibillion dollar pharmaceutical companies have no qualms about using fraudulent data to support the approval and continued sale of lethal drugs is an atrocity. That certain people within the FDA collude with pharmaceutical companies to allow dangerous and ineffective drugs on the market is an act so heinous that words do not exist to describe it.

Fighting Back

In 1994, we established the FDA Museum to document how the FDA’s failings were responsible for the needless deaths of millions of Americans.

Sadly, every assertion we made about the FDA back then has been validated by third parties and the FDA itself. I lament that we were proven correct, because this means that millions more Americans perished unnecessarily over the past 15 years… and the cost of today’s corrupt health care system threatens to financially decimate our country.

The FDA’s credibility is at an all-time low. There has never been a better time to enact legislation to reform the way health care is regulated in this country. With a new Congress in session, health freedom activists are aggressively seeking to have the law changed to allow free market forces to tear down the corrupt wall of bureaucracy that causes the needless deaths of thousands of Americans each day.

We at Life Extension are working with the American Association for Health Freedom (AAHF) to make our voices heard in Congress. AAHF is a coalition of integrative physicians, health care consumers, and health freedom activists committed to a complete reform of the FDA. Its Reform FDA Petition is available for signing at http://www.reformfda.org/. AAHF and its coalition allies will hand deliver the petition to Congress and urge immediate and comprehensive FDA reform. For this to be successful, we need your help and signature now. Please log on to www.reformfda.org and join this petition campaign.

Why Your LEF Membership is so Important

More scientific innovation is occurring in the medical field than at any time in human history. This progress is irrelevant, however, if a regulatory barrier denies the fruits of this research to people in need, or allows drugs to be sold with lethal side effects, or renders the cost of medications unaffordable.

The Life Extension Foundation has been battling FDA ineptitude for three decades. Your support through membership dues and product purchases enables us to continue this ongoing struggle to convince Congress to radically reform the way health care is controlled in this country.

For longer life,

William Faloon

References

1. Gleason PP, Walters C, Heaton AH, Schafer JA. Telithromycin: the perils of hasty adoption and persistence of off-label prescribing. J Manag Care Pharm. 2007 Jun;13(5):420-5.

2. Ross DB. The FDA and the case of Ketek. N Engl J Med. 2007 Apr 19;356(16):1601-4.

3. Graham DJ. Telithromycin and acute liver failure. N Engl J Med. 2006 Nov 23;355(21):2260-1.

4. Mathews AW. Fraud, errors taint a key study of widely used Sanofi drug; despite some faked results, FDA approves antibiotic; one doctor’s cocaine use; company defends safety. Wall St J (East Ed). 2006 May 1:A1,A12.

5. Available at: http://www.drug-injury.com/druginjurycom/2007/12/ketek-case-repo.html. Accessed December 5, 2008.

6. Available at: http://www.druginjuryblog.com/2008/06/11/ketek-fraudulent-clinical-trials-prove-fda-not-doing-its-job-congress-says/. Accessed December 5, 2008.

7. Available at: http://www.fda.gov/ora/about/enf_story2006_archive/ch3/default.pdf. Accessed December 5, 2008.

8. Available at: http://finance.senate.gov/press/Gpress/2005/prg050106.pdf. Accessed December 5, 2008.

9. Available at: http://finance.senate.gov/press/Gpress/2007/prg122007a.pdf. Accessed December 5, 2008.

10. Available at: http://us.gsk.com/docs-pdf/media-news/Paxil-CR-and-Paxil-Adult-Suicide.pdf. Accessed December 5, 2008.

11. Available at: http://www.cdc.gov/ncipc/dvp/suicide/SuicideDataSheet.pdf. Accessed December 5, 2008.

12. Available at: http://www.fda.gov/opacom/morechoices/mission.html. Accessed December 5, 2008.

13. Birge SJ. Hormone therapy and stroke. Clin Obstet Gynecol. 2008 Sep;51(3):581-91.

14. Available at: http://www.fda.gov/bbs/topics/NEWS/2008/NEW01772.html. Accessed December 5, 2008.

15. Available at: http://www.msnbc.msn.com/id/24953413/wid/7279844/. Accessed December 5, 2008.

16. Available at: http://online.wsj.com/article/SB121944789005365195.html?mod=opinion_main_commentaries. Accessed December 12, 2008.

17. Available at: http://www.pharmacistsletter.com/pl/newdrugs/FDA2007.pdf?cs=&s=PL. Accessed December 5, 2008.

18. Available at: http://online.wsj.com/article/SB123084693842347229.html. Accessed January 5, 2009.

19. Available at: http://www.ahrp.org/cms/content/view/476/28/. Accessed December 5, 2008.

20. Available at: http://www.ahrp.org/cms/index2.php?option=com_content&do_pdf=1&id=476. Accessed December 5, 2008.

21. Available at: http://finance.senate.gov/press/Bpress/2007press/prb030707a.pdf. Accessed December 5, 2008.

22. Available at: http://online.wsj.com/article/SB120355185318681367.html. Accessed December 5, 2008.

23. Available at: http://www.usatoday.com/money/industries/health/drugs/2008-08-07-costlydrugs_N.htm. Accessed December 11, 2008.

24. Available at: http://www.ustreas.gov/offices/public-affairs/hsa/pdf/pl108-173.pdf. Accessed December 5, 2008.

25. Available at: http://www.aafp.org/fpm/20050300/49what.html. Accessed December 5, 2008.

26. Available at: http://www.nytimes.com/2008/10/05/opinion/05sun4.html?ref=opinion. Accessed December 5, 2008.

27. Available at: http://www.washingtonpost.com/wp-dyn/content/article/2008/10/01/AR2008100103061_pf.html. Accessed December 5, 2008.

Atherosclerosis And The Cholesterol Controversy

William Faloon — Wed, 18 Mar 2009 21:37:00 GMT

Life Extension Magazine February 2009
Original Article: The Cholesterol Controversy

The Cholesterol Controversy

By William Faloon

As we enter the year 2009, a heated debate continues about the role of cholesterol in the development of atherosclerosis and heart disease. Based on our analysis, both sides still have it wrong!

Almost comical is the role reversal this controversy has taken. When progressive individuals first proposed that high cholesterol increases heart attack risk, the medical establishment ridiculed the idea. The FDA went so far as to make it illegal for food companies to claim that diets low in saturated fat and cholesterol had any relationship to artery disease. (Note: High-saturated fat diets cause blood cholesterol to spike.)

The dispute raged for decades until the medical establishment (and the FDA) not only embraced the concept that high cholesterol causes heart attacks, but claimed this scientific area their exclusive domain.1-5 Many of today’s complementary medicine practitioners, who would have been early proponents of low-saturated fat diets, now question the association between cholesterol and vascular disease.

The fact that confusion still exists over this straightforward medical principle helps explain why atherosclerotic disease remains today’s leading preventable killer.

Early History of Cholesterol and Arterial Disease

If we travel back to 1913, we would learn of an impressive study showing that rabbits fed a high-cholesterol diet develop atherosclerotic lesions that closely resemble those seen in humans.6 This research was initially criticized because rabbits are plant eaters whose normal diets are not the same as humans. When dogs and rats are fed high-cholesterol diets, they do not develop artery disease. It was later discovered that dogs and rats efficiently convert cholesterol to bile acids that are excreted. When these excretion mechanisms are blocked, however, dogs and rats do develop atherosclerosis in response to cholesterol feeding.

The cholesterol theory gained a bit more credibility when atherosclerotic lesions were readily induced in guinea pigs,7,8 goats,9 hens, parrots,10 and even primates11 in response to cholesterol elevation.

Interestingly, the first hints that high cholesterol caused atherosclerosis in humans occurred back in 1889.2,12 A doctor reported a case of a child with a rare genetic disorder that caused massive overproduction of cholesterol. The child died suddenly at age 11. An autopsy revealed extensive atherosclerotic-like lesions in large arteries.

It was not until 1939 that a publication in the Archives of Internal Medicine pulled together the evidence linking this rare genetic disorder (familial hyper-cholesterolemia) to coronary artery disease.2,13 It was argued back then, however, that the extraordinarily high cholesterol levels in those with this genetic defect could not be extrapolated to people with only moderate cholesterol elevations.

By 1955, the cholesterol-heart attack connection was attracting some respectability. A study was done that measured cholesterol blood levels in people from seven different countries. Citizens of Finland, who ate the most saturated fats, had an average cholesterol reading of over 260 (mg/dL). The Japanese, who consumed the least saturated fat, had average cholesterol readings of a little over 160. Over a 10-year period, the number of fatal heart attacks per 1,000 men was about 70 in Finland and a little less than 5 in Japan. Saturated fat made up 20% of the Finnish diet, but only 2.5% of the Japanese diet.2,14

These findings had a significant impact on the cholesterol debate, but the vast majority of physicians and the federal government still proclaimed that high cholesterol had nothing to do with heart attack risk.

Where Some Researchers Went Wrong

In trying to prove that diets high in saturated fats increase cholesterol levels and subsequent heart attack risk, scientists conducted studies that substituted omega-6-rich polyunsaturated fats (corn oil, safflower oil) in place of saturated fats (butter, lard, meat fats).15-17 While these studies showed reduced cholesterol levels and heart attack rates, the findings were not nearly as impressive as they could have been. This is because these kinds of polyunsaturated fats (corn oil, sunflower oil, safflower oil, etc.) rich in omega-6 fatty acids create inflammatory byproducts and induce LDL oxidation that damages arteries.

During this era of medical ignorance (the 1950s-1960s), the benefits of monounsaturated fats (such as those found in olive oil) and omega-3 fats (such as those found in cold-water fish, flaxseed, and walnut oils) in preventing heart attacks were not recognized. The best that doctors could provide in lieu of dangerous saturated fats was to substitute omega-6 polyunsaturated fats, which then created a dangerous proinflammatory state (due to an imbalance in omega-6 to omega-3 fats).18

The 1960s… More Lost Opportunities

I’ll never forget going to my first funeral and seeing a 42-year-old neighbor lying in a coffin. He had died of a sudden heart attack, but no one talked about how unusual his early death was. That’s because men over age 40 were routinely dying of heart attacks in those days.

Heart attacks and strokes claimed astronomical numbers of lives in the Western world throughout most of the past century. During the early 1960s, for example, the number of acute fatal heart attacks in younger men was substantially higher than today.19-21 A lot of this had to do with cigarette smoking and the high-saturated fat diet that was a staple in most households.

By the early 1960s, however, the theory that one could reduce their heart attack risk by avoiding saturated fats had taken hold at least in the alternative medicine community. Even the American Heart Association went on record as early as 1961 with the following closely guarded statement:

“Those people who have had one or more atherosclerotic heart attacks or strokes may reduce the possibility of recurrences by such a change in diet.”2,22

Based on a wave of studies showing reductions in heart attack incidence in those who reduced their saturated fat intake, nutritionists and alternative doctors were finally espousing heart-healthy diets. The FDA responded by criminalizing the commercial dissemination of this information by the food industry. Heart attacks claimed about seven million American lives in the 1960s.20 The FDA’s suppression of the link between poor diet and heart attack risk kept funeral businesses thriving.

The Great Cholesterol Debates

In 1969, an American Heart Association spokesperson stated that those with excess cholesterol levels should be treated medically. This doctor went on to state, “in short, we have come ... to the point where we are probably preventing a disease that was considered to be an inevitable accompaniment of aging not very long ago.”26

The American Heart Association met with fierce criticism from prominent cardiologists who continued to proclaim there was no evidence that cholesterol reduction conferred protection against heart attacks. These attacks on the cholesterol theory of heart disease were published in the leading medical journals of the day.

Regrettably, it was not until 1984 that the medical establishment formally recognized the relationship between high cholesterol and heart attack incidence.27

The First Diet-Heart Cookbook

Readers of Life Extension magazine may recall the name John Gofman, MD, PhD. This is the physicist turned medical doctor whose early work on radioactive isotopes resulted in him being recruited to work on The Manhattan Project to develop the first atomic bomb.

Dr. Gofman’s expertise on the biological effects of radiation caused him to later take a very controversial position. He meticulously documented how medical diagnostic X-rays are a cause of cancer and artery disease, something most in the medical establishment still refuse to accept.

In 1947, Dr. Gofman began research that would soon lead him to conclude that cholesterol is a cause of atherosclerosis.23,24 Dr. Gofman and his colleagues were the first to show that specific fractions of cholesterol such as LDL (low-density lipoprotein) are the most dangerous. Dr. Gofman was involved in the publication of possibly the first book in 1951 about how low-fat and low-cholesterol diets prevent heart disease.25

I am always amazed at individuals who are able to contribute so much. In Dr. Gofman’s case, he was instrumental in harnessing nuclear energy, warning of the dangers of low-level radiation, and then moved on to a completely different field to discover specific fractions of cholesterol that cause atherosclerosis.

Nathan Pritikin… An Early Hero of Mine

I will never forget as a teenager seeing a televised debate between Nathan Pritikin and a mainstream cardiologist. Pritikin explained how very low-fat diets could reverse coronary atherosclerosis, whereas the cardiologist ridiculed the notion.

I knew little about heart attacks back then, other than the fact that my family members and neighbors were having them on a regular basis. I also witnessed the poor diets these heart attack victims ate, which made Nathan Pritikin’s arguments all the more convincing to me.

What was so remarkable about Nathan Pritikin was that he had no medical training. In 1957, at age 40, Pritikin was diagnosed as having heart disease. Faced with a lifetime of ever-increasing disability, he pored over the scientific literature and formulated a diet and exercise program to treat his disease.28 After nine years of trial and error, he had cured himself.

Long before the medical establishment acknowledged that something as simple as diet might be causing serious illnesses, Pritikin had created a scientifically sound program using food and exercise as medicine. This revolutionary departure from the flawed theories of the 1950s caused him to become a public enemy of the medical establishment. Nathan Pritikin’s healthy diet program did more than reverse heart disease. Patients who came to his clinic often saw their type 2 diabetes, arthritis, and hypertension disappear.29,30

Despite these clinical successes, Nathan Pritikin was ceaselessly attacked by doctors as being a charlatan. For much of the 1970s, Nathan Pritikin waged a public battle with government and private health agencies, as well as with the American Medical Association. The medical establishment doggedly refused to accept that what one ate had anything to do with their risk of heart disease.

Pritikin was so confident that he was reversing heart disease with healthy diets that he ordered his own body autopsied after his death. Almost 30 years after being diagnosed with irreversible coronary artery disease, the autopsy showed his arteries were akin to those of a young man and clear of any signs of heart disease.31

In 1987, two years after Nathan Pritikin’s death, the Journal of the American Medical Association announced a study that showed regression of atherosclerosis in the coronary arteries of humans who reduced their blood cholesterol by a similar degree as were accomplished at the Pritikin Longevity Centers.32 Numerous subsequent studies confirmed that Nathan Pritikin was scientifically correct…and the medical establishment’s position fatally flawed.33-36

Tens of millions of Americans needlessly perished because the role of cholesterol in causing heart disease was not recognized nearly as early as it should have been.

What is Cholesterol?

Cholesterol is a lipid (fat) that is chemically classified as a sterol. It provides critically important functions in the body such as building and maintaining cell membranes. Cholesterol also functions as a precursor to hormones like testosterone and fat-soluble vitamins.

While cholesterol is essential to life, the lipoprotein it is bound to plays a role in whether it injures or protects the arterial wall. Since cholesterol is insoluble in blood, it is transported in the circulatory system by lipoproteins.

LDL (low-density lipoprotein) transports cholesterol to the cells, whereas HDL (high-density lipoprotein) transports cholesterol away from the cells.

When one has excess LDL, too much cholesterol can be deposited into the arterial wall. Insufficient HDL, on the other hand, impairs cholesterol transport away from the arterial wall (for disposal in the liver). Too much LDL and/or not enough HDL can thus set the stage for atherosclerosis. These simple facts, however, explain only part of the problem.

Pomegranate Suppresses LDL Oxidation

LDL Atherosclerosis Risk Factor	Effect of Pomegranate61
LDL basal oxidative state	Reduced by 90%
LDL susceptibility to copper-induced oxidation	Reduced by 59%
Paraoxonase-1 (protects against LDL oxidation)	Improved by 83%
Total antioxidant status	Improved by 130%

Danger of Oxidized LDL

The over-promotion of “statin”drugs has resulted in today’s cardiologists focusing on getting their patients’ LDL and total cholesterol down as low as possible. Pharmaceutical company advertising has made it appear as if the only cause of atherosclerosis is excess LDL and cholesterol.

Beginning in 1979, however, researchers made discoveries indicating that it is the oxidation of LDL that results in the most arterial damage.37-39 Thousands of studies now reveal how oxidized LDL contributes to the atherosclerotic process from start to finish.

There are doctors who argue that atherosclerosis is all about inflammation and response to endothelial injury and has nothing to do with LDL cholesterol. What these doctors overlook is the fact that oxidized LDL injures endothelial cells and causes inflammation!40-46

Oxidized LDL causes endothelial cells to secrete “adhesion molecules” that allow white blood cells to penetrate the inner lining of the artery (the endothelium). This is where initial fatty streaks and atherosclerotic plaques develop.47

Oxidized LDL turns on white blood cell gene expression that enables them to convert into foam cells, which results in continuous accumulation of oxidized LDL in the atherosclerotic plaque.48

Oxidized LDL initiates an inflammatory process by causing foam cells to secrete molecules that attract proinflammatory cells.47

Oxidized LDL enhances the process whereby immune cells, foam cells, smooth muscle cells, and endothelial cells degrade collagen, which leads to the rupture of the fibrous plaque.49

The endothelium requires nitric oxide to function properly. A hallmark characteristic of endothelial dysfunction is a lack of nitric oxide. Oxidized LDL impairs the endothelial cells’ ability to produce nitric oxide.50

As you may surmise by now, both absolute LDL level and LDL oxidation are involved in atherosclerotic processes and heart attack risk.

Coronary Risk Following Treatment with Statin Drugs According to Achieved LDL Levels

Achieved LDL Level (mg/dL of blood)	Under 54	54-71	72-94	Over 94
	Lowest Risk	10%	30%	80%
		Greater Risk	Greater Risk	Greater Risk

The data above is a tabulation of the results from patients who had already suffered a coronary event who were then prescribed either 80 mg of Lipitor® (atorvastatin) or 40 mg of Zocor® (simvastatin) per day.

These findings show that the achieved level of LDL was strongly predictive of recurring coronary events. These relative risks are adjusted for age, smoking status, diabetes, hypertension, and body mass index (BMI).64

Common Sense Approaches to Heart Attack Prevention

Financial bias, apathy, and scientific ignorance have resulted in most Americans failing to protect themselves against today’s leading crippler and killer… atherosclerosis.

Some cardiologists erroneously believe that if all their patients took a statin drug and aspirin, coronary artery disease would disappear. Equally disturbing are doctors who claim that that aging people should not worry about their LDL levels.

