New Human Study Confirms Potent Antidepressant Effects of SAMe

By David Hoffnung

Life Extension® introduced SAMe (S-adenosylmethinone) in 1997. Back then it was enormously popular in Europe, but unknown in the United States.

The National Institute of Mental Health decided to fund a double-blind, placebo-controlled trial that would evaluate SAMe as an additive therapy in those suffering major depression who were resistant to FDA-approved drugs.

Researchers at Harvard Medical School and Massachusetts General Hospital gave patients 800 mg of SAMe twice daily along with a selective serotonin reuptake inhibiting drug (SSRI).

Relative to placebo, patients who received the SAMe showed a 105% higher response rate and a 121% higher remission rate.1 Said differently, add-on therapy with SAMe in patients with drug-resistant depression produced double the response rate AND remission rate compared with placebo within a 6-week period.

This study was published in the August 2010 issue of the American Journal of Psychiatry.1 It was a follow-up to a 2004 pilot study that showed greater benefits when antidepressant drugs were combined with SAMe than when the same drugs were taken alone.2

For the past 13 years, SAMe has been on Life Extension’s TOP TEN list of the most important steps to take to ensure optimal longevity. SAMe has been recommended to aging individuals not to just feel better, but also to protect the brain, liver, joints, and other tissues of the body like no other substance.

This article reviews and updates the many studies documenting the anti-aging properties of SAMe.

A listing of all the drugs the FDA has approved to treat depression would fill several pages of this magazine. A major problem with these antidepressant drugs is that they fail a significant number of patients—up to 30%, by some accounts.3 In many cases, the drugs make depressed individuals feel worse, and FDA-mandated labeling now requires a warning that use of some antidepressants increases suicide risk—which is an incredible contradiction considering that suicide is a leading cause of death amongst depressives.

An equally disconcerting issue is the many side effects associated with antidepressant medications such as weight gain, constipation, dry mouth, and other symptoms that cause many depressives to stop using them.

There is thus an urgent need for a new approach to treating those who fail to respond to currently available antidepressant medications. Encouraging news from a recent study shows that the addition of S-adenosylmethinone (SAMe) to a serotonin reuptake inhibitor drug markedly improves the percentage of severe depressives who are relieved of their disorder.

Unlike synthetic prescription drugs that induce unintended side effects, SAMe is a naturally-occurring agent in the body that performs a multitude of beneficial functions, such as boosting glutathione levels in the brain and liver. The anti-aging properties of SAMe are so profound that non-depressives take it each day (in lower doses) just like they do their other dietary supplements.4,5

Antidepressants Don’t Work

As a team of Harvard researchers noted in a remarkable 2010 study published in the Journal of Clinical Psychiatry,6 “The majority of depressed patients will not experience remission when treated with a first-line antidepressant.”

In other words, antidepressants don’t really work for most patients. More is needed to help depression’s victims.

This is where SAMe comes in.

In modern high-tech imaging studies of healthy human brains, SAMe produces effects typical of several classes of antidepressant drugs7—but unlike those drugs, SAMe has remarkably few side effects and is well-tolerated even in elderly subjects.8

People with depression may exhibit a variety of biochemical imbalances, but the most common and best-known has to do with neurotransmitters like serotonin (involved in mood, sleep, appetite, and learning) and norepinephrine (involved in heart rate, blood pressure, and the fight-or-flight response). These chemical messengers belong to a class of molecules known as monoamines, and their synthesis in brain cells is largely controlled by the presence of folic acid, vitamin B12—and SAMe.9-12 When released into the space between brain cells (the synapse), monoamines exert stimulating or inhibiting effects on postsynaptic neurons.

With too little serotonin or norepinephrine available, the brain cannot sustain a positive mood—and depression results. Virtually all antidepressant drugs work to boost levels of these neurotransmitters within the synapse. And therein lie many of their limitations—and the causes of many of their side effects.13

SAMe operates through a completely different mechanism than these drugs. A molecule derived from the sulfur-containing amino acid methionine, SAMe is found in every living cell and plays a central role in cellular function.14,15 In addition to being required for monoamine synthesis, it also affects cell membrane fluidity, which may in turn influence how well a neuron transmits an electrical signal.16 Recent studies have shown that SAMe is also involved in the so-called “epigenetic” control of cellular function—the ability of cells to activate or suppress specific genes based on environmental influences—by its effects on proteins associated with chromosomes.17

These multi-targeted effects, coupled with an extraordinary safety profile, make SAMe a compelling treatment for a wide variety of brain disorders, from depression and cognitive decline to congenital metabolic dysfunction.18,19 SAMe crosses the blood-brain barrier, making it readily available to the brain and nervous system.10 This is vital: SAMe levels in the spinal fluid of depressed individuals have been shown to be significantly lower than those of healthy people.11

Animal models of depression shed additional light on how SAMe works in the brain. More than two decades ago Japanese scientists demonstrated a reduction in aggression in rats treated with SAMe as a result of its action in the central nervous system.20 By the turn of this century, researchers in Italy and Spain showed that SAMe reverses experimentally-induced depression in rats, at a rate faster than that of the prescription antidepressant imipramine, the first tricyclic antidepressant developed, and without apparent side effects.21,22 And in a remarkably detailed study, the Italian group showed that SAMe restored diminished brain levels of “polyamines,” essential brain molecules that are reduced in depressed patients.23

In 2007 a team of scientists at the University of Massachusetts launched a study using a combination of SAMe with N-acetyl cysteine (NAC) and acetyl-L-carnitine.24 Their subjects were aging mice with neurodegeneration similar to Alzheimer’s disease, in which depression is often a major manifestation. The combination rapidly enhanced cognitive function and prevented or reduced aggression in the animals, an effect that was rapidly reversed when the combination was withdrawn. The combination also prevented a decline in levels of the neurotransmitter acetylcholine, while contributing important antioxidant effects as well.

What You Need to Know: SAMe

• A landmark study funded by the National Institute of Mental Health revealed that the addition of S-adenosylmethionine or SAMe produces compelling results in people taking SSRIs, the majority of whom do not experience relief when taking the drug alone.
• SAMe is a naturally occurring molecule found in all living cells; it supports a host of chemical functions necessary for normal brain activity.
• SAMe acts by several distinct and independent mechanisms to target multiple sites of action in brain cells that are involved in producing depression.
• In clinical trials, SAMe has been shown to be at least as effective as prescription antidepressants, but with far fewer side effects.
• Because of its strong safety record, SAMe should be part of any regimen for brain health, particularly when depressive symptoms are present—and when prescription drugs alone don’t work.
• SAMe has also been shown to confer enormous benefits to the brain, liver, and joints, halting and even reversing various degenerative conditions, from osteoarthritis and neurodegeneration to nonalcoholic fatty liver disease.

Let’s turn now to the clinical realm and examine how well SAMe actually functions in humans suffering from depression.

SAMe Dramatically Improves Therapeutic Outcomes

Clinical trials have repeatedly demonstrated the benefits of SAMe in patients with major depression in a variety of populations: doses of 400-1,600 mg daily consistently resulted in rapid improvement in depressive symptoms and side effects that were mild and transient.25-27

SAMe is even effective in patients previously labeled “nonresponders” to conventional drug treatment.25 This led first to additional studies of SAMe compared with standard drugs rather than placebos, and later to studies in which SAMe was used in addition to such drugs.

SAMe consistently performs as well as or better than older-generation antidepressants such as imipramine and desipramine, drugs which are highly effective but have an unfavorable safety profile.28-30 In every case, the side effects of SAMe were trivial or mild. Interestingly, one such study found that regardless of whether patients received SAMe or the drug, their levels of SAMe in blood rose significantly as their depressive symptoms improved.28

Support for the Aging Brain

Experts have known for more than a decade that severely reduced brain levels of SAMe are directly linked to Alzheimer’s disease.1 More recent research reveals a direct correlation between levels of SAMe in the brain and Parkinson’s disease. In aging individuals stricken with Parkinson’s disease, parkinsonian symptoms (including increased levels of neurodegeneration) have been shown to be worse when SAMe levels are low, while cognitive function is markedly better when levels of SAMe are higher.2 At the core of SAMe’s ability to support brain function and neuronal health is its role in boosting levels of glutathione (GSH) and enhancing the antioxidant power of superoxide dismutase (SOD).3

Scientists have noted that these twin capabilities underscore SAMe’s importance as a neuroprotective compound, given the extraordinarily high metabolic activity and energy-intensive demands of both brain cells and neurons.3

References

1. Morrison LD, Smith DD, Kish SJ. Brain S-adenosylmethionine levels are severely decreased in Alzheimer’s disease. J Neurochem. 1996 Sep;67(3):1328-31.

