Archive for the ‘Gut Health’ Category

Understanding Candida Overgrowth: Natural Solutions for Yeast Infection

Understanding Candida Overgrowth: Natural Solutions for Yeast Infection

by Jenny Lelwica Buttaccio
Posted 6/29/18

If you’ve been in holistic health or chronic illness circles for any length of time, you’ve probably bore witness to the panic that ensues at the very mention of the word “candida.” But just what is it about this microbe that causes a particular stir among people? And, what role does it play in contributing to the health challenges so many of us struggle with?

Here, we aim to answer your most pressing questions about candida so that you can implement any changes you may need to improve your health.

What is Candida, Anyway?

Candida is a type of yeast — a single-cell microorganism — that normally takes up residence in various niches in the body such as the skin, mouth, intestinal tract, and vagina. “Candida has to have a host to survive, and it’s commensal,” says Dr. Bill Rawls, Medical Director of Vital Plan, meaning it’s opportunistic and benefits from its association with other organisms.

This is compared to the mutualistic relationship we have with our normal flora that’s been honed for millions and millions of years, explains Dr. Rawls, where the microbes are taking advantage of us, but we have also learned to take advantage of them.

For instance, there are numerous bacteria in our digestive tract that, in exchange for being well fed, aid with nutrient metabolism, vitamin production, and waste processing. Candida is an exception when it comes to providing advantages: It does nothing that we know of to support or improve our overall health and well-being.

Candida belongs to the kingdom of organisms known as fungi, which also includes mushrooms, mold, mildew, and more. Along with a spectrum of different types of microbes, everyone has some amount of candida in their gut. If you’re a healthy individual, other microorganisms that make up your body’s unique flora (the total sum of which is called your microbiome), such as bacterial constituents Lactobacillus acidophilus and Bifidobacterium bifidum, work synergistically to maintain a balance with one another so that one or more don’t become problematic to your health.

Currently, there are more than 20 known species of candida that cause infections or yeast overgrowth in humans, according to the Centers for Disease Control and Prevention (CDC). The most common type to affect humans is known as Candida albicans (C. albicans).

You may already be familiar with the more common types of candida overgrowth like oral thrush (often seen in babies and older adults) or vaginal yeast infections. Generally, a candida infection isn’t life-threatening, though it may make you feel lousy. But if overgrowth remains untreated, it can spread to the bloodstream, causing a serious infection called invasive candidiasis, which can affect the blood, certain organs, bones, and more, states the CDC.

Symptoms of Candida Overgrowth

The symptoms of a candida infection can range from mild to severe, and they vary from person to person. For instance, one person may experience bloating and nothing else; another may struggle with every possible side effect. Candida overgrowth symptoms include any number of the following:

  • Oral thrush (characterized by creamy white bumps on the inner cheeks and tongue)
  • Recurring vaginal yeast infections
  • Chronic urinary tract infections (UTIs)
  • Unrelenting fatigue or chronic fatigue syndrome (CFS)
  • Bowel disorders such as Crohn’s disease and ulcerative colitis
  • Gastric ulcers
  • Digestive issues (gas, bloating, constipation, diarrhea)
  • Abdominal pain and cramping
  • Sugar and carbohydrate cravings
  • Joint pain and muscle aches
  • Anxiety and depression
  • Mood swings and irritability
  • Recurring sinus infections
  • Chronic inflammation
  • Brain fog
  • Poor sleep

If you’re thinking that sounds like a long laundry list of symptoms that could easily be confused with a number of other health problems, you’re right. What’s more, candida infections rarely exist by themselves, says Dr. Rawls. Most likely, if you have an overgrowth of the yeast, you also have an excess of other opportunistic microbes in the gut, and it can be difficult to differentiate between them.

The Primary Causes

If we all carry some candida in our body, why do some of us experience overgrowth and miserable symptoms, but the rest of us never know the fungus is even present? Here are the common underlying causes for candida infection.

1. Impaired immune function

For candida overgrowth to occur, you must experience a disruption in your immune system, Dr. Rawls notes. We are regularly exposed to microbes that can make us sick, but often our good flora are able to keep those pathogens in check.

“It’s the balance of the microbiome that we’re finding is so important to disease,” says Dr. Rawls. “And candida overgrowth, in particular, is a symptom of someone’s immune system being trashed, and their microbiome being disturbed — which is not in itself, an illness.”

Underlying immune dysfunction can be a result of chronic illness (including chronic Lyme disease, fibromyalgia, and chronic fatigue syndrome) or any immune-weakening disease or condition. A number of lifestyle factors may also be at play, including lack of sleep, chronic stress, and inactivity—all of which can hamper immune function and upset your body’s balance of flora.

2. Gut dysfunction

In addition to immune system dysfunction, candida overgrowth is typically preceded by a breakdown in your gut health, and microbiome imbalance is soon to follow. Conditions such as leaky gut syndrome, irritable bowel syndrome, and gluten intolerance often coincide with candida overgrowth. Chronic stress is a top culprit, as is consuming excessive refined carbohydrates (candida thrive on starch—more on that below).

3. Antibiotic use

One way the gut flora can be disrupted is through the use of antibiotics, such as when treating Lyme disease and common co-infections like mycoplasma and bartonella. Antibiotics target bacteria – including the ones that are helpful to your body. Researchers discovered that when antibiotics kill off various beneficial bacterial species in the gut, the balance of microbes that normally keeps candida in check begins to shift. This creates favorable conditions for fungal communities to thrive, and can set the stage for candida overgrowth, as stated in the journal, Trends in Microbiology.

4. A carb-loaded diet

To compound the problem, says Dr. Rawls, the diet most common in modern Western society – excess carbohydrates, refined grains, and saturated fats, and minimal fresh produce, lean protein, and healthy fats – is neither natural nor nourishing to our bodies. The reason sugar and refined carbohydrates get a bad rap is that they act as fuel sources for candida. When you feed candida, you facilitate overgrowth and microbiome disruption, which further disrupts the immune system and impairs its ability to maintain a symbiotic relationship with numerous other microbes.

5. Environmental toxins

Another cause of yeast overgrowth includes exposure to environmental and chemical toxins. A prime example of an environmental toxin is mold. All houses have some mold inside of them, about half of which are at problematic levels. Both mold spores and mold metabolites, known as mycotoxins, are present in the air. When inhaled, they can suppress your immune system and allow candida overgrowth, explains Dr. Rawls. Plus, candida itself can produce its own mycotoxins that make you miserable.

