Category Archives: Disease - Page 28

Retroviruses and Chronic Fatigue Syndrome

Posted by on August 24, 2010 29 comments

One of the themes of this blog is that chronic infections, exacerbated by bad diets and malnutrition, are at the root of nearly all health problems.

With the invention of new tools for microbiology over the last 20 years, scientists are for the first time able to study chronic parasitic infections, albeit with difficulty. I mentioned a few weeks ago that this should be the dawn of a “golden era of antimicrobial medicine.” And maybe it is: careful studies are now linking specific pathogens to chronic diseases and discovering the mechanisms by which they cause disease.

A good example of emerging science is the progress made since 2002 in understanding a retrovirus family that is now firmly linked to cancer and chronic fatigue syndrome and may soon be linked to other diseases.

Beginning of the Story:  Human Anti-Viral Immunity and Chronic Fatigue Syndrome

Our story begins back in the 1970s with studies of the role of interferons in defending human cells against viruses. Interferons are a key part of the immune defense against intracellular pathogens – the ones that cause most human chronic diseases.

Following the effects of interferons, researchers discovered an enzyme known as ribonuclease L (RNase L). RNase L is upregulated by interferons and its function is to degrade RNA, both viral and human, to stop viral replication. [1]

Aside: High levels of RNase L destroy so much human RNA that the cell dies. This is probably adaptive for the host, since cell apoptosis also kills many pathogens within. However, it shortens lifespan. RNase L knockout mice have extended lifespans. [1]

In 1997, RNase L was found to be strongly upregulated in chronic fatigue syndrome patients. [2] This showed that chronic fatigue patients usually have viral infections. Whether the viruses were causing chronic fatigue, or just “hitchhiking” with a disease that suppressed the immune system (perhaps via a bacterial infection?), remained an open question.

A Link Between RNase L and Prostate Cancer

By the early 2000s it was established that a common (allele frequency 35%) gene mutation, the “R462Q” mutation which substitutes a glutamine for an arginine in the “hereditary prostate cancer 1” locus, raised the risk of prostate cancer. A man with two copies of this mutation has twice the risk of prostate cancer; one copy raises the risk by 50%. About 13% of prostate cancer cases were attributable to this mutation. [1, 3, 4]

It was important, therefore, to determine which protein this locus coded for. A breakthrough finding, made in 2002, was that the “hereditary prostate cancer 1” locus was the gene for RNase L. [5]

It was soon shown that the R462Q mutation decreased the effectiveness of RNase L at cleaving viral RNA. This placed prostate cancer in a new light: it implied that an unknown virus against which RNase L defends was a probable cause of prostate cancer. When RNase L function was impaired by the R462Q mutation, the infection became more virulent, and prostate cancer rates were higher. [1]

The search for this unknown virus was on.

The discovery of “xenotropic murine leukemia virus-related virus” (XMRV)

The strategy was basically to take prostate tumors and search for viral RNA, looking for viruses that were most common in patients who had the double R462Q mutation.

In 2006 one of these searches yielded fruit.  A new gamma retrovirus was found in 8 of 20 prostate cancer patients with double R462Q mutations, but only 1 of 66 patients without the double mutation. [6]

This gamma retrovirus shared a lot of RNA with a family known as the xenotropic murine leukemia viruses (MuLVs). It was dubbed “xenotropic murine leukemia virus-related virus” (XMRV). Despite the sound, it is not a murine (mouse) leukemia virus; it merely shares a lot of nucleic acids with those viruses.

Back to chronic fatigue syndrome

In 2009 a paper was published in Science reporting that XMRV was found in peripheral blood cells of 67% of chronic fatigue patients but only 3.7% of healthy controls. [7] This study was done by a group at the Whittemore Peterson Institute in Reno, Nevada.

Aside:  The Whittemore Peterson Institute has a nice Q&A about this virus and its role in chronic fatigue syndrome here.

A number of researchers tried and failed to reproduce these results. For instance, a group from the Centers for Disease Control failed to detect XMRV proteins in 51 chronic fatigue and 53 healthy patients. [8]

Perhaps proteins are just not the right molecules for detecting this virus. A new paper has just appeared that links XMRV more strongly than ever to chronic fatigue. It looked at DNA for viral genes inserted into the human genome and found XMRV sequences in 86.5% of chronic fatigue patients but only 6.8% of controls. [9] This paper was held back from publication since June because of its conflict with the CDC paper (see “Why I Delayed XMRV Paper”), but has now been released.

