Category Archives: Fibromyalgia and Chronic Fatigue

Beyond Standing Desks: Portable Outdoor Workstations

A note from Paul: I’m happy to introduce Kamal Patel’s first post on PHD! Kamal is the funniest and maybe smartest guy in the ancestral health movement. A Ph.D. candidate in nutrition and a leader in the Ancestral Health Society, you may know him from PaleoHacks or For more, check out Kamal’s bio on our About Us page. Welcome Kamal!

Goal: Do some computer work outside a couple times a week. Get maximal benefits from the sun in a minimum amount of time, while fitting all the necessary gear inside a backpack.

Resources: Tiny budget, free Amazon Prime shipping, access to a sunny park.

Why do computer work outside?

Hi, Kamal here (see below Shou-Ching for a short bio). I love sunlight. You probably love sunlight too. Turns out the sun is important for things outside of just vitamin D production. Ever wonder why indoor cats gravitate towards sunlight, even though they get their vitamin D from food? Probably not, since it just makes intuitive sense that animals want to be outdoors. The desire to be free of inside confines applies not just to indoor cats but also to indoor humans. Yet indoor humans sometimes need to see peer-reviewed articles before changing their habits. Don’t fret, we’ll start with a couple of those before delving into five specific steps for creating an outdoor workstation.

Escape plot foiled by hammock

My kitty’s escape to sunlight, foiled by a vicious hammock

Sun exposure increases production of endorphins and nitric oxide, which can translate into benefits for both pyschological well being as well as disease prevention. Light boxes benefit not only seasonal affective disorder but also non-seasonally linked depression. Brief but regular exposure to ultraviolet light from tanning beds can help the mysterious and painful chronic condition called fibromyalgia, and sunlight may benefit pain after surgery. The draw of UV radiation is so powerful that frequent tanners can literally get addicted to catching rays. Unfortunately, the “pro-sunshine” lobby isn’t pouring billions into research on sun exposure, so the specific mechanisms of sunlight benefit will likely remain more mysterious than the mechanisms of blockbuster medications like Viagra and Prilosec.

Step 1: Dress for success

Look at your skin. Does it look more like Paul’s, or does it look more like Kamal’s?


Debating who has worse posture

If it looks like Kamal’s, you might be getting vitamin D not-at-alls (PS: that’s a rhyming mnemonic). Let me explain. I first got my vitamin D tested in 2008, and it came in at a whopping 19 ng/ml…even with taking a multivitamin most days and getting sunlight at lunchtime! As you probably know, pigmented and/or tanned skin serves as sunscreen, making it tough for darker people to synthesize vitamin D without very long sun exposure times. Indians may also produce less active vitamin D (calcitriol) from a given amount of sun exposure due to genetic predisposition.

But my problems apply to you lighter-skinned folk as well — my outdoor lunch excursions were done while wearing business casual clothing with short sleeves. This means covered torso and legs, leaving only about 25% of my skin exposed for vitamin D production. If you factor in things that can lower vitamin D production further, such as cloud cover, not laying down horizontally, higher BMI, and increased age, then it might be worth it to create a “sunlight maximization” strategy. 

How serious are you about getting that extra sunlight? If you’re moderately serious, consider small changes like taking off your shoes and rolling up your pantlegs a bit while sitting in the park. If you’re extremely serious and okay with looking strange, consider occasional use of…mesh basketball jerseys! Yup, those cheapo mesh tops are made of thin material covered with tiny holes. One day I’ll buy a UV meter and check the actual numbers, but my suspicion is that wearing such a jersey would greatly increase skin exposure to the sun, perhaps doubling it or more. I bought my jersey for about $10 on Amazon, and sometimes change into it before leaving for the park. If you don’t already have blue-light blocking glasses to ratchet down light exposure before bedtime, you can buy a pair of those plus a jersey on Amazon in order to level up to free shipping.


Step 2: Acquire tiny chair and tiny laptop

Now that you’ve freed up enough skin to get some substantial sunlight, the next step is to assemble your outdoor office. This part is fun. Eventually you’ll want a small chair, especially if you’re planning on spending many hours working outside. To get a chair that you can stuff in your backpack, just head to REI or any place that sells camping gear. I chose a collapsible model at REI called “Flex Lite” that weighs only 1.75 pounds and folds down to 14×4 inches. 


Tiny chair and tiny laptop fit into backpack with plenty of room to spare.

Laptops are expensive, so you can totally just use whichever model you have. BUT…if you have a few bucks to spare or your current model is in need of replacement, I’d recommend getting an ultra-light laptop, at under 3 pounds. That way, you can fit the tiny laptop and tiny chair along with a hearty lunch in your backpack. Just remember that a laptop with a matte screen works much better than a glossy screen for outdoor use.