For 29 years, we at Life Extension have emphasized that atherosclerosis has many underlying causes.51 Our findings have been validated in many subsequently published studies.52-54 At the end of this article, we have reprinted an updated version showing 17 daggers aimed at the heart, each dagger representing an independent risk factor for developing coronary artery disease. Fortunately, most Life Extension members are already taking nutrients, hormones, and sometimes drugs to protect against every one of these cardiac risk factors.

When it comes to inhibiting LDL oxidation, members should find comfort in knowing they have been taking supplements that have been confirmed to dramatically inhibit LDL oxidation. A number of studies document the ability of ubiquinol CoQ10 to protect against LDL oxidation better than lycopene, alpha tocopherol, and other lipid-soluble antioxidants.55-59 Some of these studies show that alpha tocopherol (vitamin E) can turn into an LDL pro-oxidant unless ubiquinol is also present.60 These studies help explain the inability of the alpha form of vitamin E by itself to significantly reduce heart attack rates in certain populations.

Perhaps no other nutrient has demonstrated better anti-LDL oxidation effects than pomegranate. In a clinical study, human subjects taking pomegranate showed a beneficial 35% reduction in carotid intima-media thickness accompanied by a 45% improvement in carotid blood flow. As evidenced by the chart above, pomegranate improved markers related to LDL oxidation by up to 130%!61

These kinds of impressive study results, showing how LDL oxidation can be suppressed, might tempt some people to ignore dangerously high LDL blood levels. We at Life Extension strongly advise against this. The chart below vividly shows the sharp increase in coronary artery disease risk as LDL concentrations increase in the blood.62

Keep Your LDL Levels Below 100

Atherosclerosis remains the leading cause of death in the Western world.63 Eastern populations who are switching to high-fat Western diets are seeing vascular disease rates spiral upwards. We cannot ignore almost 100 years of research showing that excess LDL-bound cholesterol is a coronary risk factor.

While there may someday be a definitive finding that something as simple as pomegranate provides complete protection against LDL oxidation, and therefore excess LDL itself, we don’t have these data confirmed today.

You have entrusted us to provide you with an accurate analysis of the available scientific literature to keep you alive in good health. We therefore reiterate our 29-year recommendation that healthy members keep their LDL levels below 100 mg/dL.

Very high-risk groups (e.g., smokers or those with diabetes, abdominal obesity, a recently sustained heart attack, low HDL, high triglycerides, or known coronary artery disease) should strive for a 70-75 mg/dL LDL target level. (Note: Those who drive LDL down to these very low levels should use blood tests to make sure they are not also suppressing critical hormones like testosterone and DHEA.)

The chart on top of this page clearly demonstrates that in people who have already suffered a coronary event, each progressive LDL elevation increases the risk of a second event. In this study, cardiac disease incidence was 80% greater in those with an LDL reading over 94 mg/dL compared with those whose LDL was under 54 mg/dL.64

See How Our Presidents Died in the Past Century

To better understand the epidemic of heart disease that existed during the era of the cholesterol debates, look no further than the medical histories of the presidents of the United States.

President Dwight Eisenhower suffered his first heart attack in 1955. That same year, Senator Lyndon Johnson suffered his first heart attack. Back in those days, recovery from a heart attack was a slow and arduous process.

Dwight Eisenhower smoked four packs a day of cigarettes until he quit in 1949. Combined with his high-saturated fat intake, he was at great cardiac risk. Here is what President Eisenhower ate the day of his first heart attack:77

Breakfast: sausage, bacon, mush, hotcakes
Lunch: hamburger with raw onion
Dinner: roast lamb

In 1957, President Eisenhower suffered a stroke. By the time of this death in 1969, Eisenhower had suffered at least seven heart attacks, along with multiple other diseases that can be related to the unhealthy nature of the typical American diet of his era.77

Three years later, former President Harry Truman died at age 88 from atherosclerotic coronary artery disease.

Lyndon Johnson was only 46 years old when he suffered his first coronary occlusion heart attack. He too had been a heavy smoker, but quit after his first heart attack. Shortly after leaving the presidency, Lyndon Johnson resumed cigarette smoking and continued eating foods that we know today damage arterial linings (the endothelium). Johnson developed severe angina pain that crippled him until he suffered his final heart attack in 1973 at age 65.78

So while the FDA and the medical establishment were ridiculing the notion that high-saturated fat diets caused artery disease, the most famous political leaders of the day were keeling over from heart attacks right before the public’s eyes.

Heart attack and/or stroke claimed the lives of most of the presidents in the past century including Theodore Roosevelt, William Taft, Woodrow Wilson, Calvin Coolidge, Franklin Roosevelt, and Richard Nixon.

Tying it all Together

In reviewing the history of dietary fats and heart disease risk, a number of interesting facts emerge. Nathan Pritikin put a lot of the pieces together when he mandated that virtually all dietary fat should be eliminated (less than 10% total calories from fat). This protected his followers against the atherogenic effects of both saturated fat and dangerous omega-6-rich polyunsaturated fat sources like corn, soybean, safflower, and sunflower oils. The problem is that adhering to Pritikin’s very strict diet is difficult for the vast majority of people.

Fortunately, we know today that following a low-saturated fat, Mediterranean-type diet with lots of natural polyphenol antioxidants provides huge cardioprotective benefits.65 We have also acquired the knowledge that specific fats (omega-3s and certain monounsaturated fats) are extremely beneficial in reducing vascular disease risk.66,67

As we report in this issue of Life Extension, a large number of studies continue to validate the ability of low-cost plant polyphenols to not only protect against LDL oxidation, but to also boost beneficial HDL and lower absolute LDL levels in the blood.68-76

It may thus be possible for many aging humans to achieve optimal blood lipid status using an integrative approach to support healthy cholesterol levels and reduce oxidant stress… without resorting to prescription drugs.

For longer life,

William Faloon

References

1. Steinberg D. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy: part I. J Lipid Res. 2004 Sep;45(9):1583-93.

2. Steinberg D. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy: part II: the early evidence linking hypercholesterolemia to coronary disease in humans. J Lipid Res. 2005 Feb;46(2):179-90.

3. Steinberg D. Thematic review series: the pathogenesis of atherosclerosis: an interpretive history of the cholesterol controversy, part III: mechanistically defining the role of hyperlipidemia. J Lipid Res. 2005 Oct;46(10):2037-51.

4. Steinberg D. The pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy, part IV: the 1984 coronary primary prevention trial ends it—almost. J Lipid Res. 2006 Jan;47(1):1-14.

5. Steinberg D. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy, part V: the discovery of the statins and the end of the controversy. J Lipid Res. 2006 Jul;47(7):1339-51.

6. Fleissig J. Uber die bisher als Riesenzellensarkome (Myelome) bezeichneten Granulationsgeschwulste der Sehnenschiden. Dtsch Z Chir. 1913;122:239-65.

7. Bailey CH. Observations on cholesterol-fed guinea pigs. Proc Soc Exper Biol. 1915;13:60-2.

8. Anitschkow N. Ueber die experimentelle Atherosklerose der Aorta beim Meerschwinchen. Beitr Pathol Anat. 1922;70:265-81.

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22. Anon. Diet and the possible prevention of coronary atheroma; a council statement. JAMA. 1965 Dec 6;194(10):1149-50.

23. Gofman JW, Lindgren F. The role of lipids and lipoproteins in atherosclerosis. Science. 1950 Feb 17;111(2877):166-71.

24. Gofman JW. Serum lipoproteins and the evaluation of atherosclerosis. Ann NY Acad Sci. 1956 Nov 16;64(4):590-5.

25. Dobbin EV, Gofman HF, Jones HC, Lyon L, Young C. The Low-Fat, Low-Cholesterol Diet. Garden City, NY: Doubleday; 1951.

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28. Pritikin N. The Pritikin diet. JAMA. 1984 Mar 2;251(9):1160-1.

29. Barnard RJ, Lawani LO, Martin DA, et al. Effects of maturation and aging on the skeletal muscle glucose transport system. Am J Physiol. 1992 May;262(5 Pt 1):E619-26.

30. Roberts CK, Barnard RJ. Effects of exercise and diet on chronic disease. J Appl Physiol. 2005 Jan;98(1):3-30.

31. Hubbard JD, Inkeles S, Barnard RJ. Nathan Pritikin’s heart. N Engl J Med. 1985 Jul 4;313(1):52.

32. Blankenhorn DH, Nessim SA, Johnson RL, et al. Beneficial effects of combined colestipol-niacin therapy on coronary atherosclerosis and coronary venous bypass grafts. JAMA. 1987 Jun 19;257(23):3233-40.

33. Roberts CK, Chen AK, Barnard RJ. Effect of a short-term diet and exercise intervention in youth on atherosclerotic risk factors. Atherosclerosis. 2007 Mar;191(1):98-106.

34. Roberts CK, Won D, Pruthi S, et al. Effect of a short-term diet and exercise intervention on oxidative stress, inflammation, MMP-9, and monocyte chemotactic activity in men with metabolic syndrome factors. J Appl Physiol. 2006 May;100(5):1657-65.

35. Roberts CK, Vaziri ND, Barnard RJ. Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress, and nitric oxide availability. Circulation. 2002 Nov 12;106(20):2530-2.

36. Anderson JW, Konz EC, Jenkins DJ. Health advantages and disadvantages of weight-reducing diets: a computer analysis and critical review. J Am Coll Nutr. 2000 Oct;19(5):578-90.

37. Henriksen T, Mahoney EM, Steinberg D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptors for acetylated low density lipoproteins. Proc Natl Acad Sci USA. 1981 Oct;78(10):6499-503.

38. Hessler JR, Morel DW, Lewis LJ, Chisolm GM. Lipoprotein oxidation and lipoprotein-induced cytotoxicity. Arteriosclerosis. 1983 May;3(3):215-22.

39. Quinn MT, Parthasarathy S, Fong LG, Steinberg D. Oxidatively modified low density lipoproteins: a potential role in recruitment and retention of monocyte/macrophages during atherogenesis. Proc Natl Acad Sci USA. 1987 May;84(9):2995-8.

40. Ross R. Atherosclerosis--an inflammatory disease. N Engl J Med. 1999 Jan 14;340(2):115-26.

41. Ross R. The pathogenesis of atherosclerosis—an update. N Engl J Med. 1986 Feb 20;314(8):488-500.

42. Yla-Herttuala S, Palinski W, Rosenfeld ME, et al. Evidence for the presence of oxidatively modified low density lipoprotein in atherosclerotic lesions of rabbit and man. J Clin Invest. 1989 Oct;84(4):1086-95.

43. Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med. 1989 Apr 6;320(14):915-24.

44. Berliner JA, Navab M, Fogelman AM, et al. Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics. Circulation. 1995 May 1;91(9):2488-96.

45. Suits AG, Chait A, Aviram M, Heinecke JW. Phagocytosis of aggregated lipoprotein by macrophages: low density lipoprotein receptor-dependent foam-cell formation. Proc Natl Acad Sci USA. 1989 Apr;86(8):2713-7.

46. Palinski W, Rosenfeld ME, Yla-Herttuala S, et al. Low density lipoprotein undergoes oxidative modification in vivo. Proc Natl Acad Sci USA. 1989 Feb;86(4):1372-6.

47. Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr. 2006 Feb;83(2):456S-60S.

48. Tontonoz P, Nagy L, Alvarez JG, Thomazy VA, Evans RM. PPARgamma promotes monocyte/macrophage differentiation and uptake of oxidized LDL. Cell. 1998 Apr 17;93(2):241-52.

49. Libby P. The molecular mechanisms of the thrombotic complications of atherosclerosis. J Intern Med. 2008 May;263(5):517-27.

50. Zhang WZ, Venardos K, Finch S, Kaye DM. Detrimental effect of oxidized LDL on endothelial arginine metabolism and transportation. Int J Biochem Cell Biol. 2008;40(5):920-8.

51. Faloon W. A lethal misconception of epidemic proportion. Life Extension. 2007 May;13(5):7-14.

52. Danesh J, Lewington S, Thompson SG, et al. Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis. JAMA. 2005 Oct 12;294(14):1799-809.

53. Malkin CJ, Pugh PJ, Jones RD, Jones TH, Channer KS. Testosterone as a protective factor against atherosclerosis—immunomodulation and influence upon plaque development and stability. J Endocrinol. 2003 Sep;178(3):373-80.

54. Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA. 2001 May 16;285(19):2481-5.

55. Stocker R, Bowry VW, Frei B. Ubiquinol-10 protects human low density lipoprotein more efficiently against lipid peroxidation than does alpha-tocopherol. Proc Natl Acad Sci USA. 1991 Mar 1;88(5):1646-50.

56. Frei B, Kim MC, Ames BN. Ubiquinol-10 is an effective lipid-soluble antioxidant at physiological concentrations. Proc Natl Acad Sci USA. 1990 Jun;87(12):4879-83.

57. Thomas SR, Neuzil J, Stocker R. Inhibition of LDL oxidation by ubiquinol-10. A protective mechanism for coenzyme Q in atherogenesis? Mol Aspects Med. 1997;18(Suppl):S85-103.

58. Mohr D, Bowry VW, Stocker R. Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. Biochim Biophys Acta. 1992 Jun 26;1126(3):247-54.

59. Kontush A, Hubner C, Finckh B, Kohlschutter A, Beisiegel U. Antioxidative activity of ubiquinol-10 at physiologic concentrations in human low density lipoprotein. Biochim Biophys Acta. 1995 Sep 14;1258(2):177-87.

60. Bowry VW, Mohr D, Cleary J, Stocker R. Prevention of tocopherol-mediated peroxidation in ubiquinol-10-free human low density lipoprotein. J Biol Chem. 1995 Mar 17;270(11):5756-63.

61. Aviram M, Rosenblat M, Gaitini D, et al. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr. 2004 Jun;23(3):423-33.

62. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004 Jul 13;110(2):227-39.

63. Available at: http://www.cdc.gov/nchs/data/nvsr/nvsr56/nvsr56_16.pdf. Accessed October 15, 2008.

64. Ridker PM, Cannon CP, Morrow D, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005 Jan 6;352(1):20-8.

65. de Lorgeril M, Salen P, Martin JL, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation. 1999 Feb 16;99(6):779-85.

66. Harris WS, Miller M, Tighe AP, Davidson MH, Schaefer EJ. Omega-3 fatty

acids and coronary heart disease risk: clinical and mechanistic perspectives. Atherosclerosis. 2008 Mar;197(1):12-24.

67. Pérez-Jiménez F, Ruano J, Perez-Martinez P, Lopez-Segura F, Lopez-Miranda J.

The influence of olive oil on human health: not a question of fat alone. Mol Nutr Food Res. 2007 Oct;51(10):1199-208.

68. Aviram M, Fuhrman B. Wine flavonoids protect against LDL oxidation and atherosclerosis. Ann NY Acad Sci. 2002 May;957:146-61.

69. Martin-Nizard F, Sahpaz S, Furman C, et al. Natural phenylpropanoids protect endothelial cells against oxidized LDL-induced cytotoxicity. Planta Med. 2003 Mar;69(3):207-11.

70. Janisch KM, Williamson G, Needs P, Plumb GW. Properties of quercetin conjugates: modulation of LDL oxidation and binding to human serum albumin. Free Radic Res. 2004 Aug;38(8):877-84.

71. Sies H, Stahl W, Sevanian A. Nutritional, dietary and postprandial oxidative stress. J Nutr. 2005 May;135(5):969-72.

72. Mursu J, Voutilainen S, Nurmi T, et al. Dark chocolate consumption increases HDL cholesterol concentration and chocolate fatty acids may inhibit lipid peroxidation in healthy humans. Free Radic Biol Med. 2004 Nov 1;37(9):1351-9.

73. Baba S, Osakabe N, Kato Y, et al. Continuous intake of polyphenolic compounds containing cocoa powder reduces LDL oxidative susceptibility and has beneficial effects on plasma HDL-cholesterol concentrations in humans. Am J Clin Nutr. 2007 Mar;85(3):709-17.

74. Covas MI, Nyyssonen K, Poulsen HE, et al. The effect of polyphenols in olive oil on heart disease risk factors: a randomized trial. Ann Intern Med. 2006 Sep 5;145(5):333-41.

75. Baba S, Natsume M, Yasuda A, et al. Plasma LDL and HDL cholesterol and oxidized LDL concentrations are altered in normo- and hypercholesterolemic humans after intake of different levels of cocoa powder. J Nutr. 2007 Jun;137(6):1436-41.

76. Zern TL, Wood RJ, Greene C, et al. Grape polyphenols exert a cardioprotective effect in pre- and postmenopausal women by lowering plasma lipids and reducing oxidative stress. J Nutr. 2005 Aug;135(8):1911-7.

77. Available at: http://www.doctorzebra.com/prez/z_x34mirx_g.htm#zree6#zree6. Accessed October 15, 2008.

78. Available at: http://www.nps.gov/archive/lyjo/ourheartshome/lbj3.htm. Accessed October 15, 2008.

Vitamin D Deficiency

William Faloon — Tue, 03 Feb 2009 23:15:00 GMT

Life Extension Magazine January 2009
Original Article: Millions of Needless Deaths

Millions of needless deaths

By William Faloon

It is hard to imagine, but it was not until 1867 that Joseph Lister published his findings about the critical need of using sterile procedures in the surgical setting. Back then, doctors seldom washed their hands prior to surgery, let alone sterilize the instruments they had used on the previous patient.

Before Dr. Lister’s sterile techniques were adopted, patients frequently died from infections introduced during surgery.

Joseph Lister had little interest in financial or social success. These traits enabled him to endure the criticisms hurled by the medical establishment about the extra steps he took to ensure his surgical environments were clean.

One of Dr. Lister’s greatest challenges was to persuade his colleagues that germs did in fact exist. Back then, most doctors still believed in the theory of spontaneous generation.1

Convincing today’s medical establishment about proven methods to save lives may be less daunting than what Dr. Lister encountered, but it is still nonetheless challenging.

Today’s Body Count

Back in 2007, I urged the federal government to declare a national emergency. My rationale was that millions of Americans were going to needlessly die if the epidemic of vitamin D insufficiency was not immediately corrected.2

My article was based on irrefutable scientific evidence documenting how vast numbers of lives could be spared if everyone took at least 1,000 IU of vitamin D3 each day.2

I went a step further and showed how mandatory vitamin D supplementation could resolve today’s health care cost crisis by slashing the need for expensive prescription drugs and hospitalizations.2

I took it two steps further and offered to donate 50,000 one-year-supply bottles of vitamin D3 so the government could give these away to those who could not afford this ultra-low cost supplement.2

It is now 16 months later. The federal government has done nothing to inform the public of the opportunity to radically reduce their risk of dying by taking a supplement that costs less than 6 cents a day!

Vitamin D More Effective Than Previously Known

A large number of new vitamin D studies have appeared in the scientific literature since I wrote my plea to the federal government. These studies don’t just confirm what we knew 16 months ago—they show that optimizing vitamin D intake will save even more lives than what we projected.