Regarding chemical toxins, Dr. Rawls suggests that people are often unaware of the barrage of hidden, chemical exposures present in homes and the environment, which can contribute to hormone imbalances, and ultimately, immunosuppression. Top sneaky toxins found in homes include:

  • Phthalates, endocrine-disrupting chemicals used to make plastics flexible
  • Bisphenol A, another endocrine-disruptor found in food and drink containers, can linings, and receipts
  • Formaldehyde, often found in building materials and pressed-wood furniture products
  • Radon, an odorless, radioactive gas that can seep into homes from the ground
  • Parabens, estrogen imitators used in cosmetics and other beauty products
  • Chlorine, a disinfectant used in municipal water systems
  • Perfluorochemicals (PFCs), used on stain-resistant fabrics (Scotchgard, Goretex), cooking pans (Teflon), food wrappers, and microwave popcorn bags
  • Flame retardants in building materials, cushions, and more
  • Lead in paint made prior to 1978 and old plumbing

Testing and Diagnosis

In many cases, candida overgrowth can be assumed based on an assessment of your symptoms and a risk factor analysis—no separate candida-focused testing needed, says Dr. Rawls.

But in severe cases where symptoms are persistent and life-disrupting, there might be a need to gather additional medical information, such as the strain or species of yeast you’re trying to combat. Other people simply feel more comfortable with an official diagnosis. In those instances, work with your doctor to determine whether the following tests may be appropriate:

Stool Analysis

There are a variety of specialty labs offering a comprehensive stool analysis, which checks for the strain and species of yeasts that reside in your gut. They can tell you whether your candida levels fall within the normal range (though not what might be a normal for your particular microbiome).

Blood Antibody Testing

Blood work examines the IgG, IgM, and IgA antibody levels of candida. Elevated antibody levels can indicate a candida overgrowth somewhere in the body. But similar to antibody tests that check for Lyme disease, it’s possible to get a false negative. That’s because when candida suppresses the immune system, your body may not be able to yield a sufficient response and produce measurable levels of antibodies for the test.

Urine Organic Acids Testing

If an overgrowth of candida is present in the gut, it creates a metabolite known as D-Arabinitol, which will be excreted in the urine as a byproduct.

Complete Blood Count (CBC) with Differential

Another way to assess immune function, a CBC can detect a low white blood cell count, which has been associated with yeast overgrowth. But it’s important to note that results are very non-specific, says Dr. Rawls. A low white blood cell count could indicate any number of other illnesses, so a CBC test alone will not help you pinpoint candida infection.

DNA Testing

This detects the DNA of certain specific candida species. A negative test indicates that either the species-specific DNA is not present, or that levels are present at a concentration below the detectable limit.

It’s important to note that no testing methods provide a foolproof way to detect the presence of candida overgrowth. Positive test results or no, if you suspect you’re suffering from yeast overgrowth, treatment aimed at restoring immune and gut health and balancing the microbiome will address yeast overgrowth along with too-high levels of other problematic microbes and related health concerns.

How to Overcome Candida Overgrowth

While there may be instances where a short course of antifungal medication is warranted to jumpstart the treatment, over time, candida can become resistant to conventional therapies. To get well, Dr. Rawls emphasizes the importance of treating the underlying illness, which includes restoring healthy immune function and balance in the microbiome.

Step one? Herbal interventions. “Virtually any herb is going to have some effect on yeast,” says Dr. Rawls. “One of the nice properties of herbs is they tend to suppress pathogens without affecting the normal flora. So herbs have a balancing effect on the gut, which is very different than prescription antifungals and antibiotics.”

Certain herbs have been shown to be particularly effective against yeast. They include berberine, andrographis, cat’s claw, garlic, and Japanese knotweed. Additionally, herbs like Reishi mushroom and cordyceps are highly helpful. Both Reishi and cordyceps are fungal species, and some people are hesitant to pit fungus against fungus, but Dr. Rawls assures that both are especially beneficial for balancing the immune system and normalizing immune response.

Also key is reassessing your diet and nixing excess sugar, refined carbohydrates, and starch—yeast’s favorite foods. “If you don’t feed candida, they can’t thrive—simple as that,” says Dr. Rawls.

That means staying away from sweets, fruits, alcohol, processed foods, and grains, and avoiding starchy vegetables such as potatoes, acorn and butternut squash, peas, corn, pumpkin, parsnips, and plantains. Stick with this candida diet until your symptoms subside, then gradually add foods back in — one every few days or so—and watch to be sure your symptoms don’t flare up again.

Beyond that comes adopting all the habits that are vital to supporting a strong immune system, one that’s capable of maintaining healthy balance in your microbiome and keeping yeast and other troublemakers at bay. That includes cultivating eight hours of sleep each night, taking steps to minimize the stress in your life, and reducing your exposure to toxins.

Finally, empower and educate yourself about your condition. While most people with candida overgrowth are able to get a handle on the problem all on their own, sometimes a stubborn infection calls for additional support. So if you do consult with a physician, you’ll be armed and ready with plenty of information to discuss your needs and treatment options with them.


Jenny Lelwica Buttaccio, OTR/L, is a medical, health, and lifestyle writer and editor, and a licensed occupational therapist. Her work has been found in leading publications like HuffPost, Men’s Health Magazine, Prevention Magazine, and many others. Her areas of expertise include chronic health conditions, wellness, mind-body fitness, and chronic illness management. You can find her personal Lyme story on her blog, The Lyme Road or diving into the grassroots, Lyme disease awareness movement, Lyme Disease Challenge. Follow her on Twitter and Instagram.

1. Bennett JW, Klich M. Mycotoxins. Clinical Microbiology Reviews. 2003 Jul; 16(3): 497–516.
2. Candidiasis. Centers for Disease Control and Prevention website.
3. Cater RE 2nd. Chronic intestinal candidiasis as a possible etiological factor in the chronic fatigue syndrome. Medical Hypotheses. 1995 Jun;44(6):507-15.
4. Crook, W G. The Connection And Women’s Health. Jackson, TN: Professional Books, Inc; 2005.
5. Huffnagle GB, Noverr MC. The emerging world of the fungal microbiome. Trends in Microbiology. 2013 Jul; 21(7): 334–341.
6. Kumamoto KA. Inflammation and gastrointestinal Candida colonization. Current Opinion in Microbiology. 2011 Aug; 14(4): 386–391.
7. Silva Dantas A, Lee K K, Raziunaite I, et al. Cell biology of Candida albicans–host interactions. Current Opinion in Microbiology. 2016 Dec; 34: 111-118.


Candida – Signs You Have it & What to Do! The Candida Summit Online & FREE July 9-15, 2018

Candida – Signs You Have It and What To Do!

Published on May 29, 2018
Dr. Tom O’Bryan

Educator and Physician at | Celiac Disease/Non-Celiac Gluten Sensitivity/Autoimmunity | Functional Medicine

A Candida overgrowth can be serious, progress to an infection, is often resistant to drug protocols, and it can show up in unexpected symptoms, like cravings, depression, autoimmune diseases…

Click this link to save your seat, and please share this invitation with those you love:

In my upcoming interview on The Candida Summit, I will discuss how candida can become systemic and show up in a long list of easily misunderstood symptoms, but how it’s home base is always in your gut.

