Category Archives: Disease - Page 31

Multiple Sclerosis: A Curable Infectious Disease?

Posted by on July 7, 2010 46 comments

For more than a century many strands of evidence have pointed toward an infectious cause for MS.

Pierre Marie, lecturing in 1892, said that “the causative agent in multiple sclerosis is manifestly of an infective nature.  What is its precise nature?  No one so far has been able to isolate it but one day this goal will be achieved.” [1]

For a long time, little progress was made. In the 1950s, however, Paul Le Gac noticed similarities between multiple sclerosis and symptoms developed in the aftermath of diseases like Rocky Mountain spotted fever and typhus caused by Rickettsia bacteria. [2]  Rickettsia are obligate intracellular parasites that cannot survive outside a host. By 1966, Le Gac recognized that the Chlamydiae, another order of intracellular parasitic bacteria, might be responsible for MS. [3]

Le Gac tried treating multiple sclerosis with tetracyclines and other broad spectrum antibiotics, and reported a number of cures. Here is one of his case studies:

Mr. Maurice Q., a Belgian citizen, 46 years of age. Multiple sclerosis was manifested in 1955 by transient retrobulbar neuritis. In 1956 he became bedridden. As of November 1961, [he had been] totally quadriplegic for three years….

Antibiotic treatment and alginated baths were followed, within a few months, by a spectacular improvement.

In May 1962, Mr. Q. was walking normally. He was able to discard all assistive devices, and soon afterward went back to work as a freight–truck driver. [3]

However, Le Gac’s work was criticized on the ground that MS patients generally lacked antibodies to Rickettsia, not all MS patients responded to Le Gac’s treatment, and no controlled clinical trials had been conducted. [4]

Meanwhile, epidemiological evidence was accruing in support of the idea of an infectious origin.  For instance, MS was virtually unknown in the Faeroe Islands until British troops were stationed there in 1940, after which an epidemic of MS occurred.  Nearly all the MS cases diagnosed between 1943 and 1960 were in people who had resided as children in the towns where the British were stationed. [5] In general, MS risk is increased in populations with low vitamin D and poor hygiene; both associations are suggestive of an infectious origin, since vitamin D is so crucial for intracellular immunity. [6]

Technological advances in molecular biology in the 1980s and 1990s finally made possible a robust investigation into microbial causes. A key invention was real-time PCR, which was honored by the Nobel Prize for Chemistry in 1993. This technique permitted sensitive detection of bacterial DNA from tissue or fluid samples, and enabled for the first time reliable detection (and species identification) of intracellular bacteria. PCR entered research use in the 1990s.

Some scientists at Vanderbilt, who had previously been studying the role of Chlamydia pneumoniae in chronic fatigue, discovered its presence in the cerebrospinal fluid of MS patients. [7] PCR showed that DNA from C. pneumoniae was present in the cerebrospinal fluid of up to 97% of MS patients. [8] In 2002, the Vanderbilt scientists patented a combination-antibiotic therapy for C. pneumoniae [9]. They established a clinic at Vanderbilt specializing in antibiotic treatment of chronic fatigue syndrome and MS.

In medicine, some of the most important progress has been made by doctors and scientists trying to cure their own conditions. The combination of high motivation, intimate familiarity with the disease, and technical expertise is hard to beat. For this reason, I think the story of Dr. David Wheldon, a clinical microbiologist from Britain, and his wife Sarah is significant in the history of MS.  I will abridge their story from various accounts they have published. [10, 11, 12, 13]

In 1999, the Wheldons contracted a respiratory infection which produced a mild pneumonia. In its aftermath, Sarah developed asthma and David developed a myalgia which prevented him from turning his head. By 2003, Sarah had developed full-blown multiple sclerosis: she could not walk unaided, her speech was slurred, she was numb from the waist down, and an MRI revealed numerous white-matter brain lesions. 