2. Obeid R, Schadt A, Dillmann U, Kostopoulos P, Fassbender K, Herrmann W. Methylation status and neurodegenerative markers in Parkinson disease. Clin Chem. 2009 Oct;55(10):1852-60.

3. Cavallaro RA, Fuso A, Nicolia V, Scarpa S. S-adenosylmethionine prevents oxidative stress and modulates glutathione metabolism in TgCRND8 mice fed a B-vitamin deficient diet. J Alzheimers Dis. 2010;20(4):997-1002.

A study conducted in 1992 demonstrated the benefits of combining SAMe and imipramine for speeding the onset of the drug31—a critical benefit since almost all antidepressants take three or more weeks to manifest their effects, during which time patients often become discouraged and may discontinue treatment.

In 2004, a Harvard team of psychiatrists used SAMe in patients who were resistant to treatment with more modern drugs.2 In this open study design, the Harvard group provided 800-1,600 mg per day of SAMe orally to 30 patients who remained depressed despite adequate doses of their medications. Using even a highly conservative statistical analysis, they found that 50% of these previously resistant patients responded to treatment, with an impressive 43% experiencing complete remission of symptoms.2 These compelling results prompted the same Harvard group to design a larger study to more rigorously examine SAMe’s benefits in augmenting existing drug treatments.1,32

The outcome of this study was revelatory, creating a sensation within the scientific community. The group studied 73 patients who were “nonresponders” to standard treatment with selective serotonin reuptake inhibitor (SSRI) antidepressants. Subjects stayed on their SSRI for the entire 6-week study period, and took 800 mg of SAMe, or a placebo, twice daily. Their depressive symptoms were monitored using the standard Hamilton Depression Rating Scale. Thirty-six percent of the supplemented patients responded to treatment, and 26% experienced complete remission of their depression—patients who had not felt any difference with standard medications. The placebo recipients had a much worse response rate; just 18% felt a difference and a dismal 12% experienced complete remission.1

Arthritis Defense

A comprehensive 2002 SAMe study conducted by the US Department of Health and Human Services confirmed SAMe’s power not only to sustain mood, but also to optimize joint function.1 Clinical trials have shown reduced pain and stiffness in aging individuals stricken with osteoarthritis, while in vitro and animal studies have shown SAMe can stimulate the production of cartilage—a crucial factor in halting and reversing arthritis’s progression.2 Scientists have even found SAMe to be as effective as ibuprofen at reducing morning stiffness, pain at rest, pain during motion, swelling, “cracking” or “popping” sounds, and limited range of motion in arthritic joints.3

References

1. Available at: http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=erta64. Accessed September 22, 2010.

2. Hosea Blewett HJ. Exploring the mechanisms behind S-adenosylmethionine (SAMe) in the treatment of osteoarthritis. Crit Rev Food Sci Nutr. 2008 May;48(5):458-63.

3. Muller-Fassbender H. Double-blind clinical trial of S-adenosylmeth onine versus ibuprofen in the treatment of osteoarthritis. Am J Med. 1987 Nov 20;83(5A):81-3.

The lead author of the Harvard study, Dr. George Papakostas, noted “SAMe can be an effective, well-tolerated, and safe adjunctive treatment strategy for serotonin reuptake inhibitor nonresponders with major depressive disorder.”1

Summary

A landmark study funded by the National Institute of Mental Health revealed that the addition of S-adenosylmethionine or SAMe produces compelling results in major depression sufferers taking SSRIs, the majority of whom do not experience relief with prescription drugs alone. SAMe is a naturally occurring molecule found in all living cells, where it supports a host of chemical functions necessary for normal brain activity. It has been found to be safe at very high doses. Despite a wealth of data from the early 1990s, SAMe hadn’t found clinical acceptance until very recently, when new, rigorously controlled trials demonstrated its effectiveness in instances where drugs don’t work. Given SAMe’s impressive safety record, virtually anyone suffering from depressive symptoms should consider it, whether currently taking medication or not.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.

Optimal Liver Protection

SAMe’s extraordinary capacity to protect and enhance liver function has been well-documented in a wealth of studies. To take one dramatic example, blood alcohol levels among binge drinkers who ingest SAMe at the point of consumption have been shown to be significantly lower than controls.1 In 2010, researchers were able to determine why: SAMe boosts the liver’s alcohol elimination rate by increasing expression of genes within liver cells that are specifically involved in alcohol metabolism.1 Insufficient levels of SAMe have also been linked to a variety of liver diseases, including nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, both increasingly common disorders characterized by fat deposits in liver tissue that may progress to cirrhosis and full-blown liver failure.2,3 Scientists believe SAMe supplementation can prevent the onset and progression of these potentially fatal conditions.

References

1. Bardag-Gorce F, Oliva J, Wong W, et al. S-adenosylmethionine decreases the peak blood alcohol levels 3h after an acute bolus of ethanol by inducing alcohol metabolizing enzymes in the liver. Exp Mol Pathol. 2010 Sep 7.

2. Wortham M, He L, Gyamfi M, Copple BL, Wan YJ. The transition from fatty liver to NASH associates with SAMe depletion in db/db mice fed a methionine choline-deficient diet. Dig Dis Sci. 2008 Oct;53(10):2761-74.

3. Caballero F, Fernandez A, Matias N, et al. Specific contribution of methionine and choline in nutritional nonalcoholic steatohepatitis: impact on mitochondrial S-adenosyl-L-methionine and glutathione. J Biol Chem. 2010 Jun 11;285(24):18528-36.

Harvard Clinical Trials of SAMe

In a recent study published in the American Journal of Psychiatry, the results of a clinical trial conducted at Harvard Medical School and Massachusetts General Hospital were announced. The researchers found a significant benefit in male and female patients taking S-adenosylmethionine (SAMe) as an additive therapy to treat major depressive disorders.1

What made the findings of this study so remarkable is that this favorable response was observed in those who had already failed to respond to standard antidepressant drugs.1

This double-blind, randomized controlled trial to evaluate SAMe as an additive therapy against major depression in this drug-resistant population was funded by The National Institute of Mental Health.1

The trial is a follow-up to a smaller study in 2004 that found greater benefit when antidepressant drugs were combined with SAMe than when these drugs were used alone.2 In the current investigation, Harvard Medical School researchers assigned adult depressives taking serotonin reuptake inhibitor drugs (like Prozac®, Effexor®, Celexa®, Zoloft®, Paxil®, and Cymbalta®) to receive 800 mg SAMe or a placebo twice per day for six weeks. Those who received SAMe experienced a 36.1% response rate and a 25.8% remission rate, compared to a 17.6% and a 11.7% response and remission rate in the placebo group.1 This translates into a beneficial response and remission rate that was double for those receiving SAMe compared with placebo.

An accompanying editorial written by University of California-San Francisco professor of psychiatry J. Craig Nelson, MD stated that the Harvard findings are “persuasive” and that “SAMe offers a novel mechanism of treatment action and opens up a new area for future exploration.” 3

References

1. Papakostas GI, Mischoulon D, Shyu I, Alpert JE, Fava M. S-adenosyl methionine (SAMe) augmentation of serotonin reuptake inhibitors for antidepressant nonresponders with major depressive disorder: a double-blind, randomized clinical trial. Am J Psychiatry. 2010 Aug;167(8):942-8.

2. Alpert JE, Papakostas G, Mischoulon D, et al. S-adenosyl-L-methionine (SAMe) as an adjunct for resistant major depressive disorder: an open trial following partial or nonresponse to selective serotonin reuptake inhibitors or venlafaxine. J Clin Psychopharmacol. 2004 Dec;24(6):661-4.

3. Nelson JC. S-adenosyl methionine (SAMe) augmentation in major depressive disorder. Am J Psychiatry. 2010 Aug;167(8):889-91.