To make it worse, candida can be extremely difficult to test for and diagnose — and it can cause major health problems and even autoimmune diseases, such as Hashimoto’s thyroiditis, rheumatoid arthritis, ulcerative colitis, lupus, psoriasis, scleroderma, or multiple sclerosis.

So what are common symptoms of candida overgrowth?

* Fatigue, joint pain or Fibromyalgia

* Digestive issues, such as bloating, constipation, or diarrhea

* Difficulty concentrating, poor memory, or brain fog

* Lack of focus, ADD or ADHD

* Irritability, mood swings, anxiety, or depression

* Vaginal infections, urinary tract infections

* Severe seasonal allergies

* Strong sugar and refined carbohydrate cravings

* Skin issues like eczema, psoriasis, hives, and rashes or fungal infections, like athlete’s foot

Click this link to save your seat, and please share this invitation with those you love:

Candida overgrowth is not just an innocent “yeast” infection. It interacts with your body’s organs, like your brain, your hormone balance and your body’s ability to detoxify through your liver.

It is NOT your fault. There are so many causes behind candida overgrowth, like the use of antibiotics, a high sugar diet, allergies and food sensitivities, stress, alcohol, immunosuppressive illnesses, use of NSAIDs, and even birth control.

At this event, you will learn how to identify if you or a loved one may be suffering from an overgrowth, or worse. And strategies for addressing candida and the issues that often accompany it, like heavy metals and parasites.

If you have wondered about this, or if you have health concerns that are not getting answers yet, this Summit may be the answer.

To your health,

Dr. Tom O’Bryan

PS: Even if you can only listen to two or three of the interviews – or just one per day, this event addresses a condition so stealth and often even found at the heart of conditions like cancer and dementia. Click here to save your seat at this event, at no cost, as my guest:


Candida Summit – FREE  (Go here to register and to see video)

Candida is a naturally occurring, yet “opportunistic” fungus.

With the right conditions, there’s no limit to where it will spread and, when rampant, it can cause intense sugar cravings, brain fog, bloating, depression, anxiety, digestive issues, low energy or worse…

…chronic diseases.

Learn to overcome candida and reclaim your health at The Candida Summit

Even though candida is an important part of your digestive process, if unchecked, it can cause serious damage to your health.

Certain lifestyle choices and/or illness can deplete the “good” bacteria in your body to create room for candida growth:
• Use of antibiotics
• A high sugar diet
• Allergies
• Years of drinking alcohol
• An immunosuppressive illness
• Use of NSAIDs
• Birth control

Evan Brand, your host, also suffered (and healed!) from candida, parasite infections and bacterial overgrowth. In his health practice, upwards of 95% of his clients have some degree of candida overgrowth — time and time again, he sees debilitating and mysterious symptoms disappear once candida overgrowth is addressed. Join us to learn more!

Learn to overcome candida and reclaim your health at The Candida Summit

The Candida Summit is online and FREE from July 9-15, 2018!



Palsy of the Gut & Other GI Manifestations of Lyme/MSIDS

This 2008 article is full of nuggets for those of you who suffer with GI issues and Lyme/MSIDS.  It has natural options as well as pharmaceutical options.

“Palsy Of The Gut” And Other GI Manifestations Of Lyme And Associated Diseases​

March 1, 2008 in Science/Research by Dr. Virginia T. Sherr, MD

Bell’s palsy signifies paralysis of facial muscles related to inflammation of the associated seventh Cranial Nerve. Physicians may not realize that this syndrome is caused by the spirochetal agent of Lyme disease until proven otherwise. Whether it is a full or hemifacial paralysis, Bell’s palsy is cosmetically disfiguring when fully expressed. Sudden loss of normal facial expression terrifies patients who naturally fear they are having a stroke. When a smile is asked for, normal countenances warp into bizarre grimaces. The amount of tooth area exposed in this attempt to smile helps doctors evaluate the degree of paralysis and its change over time (Figure 1). In every case of Bell’s, doctors need to carefully investigate by history, physical, and laboratory work every shred of evidence that might suggest the presence of cryptic tertiary Lyme, a serious multisystem, gut and neuro-brain infection even though about half of fully diagnosed patients have no evidence whatsoever of having had a tick-bite.

Gastrointestinal Lyme disease may cause gut paralysis and a wide range of diverse GI symptoms with the underlying etiology likewise missed by physicians. Borrelia burgdorferi, the microbial agent often behind unexplained GI symptoms—along with numerous other pathogens also contained in tick saliva—influences health and vitality of the gastrointestinal tract from oral cavity to anus. Disruptions caused by GI borreliosis (Lyme) may include, amongst many others, distortions of taste, failure of other neural functions that supply the entire GI tract—paralysis or partial paralysis of the tongue, gag reflex, esophagus, stomach and nearby organs, small and/or large intestines (“ileus”), bowel pseudo-obstruction, intestinal spasms, excitability of gut muscles, inflammation of lumen lining tissues, spirochetal hepatitis, possibly cholecystitis, dysbiosis, jejunal or ileal incompetence with resultant small intestine bacterial overgrowth (SIBO), megacolon, encopresis and rectal muscle cramping (proctalgia fugax).

In cerebral hypothalamic and pituitary centers, usual sites of borrelial disruptions of the brain’s normal hormonal cascades, there are strong influences on human attitudes, ideation, and behavior relating to gastronomic issues. Newly discovered Lyme endangered cerebral hormones and renegade cytokines regulate brain-gut interactions thus initiating behavioral tendencies such as anorexia or a failure of satiety with resultant obesity.

Ticks and other vectors of Lyme disease attract their own infections from many microbes, some known and some unknown (viruses, amoebas, bacteria, and possibly parasitic filaria), which they then also can pass on to humans. The GI tract is especially vulnerable to machinations of such co-infections as bartonellosis, mycoplasmosis, human anaplasmosis (HA), and human monocytic ehrlichiosis (HME). Syndromes exactly similar to Irritable Bowel Syndrome (IBS), Crohn’s Disease, and cholecystitis, for example, may not have readily suggested a borrelial etiology to the diagnostician but Lyme increasingly is known to be a potential contributor to each.

All known Lyme-gut syndromes are treated by combining several effective antimicrobials (including use of azole medications with specific antibiotics) with agents that boost gut lining repairs and overall immunity enhancement. Azole medications are borreliacidal (against the anti-Bb spirochetal cyst form) medications such as metronidazole (Flagyl). Needed GI healing agents may include gut stimulants or relaxants, Ph agents, bile salts, nutriceuticals, immunity-enhancers, neurotoxin absorbents, and sterilizers of gut-specific microbes.