Dr. Wheldon searched the literature and found the Vanderbilt work.  He gave his wife doxycycline and roxithromycin, both effective anti-chlamydial agents.  He writes:

What followed was dramatic. For a few days, Sarah had a Herxheimer-like reaction, with a fever and night-sweats. After this, her mental fog and cognitive deficits speedily began to vanish. Slowly, the disease was rolled back … [12]

Sarah improved from a grade of 7 on the Kurtzke Expanded Disability Status Scale (EDSS) to a grade of 2, and remains at that grade seven years later. The same antibiotics cured David’s myalgia.

Dr. Wheldon and Dr. Stratton of the Vanderbilt group have since collaborated on papers summarizing the evidence for C. pneumoniae as the causal agent of MS.  [14] Dr. Wheldon now treats MS patients, and he and his wife also helped popularize a site, cpnhelp.org, set up by a chronic fatigue and fibromyalgia patient, Jim Kepner, to help chronic disease suffers defeat C. pneumoniae infections. This site has a rich lode of MS patients recounting their experiences with antibiotics.

On the clinical research side, pilot trials of antibiotic therapies for MS have been undertaken by several groups, with promising results. [15, 16, 17] It seems only a matter of time, patient pressure, and perhaps a few funerals before large-scale trials are funded.

The experience of MS patients shows that combination antibiotic treatments targeted at C. pneumoniae often halt MS progression and sometimes, as in the case of Sarah Wheldon, bring about substantial recovery.

In an upcoming post, I’ll talk about dietary reasons why antibiotics may fail, or succeed only after a protracted struggle with exceptionally difficult side effects.

[1] Marie, P., Leçons sur les Meladies de la Moelle, Paris, Masson, 1892. Cited in: “Cures” for multiple sclerosis. Br Med J. 1970 Jan 10;1(5688):59-60. http://pmid.us/5411441.

[2] “Cures” for multiple sclerosis. Br Med J. 1970 Jan 10;1(5688):59-60. http://pmid.us/5411441.

[3] Le Gac P et al. The psittacosis virus in the etiology of multiple sclerosis. C R Acad Sci Hebd Seances Acad Sci D. 1966 Nov 28;263(22):1793-5. http://pmid.us/4963916. A translation of the full text is available here:  http://www.davidwheldon.co.uk/Le%20Gac%204.pdf. More case studies may be found here: http://www.davidwheldon.co.uk/Le%20Gac%206.pdf.

[4] Field EJ, Chambers M. Rickettsial antibodies in multiple sclerosis. Br Med J. 1970 Jan 3;1(5687):30-2. http://pmid.us/4983591.

[5] Kurtzke JF, Hyllested K. Multiple sclerosis in the Faroe Islands: I. Clinical and epidemiological features. Ann Neurol. 1979 Jan;5(1):6-21. http://pmid.us/371519. Kurtzke JF, Heltberg A. Multiple sclerosis in the Faroe Islands: an epitome. J Clin Epidemiol. 2001 Jan;54(1):1-22. http://pmid.us/11165464.

[6] Cantorna MT. Vitamin D and multiple sclerosis: an update. Nutr Rev. 2008 Oct;66(10 Suppl 2):S135-8. http://pmid.us/18844840.

[7] Sriram S et al. Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS. Neurology. 1998 Feb;50(2):571-2. http://pmid.us/9484408. Stratton CW et al. Does Chlamydia pneumoniae play a role in the pathogenesis of multiple sclerosis? J Med Microbiol. 2000 Jan;49(1):1-3. http://pmid.us/10628821.

[8] Sriram S et al. Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis. Ann Neurol. 1999 Jul;46(1):6-14. http://pmid.us/10401775.

[9] Mitchell, William M. & Stratton, Charles W. “Diagnosis and management of infection caused by Chlamydia,” U.S. Patent Number 6,884,784, http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=1&f=G&l=50&co1=AND&d=PTXT&s1=6884784.PN.&OS=PN/6884784&RS=PN/6884784.