These percentages are impressive and, if they hold up, would seem to make it unlikely that XMRV is merely a “passenger” virus hitchhiking on a suppressed immune system. It may be causal for chronic fatigue.

Will anti-retroviral therapies be effective?

Clinical trials are extremely expensive and the drug companies seem to be waiting for XMRV to be proven as the cause of chronic fatigue before undertaking trials. From the Wall Street Journal:

Norbert Bischofberger, chief scientific officer at Gilead Sciences Inc., the leading maker of HIV drugs, said the company might consider a small pilot trial but would like to see stronger evidence that the viruses cause CFS before launching a large trial. Still, “I’m very open, and this would be a great opportunity,” he said.

A spokesman for Merck & Co., another major manufacturer of HIV drugs, said: “A clinical trial program would be possible to develop only after further substantial evidence of an association with CFS.” [10]

But some aren’t waiting for trials. Anti-retroviral drugs developed for AIDS are being prescribed off-label:

Jamie Deckoff-Jones, 56 years old, a doctor and CFS patient in New Mexico, has been blogging about her experiences and those of her 20-year-old daughter. Both tested positive for XMRV and are taking a combination of three anti-retrovirals.

Dr. Deckoff-Jones said a year ago she could only get up for short periods during the day. After five months on the drugs, she flew last week to Reno for an XMRV conference. Her daughter was able to go to a party and is enrolling in community college. “This is all very new, and there is no way to know if improvement will continue,” Dr. Deckoff-Jones wrote in an email, “but we appear to be on an uphill course.” [10]

Chronic fatigue patients are celebrating the progress:

Many [CFS patients] were ecstatic at news that the second study was being published.

“We’re really hoping this will blow the lid off,” said Mary Schweitzer, a historian who has written and spoken about having the illness. “Patients are hopeful that now the disease itself might be treated seriously, that they’ll be treated seriously, and that there might be some solution.” [11]

It’s sad that for decades many haven’t taken chronic diseases seriously. The absence of a known cause reflected only the lack, until recently, of microbiological tools capable of detecting and characterizing intracellular pathogens.

Had doctors taken these diseases seriously, the accumulating evidence that these were chronic infectious diseases caused by intracellular parasites might have encouraged them to look for the sort of dietary and nutritional therapies for chronic disease that we advocate on this blog. Though diet and nutrition by themselves will probably not cure these diseases, they can greatly slow disease progression and improve the odds of a cure.

A new name for XMRV: Human Gamma Retrovirus

The Whittemore Peterson Institute recently hosted the first official scientific symposium on XMRV. Dr. Joseph J. Burrascano reported from the symposium:

We formed a working group to be in constant touch and we plan to meet regularly because advances are coming so rapidly.

Big news that everyone should know and adopt is that we have proposed a name change for the virus.

This virus is a human, not mouse virus, and it is the first and so far only gamma-retrovirus known to infect people. Also, it is clearly not an “endogenous” retrovirus (one that is present in all genomes due to ancient infection).

Because of all of this, and because of the desire to begin on the right track, the new name of the virus is HGRV- Human Gamma Retro Virus. The illness caused by this infection is named HGRAD- Human Gamma Retrovirus Associated Disease.

We plan to announce this at the upcoming NIH retroviral conference this September.

Definitely stay tuned- the volume of new and important information about this virus and its disease associations is increasing rapidly and in my opinion should be a concern to every patient with chronic neuro-immune diseases, including those with chronic Lyme. [12]

It sounds like some exciting findings may be on the way.

Conclusion

This case is a fascinating illustration of the twisting turns that scientific research can take. The early discovery of a link between anti-viral immunity and prostate cancer may now lead to a cure for chronic fatigue syndrome. At least, we can hope so.

As one of the pioneers, Dr. Robert Silverman, describes it,

One of the remarkable aspects of being a scientist, is that you never know where your scientific journey will lead. [1]

Science takes a lot of patience, diligence, and persistence. It’s gratifying when all that work is rewarded by discovery.

References

[1] Silverman RH. A scientific journey through the 2-5A/RNase L system. Cytokine Growth Factor Rev. 2007 Oct-Dec;18(5-6):381-8. http://pmid.us/17681844.

[2] Suhadolnik RJ et al. Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome. J Interferon Cytokine Res. 1997 Jul;17(7):377-85. http://pmid.us/9243369.