Parallelism between Lyme borreliosis-caused paresis of facial muscles supplied by Cranial Nerve VII and Lyme-caused gastrointestinal paralyses suggested a pseudonym to the author–Bell’s palsy of the Gut—despite the fact that these syndromes are related to different types of neural fibers and only occasionally occur together. Since similar injury to all sites may be etiologically related, however, otherwise unexplained gastrointestinal symptoms should be considered as possibly related to Lyme borreliosis and/or its co-infections until proven otherwise.

Until proven otherwise, a patient’s unexplained facial paralysis is caused by the tick-borne spirochetes of Lyme disease (LYD) (1). The widely endemic bacteria are easily capable of inducing distal inflammation of the Seventh Cranial (Facial) Nerve (2). “Considering the incidence of Bell’s palsy in Lyme, it is improper to treat it as viral in origin without a work-up for Lyme disease” (3). In an early study with nearly 1000 LYD cases studied, Bell’s palsy occurred in at least 10% of validated cases (4). The frequency of Lyme’s Bell’s palsy etiology is unfamiliar to many physicians. Likewise many physicians are unfamiliar with the spirochetal cause of paralyses of muscles that facilitate normal gastrointestinal transit. Yet, these vital muscles also may be greatly compromised by the same offending neurotropic spirochete, Borrelia burgdorferi (Bb) in patients who are totally unaware of having Lyme disease. Their physicians are often surprised to learn that persistent Lyme disease is outstandingly a disease of the brain as well as involving one or all components and sub-systems of the entire nervous system (5). It is not yet widely understood by clinicians that at least 40% or more of Lyme-infected patients have major, handicapping, neurological manifestations (6,7) with the likelihood that 100% have some brain involvement. It remains to be clarified which Bb neuritides are involved in specific GI sequelae of the infection or if inflamed nerves are, indeed uniformly at fault.

“The vagi (10th Cranial Nerves) are major suppliers of the gut’s external nervous system and being very long and complex, are vulnerable to neuropathies such as Lyme disease or diabetes which can cause them serious damage.” (Personal communication from Neurologist, Richard Rhee, M.D., F.A.A.N., Neptune, NJ)

“Vagus nerve paralyses are more commonly diagnosed when caused by Herpes (varicilla) zoster or Herpes simplex viruses wherein most patients I have seen are nauseated and have no appetite. I have not observed paralytic ileus in these cases. Should vagal paralysis occur in a Lyme patient, I think the patient would complain of hoarseness and dysphagia.” (Personal communication from Dr. Hidecki Nakagawa, Japan) Indeed, both of these problems are common symptoms of neuro-Lyme.

“The autonomic nervous system supplies the gut . . . sympathetic fibers inhibiting peristalsis and secretion and parasympathetic fibers increasing them . . . Functions of the sympathetic nerves include vasomotor, motor to the sphincters, inhibition of peristalsis, and transport of sensory fibers from all of the abdominal viscera. . . . Functions of the parasympathetic nerves comprise motor and secretomotor to the gut and glands” (8).

Borreliosis-caused, gastrointestinal tract paralysis and related abnormalities can occur anywhere along the entire length of the tract (9,10)—involving, for example, functionality of taste buds (11,12), muscular strength of the tongue, gag reflex, ability to swallow, gastroparesis, peristaltic retardation (or excitation) related to small bowel competency, dysbiosis, total arrest of peristalsis (“ileus”), pseudo-obstruction (sometimes associated with Bell’s palsy) (13), colon dysfunctions, encopresis, proctalgia fugax and the final act of defecation. “In 5%–23% of patients with early Lyme borreliosis, there can be gastrointestinal symptoms such as anorexia, nausea, vomiting, severe abdominal pain, hepatitis, hepatomegaly and splenomegaly. Diarrhea occurs but is seen in only 2% of cases” (14). Regardless of the site, spirochetes’ disturbing symptoms may come and go spontaneously, often temporarily resolving in a matter of hours to days, although resolution does not imply cure. As with Bell’s palsy of the face, these gastrointestinal conditions may endure or only partially remit (15).

Similarities between Bb-caused paralyses of muscles supplied by the Facial Nerve and Lyme-caused GI neurogenic paralyses suggested a pseudonym to this writer–Bell’s palsy of the gut—despite the fact that the two manifestations of the infection may not be synchronous. Yet, they are etiologically related, which suggests need for a high index of suspicion regarding presence of borrelial disease in all perplexing gastrointestinal syndromes.

Potent Microbial Co-infections As Related To Geographic Factors

Endemic areas for tick-borne diseases include the entire Eastern and Western coasts of North America with their internally contiguous states as well as Midwestern states that support migratory bird North-South flyways (16). Infected deer ticks (Ixodes scapularis and similar hard-bodied ticks), vectors of many diseases including the ones discussed below, are thus most widely distributed by birds, geographically. There are few places in the United States that are totally safe from the risk of microbes thus ferried. In 2002, the CDC estimated the existence of nearly one-quarter million new cases in USA’s rapidly expanding LYD epidemic.

Very common co-infections from infected Ixodes sp. ticks (Figure 2) include the ehrlichioses—Human Granulocytic Ehrlichiosis, which recently was renamed Human Anaplasmosis (HA) and Human Monocytic Ehrlichiosis (HME). Human babesiosis, a tick-borne, one-celled parasite of erythrocytes, is widely misdiagnosed in its endemic, chronic form (17,18). A Bartonella-like bacteria, mycoplasma spp, and other viral and opportunistic infectors are now known to be tick-borne (19), existing in the full territorial range ofI. and other ticks (20–22). Resultant illnesses include two that have been found to be the most common tick-borne invaders of children’s gastrointestinal tracts—the combination of bartonellosis and Lyme borreliosis gut infections (23).

As with the spirochetes of Lyme, Bartonella is an increasingly common (perhaps the most common) tick infector (21). “PCR analysis of Ixodes scapularis ticks collected in New Jersey identified infections with Borrelia burgdorferi (33.6%), Babesia microti (8.4%), Anaplasma phagocytophila (1.9%), and Bartonella spp. (34.5%). The I. Scapularis tick (Figure 3) is a potential pathogen vector that can cause coinfection and contribute to the variety of clinical responses noted in some tick-borne disease patients” (24). As more experience has been gained with Bartonella henselae and its related species, bartonellosis has been found capable of causing severe gastrointestinal pain and malfunction as well as specific skin eruptions. Both of these sites involve vasculopathy— enteric and dermal as well. Scar-like stripes on the patient’s torso are telltale “stretch marks” or “scratch marks” of the disease, easily notable. This external and visible sign (the seemingly mysterious but diagnostically pathognomonic striae) may make the GI bartonellosis diagnosis less complicated for gastroenterologists and other specialists (25).