[10] David’s story told by himself: http://www.cpnhelp.org/?q=david_wheldons_story_cpn_treatment_of_cardiac_myalgic_symptoms

[11] Sarah’s story told by herself:  http://www.cpnhelp.org/?q=node/4

[12] Sarah’s story told by David: http://avenues-of-sight.com/Ignoring-the-Evidence.html

[13] http://www.davidwheldon.co.uk/ms-treatment.html

[14] Stratton CW, Wheldon DB. Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. Trends Microbiol. 2006 Nov;14(11):474-9. http://pmid.us/16996738.  Stratton CW, Wheldon DB. Antimicrobial treatment of multiple sclerosis. Infection. 2007 Oct;35(5):383-5; author reply 386. http://pmid.us/17882356.

[15] Sriram S et al. Pilot study to examine the effect of antibiotic therapy on MRI outcomes in RRMS. J Neurol Sci. 2005 Jul 15;234(1-2):87-91. http://pmid.us/15935383.

[16] Minagar A et al. Combination therapy with interferon beta-1a and doxycycline in multiple sclerosis: an open-label trial. Arch Neurol. 2008 Feb;65(2):199-204. http://pmid.us/18071030.

[17] Metz LM et al. Glatiramer acetate in combination with minocycline in patients with relapsing–remitting multiple sclerosis: results of a Canadian, multicenter, double-blind, placebo-controlled trial. Mult Scler. 2009 Oct;15(10):1183-94. http://pmid.us/19776092.

Is Multiple Sclerosis an Autoimmune Disease?

Posted by on July 5, 2010 8 comments

Multiple sclerosis is almost universally labeled an “autoimmune disease.” Yet after decades of research, there is still no proof that MS is the result of autoimmunity.

Several papers by Drs. Abhijit Chaudhuri and Peter Behan [1,2] discuss problems with the conventional explanation:

  1. Unlike other diseases which are known to have an autoimmune component (rheumatoid arthritis, systemic lupus erythematosus, and myasthenia gravis), MS has no specific immunological marker. This after 60 years of search for such a marker.
  2. The standard animal model for MS, experimental allergic encephalomyelitis (EAE), is generated by inducing autoimmunity against myelin basic protein in mice.  However, EAE symptoms do not closely resemble those of MS; rather, EAE mice look like humans with a different disease — acute disseminated encephalomyelitis (ADEM). Some differences: EAE and ADEM lack the characteristic large plaques radiating from a central focus seen in the brains of MS patients. EAE and ADEM both feature destruction of endothelial cells lining blood vessels, a pattern not seen in MS. 
  3. The autoimmune model does not explain the neurodegeneration and loss of brain matter in the brains of MS patients; the observation that widespread neuronal loss is present even at the earliest clinical stage of the disease; the absence or slight infiltration of lymphocytes in MS plaques; the role of vitamin D in MS prevention; and the general failure of immunotherapies.

Whether MS is an autoimmune disease has implications for treatment.  Autoimmune diseases are commonly treated by immunosuppression.  But if MS is an infectious disease, immunosuppression would be a terrible mistake.

After 60 years of research, the autoimmune model has failed to produce a single effective treatment for MS. Drugs have been found that improve mice with EAE, but none does much to help MS patients. Chaudhuri and Behan note:

The two most widely prescribed therapies for MS (interferon and glatiramer acetate) have no effect on the progressive forms of the disease (primary or secondary MS), although relapse rates may be reduced by about one third in some patients. A response rate of one third is considered to be a powerful placebo effect in treatment trials. [2]

The continued dominance of the autoimmune paradigm in MS research calls to mind Einstein’s definition of insanity. 

Meanwhile, other work has established that at least some cases of MS are infectious in origin, and can be cured with antibiotic and dietary therapies. That will be the subject of tomorrow’s post.