[3] Silverman RH. Implications for RNase L in prostate cancer biology. Biochemistry. 2003 Feb 25;42(7):1805-12. http://pmid.us/12590567.

[4] Casey G et al. RNASEL Arg462Gln variant is implicated in up to 13% of prostate cancer cases. Nat Genet. 2002 Dec;32(4):581-3. http://pmid.us/12415269.

[5] Carpten J et al. Germline mutations in the ribonuclease L gene in families showing linkage with HPC1. Nat Genet. 2002 Feb;30(2):181-4. http://pmid.us/11799394.

[6] Urisman A et al. Identification of a novel Gammaretrovirus in prostate tumors of patients homozygous for R462Q RNASEL variant. PLoS Pathog. 2006 Mar;2(3):e25. http://pmid.us/16609730.

[7] Lombardi VC et al. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Science. 2009 Oct 23;326(5952):585-9. http://pmid.us/19815723.

[8] Switzer WM et al. Absence of evidence of xenotropic murine leukemia virus-related virus infection in persons with chronic fatigue syndrome and healthy controls in the United States. Retrovirology. 2010 Jul 1;7:57. http://pmid.us/20594299.

[9] Lo S et al. Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors. PNAS Epub before print August 23, 2010. http://www.pnas.org/content/early/2010/08/16/1006901107.abstract.

[10] Amy Dockser Marcus, “New Hope in Chronic Fatigue Fight,” Wall Street Journal, Aug 23, 2010, http://online.wsj.com/article/SB10001424052748703846604575447744076968322.html.

[11] David Tuller, “Study Links Chronic Fatigue to Virus Class,” New York Times, Aug 23, 2010, http://www.nytimes.com/2010/08/24/health/research/24fatigue.html.

 [12] http://www.forums.aboutmecfs.org/showthread.php?7001-News-from-WPI-symposium-Name-change-to-be-proposed-for-XMRV (hat tip http://health.groups.yahoo.com/group/infection-cortisol/message/1753).

Vitamin D Dysregulation in Chronic Infectious Diseases

Posted by on August 21, 2010 45 comments

Commenter qualia recently got his serum 25-hydroxy vitamin D levels tested and found a surprising result: He had doubled his vitamin D intake from 5,000 IU to 10,000 IU per day, but his 25(OH)D levels didn’t budge – they were at 61 and 62 nmol/l, equivalent to 24.4 ng/ml in American units.

24 ng/ml is well below the optimal level for healthy people of 40 ng/ml. When a healthy person supplements vitamin D, the serum 25(OH)D level usually rises linearly with dose up to about 40 ng/ml, then it rises very slowly thereafter as the body tries to keep 25(OH)D from rising by putting vitamin D into storage.

So it was natural for qualia to expect his serum 25(OH)D level to rise when he doubled his dose.

But it didn’t. The stability of his 25(OH)D levels suggests that his body has reached an equilibrium at 24 ng/ml. Instead of plateauing at 40 ng/ml with abundant vitamin D3 as a healthy person would, he is plateauing at a lower level.

Why does that happen?

Well, I don’t know. But I would like to provide qualia with a little bit of background, because this could be a clue that helps diagnose his condition and optimize treatments.

Normal vitamin D regulation strictly controls 1,25D levels

I suggested in the comment thread that qualia get his 1,25D levels measured as well as 25(OH)D.

Levels of 1,25D are not routinely measured, even in scientific studies, because they rarely vary. Blood levels of 1,25D control calcium homeostasis and are tightly regulated. In healthy people, as vitamin D intake rises from zero, serum 1,25D levels shoot up to normal levels before 25(OH)D levels reach 12 ng/ml. They then stay in a normal range no matter how high 25(OH)D levels rise. The kidney is the primary controller of blood 1,25D levels. The normal range is about 16 to 42 pg/ml (42 to 110 pmol/L).

While all human cells can convert 25(OH)D to 1,25D, most cannot release 1,25D into the blood. 25(OH)D freely crosses cell membranes and maintains the same level throughout the body; but 1,25D does not cross membranes. This allows every cell in the body to “personalize” its 1,25D levels to its own needs.