For instance, a study published in June 2008 showed that men with low vitamin D levels suffer 2.42 times more heart attacks. Now look what this means in actual body counts.3

Each year, about 157,000 Americans die from coronary artery disease-related heart attacks.4 Based on this most recent study, if every American optimized their vitamin D status, the number of deaths prevented from this kind of heart attack would be 92,500.

To put the number of lives saved in context, tens of millions of dollars are being spent to advertise that Lipitor® reduces heart attacks by 37%. This is certainly a decent number, but not when compared with how many lives could be saved by vitamin D. According to the latest study, men with the higher vitamin D levels had a 59% reduction in heart attacks.3

This does not mean that you should stop taking medications if you can’t get your cardiac risk factors under control by natural methods. It does mean that you should make certain you are not vitamin D-insufficient.

Please note that all forms of heart disease kill over 869,700 Americans each year.4 These lethal forms of heart disease include cardiomyopathy, valvular insufficiency, congestive heart failure, arrhythmia, coronary thrombosis (blood clot in coronary artery), and coronary atherosclerosis (narrowing or blockage of coronary arteries). There is reason to believe that vitamin D could help protect against most of these forms of cardiac-induced death.5

Billions of Dollars in Health Care Savings

There are 920,000 heart attacks suffered in the United States every year.4 According to the American Heart Association, the annual cost of health care services, medications, and lost productivity related to these heart attacks is over $156 billion.4

The annual retail cost of all 300 million Americans (including children) supplementing with 1,000 IU of vitamin D per day is $6.6 billion.

So if vitamin D’s only benefit was to reduce coronary heart attack rates by 59%, the net savings (after deducting the cost of the vitamin D) if every American supplemented properly would be around $85 billion each year. That’s enough to put a major dent in the health care cost crisis that is forecast to bankrupt Medicare and many private insurance plans.

Sparing Countless Numbers From the Agonies of Cancer

The evidence supporting the role of vitamin D in preventing common forms of cancer is now overwhelming.2

Vitamin D-deficient women, for example, have a 253% increased risk of colon cancer.6 Colon cancer strikes 145,000 Americans each year and 53,580 die from it.7 Based on these studies, if everyone obtained enough vitamin D, 38,578 lives could be saved and medical costs would be reduced by $3.89 billion.8,9

A study published in January 2008 showed that women with the lowest level of vitamin D were at a 222% increased risk for developing breast cancer.10 Most studies show that higher levels of vitamin D can reduce breast cancer incidence by around 30-50%.11-14

Each year, approximately 186,800 women are diagnosed with breast cancer and 40,950 perish from it in the United States.15 This needless toll of suffering and death caused by insufficient intake of vitamin D is unconscionable.

Prostate cancer will be diagnosed in an estimated 189,000 American men this year. Almost 30,000 will die from it.16 Men with higher levels of vitamin D have a 52% reduced incidence of prostate cancer.17

The first-year costs of prostate cancer treatment are approximately $14,540.18 If all aging men achieved sufficient vitamin D status, about $1.4 billion could be saved each year.

So as you can see, there is no real health care cost crisis. What the population suffers from is frighteningly low blood levels of vitamin D. During winter months in Canada, for instance, an estimated 97% of the population is vitamin D-deficient.19

Vitamin D Protects Against Stroke

Stroke is the number three cause of death in the United States.20 It is also one of the most feared diseases because of its high incidence of permanent disability.

In a study published in September 2008, blood indicators of vitamin D status were measured in 3,316 patients with suspected coronary artery disease. The subjects were followed for 7.75 years. For every small decrease in blood indicators of vitamin D status, there was a startling 86% increase in the number of fatal strokes.21

The doctors who conducted this study concluded: “Low levels of 25(OH)D* and 1,25(OH)2D* are independently predictive for fatal strokes, suggesting that vitamin D supplementation is a promising approach in the prevention of strokes.”21

*Note: 25 [OH] D and 1,25[OH]2D are blood markers that measure vitamin D status in one’s body.

If all that vitamin D did was to reduce stroke risk, it would be critically important for every American to ensure optimal blood levels.

Low Vitamin D Doubles Death Rate

Vitamin D deficiency is a worldwide problem. Yet no conventional medical organization or governmental body has declared a health emergency to warn the public about the urgent need of achieving sufficient vitamin D blood levels.

According to John Jacob Cannell, MD, founder of the non-profit Vitamin D Counsel: “Current research indicates vitamin D deficiency plays a role in causing seventeen varieties of cancer as well as heart disease, stroke, hypertension, autoimmune diseases, diabetes, depression, chronic pain, osteoarthritis, osteoporosis, muscle weakness, muscle wasting, birth defects, and periodontal disease.

This does not mean that vitamin D deficiency is the only cause of these diseases, or that you will not get them if you take vitamin D. What it does mean is that vitamin D, and the many ways in which it affects a person’s health, can no longer be overlooked by the health care industry nor by individuals striving to achieve and maintain a greater state of health.”22

Vitamin D seems to reduce the risk of almost every killer disease of aging. In fact, a recent study shows that humans with low vitamin D status are twice as likely to die over a seven-year time period!5

Each year, the federal government spends $1 billion in research aimed at finding ways to prevent or cure the killer diseases of aging.23 Yet the government is oblivious to the most medically effective and cost-effective way of preventing needless death. This is analogous to how the establishment ignored Joseph Lister’s pleas for a sterile environment in the surgical arena.

Difference Between “Deficiency” and “Insufficiency”

Doctors are not trained to recognize a vitamin D deficiency until rickets develop in children or osteomalacia (softening of the bones) develops in adults. Clinical vitamin D deficiency is diagnosed when blood levels of a vitamin D metabolite (25-hydroxyvitamin D) drop below 12 ng/mL.

According to the world’s foremost experts, however, optimal blood levels of vitamin D are between 30 and 50 ng/mL and higher.24,25 Those with blood levels below 30 ng/mL are considered to have insufficient vitamin D.

These widely varying numbers explain why mainstream medicine is at a loss to understand the widespread health problem created by less than optimal vitamin D levels. If physicians view a patient’s medical chart and see a vitamin D blood level of 18 ng/mL, they will think this person has adequate vitamin D. The reality is that a vitamin D blood level this low predisposes this patient to virtually every killer disease of aging and may in fact be the reason that individual has become a “patient” instead of remaining healthy.

There clearly is a need for a new consensus in the medical community to redefine vitamin D deficiency as a blood reading below 30 ng/mL. As we at Life Extension long ago learned, it can take decades for the establishment to change its reference ranges to reflect scientific reality.

What Can be Done?

Despite the startling number of needless deaths, the federal government has done nothing to warn the public of the lethal dangers associated with vitamin D insufficiency.

We will distribute my original 2007 article along with this editorial to every member of the new Congress and the President in January 2009. Hopefully someone will understand the urgency of declaring a health emergency and advise that every American maintain a vitamin D blood level of at least 30 ng/mL.

If the government continues to ignore our pleas, perhaps private insurance companies will consider sending free bottles of vitamin D supplements to all of their subscribers. The outlays for medical procedures and prescription drugs would be expected to plummet in groups who took their vitamin D supplement each day.

The media has done a good job in reporting on the numerous positive findings about vitamin D over the past two years. Sales of vitamin D supplements have been increasing, so at least some Americans are getting the message and taking steps to guard against vitamin D insufficiency.

In the meantime, Life Extension will continue to report on new findings about vitamin D. We have found that if we repeat a message long enough, much of the public will wake up to scientific reality and the desire for self-preservation.

All Hospitalized Patients Should be Tested For Vitamin D

The pioneer of antiseptic procedures in the hospital setting was a Hungarian physician named Ignaz Semmelweis. In one of the world’s great detective stories, Dr. Semmelweis went back 100 years to find out why there was such an increase in puerperal fever (childbed fever) that had killed thousands of mothers in obstetric units.

Dr. Semmelweis correlated increases in autopsies performed at hospitals with greater incidences of lethal puerperal fever. It turned out that doctors would leave an autopsy room with their hands covered in decomposing human tissues (and lots of bacteria) and deliver babies with their fetid hands.

Semmelweis instructed his interns to wash their hands with chlorinated lime solutions and documented an immediate reduction in puerperal fever incidence.

Despite the logic of his arguments and concrete proof shown by the reduction in mortality when hand-washing procedures were followed, Semmelweis faced a wall of opposition. Back in those days, maternity hospitals had horrendous reputations and were sometimes referred to as deathtraps. Some suggested that lives could be saved simply by closing the clinics where people went in with minor problems and ended up dying agonizing deaths. Doctors of the day refused to accept that they were the ones responsible for the deaths of thousands of young woman. Semmelweis was eventually committed to an insane asylum where he died.

Move forward to 2009, and hospitals are still places to avoid. Medical errors, antibiotic-resistant infections, sleep interruption, pneumonia, and malnutrition continue to ravage those confined to the hospital setting.

An overlooked problem with institutional confinement is that patients admitted with insufficient vitamin D can rapidly develop severe vitamin D deficiency due to complete lack of sunlight and malnutrition caused by commotion in the hospital environment.

A strong argument could be made that every patient admitted to a hospital should have their blood tested for vitamin D and supplements administered to ensure that blood levels remain considerably above 30 ng/mL. The improvement in immune function along with reduced inflammatory responses alone could result in many more patients leaving via the hospital lobby rather than its morgue.

There are respected medical authorities today advocating universal vitamin D supplementation, but their pleas are all but ignored by most practicing doctors. Unlike the plight of women in childbirth exposed to puerperal fever by ignorant doctors in the past, no informed person has to suffer from lack of vitamin D. More and more people are taking their supplements with them when they go to the hospital because they know they will need them there more than in any other place.

Where to Purchase Vitamin D

Fortunately, the patent for synthesizing vitamin D expired long ago. It is an ultra-low-cost supplement available at any health food store, pharmacy, and most grocery stores. There is no economic impediment precluding immediate widespread supplementation.

I want to thank loyal Life Extension members for purchasing most of their supplements from our Buyers Club over the past 12 months. We use proceeds from these sales to fund critical research projects aimed at eliminating needless disease and death. We also support an ongoing campaign to reform incompetent government policies that deprive Americans of life-saving medical therapies.

Just once a year, we discount the price of every product we offer. During our annual Super Sale, members stock up on our most advanced formulations and enjoy considerable savings.

Please know we remain relentless in tearing down the walls of medical ignorance that are by far the leading causes of disability and death in the United States.

For longer life,

William Faloon

References

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2. Faloon W. Should the president declare a national emergency? Life Extension. 2007 Oct;13(10):7-17.

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11. Rossi M, McLaughlin JK, Lagiou P, et al. Vitamin D intake and breast cancer risk:
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As We See It - December, 2008

William Faloon — Wed, 07 Jan 2009 16:16:00 GMT

LE Magazine December 2008
Vindication

Vindication

By William Faloon

When we first recommended that aging men restore their testosterone to youthful levels, a firestorm of criticism erupted.

The medical establishment proclaimed that by interfering with the natural decline in testosterone secretion, that men risked all kinds of terrible fates. When Life Extension members asked their doctors for testosterone prescriptions, they ran into objections such as, “I don’t prescribe steroids,” “testosterone causes heart attacks,” and “testosterone causes prostate cancer.”

We countered these criticisms with hundreds of scientific citations showing that testosterone deficiency is an underlying cause of age-related disease. We also demonstrated that none of the paranoid fears about natural testosterone had ever been substantiated.

To this day, a huge number of doctors view testosterone as if it were a narcotic. Other physicians admit they don’t know how to prescribe testosterone to their patients. All of that is about to change.

Harvard Medical School

A new book authored by the “experts at Harvard Medical School” should bury once and for all the biased and ignorant misconceptions about natural testosterone restoration therapy.

Testosterone for Life (McGraw-Hill; 2008) is an exceptionally well-written book that validates what we long ago published about the safety, testing, method of delivery, and multiple benefits of testosterone.

While this information has been widely circulated in the anti-aging community, the fact that it has been so eloquently compiled by the “experts at Harvard Medical School” should forever dispel the myths that have misled mainstream doctors for decades.

Testosterone for Life reminds the reader of what the medical community erroneously thought, and then presents the scientific truths in such a way that it is difficult to imagine anyone regurgitating these fallacies again. The author freely admits his own mistaken beliefs about testosterone that were based on the medical establishment’s flawed dogma, and then describes how he uncovered the real facts.

Low Testosterone Increases Prostate Cancer Risk

Fear of prostate cancer is the leading reason why aging men have shied away from restoring their free testosterone to youthful ranges. To dispel this concern, Life Extension long ago analyzed every published study and found there is no basis for asserting that testosterone causes prostate cancer.1-6

Our observations from the thousands of blood tests we perform each year for members confirmed this. What we found is that men with low testosterone appear to be more likely to contract prostate cancer.

In Testosterone for Life, the misleading notion about testosterone causing prostate cancer is exposed in better detail than I have ever seen. You don’t have to buy the book to read this information. The publisher allowed us to excerpt the entire chapter that you can read in this month’s issue. "Destroying the Myth About Testosterone Replacement and Prostate Cancer."

What will come as a bombshell to the medical establishment is the compilation of scientific facts presented in this chapter showing that men with low testosterone levels have an increased percentage of prostate cancer-positive biopsies.4,7,8 This means that physicians who refused to prescribe testosterone to their aging male patients may have unwittingly contributed to today’s prostate cancer epidemic.

Testosterone May Safely Be Used in Those Who Have Had Prostate Cancer

Another revealing chapter in Testosterone for Life exposes the erroneous belief that men who have ever had prostate cancer, or are at high risk for prostate cancer, can never use testosterone.9

The prevailing dogma is that raising the concentration of testosterone is to prostate cancer like pouring gasoline onto a fire. While there are certain stages of prostate cancer where this can happen, it turns out that prostate cancer cells can thrive on relatively low concentrations of testosterone.4,7 That is why when testosterone deprivation is properly prescribed as a treatment for existing prostate cancer, the objective is to reduce testosterone to very low levels (less than 20 ng/dL of blood). That often means shutting down testosterone production from both the testes and the adrenal glands.

Life Extension still cautions that most men with prostate cancer should avoid testosterone therapy until the disease is completely eradicated. Any man (whether or not he has ever had prostate cancer) who initiates testosterone therapy and then experiences an increase in PSA should discontinue testosterone and undergo diagnostic tests to assess if prostate cancer is present. Testosterone is a stress test for latent prostate cancer and if the PSA rises in response to testosterone replacement therapy, then prostate cancer has been identified and testosterone should be stopped.

Testosterone for Life cites published studies and case reports of men with existing prostate cancer who restored their testosterone levels and experienced a reduction in clinical markers and symptoms of their disease. While we at Life Extension believe that most men with active prostate cancers should not increase their testosterone levels until their disease is brought under control, the information presented in this new book calls into question some of our previous concerns.

The major emphasis in the chapter “Treating Men Who Have a History of Prostate Cancer” is that once prostate cancer is believed to be cured, there is no reason for an aging man to suffer from a testosterone deficiency. This chapter, perhaps more than any other in this book, will turn conventional assumptions about testosterone and prostate cancer upside down.

I suggest that anyone who has had prostate cancer and now wants to restore their testosterone levels should read this chapter in Testosterone for Life. We were not able to excerpt this chapter, so one should obtain the book in order to read it.

Symptoms of Low Testosterone

Testosterone for Life heavily emphasizes the quality-of-life improvements that occur in most men who restore their testosterone to youthful ranges. Common symptoms described in men with low testosterone are:

Sexual problems such as decreased desire, erectile dysfunction, difficulty achieving orgasm, and reduced intensity of orgasm
Low energy and increased fatigue
Loss of motivation
Depressed mood
Loss of sense of well-being and vigor.

In case after case, when low testosterone is corrected, men report improvements in some or all of the above symptoms. It is interesting to note that these symptoms of low testosterone are analogous to what one would expect with normal aging.

A Generation Who Lost Their Quality of Life

Testosterone for Life discusses the many published studies showing that men with higher testosterone levels live longer and have lower rates of diabetes and heart attacks.

The emphasis of the book, however, is on the enormous quality-of-life improvements observed in men prescribed testosterone. These improvements include increased sexual desire, performance, and fulfillment, along with marked enhancements in energy and sense of well-being. These remarkable case histories, presented in meticulous detail, should ignite a stampede of aging men seeking to have their doctors prescribe them testosterone creams.

While Testosterone for Life relates many histories of men suffering common age-related afflictions who then regain their youthful vigor, the author dutifully discusses why some men do not respond to testosterone, such as being prescribed drugs that destroy libido and erection capability.

When reading Testosterone for Life, one cannot help but sympathize about an entire generation of aging men robbed of their youth because the medical establishment, federal government, and the media ignored scientific reality. We should also remember the anti-aging doctors who were persecuted and sometimes imprisoned for prescribing testosterone to their patients. The only crime these doctors committed was being ahead of their time.

Signs of Low Testosterone

“Symptoms” are something a person experiences, whereas “signs” are something that can be measured, like weight or blood pressure. Testosterone for Life describes common signs of low testosterone such as:

Loss of muscle mass and strength
Accumulation of belly fat
Low bone density
Anemia
Increased incidence of type 2 diabetes.

These signs of low testosterone are common characteristics of normal aging. Testosterone for Life confirms how most men demonstrate improvements in these pathologic signs when testosterone levels are restored.

Where Life Extension Disagrees With the “Harvard Experts”

Most of the recommendations in Testosterone for Life closely follow what Life Extension long ago published.

There are some exceptions, however, that paint an interesting picture of how differently mainstream medicine thinks when analyzing the exact same scientific data.

Life Extension has dedicated many articles to the disease-prevention potential of testosterone replacement therapy. One study, for example, showed mortality levels 88% higher in men with low testosterone, compared with men who had normal testosterone.10

Testosterone for Life acknowledges all these studies, but does not believe these studies provide enough substantiation to warrant men replacing their testosterone for the purposes of living longer. They specifically state that if a man with low testosterone has no signs or symptoms of deficiency, then he should not restore his testosterone.

We at Life Extension vehemently disagree with this line of thinking. Our position is that low testosterone contributes to the degenerative diseases of aging such as chronic inflammation,11-15 neurologic decline,16-22 diabetes,23,24 and atherosclerosis.6,25-29 Most of us take our nutrient supplements not because we suffer “signs or symptoms” of deficiency, but because we want to prevent the onset of age-related disease.

It is fascinating that the “experts of Harvard Medical School” have such a different philosophy about this critically important issue of disease prevention, though they admit they are leaning towards recommending testosterone for longevity purposes if more confirmatory studies are published.

Testosterone for Life defines low testosterone as free testosterone blood levels below 15 pg/mL. We at Life Extension suggest that aging men maintain their free testosterone at a level of 20-25 pg/mL to more closely resemble that of a healthy 21-year-old.