[1] Chaudhuri A, Behan PO. Multiple sclerosis: looking beyond autoimmunity. J R Soc Med. 2005 Jul;98(7):303-6. http://pmid.us/15994589.

[2] Chaudhuri A, Behan PO. Multiple sclerosis is not an autoimmune disease. Arch Neurol. 2004 Oct;61(10):1610-2. http://pmid.us/15477520.

Eleven Steps for Overcoming Alzheimer’s and Other Chronic Infectious Diseases

Posted by on July 1, 2010 161 comments

If Alzheimer’s is due to bacterial infection, as I suggested yesterday (https://perfecthealthdiet.com/?p=126), then it can be treated by diet, supplements, and antibiotics.

Here are eleven steps that can help defeat chronic bacterial infections, including the infections that cause Alzheimer’s. (Note:  I will justify each of these eleven steps, and cite to the scientific literature, in follow-up posts.)

1. Normalization of Vitamin D Levels.

Vitamin D is needed for the transcription of anti-microbial peptides, such as the cathelicidin LL-37 and beta-defensin, which are essential for defense against intracellular bacteria and viruses. Vitamin D deficiency is a risk factor for every chronic infection, and chronic infections tend to increase in frequency with latitude and progress most rapidly during the winter when vitamin D levels are low.  In general, a serum 25-hydroxyvitamin D3 level of 40 ng/ml (100 nmol/L in SI units) is a good target. (Some people, such as Dr. John Cannell of the Vitamin D Council, believe there may be benefits to higher levels, but this is speculative.)

2. Restriction of Carb Intake to 400 Calories Per Day.

Eating a carb-rich diet is doubly bad:  it increases blood glucose levels and triggers insulin release, both of which promote bacterial infections.

Intracellular parasitic bacteria need glucose or its glycolytic products to obtain energy. Abundant cellular glucose, caused by high blood glucose levels, enable them to reproduce and generate immune-impairing proteins more prolifically.

Insulin represses immune defenses against parasitic bacteria, by blocking production of antimicrobial peptides.

To keep both blood glucose and insulin levels low, carbohydrate consumption should be restricted to about 400 calories per day – the amount in 0.3 pounds of cooked white rice, or 1.3 pounds of sweet potatoes.

3. Restriction of Protein.

Eating minimal protein helps in two ways: it deprives bacteria of amino acids necessary for growth, like tryptophan; and it promotes autophagy, the primary means by which cells kill intracellular pathogens.

Indeed, the body’s primary defense mechanism against C. pneumoniae is tryptophan deprivation. This is why people with chronic brain infections have symptoms of serotonin deprivation, including depression, anxiety, insomnia, fatigue, impaired ability to concentrate, and low self-confidence. It’s important not to relieve this by tryptophan or 5-HTP supplementation, both of which promote bacterial growth. If symptoms are intolerable, selective serotonin reuptake inhibitor (SSRI) antidepressants, like Prozac, Paxil, or Zoloft, might be able to provide symptomatic relief. (NB: We neither recommend nor disparage these drugs.)

4. Intermittent Fasting

Autophagy is the garbage collection and recycling process of human cells.  When resources are scarce, cells turn on recycling programs and send garbage collectors known as lysosomes to engulf and digest junk proteins and damaged organelles, enabling re-use of their amino and fatty acids.

Autophagy is a key part of the immune defense against parasitic bacteria.  Lysosomes not only digest human junk, they seek out bacteria and digest them. 

Autophagy is strongly turned after about 16 hours of fasting. The longer one fasts, the more parasitic bacteria are destroyed in lysosomes.  Fasting is an easy way to improve the relative balance of power between your body and intracellular pathogens. Fasting strongly promotes autophagy in neurons, and is of therapeutic value for Alzheimer’s.

A simple strategy of intermittent fasting is to confine meals to an 8-hour window each day, thus engaging in a daily 16 hour fast.  On this strategy, one might eat only between noon and 8 pm.