Both 25(OH)D and 1,25D are active ligands for the Vitamin D Receptor (VDR), a nuclear receptor.  [1] When either 25(OH)D or 1,25D binds to the VDR, the compound is imported into the nucleus, where it combines with a vitamin A-activated Retinoid X-Receptor (RXR) to form a transcription factor which, among other roles, upregulates production of antimicrobial peptides (AMPs) that are crucial for cellular defense against intracellular pathogens.

The difference between 25(OH)D and 1,25D is that 1,25D is about fifty-fold more likely to bind to the VDR than 25(OH)D. So by converting more 25(OH)D to 1,25D, cells can upregulate their VDR activation and upregulate their immune defense against pathogens. Meanwhile, uninfected cells can keep their 1,25D levels low. Across human cells, there is a thousand-fold variation in the rate of conversion of 25(OH)D to 1,25D. [1]

In chronic infectious diseases, blood 1,25D is dysregulated

However, in people with chronic infectious diseases, 1,25D levels range all over the map, and are largely uncorrelated with 25(OH)D levels.  Here is a scatter plot from a paper by Dr. Greg Blaney [2]:

The patients in this sample were 100 chronic disease patients: 29 with fibromyalgia, 27 with chronic fatigue syndrome, 12 with post-treatment Lyme Disease, 9 with metabolic disease, 6 with osteoarthritis, 4 with irritable bowel syndrome, 4 with psoriatic arthritis, 3 with multiple sclerosis, 3 with seronegative arthritis, and 27 with other diseases.

Probably all of these diseases are caused by chronic parasitic infections.

A few things to note from this plot: (1) 25OHD levels in a lot of chronic disease patients cluster around the 61 nmol/L level that qualia has; and (2) most chronic disease patients have 1,25D levels well above the normal range, even though their 25OHD levels are mostly below the optimal level in healthy people.

What Causes 1,25D Dysregulation?

Here’s where we get into speculation. There just hasn’t been research exploring this question. Researchers are only just realizing that these diseases are infectious in origin and that vitamin-D-mediated innate immunity is critical to the intracellular immune defense.

Rather than speculate, I’m just going to mention a couple of possibilities.

First, in granulomatous diseases like sarcoidosis, it’s common to have low 25(OH)D and very high 1,25D. Granulomas are nodules where immune cells have been unable to eliminate some foreign matter and instead have built a barrier around it that walls it off from the body.  Granulomas often release 1,25D to the body. Some other granulomatous diseases: 

  • Tuberculosis
  • Leprosy
  • Schistosomiasis
  • Histoplasmosis
  • Cryptococcosis
  • Crohn’s disease

These are all infectious diseases, some of them protozoal in origin.

Second, nearly all human pathogens manufacture proteins or RNA that interfere with the innate immune response. Some are known to interfere with the VDR or with other aspects of vitamin D biology. (The HIV virus blocks the VDR entirely, one reason why it predisposes AIDS patients to infections.) It’s possible that vitamin D dysregulation is brought about by direct pathogen actions to disrupt cellular vitamin D pathways.

Conclusion

The only thing we can conclude with confidence from qualia’s vitamin D tests is that he must have a chronic infectious disease … but he knew that already.

Qualia would be best served by getting advice from an infectious disease specialist with experience in chronic diseases. Such a doctor might be able to narrow down the diagnosis. A diagnosis would help determine which antibiotics might be appropriate to help fight the infection.

Until a doctor’s diagnosis or qualia’s personal experience indicates otherwise, it’s probably prudent to continue with a reasonable intake of vitamin D and to increase iodine as quickly as possible. (Even this is not certain: the standard advice is to minimize vitamin D in granulomatous diseases.) Other infection-fighting supplements, like vitamin C, N-acetylcysteine, and glutathione are likely to be helpful also.

Finally, I always recommend that anyone with a chronic disease find a good discussion forum, like the one at http://cpnhelp.org, and try to find people with similar disease histories and learn from their experiences.

Best of luck, qualia, and please keep us posted.

References

[1] Lou YR et al. 25-Hydroxyvitamin D(3) is an agonistic vitamin D receptor ligand. J Steroid Biochem Mol Biol. 2010 Feb 15;118(3):162-70. http://pmid.us/19944755.

[2] Blaney GP et al. Vitamin D metabolites as clinical markers in autoimmune and chronic disease. Ann N Y Acad Sci. 2009 Sep;1173:384-90. http://pmid.us/19758177.

Why You Shouldn’t Supplement Calcium

Posted by on August 20, 2010 47 comments

Much of the advice handed out by medical doctors is unreliable.  One reason is that the research on which that advice is based is often conducted by specialists who overlook effects beyond their scope of professional interest.