“Clearly, many men feel more energetic, vigorous and alive with testosterone therapy, not to mention having more interest in sex and improved sexual performance. These men feel better, enjoy their lives—and their partners—more, and tend to have a better outlook on life.”

—Abraham Morgentaler, MD, FACS, Associate clinical professor,
Harvard Medical School

There are a number of delivery methods available for aging men to restore their testosterone levels. Both Life Extension and the “experts at Harvard” suggest topically applied testosterone creams or gels as the most efficient way of delivering testosterone into the body. While the Harvard experts acknowledge that patients using compounded testosterone creams achieve desired blood levels, they heavily recommend FDA-approved testosterone cream drugs because they believe these to be more reliable.

Life Extension has found that testosterone made by compounding pharmacies consistently elevates free testosterone, and that the recommended follow-up blood tests can verify that an individual using testosterone from a compounding pharmacy is achieving youthful levels.

What the Harvard people neglect to discuss is cost. The FDA-approved testosterone cream drugs can cost over $220 a month (or $2,640 a year). Compounded testosterone, on the other hand, can be obtained for around $20 a month (or $240 a year). For whatever reason, Testosterone for Life chooses not to discuss the cost differential issue.

FDA-approved testosterone drugs are unaffordable to many aging men. We at Life Extension do not hesitate to enlighten our readers that they can obtain the same benefits by spending $20 a month, as opposed to $220 a month for FDA sanctioned testosterone drugs.

Interesting Tidbits

Testosterone for Life makes compelling arguments for aging men with low testosterone to take corrective action. In rebutting critics who claim nature should not be interfered with, author Abraham Morgentaler, MD, FACS, asks whether aging people should be deprived of their eyeglasses, since visual decline is also a normal manifestation of aging. He questions why doctors who prescribe thyroid hormone drugs criticize testosterone replacement. Why, he asks, is it OK to treat low thyroid but not low testosterone?

Building muscle mass and bone density while reducing abdominal fat are well-established improvements in body composition observed in response to testosterone therapy.30-32 Testosterone for Life relates recent data showing that testosterone not only helps increase the strength and size of each muscle cell, but also influences nearby cells into becoming muscle cells.33,34

Perhaps the most detailed descriptions in Testosterone for Life are the sexual-enhancing effects that occur when this hormone is restored. Dr. Morgentaler relates numerous case reports of patients who had lost interest in sex, were unable to perform satisfactorily, and/or who no longer experienced youthful fulfillment. In most cases, these patients reported that within weeks of testosterone levels being restored, they experienced more youthful sexual urge, performance, and pleasure.

“As you know, my sex drive came back quickly. What I hadn’t expected though, was how much better I would feel… within a couple months of treatment, I felt better than I’d felt in years. I’ve started two new businesses and I’m helping a colleague with the creation of a nonprofit educational company. I’m now excited to wake up every single day.”

—Testimonial of a 52-year-old male patient who had his testosterone restored to a youthful level.

Saving Our Healthcare System

Be it the public or private sector, the United States of America does not have the economic resources to pay the health care costs of its rapidly increasing aging population.

For the past three decades, we at Life Extension have advocated free market approaches that would slash medical financial outlays by maintaining aging people in youthful states of health.

Based on an enormous amount of published scientific data, testosterone deficiency is a major risk factor in the development of expensive-to-treat degenerative diseases in the male population.

If most men restored their testosterone, the savings to Medicare alone in hospital and other medical service expenditures would be incalculable.

How to Safely Restore Youthful Testosterone Balance

Since most doctors still don’t know how to properly prescribe testosterone, I will make the following recipe as simple as possible:

1. Have your blood tested for free testosterone, estradiol, and prostate-specific antigen (PSA), along with complete blood counts and blood chemistries. These blood tests are all included in the comprehensive Male Life Extension Panel Blood Test that most members have performed annually.

2. If your blood test results reveal free testosterone below 20-25 pg/mL, find a doctor with experience in prescribing natural testosterone cream. Life Extension maintains lists of doctors who have knowledge about male hormone restoration. To locate a doctor in your area, log on to our directory of Anti-Aging Doctors

3. To obtain natural testosterone cream at the lowest price, ask your doctor to write a prescription for compounded natural testosterone cream. The exact dose you need is based on your blood test results, body mass, and later may be based on your rate of absorption and internal metabolism. Your doctor will determine what dose of testosterone cream is most appropriate for you.

4. If your estradiol level is over 30 pg/mL, your doctor may also prescribe a very low-dose aromatase-inhibiting drug such as 0.5 mg of Arimidex® twice per week. This will usually bring estradiol into the optimal range of 20-30 pg/mL.

5. Within 45 days, have your blood re-tested to verify proper testosterone dosing and rule out prostate cancer. These blood tests also enable you to guard against excess red blood cell production and excess conversion of testosterone to estradiol, as well as to ensure that liver enzymes are in normal ranges.

Life Extension members have the advantage of requesting their blood to be drawn ahead of time so their doctor can properly prescribe them testosterone during their first visit. To order the Male Panel that includes all these blood tests and a lot more at a new lower price, call 1-800-208-3444.

Compounded testosterone cream can be obtained for as little as $40 for a 60-day supply. There are also non-prescription methods that restore free testosterone to youthful ranges in some men. To inquire about these, call a Life Extension Health Advisor at 1-800-226-2370.

Will Testosterone for Life Become a Best-Seller?

Testosterone for Life is not the first book to reveal the profound age-reversal benefits observed when testosterone levels are properly restored.

A decade ago, Jonathan Wright, MD, authored a similar book called Maximize Your Vitality and Potency (Smart Publications; 1999). This book was based on the impressive clinical results Dr. Wright obtained in the 1980s when youthful testosterone levels were restored in his male patients. As some of you will remember, the FDA spent a tremendous amount of taxpayer dollars trying to destroy Dr. Wright’s medical practice.

As we move forward towards 2009, it is unlikely the FDA will repeat its ludicrous abuse of scientific reality again.

Additional Biological Inputs to Assess the Presence of Prostate Cancer

There are additional diagnostic tools beyond a one-time PSA blood test reading to more optimally assess whether or not prostate cancer is present. These include:

Serial increases over time of the PSA, despite levels in the so-called normal range of 0.0-4.0 ng/mL. Prostate cancer may be present if such increases point to a PSA velocity of 0.3 ng/mL/year or higher, or to a PSA doubling time of less than 10 years, or to a rising PSA slope or abnormal natural logarithm of the PSA slope.
A free PSA percentage of 15% or less.
An abnormal PCA3 urine test after attentive digital rectal exam.
A PSA density (PSAD) of 0.15ng/mL/cm3 or higher.

In other words, before subjecting a man to transrectal ultrasound-guided biopsies to rule out prostate cancer prior to testosterone supplementation, look at the biological declarations that declare a problem with prostate cancer is likely. The tests mentioned in this section, in all, are far more scientifically sound approaches to direct a man to an invasive procedure or to lead him away from one. Men with low testosterone may not feel compelled to do prostate biopsies prior to the use of testosterone supplementation because a biopsy.

Is a sampling of only a portion of the prostate,
Is very much dependent on the skill of the ultrasonographer
Depends on the nature and quality of the ultrasound equipment.

Once testosterone therapy has been initiated, tests as frequently as once a month are optimal until a trend indicating a flat PSA response is clearly discerned. Afterwards, reducing the frequency of PSA testing to every three to four months is reasonable, and pending those findings a further reduction in the testing interval is justifiable.

With the endorsement of doctors from Harvard Medical School, perhaps the aging male population will awaken to the fact that they have an opportunity to restore youthful mental and physical functions, while adding decades of healthy life span, just by restoring their free testosterone blood levels.

It is my sincere hope that Testosterone for Life becomes a bestseller. It may be the greatest vindication of anti-aging medicine that the establishment has ever admitted to.

Any Life Extension member who has a question about natural testosterone restoration therapy is free to call our Health Advisors at 1-800-226-2370.

For longer life,

William Faloon

References

1. Rhoden EL, Averbeck MA, Teloken PE. Androgen replacement in men under-going treatment for prostate cancer. J Sex Med. 2008 Sep;5(9):2202-8.

2. Morgentaler A. Testosterone replacement therapy and prostate cancer. Urol Clin North Am. 2007 Nov;34(4):555-63.

3. Miner MM, Seftel AD. Testosterone and ageing: what have we learned since the Institute of Medicine report and what lies ahead? Int J Clin Pract. 2007 Apr;61(4):622-32.

4. Raynaud JP. Prostate cancer risk in testosterone-treated men. J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):261-6.

5. Tan RS, Salazar JA. Risks of testosterone replacement therapy in ageing men. Expert Opin Drug Saf. 2004 Nov;3(6):599-606.

6. Gooren L. Androgen deficiency in the aging male: benefits and risks of androgen supplementation. J Steroid Biochem Mol Biol. 2003 Jun;85(2-5):349-55.

7. Schatzl G, Madersbacher S, Thurridl T, et al. High-grade prostate cancer is associated with low serum testosterone levels. Prostate. 2001 Apr;47(1):52-8.

8. Hoffman MA, DeWolf WC, Morgentaler A. Is low serum free testosterone a marker for high grade prostate cancer? J Urol. 2000 Mar;163(3):824-7.

9. Marks LS, Mazer NA, Mostaghel E, et al. Effect of testosterone replacement therapy on prostate tissue in men with late-onset hypogonadism: a randomized controlled trial. JAMA. 2006 Nov 15;296(19):2351-61.

10. Shores MM, Matsumoto AM, Sloan KL, Kivlahan DR. Low serum testosterone and mortality in male veterans. Arch Intern Med. 2006 Aug 14; 166(15):1660-5.

11. Available at: http://health.ucsd.edu/news/2007/6-5-Testosterone.htm. Accessed August 17, 2008.

12. Tang YJ, Lee WJ, Chen YT, et al. Serum testosterone level and related metabolic factors in men over 70 years old. J Endocrinol Invest. 2007 Jun;30(6):451-8.

13. Maggio M, Basaria S, Ceda GP, et al. The relationship between testosterone and molecular markers of inflammation in older men. J Endocrinol Invest. 2005;28(11 Suppl Proceedings):116-9.

14. Laaksonen DE, Niskanen L, Punnonen K, et al. Sex hormones, inflammation and the metabolic syndrome: a population-based study. Eur J Endocrinol. 2003 Dec;149(6):601-8.

15. Cutolo M, Seriolo B, Villaggio B, et al. Androgens and estrogens modulate the immune and inflammatory responses in rheumatoid arthritis. Ann NY Acad Sci. 2002 Jun;966:131-42.

16. Lu PH, Masterman DA, Mulnard R, et al. Effects of testosterone on cognition and mood in male patients with mild Alzheimer disease and healthy elderly men. Arch Neurol. 2006 Feb;63(2):177-85.

17. Cherrier MM, Plymate S, Mohan S, et al. Relationship between testosterone supplementation and insulin-like growth factor-I levels and cognition in healthy older men. Psychoneuroendocrinology. 2004 Jan;29(1):65-82.

18. Moffat SD, Zonderman AB, Metter EJ, et al. Free testosterone and risk for Alzheimer disease in older men. Neurology. 2004 Jan 27;62(2):188-93.

19. Hogervorst E, Combrinck M, Smith AD. Testosterone and gonadotropin levels in men with dementia. Neuro Endocrinol Lett. 2003 Jun;24(3-4):203-8.

20. Moffat SD, Zonderman AB, Metter EJ, et al. Longitudinal assessment of serum free testosterone concentration predicts memory performance and cognitive status in elderly men. J Clin Endocrinol Metab. 2002 Nov;87(11):5001-7.

21. Cherrier MM, Anawalt BD, Herbst KL, et al. Cognitive effects of short-term manipulation of serum sex steroids in healthy young men. J Clin Endocrinol Metab. 2002 Jul;87(7):3090-6.

22. Gouras GK, Xu H, Gross RS, et al. Testosterone reduces neuronal secretion of Alzheimer’s beta-amyloid peptides. Proc Natl Acad Sci USA. 2000 Feb 1;97(3):1202-5.

23. Traish AM, Saad F, Guay AT. The Dark Side of Testosterone Deficiency: II. Type 2 Diabetes & Insulin Resistance.J Androl. 2008 Sep 4.

24. Chandel A, Dhindsa S, Topiwala S, Chaudhuri A, Dandona P. Testosterone concentrations in young patients with diabetes mellitus. Diabetes Care. 2008 Jul 23.

25. Debing E, Peeters E, Duquet W, et al. Men with atherosclerotic stenosis of the carotid artery have lower testosterone levels compared with controls. Int Angiol. 2008 Apr;27(2):135-41.

26. Khaw KT, Dowsett M, Folkerd E, et al. Endogenous testosterone and mortality due to all causes, cardiovascular disease, and cancer in men: European prospective investigation into cancer in Norfolk (EPIC-Norfolk) Prospective Population Study. Circulation. 2007 Dec 4;116(23):2694-701.

27. Muller M, van den Beld AW, Bots ML, et al. Endogenous sex hormones and progression of carotid atherosclerosis in elderly men. Circulation. 2004 May 4;109(17):2074-9.

28. Zmuda JM, Cauley JA, Kriska A, et al. Longitudinal relation between endogenous testosterone and cardiovascular disease risk factors in middle-aged men. A 13-year follow-up of former Multiple Risk Factor Intervention Trial participants. Am J Epidemiol. 1997 Oct 15;146(8):609-17.

29. Hak AE, Witteman JC, de Jong FH, et al. Low levels of endogenous androgens increase the risk of atherosclerosis in elderly men: the Rotterdam study. J Clin Endocrinol Metab. 2002 Aug;87(8):3632-9.

30. Isidori AM, Giannetta E, Greco EA, et al. Effects of testosterone on body composition, bone metabolism and serum lipid profile in middle-aged men: a meta-analysis. Clin Endocrinol (Oxf). 2005 Sep;63(3):280-93.

31. Moretti C, Frajese GV, Guccione L, et al. Androgens and body composition in the aging male. J Endocrinol Invest. 2005;28(3 Suppl):56-64.

32. Wang C, Cunningham G, Dobs A, et al. Long-term testosterone gel (AndroGel) treatment maintains beneficial effects on sexual function and mood, lean and fat mass, and bone mineral density in hypogonadal men. J Clin Endocrinol Metab. 2004 May;89(5):2085-98.

33. Choong K, Lakshman KM, Bhasin S. The physiological and pharmacological basis for the ergogenic effects of androgens in elite sports. Asian J Androl. 2008 May;10(3):351-63.

34. Bhasin S, Taylor WE, Singh R, et al. The mechanisms of androgen effects on body composition: mesenchymal pluripotent cell as the target of androgen action. J Gerontol A Biol Sci Med Sci. 2003 Dec;58(12):M1103-10.

Life Extension Consumer Alert - December, 2008

William Faloon — Thu, 18 Dec 2008 16:14:00 GMT

Life Extension Consumer Alert - December 2008
Original Article: Response to SELECT Study Published December 9, 2008 in JAMA

Response to SELECT Study Published December 9, 2008 in JAMA

The Selenium and Vitamin E Cancer Prevention Trial (SELECT) examined the effects of L-selenomethionine and all-racemic alpha--tocopherol acetate, alone or in combination, on the risk of prostate cancer and other health outcomes in relatively healthy men. The trial included 35,533 men (age 50 years or older for African-American men and age 55 years or older for other men at the start of the study), from the U.S. and Canada, and Puerto Rico. The participants were randomly assigned to receive one of four interventions between August 2001 and June 2004 for a planned minimum follow-up of 7 years: L-selenomethionine (200 micrograms per day) and a vitamin E placebo; all-racemic alpha--tocopheryl acetate (400 IU/day) and a selenium placebo; L-selenomethionine plus all-racemic alpha--tocopheryl acetate; or a placebo.

The researchers reported that there were no statistically significant differences in the absolute number (or 5-year incidence rate) of prostate cancer diagnosis between the four groups.

In January, 2008, as part of the article “Merv Griffin’s Tragic Death From Prostate Cancer,” Life Extension predicted that SELECT would fail, and furthermore, that this flawed trial would be misused by the pharmaceutical monopoly and the mainstream medical establishment to “prove” to the lay public that low-cost, efficacious nutrients like vitamin E and selenium do not reduce prostate cancer risk,1 and by extrapolation, to impugn other low-cost, efficacious nutrients like vitamin D, selenium, fish oil, and soy as having no benefit.

For example, other clinical studies with selenium supplements show strong benefit in prostate cancer as well as a variety of other deadly cancers:

A study of 1,312 individuals who received 200 mcg of selenium daily or a placebo showed almost 50% lower risk of prostate cancer in the supplemented group than in the control group in men who had relatively low prostate-specific antigen (PSA) levels and low initial selenium levels.2
A study of 5,141 men taking a selenium-containing supplement or a placebo for eight years, with biochemical markers of prostate disease measured at the beginning and end of the study, showed that among men who had normal PSA levels at the study’s outset, a significant risk reduction of nearly 50% was recorded.3
A 2005 study focusing on selenium’s effects in preventing prostate cancer in patients with early prostate cancer took selenium, vitamin E, both L-selenomethionine and vitamin E, or a placebo for three to six weeks before undergoing prostatectomy (removal of the prostate). Levels of cancer markers were measured and compared with healthy control subjects. The result was a change in classification from cancerous to healthy in the serum markers of disease in the men who took supplements compared to those who did not.4
A study in men at high risk of lung cancer with low dietary selenium intake were randomly assigned to receive either 300 mcg of selenium or a placebo daily for one year. As expected, selenium blood levels rose dramatically in the supplemented group, while serum levels of the antioxidant enzyme glutathione peroxidase increased by 156%. At the same time, levels of lipid peroxide (a measure of cell membrane damage that leads to cancer) were reduced by 75% in the supplemented group, and there was laboratory evidence of protection from DNA damage, another prerequisite for cancer formation.5
The US Nutritional Prevention of Cancer Trial demonstrated a statistically significant reduction in lung cancer incidence with selenium supplementation, with 200 micrograms per day cutting the incidence of cancer by nearly 50%.6 A later re-analysis with additional data showed the effect to be most significant in people with low baseline selenium levels, again suggesting that supplementation is preventive when initiated early.7

Life Extension has conducted a thorough review of this latest study used to attack dietary supplements. In fact, Life Extension’s members were made aware of a fundamental fact 8 years ago that all but guaranteed trial failure of this latest attack against dietary supplements.

In the current JAMA trial, men supplemented with all-racemic alpha-tocopherol experienced significant gamma-tocopherol depletion. A careful review of the actual full-text JAMA publication reveals gamma-tocopherol depletion among those men supplemented with all-racemic alpha-tocopherol. Men supplemented with all-racemic alpha-tocopherol and alpha-tocopherol plus selenium experienced a 45% and 48%, respectively, depletion in gamma-tocopherol levels by 6 months that was sustained during the course of this 5-year trial.

