Category Archives: Multiple sclerosis - Page 2

The Vanderbilt Protocol for Multiple Sclerosis

The antibiotic approach to MS therapy was developed at Vanderbilt by Drs. Stratton and Mitchell. They have patented multiple versions of their protocol, most recently in 2005. (Since patents are publicly available and the “Description of the Invention” is often an excellent overview of the science, we’ve put links to patents at the end of this post.)

Since we have some readers with MS, including Alexander, I thought I would post a summary of the Vanderbilt protocol. This was written by Dr. Stratton in 2009:

Treatment Protocol for Chronic Infections Caused by C. pneumoniae

As far as the Cpn Antimicrobial Regimen is concerned, my thoughts (as of 2009) are as follows:

First, as a general rule, the sicker a patient is, the slower they should go. This is why our early protocol started out with only one antibiotic and one dose, and then gradually adding the next dose/antibiotic as the reactions to each dose/antibiotic became apparent. These reactions appear to be caused by destruction of Chlamydia organisms as well as by the death of some of the infected host cells. Even destruction of elementary bodies by reducing agents such as N-acetyl-cysteine (NAC) can cause these reactions as chlamydial major outer membrane protein (MOMP) is released. MOMP is known to interact with Toll-like receptors (TLRs) and can thus induce the production of cytokines. Moreover, chlamydial cell wall contains LPS, which also interacts with TLRs and induces the production of cytokines. The reaction to anti-chlamydial therapy is sometimes referred to as “die-off” as presumable both chlamydial organisms and host cells are dying. These reactions can be delayed by days to weeks and may include “flu-like symptoms”, arthralgias and myalgias, “hangover-like symptoms (“brain-fog”, nausea, malaise), gastroenteritis (including diarrhea), and (rarely) fever. These reactions are akin to the “leprosy reaction” well described with the therapy of leprosy. The use of prednisone (10-20 mg per day) and/or pentoxifylline (Trental, 400 mg bid or tid), as done for the leprosy reaction, may be beneficial.

I think that all patients should start with supplements/vitamins before they start any antibiotics. Baseline lab studies, including CBC and liver function studies, should be done and these parameters followed every 3-4 months, more frequently (i.e., monthly) for sicker patients. As C. pneumoniae can infect white blood cells and liver cells, potential death of these cells should be monitored in sicker patients. Our initial protocol recommended this. I would add NAC to the supplements. We used amoxicillin, which is degraded in the body to penicillamine (a reducing agent) in our regimen as an anti-elementary body agent, but NAC seems to work equally well and may offer additional benefits in boosting the immune system as well as protecting the liver. As far as supplements/vitamins are concerned, I think Professor David Wheldon’s supplement/vitamin suggestions are very complete and should be the benchmark. Once antibiotics are ready to be started, I would start with a macrolide. We have used Azithromycin because it is easy to give and has become somewhat cheaper since it went off patent. Clarithromycin (500 mg twice a day) or Roxithromycin (300 mg once a day) can be used instead of Azithromycin. I would still give just one 250 mg azithromycin tablet and then wait two weeks to see if there is any reaction to it. Then I would give two tablets, one on Monday and one on Wednesday. Once again I would wait two weeks. I’d continue in this way, adding each dose until the patient was taking 250 mg of azithromycin MWF. If the patient has severe reactions (meaning they can’t work – most people are trying to work and take care of a family while they are on this therapy), I’d slow down the process. After the azithromycin, I’d add doxycycline – again doing this very slowly. Once the patient was taking both azithromycin (250 mg MWF) and doxycycline (100 mg twice a day), I’d start the metronidazole pulses – again, doing these slowly and working up to a once a month pulse of 7 days of metronidazole (500 mg twice a day). Once the patient could do the monthly pulse of metronidazole, I’d add rifampin (300 mg twice a day). Once this was tolerated, I would increase the metronidazole pulse to 14 days, doing so slowly. Eventually, the patient should be able to tolerate metronidazole (500 mg twice a day) on a daily basis. Once a patient could do this regimen without any reactions, I would continue it for at least a year and probably three years for MS patients. It might take a year or two (or longer) to get to the point where there is no reaction to the daily metronidazole, depending on the chlamydial load, followed by 1-3 years of therapy. This might be a 5-year program, but should allow the patient to continue to work with minimal disruption. Patients should also be gradually improving during this time. The sicker the patient is, the longer the therapy is going to be. There is no shortcut. Younger patients who have not been sick as long tend to respond more quickly. ?