We’ve mentioned previously the example of statin research. Statin studies are generally performed by cardiologists and in the U.S., many statin studies reported only heart attacks and other cardiovascular events as endpoints, not total mortality, cancer, or infectious disease. This method of evaluating drugs would show a lethal neurotoxin to be the best cardiac treatment ever:  In the neurotoxin group not a single patient would die of a heart attack!

A similar myopia has occurred in osteoporosis research, where doctors have focused on the effect of calcium supplements on bone density or fracture rates but often do not evaluate the effect of the supplements on overall health.

But other effects have to be considered, given that:

  • Calcification of coronary arteries may be the best single indicator of heart attack risk. [1]
  • In the Nurse’s Health Study, supplementation of calcium increased the risk of calcium oxalate kidney stones by 20%. [2]
  • Calcium is a strong promoter of biofilm formation in most pathogenic bacterial species. [3] It also likely promotes formation of Candida albicans (fungal) biofilms. As a result, it can aggravate bowel disorders and infectious diseases.

Clearly, calcium in the wrong places – a problem that could be exacerbated by calcium supplementation – is a major health risk.

What causes calcium to go in the wrong places? Deficiencies of vitamin D and vitamin K2 are common reasons. Deficiencies of both are widespread. Vitamin K2 deficiency is a known cause of vascular calcification.

A few years ago, a group of New Zealand researchers conducted a randomized clinical trial that found that over five years, older women taking calcium supplements doubled their risk of heart attack compared to women taking a placebo. [4]

Now, the same group has conducted a systematic review of calcium supplementation studies which confirms the link between calcium supplementation and heart attacks. Dr. Mark Bolland of the University of Auckland, New Zealand, and colleagues report that calcium supplementation increases the risk of heart attack by 31%, the risk of stroke by 20% and the risk of death by 9%. [5]

In an accompanying editorial, Dr. John Cleland writes:

Calcium supplements, given alone, … are ineffective in reducing the risk of fractures and might even increase risk, they might increase the risk of cardiovascular events, and they do not reduce mortality. They seem to be unnecessary in adults with an adequate diet. Given the uncertain benefits of calcium supplements, any level of risk is unwarranted. [6]

We concur. A healthy diet, including dairy and green leafy vegetables, not to mention a daily multivitamin (ours contains 200 mg calcium), should provide a sufficiency of calcium as long as vitamin D levels are normal. If you’re worried about bone health, supplement with vitamins D, K2, and magnesium citrate – not calcium.

[1] Budoff MJ et al. Long-term prognosis associated with coronary calcification: observations from a registry of 25,253 patients. J Am Coll Cardiol 2007;49:1860-1870. http://pmid.us/17481445. 

[2] Curhan GC et al. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med. 1997 Apr 1;126(7):497-504. http://pmid.us/9092314.

[3] Kierek K, Watnick PI. The Vibrio cholerae O139 O-antigen polysaccharide is essential for Ca2+-dependent biofilm development in sea water. Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14357-62. http://pmid.us/14614140.  Geesey GG et al. Influence of calcium and other cations on surface adhesion of bacteria and diatoms: a review. Biofouling 2000; 15:195–205.

[4] Bolland MJ et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ. 2008 Feb 2;336(7638):262-6. http://pmid.us/18198394.

[5] Bolland MJ et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ. 2010 Jul 29;341:c3691. doi: 10.1136/bmj.c3691. http://pmid.us/20671013.

[6] Cleland JG et al. Calcium supplements in people with osteoporosis. BMJ. 2010 Jul 29;341:c3856. http://pmid.us/20671014.

The FDA Is On The Side of the Microbes

Posted by on August 11, 2010 12 comments

This should be the golden era of antimicrobial medicine. Molecular biology has over the last two decades created new diagnostic tools like real-time PCR which can isolate and amplify minute quantities of bacterial DNA to identify individual species. Today’s researchers can design antimicrobial drugs that specifically target proteins, RNA, and DNA of individual pathogens.

Existing antibiotics obtained from fungi and plants often interfere with human biology, creating side effects that limit doses. Tomorrow’s antibiotics should defeat pathogens with minimal side effects, by acting only against molecules specific to bacteria, fungi, viruses, and protozoa.