Quite surprising to many physicians, bartonellosis can cause major central nervous system damage, similar in some aspects to the aforementioned Lyme neuroborreliosis. Lyme and bartonellosis symptoms may include encephalitis signified by headaches, major memory loss, rages, seizures, and coma, as well as inflammation of the heart, abdominal pain, bone lesions, and loss of vision. Until recent years, Bartonella, at onset of infection an endothelial and subsequent red blood cells infector, was considered to cause a relatively benign and common disease otherwise known as cat scratch disease (26–28). Now that ticks have become significant transmitters of Bartonella infections into humans, this vectoring appears to amplify victims’ general Lyme symptoms (26), and quite likely amplifies GI tract lining symptoms as well.

Often Unsuspected Presentations Of GI Tract Lyme—diagnostic Usefulness Of PCR Tests On Specimens Harvested From Endoscopy/Colonoscopy Biopsies (With Illustrative Cases)

One of the blessings of modern medical investigation is a positive PCR (A direct test—polymerase chain reaction— capable of pinpointing an offending microbe’s DNA). This test can be performed on specimens from the patient’s blood, serum, plasma, CSF, urine, mothers’ milk, and all biopsy tissues. PCRs can play a vital role in diagnosing tick-borne diseases especially those affecting any organs or associated tissues. “Lyme disease is usually diagnosed and treated based on clinical manifestations. However, laboratory testing is useful for patients with confusing presentations and for validation of disease in clinical studies” (29).

DNA tests are especially handy because they can be utilized by way of biopsies harvested from inside the gut during otherwise routine colonoscopies and endoscopies in cases where the diagnosis is uncertain. PCR’s are highly specific although they are less than ideally sensitive so that a positive test is a reliable indicator of Bb infection while a negative test simply does not exclude Lyme and does not indicate a lack of infection (30).

An illustrative case history is that of “Mr. F,” a mature man thought to have been mentally retarded most of his life. His father had ascribed his youth’s sudden headaches, stiff neck, and cognitive losses to the will of God. No further evaluation or treatment was allowed. They lived in endemic tick territory at the time. Decades later the patient realized that his symptoms back then followed a series of bites by minute ticks). Now an adult, the patient’s chronic “ulcerative colitis” and depression kept him from his job as a school janitor. (Antidepressant medication had mostly just helped his anxiety) When a colonoscopy was needed, a generous gastroenterologist biopsied Mr. F’s luminal tissues, which the referring doctor then sent for testing to a reference lab specializing in tick-borne diseases. Specimen analysis returned as PCR positive for etiologies of 3 diseases that infected his colon: Borrelia burgdorferi (Lyme disease), Mycoplasma fermentans (suspected of causing GI injury via proinflammatory cytokines) (25), and B. henselae (bartonel bartonellosis). Each disease required its own unique treatment, all of which were successful and the patient’s GI symptoms resolved. Mr. F’s depression also cleared and in its place there was a kind of chronic good cheer, off and on resembling mild hypomania.

The case of “Mrs. M” illustrates another important method of detecting the presence of an active Lyme infection as well as uncovering a possible contributing cause of cholecystitis. Gall bladder (GB) tissue was tested for Bb spirochetal DNA following a cholecystectomy on this seronegative patient: A middle-aged woman with a known diagnosis of pre-existing, asymptomatic gallstones, experienced episodes of allergies, severe headaches and extreme chronic fatigue. She was treated for 2 tick-borne diseases—- LYD and babesiosis, having had symptoms of both and a positive PCR blood test for babesiosis. The LYD was treated with oral antibiotics and then 3 months of IV ceftriaxone (Rocephin) following which she showed improvement.

About a year later, Mrs. M, again fatigued, developed right shoulder blade pain and afebrile nausea after eating greasy foods. Surgery to remove her diseased gallbladder was scheduled. Treatment (doxycycline) for suspected but unproven persistent Lyme was begun. The family physician asked that biopsy specimens of the removed gall bladder be tested in a reference laboratory specializing in tick-borne diseases (31). The resultant PCR test on her gall bladder tissue was positive for DNA of the causative Bb spirochete of Lyme disease. This PCR biopsy confirmation of a seronegative patient’s Lyme diagnosis illustrates that, while Western Blot and PCR blood sample testing, especially for active late stage LYD, may not show a positive antibody response, a tissue PCR analysis may confirm the diagnosis, even when the patient has previously been treated. PCR’s done on blood are less satisfactory since Bb prefers an in-tissue environment. Treatment of Lyme disease by IV Rocephin can lead to gall bladder sludging. In this case the GB stones were considered to have predated the IV treatment. Of interest, a similar spirochetal disease (leptospirosis) has been reported as simulating symptoms of cholecystitis (32). This may be the first confirmation of a diagnosis of Lyme disease performed on GB tissue to be published—its write-up has been submitted for publication. (Case and personal correspondence from Sabra Bellovin, M.D., Portsmouth, VA)

In another instance, “Mrs. E” was evaluated in a psychiatrist’s office for severe depression, anxiety, and fatigue some months following successful removal of a colonic polyp. She mentioned that she had been experiencing chronic, depleting, diarrhea and severe insomnia. Biopsy tissue was then obtained from a repeat colonoscopy by a cooperating gastroenterologist. The specimen was PCR positive for an unspecified Mycoplasma. M. Pneumoniae is a known gut epithelial lining pathogen (33) and M. fermentanshas been found in inflamed gastro-enteric linings (19). Both potentially pathogenic mycoplasmas have been documented as carried by ticks. In addition, Mrs. E’s blood tests revealed the presence of high antibody titers for ehrlichiosis (Human Anaplasmosis—HA) as well as positive Western Blot (WB) tests for Lyme disease, indicating active cases of both when tested in a related specialty laboratory (34). Interestingly, Mrs. E’s family physician in Pennsylvania was willing to treat the ehrlichiosis but unlike some more southerly PCP’s (35) she thought Lyme was confined to New England and was unwilling to treat her patient’s borreliosis.

Treatment of active Lyme disease is often denied to very sick patients with or without the presence of positive test findings. Serologic testing for Lyme disease as routinely performed by local laboratories is well known for insensitivity. The CDC surveillance case definition excludes, for example, as many as 78% for IgG of known positive cases (36,37). More modern guidelines are currently available for diagnosis and treatment of tick-borne diseases (38,39).

Because the recommended first-use enzyme-linked immunosorbent assay (ELISA) test tends to miss at least 50% of authentically positive Lyme cases, it is less likely to be relied on (29,40). ELISA tests were not performed in any of the cases presented here.