REFERENCES:

1. Papakostas GI, Mischoulon D, Shyu I, Alpert JE, Fava M. S-adenosyl methionine (SAMe) augmentation of serotonin reuptake inhibitors for antidepressant nonresponders with major depressive disorder: a double-blind, randomized clinical trial. Am J Psychiatry. 2010 Aug;167(8):942-8. 2. Alpert JE, Papakostas G, Mischoulon D, et al. S-adenosyl-L-methionine (SAMe) as an adjunct for resistant major depressive disorder: an open trial following partial or nonresponse to selective serotonin reuptake inhibitors or venlafaxine. J Clin Psychopharmacol. 2004 Dec;24(6):661-4. 3. Perovic B, Jovanovic M, Miljkovic B, Vezmar S. Getting the balance right: Established and emerging therapies for major depressive disorders. Neuropsychiatr Dis Treat. 2010 Sep 7;6:343-64. 4. Panza F, Frisardi V, Capurso C, et al. Polyunsaturated fatty acid and S-adenosylmethionine supplementation in predementia syndromes and Alzheimer’s disease: a review. ScientificWorldJournal. 2009 May 22;9:373-89. 5. Gregory PJ, Sperry M, Wilson AF. Dietary supplements for osteoarthritis. Am Fam Physician. 2008 Jan 15;77(2):177-84. 6. Fava M. Switching treatments for complicated depression. J Clin Psychiatry. 2010 Feb;71(2):e04. 7. Saletu B, Anderer P, Di Padova C, Assandri A, Saletu-Zyhlarz GM. Electrophysiological neuroimaging of the central effects of S-adenosyl-L-methionine by mapping of electroencephalograms and event-related potentials and low-resolution brain electromagnetic tomography. Am J Clin Nutr. 2002 Nov;76(5):1162S-71S. 8. Saletu B, Anderer P, Linzmayer L, et al. Pharmacodynamic studies on the central mode of action of S-adenosyl-L-methionine (SAMe) infusions in elderly subjects, utilizing EEG mapping and psychometry. J Neural Transm. 2002 Dec;109(12):1505-26. 9. Miller AL. The methylation, neurotransmitter, and antioxidant connections between folate and depression. Altern Med Rev. 2008 Sep;13(3):216-26. 10. Carney MW, Toone BK, Reynolds EH. S-adenosylmethionine and affective disorder. Am J Med. 1987 Nov 20;83(5A):104-6. 11. Bottiglieri T, Laundy M, Crellin R, Toone BK, Carney MW, Reynolds EH. Homocysteine, folate, methylation, and monoamine metabolism in depression. J Neurol Neurosurg Psychiatry. 2000 Aug;69(2):228-32. 12. Herrmann W, Obeid R. Biomarkers of folate and vitamin B(12) status in cerebrospinal fluid. Clin Chem Lab Med. 2007;45(12):1614-20. 13. Racagni G, Popoli M. The pharmacological properties of antidepressants. Int Clin Psychopharmacol. 2010 May;25(3):117-31. 14. Bottiglieri T. S-Adenosyl-L-methionine (SAMe): from the bench to the bedside--molecular basis of a pleiotrophic molecule. Am J Clin Nutr. 2002 Nov;76(5):1151S-7S. 15. Scott JM, Molloy AM, Kennedy DG, Kennedy S, Weir DG. Effects of the disruption of transmethylation in the central nervous system: an animal model. Acta Neurol Scand Suppl. 1994;154:27-31. 16. Baldessarini RJ. Neuropharmacology of S-adenosyl-L-methionine. Am J Med. 1987 Nov 20;83(5A):95-103. 17. McGowan PO, Kato T. Epigenetics in mood disorders. Environ Health Prev Med. 2008 Jan;13(1):16-24. 18. Bottiglieri T, Hyland K, Reynolds EH. The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. Drugs. 1994 Aug;48(2):137-52. 19. Paul RT, McDonnell AP, Kelly CB. Folic acid: neurochemistry, metabolism and relationship to depression. Hum Psychopharmacol. 2004 Oct;19(7):477-88. 20. Yamamoto T, Yatsugi S, Ohno M, Ueki S. Inhibition of mouse-killing behavior by S-adenosyl-L-methionine in midbrain raphe-lesioned and olfactory-bulbectomized rats. Pharmacol Biochem Behav. 1989 Oct;34(2):395-8. 21. Benelli A, Filaferro M, Bertolini A, Genedani S. Influence of S-adenosyl-L-methionine on chronic mild stress-induced anhedonia in castrated rats. Br J Pharmacol. 1999 Jun;127(3):645-54. 22. Bellido I, Gomez-Luque A, Plaza A, Rius F, Ortiz P, Sanchez de la Cuesta F. S-adenosyl-L-methionine prevents 5-HT(1A) receptors up-regulation induced by acute imipramine in the frontal cortex of the rat. Neurosci Lett. 2002 Mar 15;321(1-2):110-4. 23. Genedani S, Saltini S, Benelli A, Filaferro M, Bertolini A. Influence of SAMe on the modifications of brain polyamine levels in an animal model of depression. Neuroreport. 2001 Dec 21;12(18):3939-42. 24. Chan A, Shea TB. Effects of dietary supplementation with N-acetyl cysteine, acetyl-L-carnitine and S-adenosyl methionine on cognitive performance and aggression in normal mice and mice expressing human ApoE4. Neuromolecular Med. 2007;9(3):264-9. 25. Rosenbaum JF, Fava M, Falk WE, et al. The antidepressant potential of oral S-adenosyl-l-methionine. Acta Psychiatr Scand. 1990 May;81(5):432-6. 26. Salmaggi P, Bressa GM, Nicchia G, Coniglio M, La Greca P, Le Grazie C. Double-blind, placebo-controlled study of S-adenosyl-L-methionine in depressed postmenopausal women. Psychother Psychosom. 1993;59(1):34-40. 27. Fava M, Giannelli A, Rapisarda V, Patralia A, Guaraldi GP. Rapidity of onset of the antidepressant effect of parenteral S-adenosyl-L-methionine. Psychiatry Res. 1995 Apr 28;56(3):295-7. 28. Bell KM, Potkin SG, Carreon D, Plon L. S-adenosylmethionine blood levels in major depression: changes with drug treatment. Acta Neurol Scand Suppl. 1994;154:15-8. 29. Delle Chiaie R, Pancheri P, Scapicchio P. Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies. Am J Clin Nutr. 2002 Nov;76(5):1172S-6S. 30. Pancheri P, Scapicchio P, Chiaie RD. A double-blind, randomized parallel-group, efficacy and safety study of intramuscular S-adenosyl-L-methionine 1,4-butanedisulphonate (SAMe) versus imipramine in patients with major depressive disorder. Int J Neuropsychopharmacol. 2002 Dec;5(4):287-94. 31. Berlanga C, Ortega-Soto HA, Ontiveros M, Senties H. Efficacy of S-adenosyl-L-methionine in speeding the onset of action of imipramine. Psychiatry Res. 1992 Dec;44(3):257-62. 32. Papakostas GI. Evidence for S-adenosyl-L-methionine (SAM-e) for the treatment of major depressive disorder. J Clin Psychiatry. 2009;70 Suppl 5:18-22

Don’t worry too much about radiation from airport X-ray screening

Due to media headlines, we at Life Extension® have been inundated by calls from members who are worried about the risks of the radiation emitted from new airport X-ray screening devices.

No organization has been more vocal about avoiding unnecessary exposure to radiation than Life Extension. We have long warned members to say NO to unnecessary X-rays and especially certain types of CT or CAT scans that can poison the body with the equivalent radiation of more than 400 regular chest X-rays.

Radiation exposure not only increases the risk of certain cancers, but also damages endothelial DNA, thus accelerating pathological atherosclerotic processes. When it comes to radiation exposure, there is no safe dose.

As far as the amount of radiation emitted from the new airport screening devices, however, the amount is so trivial that you probably should not worry about it. As you will read below, we are exposed to far more radiation as part of ordinary living — which is why it is so important to protect our precious DNA with antioxidants such as resveratrol, N-acetyl cysteine, green tea and others each day.

Here is a brief summary on the radiation emitted by X-ray airport security screening systems:

1. Naturally occurring ionizing radiation is all around us. We are continuously exposed to this background radiation during ordinary living. In 42 minutes of ordinary living, a person receives more radiation from naturally occurring sources than from screening with any general-use X-ray security system.
   