As far back as March, 2001 in the article “Avoiding Prostate Cancer,”8 Life Extension identified the importance of gamma-tocopherol supplementation in dramatically lowering the risk of developing prostate cancer — in fact, a study of 10,456 men showed that men who had the highest blood levels of gamma-tocopherol were five times less likely to get prostate cancer.9

What made this study particularly significant was that it was conducted at the prestigious Johns Hopkins School of Public Health and it evaluated a large group of men over a seven-year period. In addition to the finding that higher levels of gamma-tocopherol significantly reduced prostate cancer risk, the study showed that selenium and alpha-tocopherol also reduced prostate cancer incidence, but only when gamma-tocopherol levels are high.

Gamma-tocopherol is a form of vitamin E that is lacking in almost all commercial vitamin E supplements. When high doses of alpha-tocopherol vitamin E are consumed, it displaces critically important gamma-tocopherol in the cells. While alpha-tocopherol inhibits the production of free radicals, it is the gamma-tocopherol form of vitamin E that is required to trap and neutralize free radicals. In a study published in the Proceedings of the National Academy of Sciences,10 researchers reported that it could be dangerous to take high levels of alpha-tocopherol vitamin E without also consuming gamma-tocopherol. The reason for this is that too much alpha-tocopherol could deprive the cells of the gamma form of vitamin E that is needed to neutralize existing oxidizing agents such as the peroxynitrite radical, which can be especially damaging.

The scientists who wrote the National Academy of Sciences article suggested that alpha-tocopherol vitamin E supplements should contain at least 20% tocopherol. In response to these recommendations, Foundation members began taking one capsule a day of a supplement called Gamma E Tocopherol that provided 210 mg of gamma-tocopherol in each capsule. This same amount of gamma-tocopherol (210 mg) was later added to the Life Extension Booster formula. Foundation members obtained additional protection in the Super CoQ10 softgel caps that are fortified with a tocotrienol complex that provides the gamma-tocotrienol vitamin E fraction.

The average Life Extension member takes at least 400 IU a day of alpha-tocopherol. The 237 mg of gamma-tocopherol found in ‘Gamma E Tocopherol with Sesame Lignans’ or the 215–244.2 mg gamma-tocopherol found in our ‘Super Booster’ helps our members easily exceed the 20% gamma-tocopherol threshold. Furthermore, many of our members achieve a 1:1 ratio of alpha-gamma-tocopherol ingestion, a ratio suggested as ideal by expert research groups in vitamin E such as Bruce Ames’ laboratory at UC Berkeley.11

Other nutrients like vitamin D, along with what a man eats, have a huge impact on prostate cancer incidence. Unless these powerful confounding factors are carefully accounted for, the findings from this selenium-alpha-tocopherol study will have little value.

The landmark article “Eating Your Way to Prostate Cancer” published February, 2007 in Life Extension magazine (reviewed and critiqued by Scientific Advisory Board member Stephen Strum, MD a recognized authority on prostate cancer prevention and treatment) reported the importance of controlling dietary intake of arachidonic acid and the grave consequences of failing to mitigate up-regulation of the 5-LOX enzyme by poor dietary choices.12

This fact reveals a fundamental problem confronting all researchers who seek to “prove” whether a certain supplement prevents a disease. There are too many factors involved in the development and progression of prostate cancer including low levels of testosterone, increased levels of estrogen, co-existing diabetes or metabolic syndrome, and increased dietary saturated fats.13 These confounding factors therefore make it difficult to study just one or two compounds and expect to come up with a validated finding. To make matters worse, the aging population will contract prostate cancer at epidemic levels unless aggressive changes are implemented immediately.

This is why we encourage Foundation members to consume the healthy diets and safe supplements that have been shown to sharply reduce prostate cancer incidence. There is simply not enough time left in our generation’s projected life spans to withstand scientific study design flaws, the mainstream medical establishment’s bias against supplements, and arbitrary standards set by the pharmaceutical monopoly.

References

1. http://www.lef.org/magazine/mag2008/jan2008_awsi_01.htm

2. Combs GF, Jr., Clark LC, Turnbull BW. Reduction of cancer risk with an oral supplement of selenium. Biomed Environ Sci. 1997 Sep;10(2-3):227-34.

3.Meyer F, Galan P, Douville P, et al. Antioxidant vitamin and mineral supplementation and prostate cancer prevention in the SU.VI.MAX trial. Int J Cancer. 2005 Aug 20;116(2):182-6.

4. Kim J, Sun P, Lam YW, et al. Changes in serum proteomic patterns by presurgical alpha--tocopherol and L-selenomethionine supplementation in prostate cancer. Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1697-02.

5. Yu SY, Mao BL, Xiao P, et al. Intervention trial with selenium for the prevention of lung cancer among tin miners in Yunnan, China. A pilot study. Biol Trace Elem Res. 1990 Feb;24(2):105-8.

6. Clark LC, Combs GF, Jr., Turnbull BW, et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group. JAMA. 1996 Dec 25;276(24):1957-63.

7. Reid ME, Duffield-Lillico AJ, Garland L, et al. Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1285-91.

8. http://www.lef.org/magazine/mag2001/mar2001_awsi.html

9. Helzlsouer KJ, et al. Association Between alpha--Tocopherol, gamma-Tocopherol, Selenium, and Subsequent Prostate Cancer. J Natl Cancer Inst 2000 Dec 20;92(24):2018-2023.

10. Christen S, et al. gamma-tocopherol traps mutagenic electrophiles such as NO(X) and complements alpha--tocopherol: physiological implications. Proc Natl Acad Sci U S A 1997 Apr 1;94(7):3217-22

11.http://berkeley.edu/news/media/releases/97legacy/christen.html

12. http://www.lef.org/magazine/mag2007/feb2007_cover_prostate_01.htm

13. O’Malley RL, Taneja SS. Obesity and prostate cancer. Can J Urol. 2006 Apr;13 Suppl 2:11-7.

As We See It - November, 2008

William Faloon — Wed, 03 Dec 2008 17:11:00 GMT

LE Magazine November 2008
Dangers of Excess Estrogen In the Aging Male

Dangers of Excess Estrogen In the Aging Male

By William Faloon

We at Life Extension are sometimes asked why we check estrogen levels when testing the blood of our male members.

Long ago, we published data showing that estrogen levels are often elevated in aging men and discussed the insidious health risks associated with excess estrogen. Since it is so easy for men to correct estrogen overload, it made sense to test for it and recommend the appropriate corrective actions if blood results reveal excessive (or deficient) estrogen.

A presentation at a recent anti-aging conference suggested that higher estrogen levels are beneficial to aging men. This prompted us to search the published scientific literature to see if we had overlooked some recent findings.

What we uncovered not only confirmed our original recommendation, but revealed that excess estrogen in aging men is more dangerous than what we even thought.

Double the Stroke Risk

Stroke is the third leading cause of death and the leading cause of age-related disability. Abnormal blood clotting in the cerebral blood vessels is the most common cause of stroke. Excess estrogen promotes abnormal blood clots.1

In a study published just last year, blood levels of estradiol (a potent estrogen) were measured in a group of 2,197 men aged 71 to 93 years of age. Adjustment for age, hypertension, diabetes, adiposity, cholesterol, atrial fibrillation, and other characteristics were made. During the course of follow-up, men with the highest blood levels of estradiol had a 2.2-fold greater risk of stroke compared with those whose estradiol levels were lower.2

This study revealed that estradiol blood levels greater than 34.1 pg/mL resulted in this more than doubling of stroke incidence. Life Extension long ago warned men to keep their estradiol levels below 30 pg/mL, and this recent stroke study clearly validates our prior recommendation.

Excess Estrogen in Middle-Aged Men

One way to evaluate the health of the arterial system is to measure the inner and medial wall of the carotid artery using an ultrasound test.

In a study published two years ago, blood levels of estradiol were measured in 313 men whose average age was 58. Carotid artery intima-media thickness was measured at baseline and then three years later. After adjusting for other risk factors, men with higher levels of estradiol suffered a worsening thickening of their carotid artery wall. This led the researchers to conclude, “circulating estradiol is a predictor of progression of carotid artery intima-media thickness in middle-aged men.”3

This study of middle-aged men was initiated based on findings that treatment of men with prostate cancer using orally ingested estrogen drugs is associated with increased cardiovascular events and deaths.

Ultrasound measurement of the carotid artery wall provides an accurate prognostic indicator of arterial disease. The findings in this study show progression of carotid artery intima-media thickness in men with higher estradiol levels. Greater carotid artery intima-media thickness sharply correlates with increased risks of heart attack and stroke.

Estradiol Higher in Male Heart Attack Victims

A study published just last year compared blood levels of testosterone and estradiol in men suffering acute myocardial infarction (heart attack) with those who had previously suffered a heart attack.

Sex hormones were measured in patients presenting with acute heart attack, patients with old heart attack, and patients with normal coronary arteries. The results showed significantly higher levels of estradiol in both groups of heart attack patients compared with those without coronary disease.4 As would be expected from numerous prior studies, heart attack victims also had decreased testosterone levels.

The reason many men suffer from excess estradiol and deficient testosterone is that their aging bodies produce less testosterone while more of their beneficial testosterone is converted (aromatized) into estradiol. The pathological result is an altering of the ratio of testosterone to estrogen, creating estrogen dominance.5 This imbalance of estrogen overload and testosterone insufficiency is an often overlooked cause of cardiovascular disease.

Fortunately, there are safe methods to block the aromatase enzyme in order to lower excess estrogen while boosting free testosterone levels.

High Estrogen in Men With Coronary Atherosclerosis

An invasive diagnostic procedure known as a coronary angiogram can measure the degree of atherosclerosis present in the arteries feeding the heart muscle.

Researchers used angiogram-confirmed cases of coronary atherosclerosis to ascertain the effects of sex hormones and other metabolic factors in a group of men aged 40-60 years.

Compared with healthy age-matched controls, men with coronary atherosclerosis had low testosterone, higher levels of estrone (another potent estrogen), and a low level of testosterone in the presence of a high level of estradiol.6 These findings led the researchers to conclude their study by stating, “low levels of total testosterone, testosterone/estradiol ratio and free androgen index and higher levels of estrone in men with coronary artery disease appear together with many features of metabolic syndrome and may be involved in the pathogenesis of coronary atherosclerosis.”

In a study conducted a year later by another research group, angiograms were used to measure the extent of coronary atherosclerosis in a group of men with stable coronary artery disease. The finding showed significant positive correlations between estradiol levels and other known atherosclerotic risk factors.7 The scientists concluded their study by stating, “our results indicate a possible role of estradiol in promoting the development of atherogenic lipid milieu in men with coronary artery disease.”

These two recent studies validate other reports showing that excess estrogen promotes atherosclerosis in men.

Peripheral Artery Disease and Sex Hormones

Peripheral artery disease occurs when there is partial or total blockage of an artery, usually one leading to a leg or arm. Leg artery disease is usually due to atherosclerosis that impairs blood circulation. Those afflicted with this condition find that walking can bring on fatigue, cramping, and pain in the hip, buttock, thigh, knee, shin, or upper foot.

A study published last year sought to determine whether blood levels of testosterone and estradiol are associated with lower extremity peripheral arterial disease in elderly men.

The participants consisted of 3,014 men with peripheral artery disease who averaged 75.4 years of age. After factoring in age, current smoking, previous smoking, diabetes, hypertension, and body mass index, the findings showed that low levels of testosterone were independently and positively associated with peripheral artery disease as were high levels of estradiol.8

The doctors who conducted this study concluded, “this cross-sectional study shows for the first time that low serum testosterone and high serum estradiol levels associate with lower extremity peripheral artery disease in elderly men.”

The pharmaceutical industry makes a fortune treating those with peripheral artery disease. Common drugs prescribed include those that lower blood sugar, lower cholesterol (statins), lower blood pressure, and lower risk of blood clot. A popular drug called Plavix® has been heavily advertised to treat peripheral and other arterial diseases.

Based on what is known about the atherogenic and thrombotic risks of low testosterone and high estradiol, it is conceivable that men suffering from peripheral artery disease could discard many of their drugs if they restored their testosterone to youthful ranges and reduced excess estradiol.

High Estradiol Levels Seen in Male Chronic Inflammation Patients

Rheumatoid arthritis is a severe chronic inflammatory state that results in increased risks of heart attack, cancer, and stroke. A study of men with rheumatoid arthritis evaluated blood levels of sex hormones compared with healthy controls.9

Levels of estradiol in rheumatoid arthritis patients were higher and DHEA levels lower compared with subjects who were not suffering from chronic inflammation.9 This corresponds to studies showing that high estrogen levels (in women) can increase C-reactive protein, which is the most accurate marker for systemic inflammation.10-12 Elevated C-reactive protein is an independent risk factor for coronary heart disease in healthy individuals.

Another Lethal Mechanism of Excess Estrogen

The number one cause of death in persons over age 50 is the development of an abnormal blood clot (thrombus) in an artery that blocks blood flow to a critical region of the body such as the heart, lungs, or brain. Elevated estrogen predisposes people to these lethal thrombotic events.

It has been found that men admitted in hospitals with myocardial infarcts have elevated estradiol and lower testosterone levels.13 This was shown in an interesting study done on men admitted to the hospital with acute heart attacks whose levels of sex hormones were evaluated. Compared with control patients, estradiol levels in these heart attack patients were 180% higher, while bioavailable testosterone levels were nearly three times less than those of control patients.14

These findings reveal the higher heart attack incidences associated with high estrogen and low testosterone. It is possible, however, that these low levels of testosterone and high levels of estradiol occurred in response to the heart attack itself.14

Estrogen and Prostate Cancer

The role that estrogen plays in malignant prostate disease is contradictory and complex. Some studies indicate that estrogen and its toxic metabolites are a cause of prostate cancer.15,16 Yet once prostate cancer develops, certain estrogen compounds demonstrate anticancer effects.

This paradox can be explained by the mechanisms that estradiol (and its toxic metabolites) uses to damage prostate cell DNA,17 causing gene mutations that result in the loss of cell growth regulatory control, i.e. cancer. Interestingly, once a prostate tumor manifests, estrogen may exert anti-tumor effects, though cancer cells eventually become resistant to estrogen drugs and then even use endogenous estrogen to fuel their growth.

The fact that estrogen may temporarily exert anti-tumor effects in certain types of prostate cancer cells does not diminish the argument that estrogen may have contributed to the initiation of the same cancer. For example, in a study published two years ago, researchers discovered that when “estradiol is added to testosterone treatment of rats, prostate cancer incidence is markedly increased and even a short course of estrogen treatment results in a high incidence of prostate cancer.” These scientists hypothesize that metabolites of estrogens can be converted to reactive intermediates that can adduct to DNA and cause generation of reactive oxygen species; thus, estradiol is a weak DNA-damaging carcinogen that causes DNA damage to prostate cell genes.18 This kind of damage to DNA regulatory genes is what initiates prostate cancer.

Many published studies, however, show no association between high blood estradiol levels and diagnosed prostate cancers.19 One reason there are not more diagnosed prostate cancers in men with high estrogen may be that the high estradiol level that initiated DNA damage then serves to keep prostate cancer temporarily under control once it develops.

An interesting mechanism by which certain prostate cancer cells become resistant to estradiol therapy is the development of components in cancer cells that selectively remove estradiol from the tumor cells. If our normal cells were only as adaptive as cancer cells, we could possibly become biologically immortal.

Another reason why estradiol blood levels may not correlate with prostate cancer incidence is the ability of prostate cells to produce their own estradiol (by making their own aromatase enzyme). Although evidence is conflicting, there is a clear indication that local synthesis of estrogen in the prostate gland itself may be significant in prostate tumor development.16 All of this helps validate the importance of nutrients Life Extension male members take to block the carcinogenic effects of estrogen within the prostate gland.

An analogy to how excess estrogen can first damage DNA regulatory genes to cause cancer and then act as a prostate cancer suppressor can be seen with chemotherapy drugs. The mechanism by which most chemo drugs kill cancer cells is to inflict massive damage to cellular DNA. While chemo drugs kill cancer cells, they simultaneously damage healthy DNA and can increase the risk of future cancers. It appears that excess estrogen damages prostate cell DNA to initiate cancer, but then acts as a temporary prostate cancer suppressor. In presenting this analogy, I am not implying that estrogen in men is as dangerous as toxic chemo drugs. I am showing that something that suppresses cancer cell propagation (like estrogen) can also cause cancer.

Our Observations

We at Life Extension have often observed aged men with symptom-free prostate cancer who have startlingly high estradiol levels. It requires a needle biopsy to confirm these slow growing tumors that were identified by only modestly high PSA levels. In fact, we often look at aging men’s estradiol and free testosterone blood levels as a potential indicator of prostate cancer. Aging men with low free testosterone and high estradiol often have prostate cancer based on these observations. Many of these men, however, will die from vascular disease (possibly caused by their high estrogen levels) before their prostate cancer is diagnosed.

In fact, a study published just this year discusses potential initiating effect of estrogens in the development of prostate cancer.15 Tumor initiation is defined by the National Cancer Institute as a process in which normal cells are changed so that they are able to form tumors. Substances that cause cancer can be tumor initiators. The latest study on this subject suggests that estrogen is a prostate cancer initiator and that anti-estrogen therapies might be an overlooked prevention strategy.

An overlooked reason so many human studies fail to show a relationship between estrogen levels and prostate cancer is the fact that men with the highest estrogen levels may have perished from heart attacks and strokes before prostate cancer had a chance to clinically manifest. Based on the vascular disease risks discussed at the beginning of this article, men who suffered from estrogen overload early in their life would be expected to die sooner and, therefore not live long enough to develop clinically diagnosed prostate cancer. From a statistical standpoint, this would falsely make it appear that higher estradiol levels in aging men do not result in greater incidences of prostate cancer, since many men with the highest estrogen levels would not be alive to even participate in the study.

Misconceptions About Prostate Cancer

While prostate cancer is not usually diagnosed until men reach older ages, it can be initiated 15-25 years prior to clinical manifestation.20 In fact, there is convincing evidence that the initiating DNA damage inflicted by estrogen to prostate cells can occur before you are even born! Studies show that as early as the second and third trimester of life, exposure to elevated estrogens in the womb can initiate prostate cancer that may not manifest for 80 years.15,21-28

Please don’t feel overly helpless about this, as it requires more than mere initiation for cancer to fully develop. What you eat and other lifestyle factors have an enormous impact on whether you develop prostate cancer, even if you are strongly genetically predisposed.