A suddenly spastic or immobile esophagus or similar paralysis of the stomach muscles may represent esophageal and/or gastric paresis or spasm from Lyme neuropathies (5). Infection influencing the vagus nerves has been documented to cause paralysis in other diseases (8). Additional Bb-related symptoms may manifest as gastroesophageal reflux disease (GERD), early or absent satiety, GI bloating, nausea, vomiting, and atypical colitis wherein the pANCA test may be helpful. If Crohn’s and colitis are considerations, a Prometheus first step may help to support this diagnosis; however tissue biopsy is necessary to confirm the diagnosis. (Personal communication from Martin D. Fried, MD, FAAP, Colt’s Neck, NJ)

As noted, neuropathies can result from the immune (cytokine) system over-activation often seen in chronic Lyme cases. This may lead to prolonged inflammation with resultant damage to the enteric nervous system and/or the autonomic nervous system supplying the gut (5). In addition, possible spirochetal paralysis of the vagal nerve(s) may cause temporary or long-lasting disruption of normal small intestinal mobility, and that, in turn, may lead to Small Bowel (or Intestinal) Bacterial Overgrowth (SBBO or SIBO) (41). SIBO can be a serious and difficult-to-eradicate infection. The colon microbes involved usually have migrated backwards to small bowel areas from their original site of benign bacterial growth following loss of competent peristaltic rhythm in a now partially compromised small bowel. This overgrowth of upwardly mobile but misplaced bacteria may greatly interfere with the normal absorption of nutrients from the small intestines causing dysbiosis and various forms of malnutrition among other mischief. Bacterial overgrowth in the small gut can result in remarkable, intermittent, immense, abdominal bloating/distention with or without eructation or flatulence (42). Such disruption may occur despite the fact that small bowel muscles have their own enteric enervation and could function independently to some degree. In many cases, the diagnosis of SIBO is verifiable by the Hydrogen-Lactulose Breath test, which can reveal excess hydrogen production from the relocated colon bacteria. Related test kits are offered to outpatients upon physicians’ requisitions by Genova (aka Great Smokies) (43) and Doctor’s Data (44) Laboratories, thus allowing the unassisted patient to complete the test at home and mail it back to the lab.

Another borrelial cause of massive increases in abdominal girth associated with “gasless” bloating may cause diagnostic confusion. Unrelated to gut symptoms from Lyme’s disruption of the body’s internal “wiring,” Bb-inflicted polyradiculopathies of T7- 12 (nerve root inflammations) may result in paralysis of external abdominal muscles such as the rectus abdominus. This in turn can also lead to the appearance, not the reality, of extensive bloating. No exercise “crunches” will alleviate this distention even for a previously well-toned individual. Antibiotic treatment for borreliosis may resolve this symptom (45, 46).

A diagnostic tip-off to the presence of LYD (and/or bartonellosis) may be a concomitant hypersensitivity of the chest or waist area skin in combination with distended belly from weakened abdominal wall muscles (47). One may hear from a child with unrecognized tick-borne disease, “I can’t stand anything touching the front of me.” Or, “My clothes have to be real tight” or “I will wear only these (very loose) clothes.” Parents of children with Lyme disease are often bewildered by apparent compulsions such children may develop while trying to get dressed in the morning. Catching the school bus on time can result in chaos as the harried parent attempts to ready a child when the child is not known to be Lyme- or bartonellacompromised.

Adynamic or paralytic ileus, a non-obstructive motility failure (suddenly “silent” intestines), may occur as a result of neuroborreliosis on an intermittent basis, with resultant abdominal distention. As mentioned, these functional lapses and pseudo-obstructions from faulty gut motility may be due to direct spirochetal or other microbial invasion with resultant tissue inflammation, or to noxious influences of cytokine (immune system) reactions, or to microbeproduced neurotoxins that can affect Central, Somatic, Autonomic (parasympathetic or sympathetic), and Enteric nervous systems that supply the GI tract.

In children and in adults who unknowingly have been inoculated with Bb spirochetes, etc. from ticks or from bites of other less common Lyme disease vectors such as horseflies, deer flies, or even mosquitoes (48), the resultant altered gastrointestinal motility symptoms may be mild to life-threatening. (Ehrlichiosis has a 5% mortality rate in children.) Students are frequently reported to the office as having persistent stomach pain (“belly aches”) (49), failure to thrive, reluctance to go to school (their behavior often incorrectly labeled psychosomatic, attention-getting or amotivational), or as adults, patients may be fearful of going out to eat or to work due to an apparent “Irritable Bowel Syndrome.” These latter borreliosis symptoms are a result of visceral hypermotility instead of paralysis. In addition, the patient may have bloody diarrhea reminiscent of Crohn’s disease, or of colitis (50). As in the case of H. pylori’s discovery as a cause of gastric ulcers, suspicion amongst researchers is growing in regard to “stress” as the cause of IBS. And, Crohn’s Disease is now considered etiologically related to a pre-existing (unspecified) gastroenteritis (51). Constipation of an unusual type can occur in a LYD patient who is not prone to having sluggish bowel movements. The stool can suddenly become puttylike, unresponsive to usual laxative treatments. Even massive efforts to relieve this obstipation using all vigorous conventional methods may not suffice. In addition, many patients with gastrointestinal Lyme disease develop symptoms reminiscent of Sprue/celiac disease and/or lactose intolerance all of which may improve somewhat when treatment for the underlying infection( s) is successfully concluded.

The Molecular Brain As A Gut-influencing Organ

Another site of Bb spirochete-caused neuron damage that likely affects the GI tract is the human brain—especially its Lyme-injured hypothalamic and brain stem melanocortin circuits. “Melanocortins are small protein molecules that carry messages between nerve cells in the brain. They are involved in regulating a variety of complex behaviors, including social interactions, stress responses and—most importantly in this context—food intake. So it is easy to see how interference with them could cause anorexia and bulimia . . . Anorexia and bulimia may be autoimmune diseases—and so may several other psychiatric illnesses” (52). This passage refers to the work of scientists from the Karolinska Institute in Stockholm, Sweden, who have been looking at possible connections between different gut bacteria and autoantibodies against melanocortins to see if they can determine which bacteria might be responsible for a variety of eating disorders. They are finding that the level of autoantibodies to melanocortins is positively correlated with anorexia, but inversely correlated with bulimia (53). When melanocortins are pathologically over or under-activated, either stimulation of hunger or of food avoidance may result. The former leads to hyperalimentation and obesity (54). The latter leads in some cases to anorexia nervosa and other health problems. Brian Fallon, MD, and other psychiatrists have long noted that when their neuro-Lyme patients are treated with antibiotics for the underlying chronic Bb infection, there is significant improvement in eating disorder symptoms (55). Bell’s 7th and the vagus’ (10th) Cranial Nerve pathologies, brain molecular distortions, gastrointestinal disruptions, and human behavioral idiosyncrasies are all perceived of as interrelated.