   
2. A full-body X-ray security system delivers less than the dose (of ionizing radiation) a person receives during 4 minutes of airline flight. The TSA has set the dose limit to ensure a person receives less radiation from one scan with a TSA general-use X-ray security system than from 2 minutes of airline flight.
   
   
3. Compared with a conventional CT scan, the dose of radiation generated by the airport screening system is very low. "A passenger would need to be scanned using a backscatter scanner, from both the front and the back, about 200,000 times to receive the amount of radiation equal to one typical CT scan," said Dr. Andrew J. Einstein, director of cardiac CT research at Columbia University Medical Center in New York City. "Another way to look at this is that if you were scanned with a backscatter scanner every day of your life, you would still only receive a tenth of the dose of a typical CT scan," he said. By comparison, the amount of radiation from a backscatter scanner is equivalent to about 10 minutes of natural background radiation in the United States, Einstein said. "I believe that the general public has nothing to worry about in terms of the radiation from airline scanning," he added. For moms-to-be, no evidence supports an increased risk of miscarriage or fetal abnormalities from these scanners, Einstein added. "A pregnant woman will receive much more radiation from cosmic rays she is exposed to while flying than from passing through a scanner in the airport."

Having said all the above, when I travel this Thanksgiving weekend, I will insist on an intrusive physical pat down as opposed to the X-ray scanners. The public has been deceived so many times by the makers of radiation equipment that I simply don’t trust their numbers. It also gives me the opportunity to educate other human beings (in this case, perfect strangers) that there is no safe dose of radiation that one should intentionally expose oneself to.

For longer life,

William Faloon

References:
http://www.fda.gov/Radiation-EmittingProducts/RadiationEmittingProductsandProcedures/SecuritySystems/ucm227201.htm
http://www.businessweek.com/lifestyle/content/healthday/634724.html
http://www.lef.org/magazine/mag2010/aug2010_Lethal-Danger-of-CT-Scans_01.htm

Inflammation and the aging brain

Inflammation and the aging brain
By Dale Kiefer

Inflammation is now thought to play a role in pathological conditions ranging from anemia and allergy to coronary heart disease, psoriasis and even stroke. From inflamed gums that may contribute to cardiovascular disease, to playing a crucial role in fanning the flames of cancer cell growth, inflammation has been implicated in many more diseases than was previously believed.

Recently, inflammation has also been recognized as playing a central role in the debilitating cognitive decline that characterizes neurological disorders such as Alzheimer’s disease and vascular dementia. Although mental decline and memory loss have long been considered inevitable hallmarks of old age, new research suggests that such inflammation/age-associated decline is avoidable. Indeed, findings reported by some scientists suggest that early intervention in low-grade inflammation may offer some protection against these dreaded brain diseases.

The many guises of inflammation
Inflammation is as familiar as an overworked muscle, and as common as your latest sunburn. Parents who have agonized over a child’s escalating fever know that inflammation occasionally transcends the merely annoying to become something far more troubling: Fever that climbs too high for too long can inflict serious, even life-threatening, damage.

But inflammation, including fever, serves a useful purpose in the body. Even sunburn is a result of the body’s attempt to repair damage inflicted by ultraviolet radiation. In fact, inflammation is an ingenious adaptation that allows the body to defend against clear and present dangers.

For instance, when virulent bacteria invade, they thrive precisely at the body’s normal temperature of 98.6 ºF (37 ºC). Once established, they pour toxins into the bloodstream, while continuing to proliferate exponentially. The immune system mounts a defense, but cellular defenders may be thwarted or simply overwhelmed. In response, the body turns up the furnace. Sensitive to the slightest temperature increases, pathogens perish. The body wins the battle. Fever breaks and all is well.

This is just one example of inflammation’s beneficial nature. But some inflammation goes too far. Fever doesn’t always vanquish the invading horde and fade back to a state of disease-free normalcy. Occasionally the cost of battle is too dear and fever damages the very body it is defending. Autoimmune diseases provide another example of inflammation gone awry. The immune system targets the body’s own tissues by its inability to differentiate between some of the body’s proteins and foreign invaders. In essence, the immune system wages war, against itself. Diseases such as rheumatoid arthritis and lupus erythematosus are the result. Clearly, inflammation can be a double-edged sword.

News from the hot zone
The inflammation of most concern, however, generally goes unnoticed. It is this low-grade chronic inflammation (as opposed to the acute, intense inflammation associated with a healing wound, for instance) that is believed to underlie the most serious neurodegenerative diseases. Huntington’s disease, for example, is characterized by chronic brain inflammation caused by the immune system’s misguided attempts to eliminate a defective protein that results from a genetic defect. And although their inflammation triggers are different, diseases such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease, or ALS) and even multiple sclerosis, are also characterized by chronic inflammation of neural tissues.

Regarding Alzheimer’s disease, one research team noted, “Inflammation is becoming increasingly substantiated as a contributor to Alzheimer’s disease pathogenesis”1 For this reason anti-inflammatory drugs, such as the non-steroidal anti-inflammatory drugs (NSAIDs, e.g. aspirin, ibuprofen and acetaminophen) and the newer COX-2-inhibitor class of prescription drugs, are under investigation as therapies for this and other inflammation-related diseases.

Inflammation and the brain
To better understand inflammation’s role in disease, it’s helpful to comprehend its more benevolent role in keeping the body healthy. Inflammation is the body’s response to a perceived threat. In the case of an invasion by bacteria, the immune system correctly identifies the unwelcome entity and attempts to neutralize it. This involves a complex chain of events and may require the cooperation of a variety of specialized cells. Their activity is generally beneficial, but the goal is always the same: to rid the body of intruders and to dispose of damaged tissue so healing may take place.

Throughout most of the body, cells known as macrophages act as living soldiers, searching for invaders, and then engulfing and neutralizing them. In the brain, supporting cells of the glial family, known as microglial cells, act as scavengers, in much the same fashion as macrophages. They engulf and eliminate dead neurons that have been damaged by injury or illness. Unfortunately, they also secrete harmful neurotoxins and toxic oxygen free radicals in an attempt to neutralize foreign or undesirable substances.2

Regrettably, the inflammatory response is occasionally worse than the stimulus that triggered it in thefirst place. Even when the original trigger is eliminated, inflammation may become self-perpetuating. Such, apparently, is the case in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, ALS and multiple sclerosis, which are characterized by a great deal of microglial activity. The presence of activated microglial cells is an indicator of chronic inflammation.3,4

Alzheimer’s and inflammation
Much remains to be elucidated regarding the onset and progression of Alzheimer’s disease, but it seems clear that an inflammation-provoking protein fragment, a peptide known as amyloid-B, triggers inflammation. Uninterrupted, the inflammation gradually accelerates, killing nerve cells and causing a drastic decline in levels of a vital brain chemical, the neurotransmitter acetylcholine. This downward spiral of neural degeneration commences with the induction of nearly undetectable inflammation, progresses to the erosion of memory, concentration and learning ability and ends with death. Upon demise, Alzheimer’s patients display abnormal spaghetti-like neuritic amyloid-B plaques and neurofibrillary tangles. Like a battleground littered with the remains of the combatants, these damaging plaques are associated with reactive microglial cells, and consist of amyloid-B protein fragments, immune system proteins such as interleukin-6 (IL-6)and other components indicating long-term, and ultimately counterproductive, inflammation.5

Microglial cells, which accompany the neuritic plaques of Alzheimer’s disease, are normally dormant. They are activated only in response to inflammation, thus their presence is a sure sign of brain inflammation. Although present in large numbers in the brains of patients with degenerative neurological diseases, such as Huntington’s6 and Alzheimer’s diseases, their numbers are also elevated in otherwise healthy elderly individuals. This implies that a certain degree of neuroinflammation is an ordinary result of nothing more than advanced age.2 Indeed, some scientists have suggested that cognitive decline begins early in the aging process and is an inevitable result of advancing age.7 Controlling inflammation, therefore, could presumably benefit anyone interested in preventing eventual memory loss and cognitive decline.