Estrogen’s Role in Benign Prostate Enlargement

Unlike prostate cancer, estrogen’s role in the development and progression of benign prostatic hyperplasia (BPH) is clearly defined. Animal studies initially led to the hypothesis that estrogens can stimulate prostate growth, resulting in hyperplasia of the gland. A large body of subsequent human research confirms the initial findings.15,20,29-32

Estrogen stimulates proliferation of the stromal cells in the prostate gland that cause so many of the urinary discomforts associated with BPH. A study published just this year documents a specific mechanism by which estradiol causes rapid proliferation of prostate stromal cells.15

Another study also published this year provides further clarification on how estradiol increases the proliferation of stromal cells and how anti-estrogen compounds block this undesirable effect. The researchers concluded that “…these findings support the hypothesis that estrogens play a role in the pathogenesis of BPH, a disease characterized predominantly by stromal overgrowth.”20

In a study published last year, researchers evaluated the association of sex hormone levels in the blood with common BPH urinary tract symptoms. Study subjects consisted of 260 men, 60 years of age or older, whose blood levels of testosterone, estradiol, and other sex hormones were measured. Of these men, 128 cases had two to four symptoms (excessive urination at night, hesitancy, incomplete emptying, and weak stream). The 132 men in the control group had no urinary symptoms. Adjustments were made for age, race/ethnicity, waist circumference, cigarette smoking, alcohol consumption, and physical activity.33

The results showed that BPH sufferers had statistically significantly greater estradiol concentrations than symptom-free controls. Men suffering from BPH symptoms also had higher levels of a marker for a metabolite for dihydrotestosterone (DHT, another documented factor in the development of BPH). After multivariate adjustments, men with the greater estradiol concentration had a 1.78 times higher incidence of urinary tract symptoms. An even greater incidence of urinary tract symptoms occurred in men with the highest levels of a dihydrotestosterone metabolite, whereas blood testosterone level showed no effect on urinary tract symptoms. The doctors who conducted this study concluded by stating, “in this cross-sectional study representative of older US men, circulating AAG, a metabolite of dihydrotestosterone, and estradiol were associated with an increased risk of having lower urinary tract symptoms.”33

These findings, reported over the past 18 months confirm what Life Extension told its members back in 1994 about estrogen’s role in benign prostatic hyperplasia (BPH). The encouraging news is that most Life Extension male members are already taking nutrients (and in some cases drugs like Arimidex® and Avodart®) that exhibit anti-estrogen and anti-DHT properties in the prostate gland itself. This is important because even when estrogen and DHT are lowered in the blood, prostate cells can compensate by synthesizing them in the prostate gland.

How Excess Estrogen Levels Occur in Aging Men

In males, the main biologically active estrogen is estradiol. The primary source of estradiol in men is from the conversion (aromatization) of testosterone. As men age, the production of androgens from the adrenals and gonads is decreased. The aromatization of testosterone to estradiol is often maintained, but due to a variety of factors, more testosterone is aromatized in fatty tissues, causing a further imbalance of the ratio of testosterone to estrogen, i.e. too much estradiol and not enough testosterone. The result is a deficiency of beneficial testosterone and an excess amount of estradiol.34

As men age, the amount of testosterone produced in the testes diminishes greatly. Yet estradiol levels remain persistently high. The reason for this is increasing aromatase activity along with age-associated fat mass, especially in the belly.5 Estradiol levels correlate significantly to body fat mass and more specifically to subcutaneous abdominal fat. The epidemic of abdominal obesity observed in aging men is associated with a constellation of degenerative disorders, including heart disease, diabetes, and cancer.9,35-38

Subcutaneous abdominal fat acts as a secretory gland, often producing and emitting excessive levels of estradiol into an aging man’s blood.39 One’s waist circumference is a highly accurate prognostic measurement of future disease risk, with excess estradiol secretion being at least one of the deadly mechanisms associated with the difficult-to-resolve problem of having too much abdominal fat.5,40

Symptoms of excess estrogen in aging men include the development of breasts, having too much abdominal weight, feeling tired, suffering loss of muscle mass, and having emotional disturbances. Many of these symptoms correspond to testosterone deficiency as well.41

Protecting Against Toxic Estrogen Metabolites

It is not just excess estradiol that poses health risks. Specific estrogen metabolites may also initiate and promote hormone-related cancers. Daily consumption of cruciferous vegetables (broccoli, cauliflower, cabbage, Brussels sprouts),54-59 along with isoflavone-rich soy foods60-64 converts these dangerous estrogen metabolites (such as 16-alpha-hydroxyestrone) to safe ones (2-hydroxyestrone) that may protect against prostate cancer.

For those who don’t eat these cancer-protective foods on a daily basis, low-cost supplements can supply the most active constituents of cruciferous vegetables (such as indole-3-carbinol and sulphoraphane)65-70 and soy (genistein and daidzein).71-74

Don’t Lower Your Estrogen Too Much!

When reviewing the studies about the multiple pathological effects of excess estrogen in aging men, it may be tempting to take high doses of an aromatase-inhibiting drug (like Arimidex®) to slash estrogen levels as low as possible. Don’t do this, as men need estrogen to maintain bone density, cognitive function, and even to maintain the inner lining of the arterial wall (the endothelium).42

Most Life Extension members know that too little cholesterol (below 150 mg/dL) can be more dangerous than too much cholesterol (levels over 200 mg/dL). The same may hold true for estrogen. We have recommended that ideal ranges for estradiol for most aging men are between 20 and 30 pg/mL of blood. Below 18 pg/mL increases osteoporosis risk, while levels greater than 30 pg/mL increase heart attack and stroke incidence.

The availability of low-cost blood tests enables aging men to optimize their estradiol levels using natural approaches and/or prescription drugs.

Estrogen and Men’s Bones

Osteoporosis is not just a risk for aging women. Men also suffer crippling fractures caused by loss of bone mineral density. When aged men suffer a bone fracture, their risk of dying is significantly higher than women.43,44

In a study published two years ago, doctors analyzed blood levels in three groups of men for estradiol only, testosterone only, and estradiol and testosterone together. In men with low estradiol (2.0-18.1 pg/mL of blood), hip fractures were more than three times higher compared with men who had estradiol levels of 18.2-34.2 pg/mL.45

Men with estradiol levels greater than 34.3 pg/mL had a slightly higher risk of hip fracture compared with those in the range of 18.2-34.2 pg/mL. This study helps confirm Life Extension’s recommended range for estrogen levels in aging men.

Interestingly, this study also showed in the group of men whose blood was measured for estradiol and testosterone, those who were low in both these hormones suffered a startling 6.5 times greater incidence of hip fractures. The authors of this study concluded, “men with low estradiol levels are at an increased risk for future hip fracture. Men with both low estradiol and low testosterone levels seem to be at greatest risk for hip fracture.”45

Conflicting Data

With the voluminous amount of scientific studies being published today, contradictions inevitably arise, and this is not always due to study design flaws.

For the past decade, Life Extension has reported on dozens of studies showing that higher testosterone levels significantly reduce a man’s risk of cardiovascular disease. In fact, we just did a comprehensive database search and identified a total of 50 studies that document the protective effects of testosterone against cardiovascular disease in men.

A study published two years ago, however, contradicts this. This study showed greater incidences of heart attacks in men with higher testosterone and lower heart attack risks in older men with higher estradiol. (In younger men, estradiol level had no impact on heart attack incidence in this study.) The authors of the study admitted a limitation to the study was only measuring baseline levels of hormones. This study nonetheless was used at the anti-aging conference to proclaim that estradiol protects against heart attack.46

There are scientific studies that demonstrate estrogen’s potential beneficial effects to a man’s vascular system. These protective mechanisms, however, have to be weighed against pathological damage the very same estrogen can induce.

As I mentioned earlier, despite the documented dangers of excess estrogen, levels that are too low also present risks, not only to bone,45,47-49 but to the vascular system as well.46,50,51 If a man were to intentionally lower his estradiol too much, he could very well suffer vascular disease because estrogen is vital to proper endothelial function.52,53

This is why it is so important for aging men to have annual blood tests. If estrogen is too low (below 18-20 pg/mL), or too high (above 30 pg/mL), corrective action should be taken.

How to Reduce Excess Estrogen

In aging men, a large percentage of estradiol is synthesized in abdominal adipose (fat) tissues.42 Reducing waist circumference confers huge health benefits, one being a lowering of estradiol levels.

One of the most effective ways for men to reduce belly fat is to restore their free testosterone to youthful ranges. Nutrients that inhibit the aromatase enzyme can help boost testosterone levels by preventing its conversion (aromatization) into estradiol.

As men grow older, however, their testicular testosterone production declines precipitously. This means that inhibiting aromatase might not sufficiently maintain testosterone levels because not enough is being produced internally. Fortunately, low-cost compounded testosterone creams are available that can be rubbed on the skin for absorption into the bloodstream.

For men with excess aromatase activity, this topically absorbed testosterone might convert into too much estradiol. If this happens, the use of very low-dose aromatase-inhibiting drugs (0.5 mg of Arimidex® twice a week) may be all that is needed to protect against estrogen overload. Some men don’t need these drugs and can use nutrient formulas that have aromatase-inhibiting properties.

There is no need to guess what you need, as a blood test taken 30-45 days after initiating testosterone-replacement not only reveals a man’s estradiol level, but also ensures that the PSA has not spiked (indicating possible pre-existing prostate cancer), that the dose of testosterone cream is appropriate, and that there are no other side effects occurring.

To view a wide range of estrogen-lowering strategies, one can view Life Extension’s Male Hormone Modulation Protocol by logging on to our male hormones page.

What if Your Estrogen Level is Too Low?

Some men are so deficient in aromatase that they do not make enough estrogen.

If a blood test reveals estradiol below 20 pg/mL, which may occur if Arimidex®, for example, is being taken at too high a dose, one should consider reducing the dose. Alternatively, applying a tiny dose of a compounded topical estradiol cream to the skin several times a week may also help increase estradiol levels. Follow-up blood tests 30-45 days later can assess if too much or too little topical estradiol cream is being used.

There is also evidence that consuming phytoestrogens from soy might provide similar benefits for the bone75-79 and vascular system.80-88

Summary

It is hard to imagine that before 1906, doctors did not even know that a hormone (estrogen) was secreted by the ovaries in women. It was not until 1930 that the isolation of the estrogen complex in pure form was published.

Less than 80 years later, scientists are debating what the optimal levels of estrogen should be in men. This exponential leap in scientific knowledge is a marvel in itself!

The role that estrogen plays in men’s health is an important topic discussed at medical conferences today. As outlined in this article, testing one’s estradiol level is critical because it can be a serious problem if it is too high or if it is too low.

I am pleased to announce that the everyday low price for the Male or Female Blood Test Panels has been reduced from $299 to $269. This price reduction is made possible by the large volume of blood testing Life Extension members have been ordering.

In addition to estradiol, the Male Panel measures PSA, free testosterone, DHEA, C-reactive protein, homocysteine, along with cholesterol lipids, glucose, and blood cell counts and chemistries.

I encourage any member who has not had this comprehensive blood test conducted over the past 12 months to take advantage of this new lower price. To order the Male or Female Panel by phone, call 1-800-208-3444.

If the results reveal estradiol levels are too high or too low, corrective measures can easily be taken to protect your precious health.

For longer life,

William Faloon

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35. Choi BG, McLaughlin MA. Why men’s hearts break: cardiovascular effects of sex steroids. Endocrinol Metab Clin North Am. 2007 Jun;36(2):365-77.

36. Kaneda Y, Ohmori T. Relation between estradiol and negative symptoms in men with schizophrenia. J Neuropsychiatry Clin Neurosci. 2005;17(2):239-42.

37. Zou B, Sasaki H, Kumagai S. Association between Relative Hypogonadism and Metabolic Syndrome in Newly Diagnosed Adult Male Patients with Impaired Glucose Tolerance or Type 2 Diabetes Mellitus. Metab Syndr Relat Disord. 2004;2(1):39-48.

38. Abu-Abid S, Szold A, Klausner J. Obesity and cancer. J Med. 2002;33(1-4):73-86.

39. Kula K, Walczak-Jedrzejowska R, Slowikowska-Hilczer J, et al. Important functions of estrogens in men—breakthrough in contemporary medicine. Przegl Lek. 2005;62(9):908-15.

40. Anderson LA, McTernan PG, Barnett AH, Kumar S. The effects of androgens and estrogens on preadipocyte proliferation in human adipose tissue: influence of gender and site. J Clin Endocrinol Metab. 2001 Oct;86(10):5045-51.

41. Lund BC, Bever-Stille KA, Perry PJ. Testosterone and andropause: the feasibility of testosterone replacement therapy in elderly men. Pharmacotherapy. 1999 Aug;19(8):951-6.

42. Gooren LJ, Toorians AW. Significance of oestrogens in male (patho)physiology. Ann Endocrinol (Paris). 2003 Apr;64(2):126-35.

43. Seeman E. The dilemma of osteoporosis in men. Am J Med. 1995 Feb 27;98(2A):76S-88S.

44. Center JR, Nguyen TV, Schneider D, Sambrook PN, Eisman JA. Mortality after all major types of osteoporotic fracture in men and women: an observational study. Lancet. 1999 Mar 13;353(9156):878-82.

45. Amin S, Zhang Y, Felson DT, et al. Estradiol, testosterone, and the risk for hip fractures in elderly men from the Framingham Study. Am J Med. 2006 May;119(5):426-33.

46. Arnlov J, Pencina MJ, Amin S, et al. Endogenous sex hormones and cardiovascular disease incidence in men. Ann Intern Med. 2006 Aug 1;145(3):176-84.

47. Nuti R, Martini G, Merlotti D, et al. Bone metabolism in men: role of aromatase activity. J Endocrinol Invest. 2007;30(6 Suppl):18-23.

48. Gennari L, Nuti R, Bilezikian JP. Aromatase activity and bone homeostasis in men. J Clin Endocrinol Metab. 2004 Dec;89(12):5898-907.

49. Khosla S, Melton LJ 3rd, Riggs BL. Estrogens and bone health in men. Calcif Tissue Int. 2001 Oct;69(4):189-92.

50. Phillips GB. Is atherosclerotic cardiovascular disease an endocrinological disorder? The estrogen-androgen paradox. J Clin Endocrinol Metab. 2005 May;90(5):2708-11.

51. Mendelsohn ME, Karas RH. The protective effects of estrogen on the cardiovascular system. N Engl J Med. 1999 Jun 10;340(23):1801-11.

52. Sader MA, McCredie RJ, Griffiths KA, et al. Oestradiol improves arterial endothelial function in healthy men receiving testosterone. Clin Endocrinol (Oxf). 2001 Feb;54(2):175-81.

53. Sudhir K, Komesaroff PA. Clinical review 110: Cardiovascular actions of estrogens in men. J Clin Endocrinol Metab. 1999 Oct;84(10):3411-5.

54. Traka M, Gasper AV, Melchini A, et al. Broccoli consumption interacts with GSTM1 to perturb oncogenic signalling pathways in the prostate. PLoS ONE. 2008;3(7):e2568.

55. Kirsh VA, Peters U, Mayne ST, et al. Prospective study of fruit and vegetable intake and risk of prostate cancer. J Natl Cancer Inst. 2007 Aug 1;99(15):1200-9.

56. Xiao D, Singh SV. Phenethyl isothiocyanate inhibits angiogenesis in vitro and ex vivo. Cancer Res. 2007 Mar 1;67(5):2239-46.

57. Chan JM, Gann PH, Giovannucci EL. Role of diet in prostate cancer development and progression. J Clin Oncol. 2005 Nov 10;23(32):8152-60.

58. Giovannucci E, Rimm EB, Liu Y, Stampfer MJ, Willett WC. A prospective study of cruciferous vegetables and prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003 Dec;12(12):1403-9.

59. Kristal AR, Lampe JW. Brassica vegetables and prostate cancer risk: a review of the epidemiological evidence. Nutr Cancer. 2002;42(1):1-9.

60. Grainger EM, Schwartz SJ, Wang S, et al. A combination of tomato and soy products for men with recurring prostate cancer and rising prostate specific antigen. Nutr Cancer. 2008 Mar;60(2):145-54.

61. Heald CL, Ritchie MR, Bolton-Smith C, Morton MS, Alexander FE. Phyto-oestrogens and risk of prostate cancer in Scottish men. Br J Nutr. 2007 Aug;98(2):388-96.

62. Kurahashi N, Iwasaki M, Sasazuki S, et al. Soy product and isoflavone consumption in relation to prostate cancer in Japanese men. Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):538-45.

63. Holzbeierlein JM, McIntosh J, Thrasher JB. The role of soy phytoestrogens in prostate cancer. Curr Opin Urol. 2005 Jan;15(1):17-22.

64. Lee MM, Gomez SL, Chang JS, et al. Soy and isoflavone consumption in relation to prostate cancer risk in China. Cancer Epidemiol Biomarkers Prev. 2003 Jul;12(7):665-8.

65. Aggarwal BB, Ichikawa H. Molecular targets and anticancer potential of indole-3-carbinol and its derivatives. Cell Cycle. 2005 Sep;4(9):1201-15.

66. Garikapaty VP, Ashok BT, Chen YG, et al. Anti-carcinogenic and anti-metastatic properties of indole-3-carbinol in prostate cancer. Oncol Rep. 2005 Jan;13(1):89-93.

67. Sarkar FH, Li Y. Indole-3-carbinol and prostate cancer. J Nutr. 2004 Dec;134(12 Suppl):3493S-8S.

68. Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. 2001 May 24;20(23):2927-36.

69. Yao H, Wang H, Zhang Z, et al. Sulforaphane inhibited expression of hypoxia-inducible factor-1alpha in human tongue squamous cancer cells and prostate cancer cells. Int J Cancer. 2008 Sep 15;123(6):1255-61.

70. Myzak MC, Tong P, Dashwood WM, Dashwood RH, Ho E. Sulforaphane retards the growth of human PC-3 xenografts and inhibits HDAC activity in human subjects. Exp Biol Med (Maywood). 2007 Feb;232(2):227-34.

71. Zhang LL, Li L, Wu DP, et al. A novel anti-cancer effect of genistein: reversal of epithelial mesenchymal transition in prostate cancer cells. Acta Pharmacol Sin. 2008 Sep;29(9):1060-8.

72. Banerjee S, Li Y, Wang Z, Sarkar FH. Multi-targeted therapy of cancer by genistein. Cancer Lett. 2008 May 18.

73. Kikuno N, Shiina H, Urakami S, et al. Genistein mediated histone acetylation and demethylation activates tumor suppressor genes in prostate cancer cells. Int J Cancer. 2008 Aug 1;123(3):552-60.

74. Nagata Y, Sonoda T, Mori M, et al. Dietary isoflavones may protect against prostate cancer in Japanese men. J Nutr. 2007 Aug;137(8):1974-9.

75. Ma DF, Qin LQ, Wang PY, Katoh R. Soy isoflavone intake inhibits bone resorption and stimulates bone formation in menopausal women: meta-analysis of randomized controlled trials. Eur J Clin Nutr. 2008 Feb;62(2):155-61.

76. Atkinson C, Compston JE, Day NE, Dowsett M, Bingham SA. The effects of phytoestrogen isoflavones on bone density in women: a double-blind, randomized, placebo-controlled trial. Am J Clin Nutr. 2004 Feb;79(2):326-33.