5. Ketogenic Fasting.

Two dangers of fasting are that it can lead to loss of muscle tissue as protein is consumed to generate ketones and glucose, and that neurons may be put under stress by glucose deprivation.

Both dangers can be ameliorated by eating ketogenic fats during the fast.  “Ketogenic” means generative of ketone bodies. Ketone bodies, which are generated from fats or some proteins during fasting, are the only neuronal energy source that bacteria can’t steal. There is a large literature showing that high circulating ketone levels are neuroprotective, and ketogenic diets have been successfully tested as Alzheimer’s therapies.

The most ketogenic fats are the short- and medium-chain fats found abundantly in coconut oil. Taking plentiful fat calories from coconut oil, but no carb or protein calories and few other fats, can enable fasts to be extended substantially longer with minimal loss of muscle tissue or neuronal stress.

On a ketogenic fast, eliminate carbs and protein for a 36-hour period, from dinner one day to breakfast on the second day.  During the intervening day, eat no protein or carbs, but do eat as much coconut oil as you like.

There is no limit on how much coconut oil may be consumed – but 12 tablespoons per day would produce a surfeit of ketones. NB: Always drink plenty of water during a fast. We also drink coffee with plentiful heavy cream.

6. Elimination of Wheat and Other Grains. 

Wheat is a toxic food that interferes with immune defenses and impairs vitamin D function. It also generates antibodies to the thyroid, which damage the thyroid status and further impair immune function.

7. Elimination of Omega-6-Rich Oils and Inclusion of Omega-3-Rich Fish.

A diet that minimizes omega-6 content by replacing soybean oil, corn oil, canola oil, and other omega-6 rich oils with butter, coconut oil, and beef tallow, and gets adequate omega-3 fats by eating salmon or other cold-water fish, optimizes the immune defense against intracellular pathogens.

A high omega-6 and low omega-3 diet weakens immune defenses against intracellular pathogens and re-directs the immune system toward extracellular threats.

Note that the combination of carbohydrate, protein, and omega-6 fat restriction necessarily means that half or more of calories should be obtained from saturated and monounsaturated fats.  It is important not to have a saturated fat phobia if you want to escape or defeat Alzheimer’s!

8. Fructose Minimization.

Fructose is a toxin and is deprecated on the Perfect Health Diet. One of its worst features is that promotes infections. In mice, blood levels of endotoxin, a bacterial waste product, are higher on a fructose-rich diet than on any other diet.

Therefore, sugary foods like soft drinks should be eliminated.  Fruit and berries are OK in moderation.  We recommend no more than 2 portions of fruit and berries per day. Most carb calories should be obtained from starchy foods, like sweet potatoes or taro or white rice.

9. Melatonin supplementation. 

Whereas vitamin D is the “daylight hormone,” melatonin is the “hormone of darkness.”  It is generated during sleep, and is favored by darkness.  Even a little bit of light at night, like the LEDs of an alarm clock or streetlights shining through a window, can disrupt melatonin production.

Melatonin is extremely important, not least because it has powerful antibiotic effects.

To maximize melatonin production, everyone should sleep in a totally darkened room, with windows covered by opaque drapes and all lights extinguished and LCD or LED clocks turned face down.

Unfortunately, people with chronic bacterial infections will generally still be melatonin-deficient, for the same reason they are serotonin-deficient:  melatonin is derived from tryptophan and serotonin. Fortunately, melatonin is easily supplemented.

A melatonin tablet can be allowed to dissolve in the mouth just before bed. High doses will generally produce a deep sleep followed by early waking; this can be remedied by using time-release capsules, or by reducing the dose.

10. Selenium and Iodine Supplementation and Thyroid Normalization.

This is basic for good health in all contexts, but optimizing thyroid hormone levels and maintaining iodine and selenium status are especially important for anyone with an infection.

Both selenium and iodine are required for proper immune function. To get iodine, white blood cells will strip iodine from thyroid hormone; for this reason, people with chronic infections are often somewhat hypothyroid, as indicated by TSH levels above 1.5.