This blog believes that nearly all diseases have an infectious origin. Infections outrun the immune system due to dietary and nutritional inadequacies. Diet, nutrition, and new antimicrobials should enable nearly all diseases to be defeated.

We are on the cusp of enabling nearly everyone to live to age 100 in good health. All we need is a renewed focus on antimicrobial research, and better diets.

Yet nothing is happening.

Via frequent commenter erp comes an excellent story that explains why (Trine Tsouderos, “Arsenal of antibiotics not being restocked: Dispute over rules for approving new drugs stalls production even as concern rises over deadly resistant bacteria,” Chicago Tribune, August 6, 2010):

Drug companies are abandoning the antibacterial business, citing high development costs, low return on investment and, increasingly, a nearly decade-long stalemate with the Food and Drug Administration over how to bring new antibiotics to market.

Soon, doctors fear, we could be defenseless against bacteria that can resist all existing antibiotics, which would mean more victims like Simon, dead from a staph infection that drugs used to conquer easily.

Dr. Brad Spellberg, an expert on antibiotic resistance, called the situation “catastrophic.”

At the core of the problem is a regulatory impasse over whether drug companies seeking FDA approval for antibiotics should be required to run much more stringent clinical trials.

The FDA says yes, citing advances in the science of clinical trial design and a series of humiliations involving trials for drugs the agency had approved, including the antibiotic Ketek….

But the pharmaceutical industry and some infectious-disease doctors say the proposed rules will make it so difficult and expensive to gain approval for new antibiotics that the few remaining companies will abandon the field altogether….

At times the debate has been so heated that the acting chairman of an FDA committee opened a 2009 meeting by warning that he didn’t want to read the next day about police “having to arrest scientists for breaking shop windows and turning over cars.”…

For years, new antibiotics often were approved based on clinical trials that didn’t have to show the new drug was better than an old one. Instead it had to fall within an acceptable margin of efficacy, which meant it could test somewhat worse and still be considered a success.

Just how much worse is OK with the FDA lies at the heart of the debate. The FDA wants the margins for these “non-inferiority trials” to be scientifically justified, and that may result in margins much tighter than before.

Whatever legal considerations may lie behind the FDA’s position, from a medical point of view its planned rules are ridiculous. To be clinically valuable, new antibiotics don’t need to be better than existing ones, just different.  Against most diseases, combinations of antibiotics are the best therapy.  Striking at a bacterium by several independent mechanisms is highly effective at impairing its activity and helping the immune system defeat it.

The fact that bacteria evolve resistance makes the need for a steady stream of new antibiotics even more critical.

Adding to the problem is that it is not feasible to organize clinical trials large enough to evaluate efficacy:

But showing one antibiotic is superior to another is hard because many antibiotics work so well, Spellberg said….

Placebo trials, in which the drug is tested against a look-alike but useless pill or injection, are also unrealistic, according to some experts. It’s nearly impossible to persuade patients with a painful sinus infection to enroll in a study with a 50 percent chance of getting a sugar pill and not a drug, they said….

Some are suggesting that for community-acquired pneumonia, antibiotics trials might require as many as 10,000 patients at a cost of about $50,000 a patient, or $500 million.

The solution is simple. Antimicrobials should be evaluated for safety only. Doctors can work out efficacy quickly through clinical experience.

Dr. David Shlaes, who worked in pharmaceutical antibiotic development for decades and is now a consultant to the industry, said it is absurd to be, in effect, questioning if antibiotics work.

“This is like asking how do I know parachutes work?… Those of us in infectious disease, we are all scratching our heads wondering: What the hell they are talking about?” said Shlaes, whose book, “Antibiotics: The Perfect Storm,” will be published this fall. “It is like proving gravity all over again.”

Soon after reading this story I learned that our next door neighbor, a 62-year-old man in seemingly fine health, died over the weekend from an MRSA infection he contracted while in the hospital for a surgical procedure. The antibiotics that might have saved him were never developed, due to clinical trial requirements that are about to become even more onerous.

“Nobody can run those trials,” said Shlaes. “[FDA administrators] live in a different world. Their world is numbers and logic. It is not patients and life.”

Dr. Shlaes is exactly right. The bureaucrats are not concerned about patients and life. They are concerned about drugs embarrassing them, as Vioxx did.

Without effective antibiotics, the whole medical system falls apart, experts say.

Yes. But when it does, how many will realize that the FDA, and the politicians who wrote their governing legislation, are to blame?