77. Harkness LS, Fiedler K, Sehgal AR, Oravec D, Lerner E. Decreased bone resorption with soy isoflavone supplementation in postmenopausal women. J Womens Health (Larchmt). 2004 Nov;13(9):1000-7.

78. Uesugi T, Fukui Y, Yamori Y. Beneficial effects of soybean isoflavone supplementation on bone metabolism and serum lipids in postmenopausal japanese women: a four-week study. J Am Coll Nutr. 2002 Apr;21(2):97-102.

79. Droke EA, Hager KA, Lerner MR, et al. Soy isoflavones avert chronic inflammation-induced bone loss and vascular disease. J Inflamm (Lond). 2007;417.

80. Seok YM, Baek I, Kim YH, et al. Isoflavone attenuates vascular contraction through inhibition of the RhoA/Rho-kinase signaling pathway. J Pharmacol Exp Ther. 2008 Sep;326(3):991-8.

81. Si H, Liu D. Phytochemical genistein in the regulation of vascular function: new insights. Curr Med Chem. 2007;14(24):2581-9.

82. Colacurci N, Chiantera A, Fornaro F, et al. Effects of soy isoflavones on endothelial function in healthy postmenopausal women. Menopause. 2005 May;12(3):299-307.

83. Liang YL, Teede H, Dalais F, McGrath BP. The effects of phytoestrogen on blood pressure and lipids in healthy volunteers. Zhonghua Xin Xue Guan Bing Za Zhi. 2006 Aug;34(8):726-9.

84. Kapiotis S, Hermann M, Held I, et al. Genistein, the dietary-derived angiogenesis inhibitor, prevents LDL oxidation and protects endothelial cells from damage by atherogenic LDL. Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2868-74.

85. Wenzel U, Fuchs D, Daniel H. Protective effects of soy-isoflavones in cardiovascular disease. Identification of molecular targets. Hamostaseologie. 2008 Feb;28(1-2):85-8.

86. Si H, Liu D. Genistein, a soy phytoestrogen, upregulates the expression of human endothelial nitric oxide synthase and lowers blood pressure in spontaneously hypertensive rats. J Nutr. 2008 Feb;138(2):297-304.

87. Chan YH, Lau KK, Yiu KH, et al. Isoflavone intake in persons at high risk of cardiovascular events: implications for vascular endothelial function and the carotid atherosclerotic burden. Am J Clin Nutr. 2007 Oct;86(4):938-45.

88. Rimbach G, Boesch-Saadatmandi C, Frank J, et al. Dietary isoflavones in the prevention of cardiovascular disease--a molecular perspective. Food Chem Toxicol. 2008 Apr;46(4):1308-19.

As We See It - October, 2008

William Faloon — Wed, 26 Nov 2008 17:17:00 GMT

LE Magazine October 2008
Suzanne Somers' Plan to Eradicate Medical Ignorance

Suzanne Somers’ Plan to Eradicate Medical Ignorance

By William Faloon

The leading cause of disease, premature aging, and death is lack of knowledge about effective technologies that already exist!

Forward-thinking physicians are making tremendous strides in identifying scientific methods for keeping aging humans healthy. The problem is that this information remains confined within these doctors’ private practices and is not yet part of the mainstream.

By virtue of her books, TV appearances, and personal lectures, actress Suzanne Somers has enlightened more people about the benefits of natural hormones than anyone else in history.

Through her in-depth discussions with the world’s most avant-garde doctors, Suzanne has uncovered an abundance of other innovations that could spare millions of Americans from the agonies of age-related disease.

Suzanne has spent the past five years interviewing doctors who “think outside the box” in order to develop practical solutions for their patients. This wealth of scientific information has been compiled into her brand new book titled BREAKTHROUGH.

Suzanne’s Unique Scientific Perspective

You may wonder why actress Suzanne Somers is in such a unique position to accurately identify effective medical therapies that conventional doctors overlook.

One reason is that she has personally derived enormous benefit from the nutritional supplements, natural hormones, and European drugs (not approved in the US) she has used to resolve her own serious health issues. Instead of listening only to what her mainstream doctors said, Suzanne took it upon herself to spend thousands of hours reviewing the medical literature to uncover what mainstream medicine has not yet embraced.

Suzanne also possesses a natural talent to comprehend scientific data and more importantly, an intense interest in health-related issues. As we have all learned, medical doctors too often lose “interest” in the health sciences, which is one reason doctors are so resistant to new ideas, no matter how logical they are.

Perhaps Suzanne’s most significant attribute is her ability to interact with pioneering doctors and scientists in a way that enables her to extract practical information that she then conveys in an easy-to-understand format in her new book called BREAKTHROUGH.

There is no question that Suzanne’s celebrity status has opened many doors for her in the scientific community. Few celebrities, however, have the ability to interact with these high-caliber researchers and clinicians and then translate what they discover into words the public can understand.

Why This Book Could Revolutionize Medical Practice

Life Extension members long ago realized that few doctors understand even basic methods of averting degenerative disease. It is as if a barrier separates the fruits of scientific discovery from its implementation into clinical medical practice.

A major reason why life-saving discoveries are suppressed is drug company influence. Pharmaceutical giants maintain such a stranglehold over the FDA, academia, and physician-prescribing practices that little in the way of medical innovation sees the light of day. Instead, consumers and doctors are exposed to endless promotions for costly, side effect-prone prescription drugs that have only minimal degrees of efficacy.

In her new book, Suzanne Somers identifies pioneering physicians who see through the charade erected by pharmaceutical interests and have instead developed non-patented, science-based approaches to preventing and treating age-related disease.

Unlike health books that are somewhat inaccurate or overly technical, each chapter of Suzanne Somers’ new book is dedicated to innovative discoveries that include physicians’ hands-on clinical experiences. It provides the reader with a virtual consultation interview with doctors at the very forefront of medical practice.

Suzanne has a unique ability to take scientific information and translate it into what she calls “people speak,” meaning the public at large can understand exactly what the book conveys.

Why We Are Optimistic About Suzanne’s New Book

A groundswell of consumer resentment is erupting in response to exposés about corrupt pharmaceutical industry practices.

The scientific data so eloquently presented in Suzanne’s book, along with her ability to get this information into the hands of so many Americans, may very well ignite a citizens’ revolt against today’s entrenched medical establishment.

Taking Action!

It’s easy to complain about problems, but few visionaries initiate the corrective action needed to triumph over life-threatening humanitarian issues.

Actress Suzanne Somers is an intuitive author determined to eradicate the barriers of medical ignorance that are the underlying cause of needless suffering and countless deaths.

We at Life Extension are enormously grateful that Suzanne dedicated so much of her time to researching and writing this new book. While our scientific boards comprise some of the world’s most brilliant physicians and researchers, all of these individuals together do not possess the mass appeal of Suzanne Somers.

In other words, even if a credentialed scientist took the time to compile a comprehensive book like Suzanne did, it would likely wallow in obscurity. Suzanne, on the other hand, has both the celebrity status and the remarkable ability to relate to aging people’s health concerns. We are optimistic that her new book will find its way into the hands of tens of millions of Americans who will then petition Congress to tear down today’s bureaucratic barriers to scientific advancement.

For almost 30 years, the Life Extension Foundation has been transforming the way medicine is viewed and practiced. While significant progress has been made in many areas, we have still not assembled the critical mass of the population needed to overthrow the bureaucracy that denies Americans access to the fruits of scientific progress.

Suzanne Somers’ brand new book BREAKTHROUGH reveals novel approaches that aging people can use today to defy age-related degenerative processes. I encourage Life Extension members to order a copy for their own personal benefit.

For longer life,

William Faloon

As We See It - September, 2008

William Faloon — Fri, 21 Nov 2008 16:06:00 GMT

LE Magazine September 2008
Would You Tolerate This Abuse?

Would You Tolerate This Abuse?

By William Faloon

Americans needlessly die while scientific discoveries that could save their lives remain trapped in bureaucratic red tape.

There is a solution to this travesty. Allow free market innovation into the health care arena, and the development of new medical therapies will progress as rapidly as other technologies.

Do you remember how expensive long distance phone calling used to be?

Back in 1980, archaic federal rules enabled the original AT&T to control national long distance dialing. You could recognize a long distance call by the hissing and crackling noise heard before the caller spoke. High-speed internet and mobile phone connections were not available.

In 1980, the Life Extension Foundation was in its infancy. Making long distance calls during the day was unaffordable to us. We waited until after 5:00 PM to make brief long distance calls. For calls that involved a lot of talk time, we scheduled these after 11:00 PM (or on weekends) when rates were at their lowest.

By 1982, we needed to install a toll-free "800" line, but feared the high cost. The 50-cent per minute rate caused concern that we might not be able to afford the monthly bill. Factoring in inflation, 50 cents in 1982 is equivalent to $1.16 today. That meant that if our 800 line was used just four hours a day, the monthly cost would be $6,960 in today's dollars.

Consumers Fought Back

There was quite a debate around 1980 as to whether consumers would benefit if other companies were allowed to compete in offering long distance services. AT&T heavily lobbied Congress arguing that all kinds of terrible problems would occur if it lost its monopoly.

AT&T pointed to its stellar record of scientific advances and threatened that if it could not charge its monopolistic rates, then further improvements in communications technology would be hindered. AT&T's track record for scientific prowess gave them a strong argument.

Fortunately, free market theory prevailed and AT&T was forced to relinquish its stranglehold over long distance calling in the United States. The transition was by no means smooth. The initial long distance competitors' services were clearly inferior to AT&T. We at Life Extension found it frustrating to initiate long distance calls over these discount carriers' networks. One newspaper columnist complained that he was tired of being solicited by these substandard discount carriers and wanted the government to reinstate AT&T's monopoly.

How Times Have Changed

Anyone who has paid attention to long distance rates over the past 28 years appreciates the enormity of the benefit brought about by abolishing AT&T's monopoly.

Consumers used to pay over 60 cents per minute for daytime long distance calls (equal to $1.39 per minute in today's depreciated dollars).1 Can you imagine if you had to pay $250 for three hours of long distance calling? This would be unthinkable today where for under $40 a month, you can have an unlimited long distance service that usually includes local connection charges.

Consumers today save a whopping 84% compared with 1980, even if they only make three hours of long distance calls a month. Unlike AT&T's threats of technological stagnation, the quality, reliability, and speed of today's long distance phone service are vastly superior.

As far as Life Extension's toll free service, our rate has dropped to 1.6 cents per minute. Back in 1982, we were paying the equivalent in today's dollars of $1.16 per minute for inferior service. When adjusted for inflation, we are saving 99% compared with what we paid in 1982.

Why Do Americans Tolerate Pharmaceutical Monopolies?

What if the federal government outlawed long distance competition and returned to the monopolistic ways of the past? If this were to occur, I am certain that every elected politician (who voted for this) would be thrown out of office.

Yet the public today tolerates federal and state laws that enable pharmaceutical companies to conduct business as a virtual monopoly. The result is that Americans pay outlandish prices for mediocre drugs that are often laden with side effects.

As AT&T did in 1980, drug companies seek to deceive Congress and the public by stating their high prices are needed in order to discover better technologies. The reality is that after decades of exorbitant drug pricing, one's odds of surviving a serious disease using conventional methods are not substantially improving. Yet drug prices are exponentially higher.

Citizen apathy has allowed this economic and medical bloodbath to occur. One of Life Extension's missions is to provide the hard facts so that today's antiquated regulatory system can be eradicated. We believe that in a free market environment, technological breakthroughs that occurred in telecommunications will also happen in medicine.

Unregulated Supplement Prices Plummet

Unlike regulated prescription drugs, the cost of dietary supplements has plummeted over the past three decades.

For example, when coenzyme Q10 (CoQ10) was first introduced to Americans in 1983, a bottle containing 1,000 mg (100 10-mg capsules) retailed for $30. In 2008, the retail price of a bottle containing 5,000 mg (100 50-mg capsules) of a superior form of CoQ10 (ubiquinol) is $58. Based on milligram potency alone, the cost in inflation-adjusted dollars for CoQ10 has come down by 83%.

If the FDA had succeeded in turning CoQ10 into a drug as it tried to do in the early 1980s, you might be paying $337.50 for what retails now for $58 (and costs Life Extension members far less).

Under the FDA's regulatory stranglehold, it is unlikely that the superior ubiquinol form of CoQ10 would have been "approved" any time soon. This would force Americans to pay the inflated price ($337.50 per bottle) for a less-than-optimal product. This illogic is what monopolies are all about, and why they cannot be allowed to exist.

If one looks at the price history of dietary supplements, costs are substantially lower now than when they were originally brought out. When SAMe was first introduced to Americans in 1996, it cost $45 for 4,000 mg (20 200-mg tablets). This was the European-regulated "drug" price. Soon after it became an unregulated supplement, the price went down a great deal. As more manufacturers competed to make SAMe, the price plummeted to where Life Extension members can obtain 8,000 mg (20 400-mg tablets) for only $21. Thus SAMe now costs 77% less than when it was originally introduced.

Prescription drug costs, on the other hand, have skyrocketed at a rate that far exceeds inflation. The difference is that prescription drugs are heavily regulated, as opposed to dietary supplements that are sold under free market conditions.

Today's Health Care Catastrophe

I accumulate so many reports about today's health care calamities that it is not possible to fit them into one issue of Life Extension magazine. To remind you of recent findings, we have reprinted a few of the appalling headlines.2-10

As you can clearly see by these reports, unless radical legal changes are made, Americans will continue to pay high prices for dangerous drugs that have limited efficacy.

More frightening is the suffocating effect that regulation has on the discovery of life-saving therapies. Just imagine if advancement in clinical medicine progressed at the same rapid rate as telecommunications. If it did, we would probably have cures for most killer diseases today!

For example, the first direct-dial transcontinental telephone call occurred in 1951.11 That first call took 18 seconds to complete, had lots of static in the background, and most consumers could not readily afford it. Move forward to 2008, and we all have access to clear phone connections across the country instantly at minimal cost.

Now look at the dire prognosis for pancreatic cancer patients today. A patient diagnosed with pancreatic cancer in 2008 typically lives just a few months longer compared with 1951.12-14 Yet the price for these additional months of life can be thousands of times higher than that in 1951.15

We need to swiftly improve medical science at a speed analogous to telecommunications, computers, and other unregulated technologies.

Scathing FDA Report Provides Basis to Revolutionize Medicine

The FDA has provided a rare opportunity to enact legislation that can enable Americans to quickly gain access to life-saving medical therapies.

As reported two months ago in my article "The FDA Indicts Itself," the FDA did a study of itself and its findings revealed that it is scientifically incompetent and incapable of doing its job.16,17 These are not mere allegations from outside critics, but are instead the FDA itself admitting that it cannot carry out its mission.

There has never been a better time for a comprehensive overhaul of the FDA. Everything about it - from its mission to its management - needs to be taken apart, reviewed, redefined, and recreated so that it helps support, rather than obstruct, a vibrant free market in health care science.

American Association for Health Freedom to Coordinate New Campaign

I am pleased to announce that the American Association for Health Freedom, an organization committed to complete reform of the FDA, is spearheading a campaign to change today's broken system.18 This is not our organization, but one that represents a coalition of integrative physicians, health care consumers, and health freedom activists around the country.

The approach that the American Association for Health Freedom is proposing will enable Americans to access affordable, safe, and effective therapies that are being denied to them now.

We at Life Extension are proud to be a sponsor of the American Association for Health Freedom and join other visionary leaders who support it.

Can Logic Prevail Over Lethal Dogma?

There are pessimists who think Americans will not be able to achieve true health freedom in the immediate future. Naysayers complain that if free market principles are extended to health care, some terminally ill patients will die sooner if experimental therapies fail.

My response is to again analogize what happened when long distance phone calling was deregulated. Sure, there were problems in the beginning, but look at where we are today with a dependable low-cost phone service affordable to all. Even more impressive are the incredible advancements in high-speed internet access and mobile phone connectivity that would have been unthinkable in the early 1980s.

A lot of my enthusiasm for a free market approach to health care is based on my own confidence in judging which novel medical therapies are truly safe and effective. A look at Life Extension's 28-year track record shows that we have been able to identify life-saving approaches to combating disease long before they are approved by the FDA.

Have we made mistakes? Yes, we have fallen victim to a few fraudulent studies that caused us to recommend products that we later found did not work. We have not, however, recommended products that killed anyone. Contrast this to regulated FDA-approved drugs that have collectively killed millions of Americans over the past three decades.

I believe the logic of letting the free market determine what therapies Americans may use to prevent and treat disease will defeat the cynics who fear changing the regulatory quagmire that exists today. Existing laws that protect against real health fraud will still enable charlatans to be stopped and prosecuted.

We Have Done it Before?

For those who don't know the history of the Life Extension Foundation, we have battled bureaucratic ineptitude since the early 1980s. Our overriding motivation is the fact that our very lives are at stake if we fail to abolish today's obsolete regulation of our health care.

One of our victories was the passage of the Dietary Supplement Health and Education Act (DSHEA).19 This legislation enabled consumers to learn about some of the benefits of dietary supplements. When the DSHEA legislation was initially proposed, it was apathetically viewed and most people thought it could never be enacted.

It took five years to pass DSHEA, but we eventually rallied so many consumers and industry leaders that Congress passed this landmark legislation. Please know that Life Extension was not the only one responsible for passage of DSHEA. Our support at its embryonic stage, however, set the stage for DSHEA to evolve from an obscure snowball in 1989 to an unstoppable avalanche in 1994.

It is now time again to educate Congress about the urgent need to reform the FDA. I plan to use the enormous success of long distance phone deregulation to help persuade the public and Congress that today's health care cost crisis will largely disappear if we return to free market principles in health care.

Congressional Petition to Reform the FDA

To persuade Congress to address this monumental problem, a Petition to Reform the FDA has been drafted.

Our first mission is to collect so many names on the Reform FDA Petition that it compels Congressional action. We will hand deliver the Petition to Congressional leaders and urge them to enact comprehensive FDA reform.

I ask every Life Extension member to put their name on this Petition so that Congress knows the citizenry is behind this groundbreaking initiative.

The easiest way to sign the Reform FDA Petition is to do so online. This new website has been set up by the American Association for Health Freedom (AAHF), an independent non-profit organization committed to the total overhaul of the FDA.

For longer life,

William Faloon

References

1. Consumer Reports. 1983. Nov;48(11): 618-20.

2. Available at: http://money.cnn.com/ 2008/03/03/news/economy/ 104239768.fortune/index.htm. Accessed June 23, 2008.

3. Available at: http://www.newsinferno.com/archives/1589. Accessed June 23, 2008.

4. Available at: http://www.cnn.com/2008/HEALTH/04/07/children.drug.errors.ap/index.html. Accessed June 23, 2008.

5. Available at: http://www.boston.com/news/education/higher/articles/ 2007/08/11/us_life_span_shorter/. Accessed June 23, 2008.