Additional Diagnostic Hints

Patients with a Lyme disease-related facial paralysis may not have positive antibody laboratory tests for borreliosis as is often also true of those with gastrointestinal neuroborreliosis. Despite those facts, it is imperative that the multi-organ infecting microbes associated with such dysfunctions be suspected and treated if they are likely to be present—but the prescription of immunity lessening steroids should never be used routinely to decrease symptoms (56). Neuro-Lyme is mid-or-latestage (tertiary) Lyme disease, which may account for the lack of positives on many antibody tests (antibodies having been depleted by Bb, an ace immune system disabler.) Commonly, active tertiary Lyme shows a diagnostic positive IgM response that is conventionally but mistakenly thought to be a marker accurate only in relatively early infection (57). Persistence of a positive IgG WB test is most often seen in those with predominantly arthritic forms of Lyme disease (58).

Although the tests should be run, attempts to check for positive DNA is time consuming with results rarely coming back inside of several weeks. Yet, the patient needs immediate treatment. That same dilemma confronts both the patient with Seventh Cranial Nerve palsy as well as the enterically compromised patient. If paresis or spasm occurs and the esophagus stops functioning, a patient may choke on recently swallowed food or fluid. If it occurs in the stomach, it may cause nausea and gnawing abdominal pain. If even a partial paralysis occurs in the small intestines, SIBO (SBBO) with bloating of immense proportions may ensue. Paresis of the colon may result in mega colon with severe constipation and/or encopresis even in very young children in Lyme-endemic regions. Diarrhea resembling an IBS-like syndrome can occur if there is Bb-sponsored gut hypermotility. Similarly, GI spasms may also result in a plethora of symptoms, including spastic colon and seeming occlusions. A trial on antimicrobials is helpful for those suspected of having tick-borne diseases despite negative tests. The “symptom intensification syndrome” known as a Herxheimer reaction needs to be anticipated by both doctor and patient as potentially distressingly difficult but is to be expected when immune systems over-respond to a spirochetal die-off. This reaction should not be confused with an allergic reaction to the antibiotic.

Most helpful diagnostic tests for Lyme disease are the direct or photographed observations of a “Bulls Eye’s” circular or oval skin rash. Unfortunately, it is only present in roughly 50% of known cases. If the lesion slowly expands (due to spirochetes multiplying in the outer edge, which fact allows easier biopsy and culture) it is perfectly diagnostic of Lyme disease or its associated “STARI” (Master’s disease—a form of Lyme disease.) In endemic areas, patients should be coached to photograph any suspect rashes and to keep the living tick for a doctor’s observation or Bb DNA testing. Western Blots (WBs) are best done in a reference lab specializing in tick-borne diseases with the doctor’s insistence that all antibody bands be counted and reported. The tests should employ the correct strains of Borrelia and also not depend on spirochetes that have lost DNA due to multiple passes through a series of hosts.

Acceptable tests have both high specificity and sensitivity. For example, the C6 Peptide/Lyme test has excellent specificity so that those tests that come back positive are valid and are confirmatory of Lyme’s presence. However, negative results from the C6 test merely show that the test was done—they do not show that Bb was absent. The negative test does not prove that the patient is free of Lyme disease.

Useful tests include a urine Bb antigen test with positive findings backed up by the highly accurate Southern Blot test. As noted, PCR tests on all appropriate tissues/fluids, especially serum, whole blood, urine, tears, mother’s milk and CSF are valuable diagnostically.

Choices of tests for several Bb’s co-infections are enhanced by awareness of the prevalent strain/species of the infection that is extant in the area where the patient was tick-inoculated. Tandem IFA and PCR tests are usually performed for co-infections. In addition, florescent microscopic views of stained slides can show babesiosis ring forms inside RBC and other tests can show cystic forms of Bb under black light. Bartonellosis can be tested for by PCR (blood and tissues) and its positive WBs are considered diagnostic when combined with history and physical evidence. As is true of Bb, however, bartonella patients may be seronegative and without PCR-DNA captured.

A Brief Overview Of Some Approaches To The Treatment Of Tick-borne Diseases Affecting The Gut

Sensations of total, dire, overwhelming, unending, weakness or fatigue in most seriously ill Lyme patients lead many Lyme patients to consider suicide. Treatment begins with educating them about the treatable, underlying diseases and about realistic expectations in order to inspire hopefulness for recovery. The physician’s listening skills and willingness to give anxious patients extra time can be life-saving.

Prescription of skillfully combined oral antibiotics in an attempt to avoid IV treatment for all but those seriously afflicted with advanced neuro-Lyme (patients that manifest MS-like or ALS-type symptoms) is the next challenge (59). In addition to the usual antibiotics advised for Lyme disease, telithromycin (Ketec) used cautiously or azithromycin (Zithromax) may successfully accomplish blood-brain tissue barrier penetration that is needed. Such patients have to be monitored closely for liver, etc. side effects. In recent years, Lyme expertise has included the combining of antibiotic(s) with those in the azole family of drugs (such as metronidazole/Flagyl) that penetrate cell wall-less cyst forms of Bb, forcing spirochetes out of cover as it were to their demise from the antibiotics. Regularly spaced “safety blood work” must be regularly ordered for all patients who require long-term use of any antibiotics. For those with Lyme-sluggishness of the gut with resultant SIBO, non-absorbable, intestinal “antimicrobials” likely will be needed (60). Current usage of rifaximin may include carefully monitored long term prescriptions.

  • Doxycycline has the advantage of being able to arrest both Lyme and the ehrlichioses in those who are multiply infected with each.
  • Bartonella (the tick-borne variant) usually responds, albeit slowly, to aggressive treatment by one of the quinolone family of antibiotics such as levofloxacin (Levaquin) or by rifampin (Rifampicin).
  • Mycoplasmas may respond best to tetracycline, rifampin, and erythromycin.
  • Babesia, the red blood cell parasite, requires different approaches for acute and chronic disease stages. In chronic babesiosis, the form incidentally seen by gastroenterologists, a combination of artemisinin, atovaquone (Mepron) or Malarone, a combination of atovaquone and proguanil hydrochloride, and azithromycin are still drugs of choice (61).
Nutraceuticals And Antimicrobials To Restore The Immune System And The GI Tract

Restoration of gastrointestinal systems damaged by tick-borne diseases can be a formidable task depending on the presentation and severity of symptoms, antimicrobial or other treatments involved, and any side effects thus incurred. The goals are to enhance gut motility or reduce spasticity, remove toxins, improve patients’ general and gut-lining immunity while killing off invaders such as tick-borne microbes, fungi, and other gut opportunists (62,63).