With MS patients, due to the possible CNS damage that might occur by going slowly, I would move more quickly unless there were major reactions. This means compressing what might have taken a year into several months. 

The reactions patients have are varied – some are severe enough that they stop the antibiotics. That, of course, defeats the purpose of the therapy. It is very tricky and each patient has to learn his own limitations. When we started our protocol, we were thinking of a hotline to answer questions that are now easily and better answered via the internet ( Finally, I don’t think this is the only regimen that will work nor do I think it will work better or faster. It is just what I do in 2009 when treating a patient.

I’ve been informed that the late stages of the protocol have been further refined in 2010. Now, once die-off reactions to the metronidazole subside, Dr. Stratton tries rifabutin or rifampin.

I would agree with Dr. Stratton that nutritional supplements should begin 3-4 months before antibiotics, but would add that our diet should be adopted 3-4 months before antibiotics begin. This is necessary to improve immune response and healing capacity; and to avoid unnecessary cell death and die-off toxicity when antibiotics begin. The eleven ways to enhance immunity, discussed in Step Four of the book, should be routinely practiced.

Simply introducing diet and nutrition alone can lead to significant die-off effects. This shows that the adoption of diet and nutritional supplements is therapeutic in its own right.

On a bad diet, antibiotics are dangerous, as they risk gut dysbiosis and introduction of new co-infections.

Like Dr. Stratton, I think being active at is essential for anyone on this protocol. Many people at have used this protocol, often for years, and their experience can be very helpful.

As Dr. Stratton notes, it takes years to cure MS. It is necessary to be patient and to balance speed of killing pathogens against allowing the body time to recover from die-off effects – toxic bacterial proteins and human cell death. Remember, “the dose makes the poison” – doubling the rate of pathogen killing may quadruple the toxicity effects, so the optimum course is not the one with highest rate of pathogen killing. Every patient has to progress at his own pace. Go as fast as you can but no faster.

There are steps that can be taken to reduce die-off toxicity, such as drinking lots of water and eating salt to help urine excretion, and taking “moppers” such as charcoal, bentonite clay, cholestyramine, or chlorella to help assure that toxins released from the liver through the bile are excreted in feces, not re-absorbed.


MS recovery is not impossible; indeed, many have recovered on this protocol. However, it is long and arduous. Optimizing diet will shorten time to recovery, but it will still take years. 

MS is not the only disease that may be caused by C. pneumoniae. Alzheimer’s dementia, atherosclerosis, stroke, rheumatoid arthritis, and rosacea are all associated with C. pneumoniae infections and may be treatable by Dr. Stratton’s protocol.


“Multiple Sclerosis:  A Curable Infectious Disease?”, July 7, 2010,

“Is Multiple Sclerosis an Autoimmune Disease?”, July 5, 2010,

“Eleven Steps for Overcoming Alzheimer’s and Other Chronic Infectious Diseases,” July 1, 2010,

A list of the Vanderbilt patents.

The 2005 patent, ID 7,094,397.

Multiple Sclerosis: A Curable Infectious Disease?

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,, 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.

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

[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. A translation of the full text is available here: More case studies may be found here:

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

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

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

[7] Sriram S et al. Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS. Neurology. 1998 Feb;50(2):571-2. 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.

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

[9] Mitchell, William M. & Stratton, Charles W. “Diagnosis and management of infection caused by Chlamydia,” U.S. Patent Number 6,884,784,

[10] David’s story told by himself:

[11] Sarah’s story told by herself:

[12] Sarah’s story told by David:


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

[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.

[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.

[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.

Is Multiple Sclerosis an Autoimmune Disease?

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.

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

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

If Alzheimer’s is due to bacterial infection, as I suggested yesterday (, 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.


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.