Step 3: Optimize ergonomics

The name of the game when working at a computer is to avoid repetitive stress injuries. Simply by being outside, it will give you more incentive to get up and walk around once in a while. But there are other ways to introduce some structured change-of-posture. You can set a timer for every 20 or 30 minutes or get an app on your phone that reminds you to get up. You could also take a break from sitting in the chair to sit on the grass. Note that sitting with feet in contact with the earth (aka “earthing” or “grounding”) is speculated to have some health benefits, which is another bonus for getting in some outdoor office time.

For those with wrist problems, consider switching up your input method every now and then. Switching from right to left hand on occasion is the easiest way to do this. Other ways are switching from trackpad to mouse or trackball and using keyboard shortcuts more. Later this summer, a motion-detecting input device called “Leap Motion” is coming out that will allow you move the cursor with your MIND! Just kidding, not with your mind. But it does allow you to move the cursor with your hands in the air, Minority Report style, reducing much pressure from overstressed wrist tendons and ligaments. Fancy gadgets aside, if you’re going to spend more time outside, it’s a perfect opportunity to think more about varying your working position and revisiting ergonomics.

Step 4: Get pumped

This is going to sound cheesy, but so be it. Working outside can make you feel more alive. The transition from typical cubicle to standing desk is exciting. Work typically takes up the majority of one’s adult life, and standing cracks the mold of being a robotic office cubicle worker. Incorporating some outside work time removes so much of the drudgery aspect from work that it can confuse the most pessimistic of brains.

Normalizing circadian rhythm is an essential part of the health equation, and a complementary factor is being outdoors in the sun. “Sick building syndrome” doesn’t get a ton of research attention, but it’s a very real thing. One reason outdoorsy vacations provide a sense of well-being could be a lack of droning artificial light, stale air with concentrated indoor pollutants, and disgruntled coworkers. Even an office full of windows isn’t perfect. Office windows filter out UVB rays (meaning no vitamin D production or improved mood through endorphin release) but allow some UVA through (meaning staying indoors behind a window doesn’t keep you risk-free from skin damage and cataracts).

Step 5: Get outside already!


Directions: Stuff into backpack, leave for park while whistling CCR’s “Lookin’ Out My Back Door”.

Above are my typical outdoor office supplies, all of which easily fit into a normal-sized backpack with room to spare. From the top left, there’s a travel-sized sunblock, laptop, collapsible chair, flipflops, coconut chips plus sardines in olive oil, and mobile wifi device. If you don’t want to get a mobile wifi device, you can usually get free or cheap mobile wifi from your smartphone.

In terms of practical recommendations, I advise people with school or office work to gradually spend more time working outside. If you find yourself able to be productive working outside, only then consider buying a chair or other outdoor accouterments. Wearing a mesh jersey might seem drastic, but it has a couple benefits. For darker-skinned individuals, it can substantially decrease the prolonged time needed to produce vitamin D. Very light-skinned individuals who are at higher risk of skin cancer could wear sunblock on parts of the body that are more prone to skin damage (like the face) and couple that with producing vitamin D from a jersey-clad torso.

To reiterate because of its importance, a critical concept for office work is VARIATION. The capital letters are to show that I’m not joking around. Combining typical indoor seated work with at least occasional standing work and occasional outdoor seated work is a solid ergonomic base. Increasing the standing to a few hours a week may result in weight loss of several pounds a year. When indoors, a “microbreak” of under a minute could be spent grabbing some water, taking a lap around the office, or climbing a set of stairs. These microbreaks have been shown to reduce muscular discomfort without compromising productivity. When outdoors, microbreaks are pretty much just awesome. Breathe in some fresh air, stare at the clouds, say hello to the doggies at the park. All the studies in the world can’t relay just how nice it is to work outside a couple times a week.

Retroviruses and Chronic Fatigue Syndrome

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

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

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

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

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

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

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

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

A Link Between RNase L and Prostate Cancer

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

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

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

The search for this unknown virus was on.

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

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

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

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

Back to chronic fatigue syndrome

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

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

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

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

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

Will anti-retroviral therapies be effective?

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

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

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

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

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

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

Chronic fatigue patients are celebrating the progress:

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

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

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

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

A new name for XMRV: Human Gamma Retrovirus

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

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

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

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

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

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

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

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


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

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

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

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


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

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

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

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

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

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

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

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

[9] Lo S et al. Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors. PNAS Epub before print August 23, 2010.

[10] Amy Dockser Marcus, “New Hope in Chronic Fatigue Fight,” Wall Street Journal, Aug 23, 2010,

[11] David Tuller, “Study Links Chronic Fatigue to Virus Class,” New York Times, Aug 23, 2010,

 [12] (hat tip

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.

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.