Dual pathways to inflammation
Just in the last decade, scientists discovered a key enzyme produced by the body in response to inflammatory provocations: cyclooxygenase-2 (better known as COX-2). COX-2 has been identified as an important link in the inflammation cascade. Unlike COX-1, COX-2 is only present in the body during inflammation Research has revealed that cells convert cell membrane phospholipids to arachidonic acid, which serves as a substrate that gives rise, in turn, to two powerful and potentially damaging classes of inflammation mediators, known as eicosanoids: the prostaglandins and leukotrienes. As one researcher noted, “Arachidonic acid release and production of eicosanoids are prerequisites for inflammation”1 The eicosanoids are synthesized from arachidonic acid by the action of two enzymes that form the crux of dual inflammatory pathways: cyclooxygenase (COX) and lipooxygenase (5-LOX).

The COX proteins take two forms: COX-1 and COX-2. The actions of COX-1 are generally beneficial. But the activity of COX-2 is generally harmful. COX-2 inserts an oxygen molecule into arachidonic acid to synthesize prostaglandins, which are powerful triggers of pain and inflammation. 5-LOX converts arachidonic acid into inflammatory leukotrienes.

NSAID medications treat inflammation by blocking the activity of both the COX-2 enzyme and its more benevolent sibling, COX-1. But COX-1 is necessary for stomach lining protection; so interfering with COX-1’s activity can cause gastric disturbances ranging from simple discomfort to dangerous bleeding ulcers. For this reason the new COX-2-inhibitor class of prescription drugs (e.g. Celebrex and Vioxx) has rocketed to popularity. Their more selective action effectively relieves inflammation while minimizing the distressing side effects that are possible with chronic use of NSAIDs.

Researchers are investigating the possibility that anti-inflammatory agents, such as the COX-2 inhibitors, may provide viable therapy not only for Huntington’s, but also for other neuro-degenerative diseases such as Alzheimer’s and Parkinson’s disease. It’s well documented that the COX pathway generates inflammatory prostaglandins. But medical research has largely ignored the potentially damaging effects of 5-LOX, the enzyme that forms the second branch of the dual arachidonic acid inflammation pathways. As a recent study reported, 5-LOX might play a significant role in the pathobiology of aging-associated neuro-degenerative diseases.8

5-LOX generates inflammatory leukotrienes, which are known to be potent inflammatory mediators that play a role in allergic reactions. They may also play a role in ischemia and atherosclerosis.9 Stroke, traumatic brain injury and Alzheimer’s disease have also been linked to the activity of 5-LOX and leukotrienes.2 The results of a recent study indicate that blocking COX-2 while ignoring the effects of 5-LOX may be counter-productive. In fact, using COX-2 inhibitors to block the activity of COX-2 may actually cause 5-LOX levels to increase further, making inflammation worse, rather than better.2 This “rebound” inflammation is evidently caused by shifting arachidonic acid toward synthesis of damaging leukotrienes through the 5-LOX pathway.

An obvious solution to this problem would be the addition of a drug to the anti-inflammatory regimen that can block 5-LOX. Fortunately, such substances exist, although they have only recently come under scrutiny as complements to far more heavily researched NSAIDs and COX-2 inhibitors.

In one 5-LOX inhibition study, researchers speculated, ‘Inhibitors of the two pathways might have additive, or even synergistic neuroprotective effects when used in combination.’ By study’s end, they had concluded that a 5-LOX inhibitor “significantly potentiated the effects of three different COX inhibitors.”2 Their findings suggest, quite simply, that while anti-inflammatory therapy with COX-inhibitors may be neuroprotective, therapy combining both COX and 5-LOX inhibitors should prove considerably more effective.

The promise of anti-inflammatory therapy
The feedback loops in the brain do not allow for simplistic approaches to the treatment of multi-factorial diseases. Not surprisingly, a recent study in the Journal of the American Medical Association found that COX-2 inhibition alone was ineffective in slowing the progression of clinically diagnosed Alzheimer’s disease. It is likely that these results reinforce a growing body of research that dual inflammatory pathway inhibition may be needed to fully realize the promise of anti-inflammatory therapy. While anti-inflammatory therapy may slow progression of some diseases, it may be necessary to begin taking anti-inflammatory agents long before symptoms appear, in order to prevent or reverse the ravages of neurodegenerative diseases.

REFERENCES:

1. Paris D, et al. AB vasoactivity: an inflammatory reaction. Ann N Y Acad Sci (no date provided) pp.97-108.

2. Klegeris A et al. Cyclooxygenase and 5 lipooxygenase inhibitors protect against mononuclear phagocyte neurotoxicity. Neurobiol of Aging 2002 (23) 787-794.

3. Teismann P, et al. Cyclooxygenase-2 is instrumental in Parkinson’s disease neurodegeneration. PNAS 2003; 100 (9):5473-5478.

4. Pompl PN, et al. A therapeutic role for cyclooxygenase-2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis. FASEB J. 2003; 10.1096/fj.02- 0876fje

5. Scali C, et al. The selective cyclooxygenase-2 inhibitor rofecoxib suppresses brain inflammation and protects cholinergic neurons from excitotoxic degeneration in vivo. Neuroscience 2003; 117:909-919.

6. Sapp et al., Early and progressive accumulation of reactive microglial in the Huntington Disease Brain. Neuropathol Exp Neurol 2001; 60(2): 161-172.

7. Jorm AF, et al. The prevalence of dementia: a quantitative integration of the literature. Acta Psychiatr Scand 1987; 76: 465-479.

8. Uz T, et al. Aging-associated up-regulation of neuronal 5- lipoxygenase expression: putative role in neuronal vulnerability. FASEB 1998; 12: 439-449.

9. Spanbroek R et al. Expanding expression of the 5-lipoxygenase pathway within the arterial wall during human atherogenesis. PNAS 2003; 100:12381243.

Mucus is a sure sign of a body in a state of extreme agitation.