6. Available at: http://money.cnn.com/2007/08/15/news/companies/fda/index.htm. Accessed June 23, 2008.

7. Available at: http://blogs.usatoday.com/oped/2007/08/our-view-on-exp.html. Accessed June 23, 2008.

8. Available at: http://www.foxnews.com/story/0,2933,296427,00.html. Accessed June 23, 2008.

9. Available at: http://www.msnbc.msn.com/id/21033714/. Accessed June 23, 2008.

10. Available at:http://www.kmov.com/justposted/stories/kmov_health_071008_ breastcancerheart.14e95c1d0.html. Accessed June 23, 2008.

11. Available at: http://www.corp.att.com/attlabs/reputation/timeline/51trans.html. Accessed June 23, 2008.

12. Stewart RJ, Stewart AW, Stewart JM, Ibister WH. Cancer of the pancreas in New Zealand 1970-1974. Aust N Z J Surg. 1982 Aug;52(4):379-84.

13. Available at: http://www.pancreatica.org/Pancreatica%20Media%20Sheet.pdf. Accessed June 26, 2008.

14. Czernichow P, Lerebours E, Colin R. Epidemiology of cancer of the pancreas. Current data. Presse Med. 1986 Feb 22;15(8):387-91.

15. Available at: http://www.medscape.com/viewarticle/409001_2. Accessed June 26, 2008.

16 Faloon W. The FDA indicts itself. Life Extension. 2008 July;14(7):7-11.

17. Available at: http://www.fda.gov/ohrms/dockets/AC/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf. Accessed June 23, 2008.

18. Available at: http://www.apma.net/aahf/default.asp. Accessed June 23, 2008.

19. Available at: http://www.fda.gov/opacom/laws/dshea.html. Accessed June 23, 2008.

As We See It - August, 2008

William Faloon — Thu, 13 Nov 2008 16:32:00 GMT

LE Magazine August 2008
Novel Drug Therapy Immediately Reverses Alzheimer's Cognitive Deficits

Novel Drug Therapy Immediately Reverses Alzheimer’s Cognitive Deficits

By William Faloon

Twenty million Americans alive today are destined to contract Alzheimer’s disease, an affliction that robs us of memory, intelligence, and eventually our most rudimentary cognitive abilities.

Newly diagnosed Alzheimer’s victims are told they will suffer a relentless decline in their neurological function until death. Initial symptoms are short-term memory lapses that worsen until patients cannot recognize their own family members. As dementia progresses, hostile emotional outbursts often manifest, while the patient loses the ability to take care of one’s self—even to the extent of going to the bathroom.

The few drugs approved to treat Alzheimer’s symptoms produce only modest short-term effects. Some patients cannot tolerate them at all.

Up until now, a diagnosis of Alzheimer’s meant one was destined to slowly be deprived of all cognitive function—a condition that tops the list of aging people’s disease fears.

Breakthrough Therapy Results in Rapid Cognitive Improvement

Scientists have linked chronic inflammatory events in the brain with the onset and progression of Alzheimer’s disease.1-14 A causative inflammatory factor in the neuronal degeneration of Alzheimer’s disease is a cytokine called tumor necrosis factor-alpha (TNF-alpha).15-22

There are several nutrients that decrease TNF-alpha levels in the body.23-45 Ingestion of these nutrients is associated with reduced Alzheimer’s disease incidence.43-45 For those already afflicted with Alzheimer’s dementia, however, more than just reducing TNF-alpha level is needed to reverse the course of the disease.

In 1998, an anti-TNF-alpha drug called Enbrel® (etanercept) was approved to treat rheumatoid arthritis. Enbrel® does not reduce TNF-alpha in the body. Instead, it functions by binding to TNF-alpha and blocking its ability to latch on to TNF-alpha receptor sites on cell membranes. By interfering with the action of TNF-alpha in this way, the toxic effects of excess TNF-alpha are diminished.

I am going to tell you how Enbrel® can be administered to Alzheimer’s patients in a special way so that it flows directly into the brain, but readers should first understand how TNF-alpha causes senile dementia.

Cognitive Test Improvement After Six Months of Enbrel® Injection

Alzheimer’s Disease Assessment Scale-Cognitive subscale	26%
Mini-Mental Status Examination	12%
Severe Impairment Battery	27%

How Excess TNF-alpha Impairs Neuronal Function and Structure

In the brain, TNF-alpha can elicit a cascade of cellular events culminating in neuronal death.11,46-51 Elevated TNF-alpha has been observed in the brain, cerebrospinal fluid, and serum in Alzheimer’s disease cases.2,50,52-54

Of particular interest is how TNF-alpha affects the “synapses” in our brains. A “synapse” is the point of connection between nerve cells. Brain cells are interconnected and communicate with each other by sending neurotransmitters through the synapses.

Excess TNF-alpha in the brain can disrupt synaptic communication.55-58 A number of findings suggest that synaptic dysregulation caused by excess TNF-alpha contributes to cognitive and behavioral dysfunction in Alzheimer’s disease.52,59-68

Elevated TNF-alpha does more than disrupt vital synaptic communication. A structural change seen in Alzheimer’s disease is the accumulation of amyloid-beta in brain cells. Amyloid-beta accumulation increases inflammation and this inflammation causes further amyloid-beta formation. One mechanism by which amyloid-beta induces inflammation is by triggering an increase in TNF-alpha production.60,69-72

Thus, excess TNF-alpha triggers a vicious cycle whereby toxic amyloid-beta is produced, resulting in greater levels of proinflammatory TNF-alpha, which cause even more amyloid-beta and TNF-alpha formation. Elevated TNF-alpha directly causes synaptic dysfunction and contributes to neuronal destruction. The result of these pathological changes is the horrific senile deficits suffered by Alzheimer’s disease patients.

As you will soon read, the rapid effect of Enbrel® in reversing cognitive impairment helps validate the role of excess TNF-alpha in the debilitating Alzheimer’s disease process.

Protect Yourself Against Excess TNF-alpha

A common consequence of “normal” aging is a state of chronic systemic inflammation. This inflammatory state can cause diseases as diverse as atherosclerosis,74-80 cancer,81,82 arthritis,83-87 and Alzheimer’s disease.88

Members of the Life Extension Foundation do not intend to age “normally.” To protect against excess proinflammatory cytokines like TNF-alpha, they supplement with nutrients like fish oil,23-33 luteolin,34-37 and curcumin.38-42 Maintaining a youthful hormone balance using DHEA89-94 and testosterone95-110 (in men), eating foods cooked at relatively low temperatures,111 and sustaining a healthy weight are also critical to suppressing inflammatory reactions.

While Alzheimer’s disease rates are projected to skyrocket with the aging population, a large number of scientific studies reveal that one’s risk can be significantly reduced by eating a healthy diet and taking the proper nutrients and hormones.

How Enbrel® is Administered as an Anti-Alzheimer’s Therapy

The approved use of Enbrel® is to self-inject it under the skin once a week to alleviate chronic inflammatory disorders. Enbrel® injected this way, however, will not sufficiently penetrate the blood-brain barrier to produce rapid cognitive improvement.

To deliver Enbrel® to the brain, researchers are injecting it into the back of the neck (in the spongy muscle area between the sixth and seventh cervical vertebrae). The patient’s head is then lowered for about five minutes at a level around their abdomen to better enable the Enbrel® injected into the neck to flow to the brain (through the cerebrospinal venous system).

The dose that had been used in clinical studies was 25-50 mg of Enbrel® in 1 cc of sterile water. Life Extension is exploring the use of Enbrel® in a larger amount of water (2 cc) to enable more Enbrel® solution to travel to the brain.

These Enbrel® injections to the back of the neck (known as interspinous injections) should be administered once a week by a competent neurologist.

The First Pilot Study of 15 Alzheimer’s Patients

Current medical treatments for Alzheimer’s disease do not prevent long-term clinical deterioration.

As discussed, tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that is implicated in the neuronal disruption and degeneration observed in Alzheimer’s patients.

An open-label study was conducted in 15 patients with mild-to-severe Alzheimer’s disease.20 Three recognized test measures of cognitive function were performed at the study’s onset. The patients received weekly Enbrel® injections to the back of the neck, and cognitive testing was repeated at one-month intervals. The following box shows the clinical improvements that were measured in this initial test group after six months:

When one considers that Alzheimer’s disease up until now has resulted in worsening of cognitive function, the fact that there was an average 22% improvement in these three mental function measurements after six months is unprecedented.

These patients continued receiving these Enbrel® injections for more than three years. The results suggest that weekly maintenance treatment produces a sustained positive effect, indicating that this novel approach can slow or even halt much of the mental deterioration that occurs in Alzheimer’s patients. This again is an unparalleled clinical phenomenon.

Surprising Findings Reveal Immediate Improvement!

The initial studies were limited to measuring the effectiveness of Enbrel® between 30-day intervals. What the researchers and caregivers of these Alzheimer’s patients noticed, however, was a rapid clinical improvement within minutes of administering the Enbrel®.

The immediate improvement in cognitive function in these demented patients was unexpected and caught researchers (and their caregivers) off guard. Just imagine how surprising it would be to bring your senile loved one to a doctor’s office and observe an instant improvement in their mental function.

The authors of the original study then decided to use several recognized tests to measure the degree of rapid improvement in a new patient treated as part of their standard practice of medicine.

The Second Pilot Study

The new patient was an 81-year-old who had been in good general health until about two years before initial presentation, at which time his wife noted progressive memory difficulties and difficulties with mathematical calculation.71

His wife took over mathematical tasks such as check writing, and the patient was evaluated by a neurologist 18 months prior. The drug Aricept® was prescribed but was not tolerated and was discontinued after four months. Two other Alzheimer’s drugs (Nameda® and Exelon®) were prescribed but also were not tolerated by the patient.

A mental status examination performed one day prior to Enbrel® injection into the neck showed this patient had difficulty recalling personal autobiographical information such as his birthday or his father’s occupation. He could not recall the names of any of the physicians who treated him. He was not oriented to the calendar date, day of the week, year, place, city, or state. Detailed examination revealed that he had marked difficulty in recalling words, and could not name nine out of 10 pictures he was just shown.

When given a test to measure his linguistic skills, i.e., asked to list all the animals he could in 60 seconds, he could only list two, dog and cat.

On memory testing, the patient could not recall the name of his physician after 90 seconds, despite repetitive introductions on at least four occasions throughout the examination. It took three trials for the patient to register five words and 90 seconds later, the patient could not retrieve any of the words even with categorical cueing.

When asked to draw a clock with the hands placed at 10 minutes after 11, he drew a square without numbers and one line for the hour or minute hand. He could not do a task that involved connecting letters and numbers and was clearly overwhelmed by it.

The patient could not perform simple calculations and could not do serial sevens (counting down from 100 by sevens). When asked to add 29 plus 11 after a marked latency he said 31. Abstract concepts such as a how a train and a bicycle, a watch and a ruler, or music and painting were similar could not be expressed by the patient.

On the Montreal Cognitive Assessment test, the patient scored 7 out of 30 possible points, consistent with moderate-to-severe dementia. Based on these and other cognitive tests, the patient clearly met the established criteria for probable Alzheimer’s disease.

Side Effects of Enbrel®

Enbrel® is NOT a drug one would take unless it is critically needed. That is because when administered systemically, it increases the potential risks of infection, low blood counts, lymphoma, demyelinating nerve disease, eye inflammation, congestive heart failure, and death.73 The long-term side effects are not known when Enbrel® is administered primarily to the brain, as is being done in this anti-Alzheimer’s treatment.

Written informed consent has been obtained from all these Alzheimer’s disease test subjects (or their family members) warning them of these potential risks. The rationale in accepting known and unknown side effect risks is that Alzheimer’s disease is a uniformly progressive and lethal disease. There is no other therapy that so rapidly and effectively reverses the clinical course of the disease.

Examination Ten Minutes After Enbrel® Injection

Immediately prior to Enbrel® injection the patient was questioned by the neurologist. He could not state the year nor could he name the state he lived in.

Ten minutes after Enbrel® dosing, the patient was re-examined. He was noticeably calmer, less frustrated, and more attentive. He was able to correctly identify the state as California, and he identified the year as 2006. His responses to questioning seemed less effortful and more rapid, with less latency. He left to go to a second neurologist for immediate further testing.

Follow-Up Neurologic Examination Two Hours After Enbrel® Treatment

The patient was re-tested by another neurologist two hours after Enbrel® administration. While he could not recall being in the treating neurologist’s office earlier in the day (before the Enbrel® injection), he did recall the name of the second neurologist he was seeing. He was now oriented to month, day of week, and place, and could again correctly name the state as California, which he could not do prior to Enbrel® injection to the back of his neck. He was off on the calendar date by two days, and the year by one year.

The patient’s ability to name pictures was markedly improved, correctly naming nine out of the first 10 pictures, a marked improvement from the day prior when he could only name one of the 10 presented pictures. On the verbal fluency test, he was able to list eight words that started with the letter “F” in 60 seconds and made only one erroneous response. On a linguistics task, he was able to list five animals in 60 seconds.

On visuospatial functioning, the patient could copy a three-dimensional cube, and when asked to draw a clock, he drew a circle with an hour and minute hand. When given a test to connect letters and numbers, the patient was clearly able to sequence and complete the task, alternating letters and numbers accurately. He was able to pantomime seven out of eight finger constructions of increasing complexity.

On memory testing, the patient could not recall any of five memoranda after five minutes even with categorical cueing. With multiple-choice cueing, he could recall one out of five memoranda. However, he could recall the examiner’s name without difficulty and without necessity of repetition of introductions throughout the entire examination.

On attentional testing, the patient could accurately list five digits in a forward fashion and three digits in a reverse sequence fashion. On a vigilance task test, he made no errors of omission or commission.

On calculations, he could subtract seven from 100 correctly, but could not perform serial sevens. He could not divide 58 by two, nor could he add 29 plus 11. He could not tell the neurologist how many nickels were in a dollar.

On ability to abstract concepts, he was able to relate how a train and bicycle were similar in that they both can be used for transportation. When asked how a watch and a ruler were similar, he related that they both give information. When asked how music and painting were similar, he related, “You draw your painting; however, music you hear.”

Montreal Cognitive Assessment performed two hours following the single dose of Enbrel® injected into the back of his neck, yielded a score of 15 out of 30 points… a 115% improvement compared with the previous score of 7 before the Enbrel® injection (only two hours before).

A collateral interview with the patient’s son and wife confirmed their validation of a marked improvement in cognitive abilities following Enbrel® administration

Neurological Effects One Week After Initial Enbrel® Injection

Upon returning for his second weekly Enbrel® injection, the patient’s wife and son confirmed that he had remained markedly improved throughout the week.

He was less reluctant to join in conversation. On re-examination by the first neurologist prior to receiving the second weekly dose, the patient correctly identified the year, month, season, day of week, and state. He appeared to answer with less frustration, and the examiner’s impression was that there was reduced latency of response, along with other observable improvements. On the test for verbal fluency, when asked to list all of the words that start with the letter “F” in 60 seconds, he listed eight words and named five animals in 60 seconds.

Sustained Improvement

The patient received a single dose of Enbrel® injected into the back of his neck for each of the first five weeks; the next dose was omitted, and the patient returned after seven weeks for retesting. At this seven-week interval (and 14 days after receiving his last dose of Enbrel®), his Montreal Cognitive Assessment score was 14 out of 30 (a 100% improvement from the baseline score of 7), with persistent improvement in the numbers-letters connecting task, and improved depiction of the clock face.

The researchers stated that the rapid cognitive improvement following Enbrel® injection to the back of the neck is not limited to this patient. It had in fact been commonly observed in multiple patients during these researchers’ more than three years of clinical experience utilizing Enbrel® for treatment of probable Alzheimer’s disease.20,71

Life Extension Foundation Helps Validate Findings

In as much as these clinical improvements are unprecedented, the Life Extension Foundation conducted a pilot study of a 91-year-old female Alzheimer’s disease patient who suffered severe cognitive deficits.

There was immediate improvement after the first Enbrel® injection. For example, she was able to follow simple commands such as “tap your fingers” that she couldn’t do before the injection. She was more animated as well.

After four weeks, the results on the Mini-Mental Status Exam showed a significant 150% improvement, and her aid described her as engaging in more accurate discussions and eating better.

The family of this Alzheimer’s patient and the treating neurologist noticed an immediate improvement after the first Enbrel® injection. According to her son, who is a medical doctor:

“My mother is doing better. Her conversations are longer. She is asking to go for walks outside. She is no longer incontinent of stool. When I told her I was going to give a talk in Boca Raton next month she said, “I am very proud of you.” She has not said anything that complex in years.”

Life Extension is continuing to fund this patient’s Enbrel® therapy and follow up on her progress. Regrettably, due to complications related to her advanced Alzheimer’s disease state, administering these weekly injections has been challenging. Every effort is being made to help this women regain some of her cognitive abilities. Future studies will be aimed at early-stage Alzheimer’s disease patients.

New Clinical Study Sponsored by the Life Extension Foundation

Based on these extraordinary findings, the Life Extension Foundation is seeking to launch an expanded study with the objective of measuring the long-term effects of weekly Enbrel® injections plus nutrients that help suppress the production of excess TNF-alpha.

Enbrel® is an extremely expensive drug. The normal cost of the Enbrel® and weekly injections is approximately $675. If you or a person you know with early-stage Alzheimer’s disease desires to participate in this new clinical study, there will be no charge for treatments.

The study site will be in south Florida. Since the Enbrel® injections will have to be administered weekly, study participants should ideally reside in the Fort Lauderdale area.

Due to the potential side effects of Enbrel®, there are bureaucratic hurdles we have to comply with before initiating this formal study. Once we have institutional approval, Life Extension will initiate this study aimed at validating a proven method to reverse Alzheimer’s disease. We hope to keep the delay in launching this study to a minimum, but many of the regulatory aspects are beyond our control.

To inquire about enrolling in this new study sponsored by the Life Extension Foundation, call 1-866-517-4536.

A New Era…

In 1907, Dr. Alois Alzheimer performed an autopsy on the brain of a deceased individual and noted the structural characteristics of the disease that now bears his name. Up until now, there has been no effective way to slow this horrific condition.

For the first time in medical history, those afflicted with Alzheimer’s disease may enjoy an immediate reversal of cognitive deficits, while potentially slowing the destruction to their precious neurons caused by TNF-alpha-induced inflammatory reactions.

Up until now, taking a loved one to a doctor’s office and learning of an Alzheimer’s disease diagnosis meant a bleak future of unrelenting neurologic decline. Based on what has been discovered, newly diagnosed patients may soon gain access to these special Enbrel® injections and enjoy a rapid and long-lasting restoration of cognitive function.

For longer life,

William Faloon

If you have any questions on the scientific content of this article, please call a Life Extension Health Advisor at 1-800-226-2370.

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