There are too many tricks and pitfalls to thyroid normalization to describe the whole issue here, but a good start is to eliminate wheat from the diet, and to obtain 200 mcg selenium and at least 400 mcg iodine per day. Do not get too much selenium as it is toxic.  Selenium and iodine may be obtained from foods:  two to three Brazil nuts a day for selenium, and seaweed for iodine.

11. Vitamin C and Glutathione or NAC Supplementation.

These are important for immune function. Vitamin C supplementation is an important safety precaution because infections greatly increase the rate of loss of vitamin C, and can generate tissue scurvy with devastating consequences.

Glutathione is destroyed by stomach acid. We recommend buying reduced glutathione and taking it with a full glass of water on an empty stomach, at least 2 hours after and 1 hour before taking food. Alternatively, N-acetylcysteine (NAC) and glycine-rich foods like gelatin may be taken to promote glutathione synthesis.

Conclusion

This is by no means an exhaustive list of dietary and nutritional steps that can help against chronic infections.  However, we believe these are the most powerful and important steps.

Alzheimer’s and other diseases caused by chronic bacterial infections – possibly including multiple sclerosis, Lyme disease, chronic fatigue syndromes, fibromyalgia, rheumatoid arthritis, and many others – are preventable, treatable, and often curable.  These dietary steps, along with appropriate antibiotic therapy, are keys to a cure.

Is Alzheimer’s Caused By a Bacterial Infection of the Brain?

Posted by on June 28, 2010 14 comments

As I noted earlier (https://perfecthealthdiet.com/?p=86), everyone gets chronic bacterial infections; infection rates are nearly 100% in the elderly.  In most people, however, the infection doesn’t progress to overt symptoms until old age. 

The first symptoms, apart from loss of athleticism and energy, often appear in the brain and nerves.  This is because neurons are a uniquely cozy home for bacteria.  Because they cannot burn fats, neurons have high levels of the energy substrates that bacteria rely on – pyruvate, lactate, and other products of glycolysis.

Loss of memory is one of the primary symptoms of bacterial infection of the brain. I myself had a chronic bacterial infection that caused loss of memory, and my memory was recovered with antibiotic treatment. (I now, thankfully, have a 100% functional brain.) The experience persuaded me that Alzheimer’s was very likely due to a bacterial infection of the brain.

Several recent findings support that inference. 

  • Alzheimer’s patients almost invariably have infections of the brain and nerves. C. pneumoniae is the most common agent.  Post-mortem autopsies found that C. pneumoniae infections in 17 of 19 Alzheimer’s brains, but only 1 of 19 non-Alzheimer’s elderly brains. [1]
  • The characteristic physical feature of the Alzheimer’s brain, clumps of amyloid-beta, are plausibly the result of the brain’s antimicrobial defenses.  It turns out that amyloid-beta is an antimicrobial peptide, part of the brain’s defense mechanisms against bacteria. [2]

These findings are consistent with a bacterial origin for Alzheimer’s. In the Alzheimer’s brain, the bacteria are parasites, stealing fuel and nutrients. This may be why the early signs of incipient Alzheimer’s are similar to the cognitive symptoms of hypoglycemia.

If Alzheimer’s is indeed caused by bacterial infection of the brain, then it is a treatable – often, curable – condition.  I’ll discuss in my next post some steps that will treat and help cure Alzheimer’s.

[1] Balin BJ et al. Chlamydophila pneumoniae and the etiology of late-onset Alzheimer’s disease. J Alzheimers Dis. 2008 May;13(4):371-80. http://pmid.us/18487846. Hat tip Stephanie Seneff, http://stephanie-on-health.blogspot.com/2009/12/10-evidence-that-infection-is.html.

[2] Soscia SJ et al. The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide. PLoS One. 2010 Mar 3;5(3):e9505. http://pmid.us/20209079.