Mucus Clearing Diet

Excerpt from NORTH AMERICAN DIET

Bug the body enough, and it’s going to react. The cold virus is a great example of a body being bugged and, boy, do you know it. Sore throat, puffy eyes, and loads and loads of you know what! Mucus is a sure sign of a body in a state of extreme agitation. The heavy, over-processed, dairy-rich makeup of the North American diet demands the human body to react as if it is fighting a viral invasion every day. In the morning we can feel its effect, foggy clogged head, puffy eyes and dulled senses. The answer, a large mug of strong coffee to kick-start the system so that we can face the rigors of the day. Most of us have forgotten what it is like to awaken, clear-minded and full of energy. Yet, within two weeks, of a changed diet, the transformation can be quite remarkable, jumping out of bed in celebration of the new day; a throwback to a younger, healthier you. The human body is an incredibly, complex system. It transfers vital fluids through miles of tubes and membrane highways. The circulatory system is 60,000 miles long. You would need a truck load of road maps to travel a small portion of your body. The kidneys, alone, contain 500 miles of internal plumbing. Each time you breathe, 300 billion—yes billion—capillaries in the lungs await to absorb life-giving oxygen. However, mucus can slow down or stop the important movements along the many pathways of the body, creating a feeding ground for viruses and pathogens (disease-producing bacteria). Let’s look at an antibody soap opera. Antibody X must seek and demolish Microbe Z, a bacterial bad guy, responsible for an irritating cold. The body is tracking his position, Agent X has been assigned to a search-and-destroy mission to intercept Microbe Z before he does greater damage to the host. On his way through the lymph, he finds himself in a traffic jam, an underpass full of mucus. In this vulnerable position, Agent X is a sitting duck. From above, he is ambushed by two million bacterial bad guys who have been feasting on the mucus for days. The last thought in Agent X’s mind before he dies is, in spite of his perfect conditioning and training, nothing had prepared him to deal with the obstruction of thick, sticky mucus. Finally, after the host had suffered for days with a raw throat, coughing, sneezing, reinforcements were able to destroy the bacterial bad guys. Not all mucus is bad. Healthy mucus is a clear, slippery, lubricating secretion, used to protect mucus membranes along the digestive, respiratory, urinary and reproductive tracts. Unhealthy mucus is cloudy, thick, and sticky. Mucus is secreted to stop irritants, pollutants, or carcinogenic compounds, created by putrefying, undigested food residues. It’s like a blanket of protection. Certain foods such as milk and bread cause an increase of mucus secretions. These foods have large protein molecules (casein and gluten) which are difficult to digest and are more prone to putrefaction, and may be toxic or an irritant to the body. For many, bread and milk cause sinus congestion. Mucoid is a mixture of large gelatinous particles, which has a sticky or jelly-like consistency. The word mucoid encompasses the terms mucin, colloid, mucoproteins and glycoproteins. Mucoid is caused by many toxins, pollutants, food additives and allergies. Mucoid can be present in any body tissue but is most commonly associated with the respiratory system, gastrointestinal tract, lymphatic system, uterus, vagina urinary system and the joints. Cartilage in a joint contains mucus membrane cells which secrete a clear slippery mucus to keep joints lubricated. When mucoid-forming substances are present, toxic mucoid builds up deposits within the joint. Mucoid within the body tissues, drains into the lymph which filters waste from the intercellular fluid. The blood absorbs 90% of this cellular waste fluid and the lymph absorbs the other 10% composed of the larger waste particles. The lymph glands contain one-way valves, lined with muscle tissues that behave like pumps. If an overload of mucoid from the cells accumulates in the lymph and is not cleansed from the system, it can become stagnant and prone to infection. Dr. Robert Gray, a nutritionist, determined, through intensive testing that certain foods are mucus-forming and others are mucus cleansing. The foods shown to cause mucus are dairy products, white flour, meat, eggs, potatoes, beans, rice, grains, fish, peanuts and fats. MAKING CELL FOOD FROM CELLS The relationship between mucus and diet is not a new theory. In 1912, Dr. Arnold Ehret released a book called, The Mucusless Diet and Healing System. He discusses in great detail, the mucus-forming effect of various foods. Ehret theorized that all disease is caused by a clogging of the tube and membrane structures within the body due to a build-up of restrictive mucus. The process of digestion is to liquefy food small enough to be infused by the absorptive cells on the villus in the intestine. For any nutrient to pass through the membrane of a cell, it must be less than 44,000,000,000 th. of an ounce. The rest of the substance not absorbed remains within the colon until elimination. Foods that form mucus have a glue-like bond, tightly holding their molecules together. In milk, it is casein, in wheat, rye, oats and barley, the glue-like substance is gluten. The dictionary defines gluten as a tough, sticky mixture of plant proteins, obtained by washing out the starch from wheat or other cereal flour and used as an adhesive and thickener. These glue-like bonds require strong stomach acids for digestion. Lack of chewing and poor food combinations make it impossible for the stomach acids to properly dissolve the bond between these molecules. After digestion, many food particles are still too large to be used by the body. In a short time, the oversized, partly-digested food particles start to putrefy and are coated with mucus to prevent further putrefaction while still in the intestine. The intestinal wall is contains over four million microvillus. Their job is the absorption of nutrients. Due to the vast number of microvilli the total effective area for absorption, within the colon is more than 2,200 square feet. On the surface of these microvillus is mucus-secreting cells. Mucus is secreted by these cells to protect the intestinal wall and to impede the absorption of harmful substances through the colon. Eighty percent of all absorption takes place in the small intestine. Only 20 percent is absorbed by the stomach and large intestine. The stomach performs very little absorption because the gastric contents are so acidic. The entire gastric epithelium must be devoted to mucus production. Without mucus to protect the stomach, ulcers would develop in a few hours. Within the duodenum (small intestine) the submucosal glands produce copious quantities of mucus. This mucus contains buffers that elevate the pH balance. The more acid forming the food, the greater the amount of mucus secreted. As the mucus and food particle solution pass through the intestines, moisture is removed. As more moisture is removed, the mucus becomes sticky and gluey. In passing, it leaves a coating on the intestinal wall. Layer after layer of gluey feces build up over the years. It forms into a tough, rubbery, black substance found in lumps in the corners of the intestinal tract. X-ray studies show that the accumulation of hardened feces badly deforms the intestines. Autopsies have shown that an average male has seven to nine pounds of this hardened feces within his intestine. This coating causes constipation, a reduction in the absorption of nutrients through the intestinal wall and is a breeding ground for parasites. Imagine a drain, clogged with human hair, dust, old soap and pieces of decaying food, all forming a sticky mass of rotting waste that cannot be removed. The medical names labeled for these diseases are diverticula, colitis, stricture, prolapsus, hemorrhoids, worms, yeast infection, chronic constipation, colon cancer and appendicitis. Colonics are given by naturopaths or colon therapists using a device to circulate water through the intestine while your stomach is being massaged. Numerous clients have been helped through this therapy. Removal of clogged waste allows the human machine to work again. But, unless there is dietary change, the symptoms will simply return. Without the natural, sponge-like properties of fruits and vegetables, intestinal diseases will continue to abound, especially amongst the elderly. Grapes and citrus fruits are some of the greatest mucus-cleansers. They help the body to remove mucus and toxins, supplying vital nutrients in the correct balance for rejuvenation and healing. The most powerful method of removing mucus from the intestines and mucoid from the organs and lymph glands is the combined cleansing effect of a non-mucus/mucoid-forming diet and fasting. Factors Which Increase Mucus LARGE MEALS. Our body's need for food is often much less than what we eat. Any foods eaten beyond our body's need is a burden. Some of this excess food will be converted into fat. Yet the body can create only so much fat per day. If you eat above digestive capacity, the excess must be eliminated. During elimination, the lymph glands are overloaded and mucoid forms in response to putrefaction. EATING WITHOUT HUNGER. When food is eaten before complete digestion of the previous meal, partially-digested food will be released into the colon thus causing mucus. GULPING FOOD. Improper chewing overworks the digestive system. If the food particles are too big to be assimilated, they must be eliminated through the colon. On the way, these particles putrefy, thus causing mucus. IMPROPER COMBINATIONS. A typical meal contains starch, protein, sugars and fats, each requiring a completely, different digestive secretion. Complex food mixtures create mucus because the food molecules cannot be dissolved efficiently.

Mucus Producing Foods While there are numerous anecdotal reports that insist milk or other dairy products increase the production of mucus, the Australian Dairy Research Council conducted a study in the early 1990s that determined milk consumption did not, in fact, contribute to excess mucus production. In fact, no foods directly produce mucus. However, mucus levels can increase as a result of allergic reactions to foods. Dairy Products There is a widespread misconception that milk can actually increase the production of mucus. However, according to a physician at the National Jewish Medical and Research Center, high-fat dairy, particularly milk, will only thicken the mucus that you already have. This may explain many people's belief that when they consume milk, their mucus output rises. Allergens Allergies can contribute to inflammation, which can cause sinusitis. One of the symptoms of sinusitis is an increase in mucus production. A common allergen for many people is food. Food allergens can come from a wide variety of products, including wheat-based food, dairy, berries, items containing gluten and many more. Sugar Sugar, and sugary drinks, can act as a diuretic, which means it boosts the removal of water from the body. Dehydration, or simply lack of water, tends to thicken mucus secretions in the throat.

Thousands of Americans died from H1N1 after receiving vaccine shots

Thousands of Americans died from H1N1 even after receiving vaccine shots

Sunday, January 17, 2010
by Mike Adams, the Health Ranger


(NaturalNews) The CDC is engaged in a very clever, statistically devious spin campaign, and nearly every journalist in the mainstream media has fallen for its ploy. No one has yet reported what I'm about to reveal here.

It all started with the CDC's recent release of new statistics about swine flu fatalities, infection rates and vaccination rates. According to the CDC:

• 61 million Americans were vaccinated against swine flu (about 20% of the U.S. population). The CDC calls this a "success" even though it means 4 out of 5 people rejected the vaccines.

• 55 million people "became ill" from swine flu infections.

• 246,000 Americans were hospitalized due to swine flu infections.

• 11,160 Americans died from the swine flu.

Base on these statistics, the CDC is now desperately urging people to get vaccinated because they claim the pandemic might come back and vaccines are the best defense.

But here's the part you're NOT being told.

The CDC statistics lie by omission. They do not reveal the single most important piece of information about H1N1 vaccines: How many of the people who died from the swine flu had already been vaccinated?

Many who died had already been vaccinated

The CDC is intentionally not tracking how many of the dead were previously vaccinated. They want you (and mainstream media journalists) to mistakenly believe that ZERO deaths occurred in those who were vaccinated. But this is blatantly false. Being vaccinated against H1N1 swine flu offers absolutely no reduction in mortality from swine flu infections.

And that means roughly 20% of the 11,160 Americans who died from the swine flu were probably already vaccinated against swine flu. That comes to around 2,200 deaths in people who were vaccinated!

How do I know that swine flu vaccines don't reduce infection mortality? Because I've looked through all the randomized, double-blind, placebo-controlled clinical trials that have ever been conducted on H1N1 vaccines. It didn't take me very long, because the number of such clinical trials is ZERO.

That's right: There is not a single shred of evidence in existence today that scientifically supports the myth that H1N1 vaccines reduce mortality from H1N1 infections. The best evidence I can find on vaccines that target seasonal flu indicates a maximum mortality reduction effect of somewhere around 1% of those who are vaccinated. The other 99% have the same mortality rate as people who were not vaccinated.

So let's give the recent H1N1 vaccines the benefit of the doubt and let's imagine that they work just as well as other flu vaccines. That means they would reduce the mortality rate by 1%. So out of the 2,200 deaths that took place in 2009 in people who were already vaccinated, the vaccine potentially may have saved 22 people.

61 million injections add up to bad public health policy

So let's see: 61 million people are injected with a potentially dangerous vaccine, and the actual number "saved" from the pandemic is conceivably just 22. Meanwhile, the number of people harmed by the vaccine is almost certainly much, much higher than 22. These vaccines contain nervous system disruptors and inflammatory chemicals that can cause serious health problems. Some of those problems won't be evident for years to come... future Alzheimer's victims, for example, will almost certainly those who received regular vaccines, I predict.

Injecting 61 million people with a chemical that threatens the nervous system in order to avoid 22 deaths -- and that's the best case! -- is an idiotic public health stance. America would have been better off doing nothing rather than hyping up a pandemic in order to sell more vaccines to people who don't need them.

Better yet, what the USA could have done that would have been more effective is handing out bottles of Vitamin D to 61 million people. At no more cost than the vaccines, the bottles of vitamin D supplements would have saved thousands of lives and offered tremendously importantly additional benefits such as preventing cancer and depression, too.

The one question the CDC does not want you to ask

Through its release of misleading statistics, the CDC wants everyone to believe that all of the people who died from H1N1 never received the H1N1 vaccine. That's the implied mythology behind the release of their statistics. And yet they never come right out and say it, do they? They never say, "None of these deaths occurred in patients who had been vaccinated against H1N1."

They can't say that because it's simply not true. It would be a lie. And if that lie were exposed, people might begin to ask questions like, "Well gee, if some of the people who were killed by the swine flu were already vaccinated against swine flu, then doesn't that mean the vaccine doesn't protect us from dying?"

That's the number one question that the CDC absolutely, positively does not want people to start asking.

So they just gloss over the point and imply that vaccines offer absolute protection against H1N1 infections. But even the CDC's own scientists know that's complete bunk. Outright quackery. No vaccine is 100% effective. In fact, when it comes to influenza, no vaccine is even 10% effective at reducing mortality. There's not even a vaccine that's 5% effective. And there's never been a single shred of credible scientific information that says a flu vaccine is even 1% effective.

So how effective are these vaccines, really? There are a couple thousand vaccinated dead people whose own deaths help answer that question: They're not nearly as effective as you've been led to believe.

They may not be effective at all.

Crunching the numbers: Why vaccines just don't add up

Think about this: 80% of Americans refused to get vaccinated against swine flu. That's roughly 240 million people.

Most of those 240 million people were probably exposed to the H1N1 virus at some point over the last six months because the virus was so widespread.

How many of those 240 million people were actually killed by H1N1? Given the CDC's claimed total of deaths at 11,160, if you take 80% of that (because that's the percentage who refused to be vaccinated), you arrive at 8,928. So roughly 8,900 people died out of 240 million. That's a death rate among the un-vaccinated population of .0000372

With a death rate of .0000372, the swine flu killed roughly 1 out of every 26,700 people who were NOT vaccinated. So even if you skipped the vaccine, you had a 26,699 out of 26,700 chance of surviving.

Those are pretty good odds. Ridiculously good. You have a 700% greater chance of being struck by lightning in your lifetime, by the way.

What it all means is that NOT getting vaccinated against the swine flu is actually a very reasonable, intelligent strategy for protecting your health. Mathematically, it is the smarter play.

Because, remember: Some of the dead victims of H1N1 got vaccinated. In fact, I personally challenge the CDC to release statistics detailing what percentage of the dead people had previously received such vaccines.

The headline to this article, "Thousands of Americans died from H1N1 even after receiving vaccine shots" is a direct challenge to the CDC, actually. If the CDC believes this headline is wrong -- and that the number of vaccinated Americans who died from H1N1 is zero -- then why don't they say so on the record?

The answer? Because they'd be laughed right out of the room. Everybody who has been following this with any degree of intelligence knows that the H1N1 vaccine was a medical joke from the start. There is no doubt that many of those who died from H1N1 were previously vaccinated. The CDC just doesn't want you to know how many (and they hope you'll assume it's zero).

Where are all the real journalists?

I find it especially fascinating that the simple question of "How many of the dead were previously vaccinated?" has never been asked in print by a single journalist in any mainstream newspaper or media outline across the country. Not the NY Times, not WashingtonPost.com, not the WSJ, LA Times or USA Today. (At least, not that I'm aware of. If you find one that does, let me know and I'll link to their article!)

Isn't there a single journalist in the entire industry that has the journalistic courage to ask this simple question of the CDC? Why do these mainstream journalists just reprint the CDC's statistics without asking a single intelligent question about them?

Why is all the intelligent, skeptical reporting about H1N1 found only in the alternative press or independent media sites?

You already know the answer, but I'll say it anyway: Because most mainstream media journalists are just part of the propaganda machine, blindly reprinting distorted statistics from "authorities" without ever stopping to question those authorities.

The MSM today, in other words, is often quite pathetic. Far from the independent media mindset that used to break big stories like Watergate, today's mainstream media is little more than a mouthpiece for the corporatocracy that runs our nation. The MSM serves the financial interests of the corporations, just as the CDC and WHO do. That's why they're all spouting the same propaganda with their distorted stories about H1N1 swine flu.

But those who are intelligent enough to ask skeptical questions about H1N1 already realize what an enormous con the pandemic was. In the end, it turned out to be a near-harmless virus that was hyped up by the CDC, WHO and drug companies in order to sell hundreds of millions of doses of vaccines that are now about to be dumped down the drain as useless.

Sources for this story include:
CNN
http://edition.cnn.com/2010/HEALTH/...

Washington Post
http://www.washingtonpost.com/wp-dy...

msnbc.com

Doctors puzzle over woman’s mystery ailment

After eight years, they still don’t know what’s wrong with Kelly Klodzinski

By Michael Inbar

TODAYshow.com contributor

updated 10:09 a.m. ET, Thurs., Jan. 14, 2010

For eight years, Kelly Klodzinski has lived through a medical hell. Her jaw clenches so tightly that she can’t eat a peanut butter sandwich; she has an inflamed heart that often makes it difficult to breathe, much less walk; and she spends so much time in hospital beds that she’s on a first-name basis with staff at seven or eight clinics.

Thankfully, though, Klodzinski is now part of a groundbreaking new program: At a clinic in Bethesda, Md., she is examined by some of the leading minds in medicine, who aren’t rushed because they only see three or four patients a week. And the charge to Klodzinski for such acute care? Not one red cent.

There is a catch, however: Patients like Kelly have to be sick, really sick, to be admitted. And what’s more, those patients have already had to suffer through years of medical maladies that don’t even have a name.

That’s the mission of the Undiagnosed Diseases Program, created by the National Institutes of Health in May 2008. And even though it sounds a bit like the medical-mystery TV show “House,” the doctors caution their work can’t be tied into a neat bow in the space of a one-hour episode.

Mysterious symptoms
Still, for Klodzinski, being treated at the UDP clinic is the first light of hope she’s seen after eight years of medical darkness. The young Louisiana wife — focus of the first of a two-part series examining medical mysteries on TODAY — has seen her body steadily break down in many ways, with doctors unable even to give her a diagnosis, much less cure her.

Appearing live on TODAY Thursday, Klodzinski told Matt Lauer she feels like a medical orphan: Concerned friends don’t understand that she suffers from maladies that have no name.

“It’s very, very frustrating,” she told Lauer. “People ask me every day, ‘What’s wrong with you, what do you have?’ And I don’t have an answer; I just tell them it’s undiagnosed. And they will say, ‘Well, what do they call it?’ And I say, ‘I don’t know, they’ve don’t have anything TO call it.’ ”

TODAY A growth on Kelly Klodzinski’s jaw was the first of a series of apparently unrelated symptoms to plague her.

Klodzinski’s health began deteriorating at age 15, when a small sore in her mouth grew so large it made it impossible to open her jaw more than a fraction of an inch. It was followed by serious but seemingly unrelated health issues: inflammation in her heart that left her struggling to walk, nodules forming on her lungs and an enlargement of her right kidney.

She’s been in and out of hospitals ever since, and she sometimes has as many as four doctor’s appointments in a week. She’s been looked at by pulmonologists, cardiologists, hematologists and oncologists. Klodzinski has undergone multiple surgeries, one of which she barely survived. But all the while, well-trained doctors have been unable to pinpoint the root cause of her health dilemma.

Now, with treatment at the UDP clinic, Klodzinski told TODAY she can finally see some progress in turning her health crisis around, even if she’s been down the road with doctors too many times to be totally confident.

“It would be a pretty big deal to get a diagnosis after eight years,” she said. “I would be in shock if [they] told me, ‘This is what you have.’ If I could just get some treatment options, how to keep it under control, how to keep it from flaring up again, that would be great.”

Not like ‘House’
The novel program undertaken by NIH can be called forward-thinking; just don’t call it “House” in the presence of Dr. William A. Gahl, one of its founders. “That’s entertainment — we’re not here for entertainment in any respect,” Gahl told TODAY. “That program essentially solves that problem, that story, within an hour. The whole premise is completely unrealistic and completely off track, and it’s intended to be drama. I think also, someone who has Dr. House’s personality characteristics would never be permitted to handle patients or would have his license taken away.”

TODAY Despite eight years of examinations by an array of doctors, there is still no diagnosis for Kelly Klodzinski’s symptoms.

Klodzinski told TODAY she knows she’s in better hands with the experts at the UDP clinic, and counts herself lucky she was accepted into the program. Since opening, the clinic has sifted through some 2,100 inquiries and accepted only 140 patients thus far.

Klodzinski feared she wouldn’t be accepted, believing “there were probably a lot weirder cases,” but says she feels like she’s finally found the right place for treatment.

“It’s weird because it’s like, ‘Do I really have the disease that nobody knows what it is?’ Klodzinski told TODAY. “I go to the hospital and there are so many sick people there and they all know what’s wrong with them. What’s so weird about my condition that they don’t know what it is or what doctor to send me to?”

Unrelated ailments
Gahl said the intriguing mystery with Klodzinski is that she suffers from multiple maladies, with one not necessarily being related to the other. She shows signs of ascites (free fluid in her abdomen), pericarditis (inflammation of her heart covering) and hydroneophrosis (enlargement of her kidney), along with mouth cysts that cause her jaw to become inflamed.

“It’s possible [she] has a genetic disorder,” Gahl said, and if “we could find the gene that is responsible and relate mutations in that gene to her symptomatology, [it would be] a great outcome for us and for the profession, too.”

Another one of Klodzinski’s physicians at UDP, pulmonologist Dr. Bernadette Gochuico, said, “Kelly is very unusual, and she’s challenging. We are doing some detective work in that Kelly has something that has not been described before, and we’re trying to identify for the first time what may be causing her disease.”

Klodzinski told Lauer she’s taken steroids and morphine for years, but the UDP clinic has put her on a new drug normally used to treat rheumatoid arthritis, lupus and malaria. She began taking the drug in December, and is due back at the clinic in March to see if it’s helping.

Symptoms first, diagnosis later
Appearing with Klodzinski on TODAY, medical correspondent Dr. Nancy Snyderman says it is good medicine to try to make Kelly feel better first, then figure out the root cause for all that ails her. “When a patient has real symptoms, sometimes doctors are better off to treat the symptoms, then wait for the diagnosis,” she said.

Snyderman also lauded the NIH program for bringing together experts from various fields. “Not everything fits into a neat package; sometimes Mother Nature has a sort of different plan, and the constellation of symptoms don’t fall into one package,” she said.

TODAY Klodzinski told TODAY that she feels ‘pretty helpless’ and still has her dark days but she's optimistic since getting accepted into the UDP clinic.

Klodzinski told TODAY her spirits are somewhat buoyed by visiting the UDP clinic, but she still has her dark days. Recurrence of severe symptoms forced her into a hospital bed last year and made her have to plan her wedding while lying on her back.

“It’s kind of scary,” she said, “especially when it first started happening. I’m never really happy that I have to take steroids to live, basically. I don’t like knowing that without a little pill every day there’s a possibility I might die. I feel pretty helpless, and it is hard knowing that no one has really gone through the same disease process as I have.”

Still, getting accepted into the UDP clinic allows her to see doctors she would never have been able to afford otherwise. “I don’t have insurance; we don’t have the money to fly around the world,” she explained. “When I found out someone was interested in finding out what was wrong with me, I was so excited.”

Undiagnosed Diseases Program

National Institutes of Health
Office of Rare Diseases Research

Undiagnosed Diseases Program

The ORDR Web site aims to answer questions about rare diseases and the activities of the ORDR for patients, their families, healthcare providers, researchers, educators, students, and anyone with concern for and interest in rare diseases. The site provides information about ORDR-sponsored biomedical research, scientific conferences, and rare and genetic diseases. It also serves as a portal to information on major topics of interest to the rare diseases community.

The ORDR Web site links to:

• Information on many of the rare diseases.
• Information about the services of the Genetic and Rare Diseases Information Center (GARD) and other rare diseases information sources.
• Planned, ongoing, or completed clinical studies and trials.
• Research funding opportunities from NIH and other sources.
• Patient recruitment and referral procedures for the NIH Clinical Center hospital.
• Rare diseases publications and reports.
• Sources for genetic testing and counseling.
• A program to develop new genetic tests and to make them available to the public.
• Information on transportation and lodging for patients and their families during diagnosis and treatment at NIH and at other research sites across the Nation.
• Information about ORDR-NIH supported scientific conferences.
• Opportunities for transfer of technology for the prevention, diagnosis, or treatment of rare diseases or conditions.

Some patients wait years for a definitive diagnosis. Using a unique combination of scientific and medical expertise and resources at the National Institutes of Health (NIH), the Undiagnosed Diseases Program pursues two goals:

• To provide answers to patients with mysterious conditions that have long eluded diagnosis
• To advance medical knowledge about rare and common diseases

The program is trans-NIH in scope. It is organized by the National Human Genome Research Institute (NHGRI), the NIH Office of Rare Diseases Research (ORDR) and the NIH Clinical Center. Many medical specialties from other NIH research centers and institutes will contribute expertise needed to conduct the program, including endocrinology, immunology, oncology, dermatology, dentistry, cardiology, and genetics, which are represented among the dozens of participating senior attending physicians who may participate in the program's clinical research.

Any longstanding medical condition that eludes diagnosis by a referring physician can be considered undiagnosed and may be of interest to this clinical research program. Of the total number of cases that may be referred to this program, a very limited number will be invited to proceed in the study at the discretion of the program’s medical team.

For more information please call (866) 444-8806

Please do not send Undiagnosed Diseases Program-related email or submit medical records to the NIH Office of Rare Diseases. All communication should be handled through the Undiagnosed Diseases Program staff at the NIH Clinical Center.

Program Information

Frequently Asked Questions (FAQ)

Information for patients (PDF - 90 KB)

Information for health-care providers (PDF - 93 KB)

News

Press Release (PDF - 51KB)

Place for Hope

Audio recording media telebriefing (MP3 - 10,799 KB)

Audio recording patient advocacy teleconference (MP3 - 18,905 KB)

Transcript: Undiagnosed Diseases Program Media Tele-Briefing (PDF - 79 KB)

NY Times Magazine describes the experiences of a UDP patient

Patient Support

In Need of Diagnosis, Inc. (INoD)

Syndromes Without A Name- USA (SWAN-USA)