Painful rectal area muscle spasms in Lyme patients usually respond to alprazolam (Xanax) 0.25 mg (1?2 to one tablet) best chewed for quick relief and Natural Calm, a formulary of instant release, water-soluble magnesium. Rectal cramps probably can be prevented most of the time by using the highest tolerated doses of daily magnesium—slow release is the recommended approach but many patients also need the quick-acting powder at bedtime to prevent all kinds of Lyme-caused muscle cramping or spasms.

Dietary intake of all sugars and non-complex carbohydrates should be totally avoided while patients take antibiotics. Probiotics—high quality lactobacillus (2 enteric-coated pearls) once or twice daily or more as needed and bifidus (at least one cap) once daily are essential for gut protection during and following antibiotic treatment. Immunity and energy enhancers such as extract from reishi mushrooms, Cordyceps sinensis (at least one 740 mg capsule daily), Co-Enzyme Q10 (100 mg twice daily), green tea, acetyl L-Carnitine (500 mg at least twice daily), Vitamin B Complex-50 to 100, folate, sublingual B12, magnesium (slow release tablets) taken to tolerance daily, gamma linolenic acid (GLA) as refrigerated Oil of Evening Primrose (1?2 tsp. daily) or borage oil (one 1,000 mg soft gel daily), Omega 3 EFA fish oil (one soft gel 3–4 times per day), selenium (200 mcg one cap daily), alpha lipoic acid (100 mg daily) and a comprehensive multivitamin (59)—all can be of great benefit.

Healing agents will be needed to repair the gut lining and restore functions damaged by Lyme-Bartonella- Mycoplasma infections. That list may include oral preparations of liquid Aloe Vera, Oil of Clove drops, Uncaria spp., anti-fungal tannins, garlic, chewable licorice tabs, betaine, Enteric-coated Oil of Peppermint, Conjugated linoleic acid CLA) (1000 mg twice daily), a-lipoic acid (100 mg one daily), Slippery Elm demulcent capsules (325 mg 1–8 three times daily), and ursodiol bile acid tablets (64). Additionally, in the treatment of SIBO, complete stool analysis with culture and sensitivity of opportunistic bowel pathogens may elucidate the choice of antibiotic. Alternatively, a trial may be undertaken with rifaximin (Xifaxan) 200 mg three times a day until symptoms have cleared (60). Cholestyramine (Questran) may be useful in reducing the recycling neurotoxins produced by tick-borne diseases.

As tick-borne-diseased GI systems and their owners heal, relief will be palpable. Physicians will partner in that gratification as well when previously grimfaced patients move to the healthy side of a bellshaped curve—a graph that would measure the degree to which both gastrointestinal tracts and lives have been restored to functional capacities. These satisfactions satisfactions will be re-experienced when wisely diagnosed and treated Lyme-sick patients will be able to smile broadly at last, knowing in their guts that zesty appetites for life really will be possible again.


Duray PH, Steere AC. Clinical pathologic correlations of Lyme disease by stage. Annals NY Academy of Sciences, 1988; 539:65-79.
Eiffert H, Karsten A, Schlott T, et al. Acute peripheral facial palsy in Lyme disease—a distal neuritis as the infection site. Neuropediatrrics, 2004; 35(5):267-273.
Bleiweiss JD. When to suspect Lyme disease, 1994. [3-23-2006].
Clark JR, et al. Bells palsy. Laryngoscope, 1985; 95:1341-1345.
Nichols TW, Pearce LA. Lyme gastroparesis suggestive of inflammatory neuropathy. Abstract presentations—14th Meeting of the American Motility Society and UICM (9-22 to 25-2005, Santa Monica CA and Lyme & Other Tick- Borne Diseases: Emerging Tick- Borne Diseases, sponsored by Columbia University College of Physicians & Surgeons and The Lyme Disease Association. 10-28-05.
Fallon B. WebMD. Neurologic Lyme disease. 1999. [3-23-06].
Barbour AG. [See “Faculty” + “Barbour” 3-23-06].
Nakagawa H, Satoh M, Kusuyama T, et al. Isolated vagus nerve paralysis caused by varicella zoster virus reactivation. Otolaryngology Head and Neck Surgery, 2005; 133(3):460-461.
Steere AC, Bartenhagen NH, Craft JE, et al. The early clinical manifestations of Lyme disease. Annals of Internal Medicine, 1983; 99(1):76-82.
De Koning J, Duray PH. In Aspects of Lyme borreliosis. Histopathology of Human Lyme borreliosis. ed. Klaus Weber, M.D., Willy Burgdorfer, Ph.D., M.D. Berlin Heidelberg: Springer-Verlag: 1993; 93-104.
Fallon BA, Nields JA, Liegner K, et al. The neuropsychiatric manifestations of Lyme borreliosis. Psychiatric Quarterly, 1992; 63(1):95-117.
Reik L, Steere AC, Bartenhagen NH, et al. Neurologic abnormalities of Lyme disease. Medicine, 1979; 58(4):281-294.
Chatila R, Kapadia CR. Intestinal pseudoobstruction in acute Lyme disease: a case report. Am J Gastroenterol, 1998; 93(7):1179-1180.
Reisinger EC,; Fritzsche C, Krause R, et al. Diarrhea caused by primarily non-gastrointestinal infections. Nat Clin Pract Gastroenterol Hepatol, 2005; 2(5):216-222. emil.reisinger@
Bagger-Sjoback D, Remahl S, Ericsson M. Long-term outcome of facial palsy in neuroborreliosis. Otol Neurotol, 2005; 26(4):790-795.
Gardner T. Lyme disease. Infectious Diseases of the Fetus and Newborn Infant, ed. Remington JS, Klein JO. Philadelphia: W.B. Saunders Co. 2001; 519-641.
Allred DR. Babesiosis: persistence in the face of adversity. Trends Parasitol, 2003; 19:51-55.
Tick-borne Diseases of Humans. Goodman JT, Dennis DT, Sonenshine DE. Ed. ASM Press, Washington, DC. [ISBN: 1-55581-23-4] 2005.
Eskow E, Adelson ME, Rao RV, Mordechai E. Evidence for disseminated Mycoplasma fermentans in New Jersey residents with antecedent tick attachment and subsequent musculoskeletal symptoms. J Clin Rheumat, 2003; 9(2):77-87.
Stricker RB, Gaito A, Harris N, Burrascano J. Coinfection in patients with Lyme disease: how big a risk? Clinical Infectious Diseases, 2003; 37:1277–1278.
Eskow E, Rao RV, Mordechai E. Concurrent infection of the central nervous system by Borrelia burgdorferi and Bartonella henselae: evidence for a novel tick-borne disease complex. Arch Neurol, 2001; 58:1357–1363.
Los Angeles County West Vector & Vector Borne Disease Control District. Bartonella. [3-20-2006]
Fried MD, Schairer J, Madigan G, et al. Bartonella henselae is associated with heartburn, abdominal pain, skin rash, mesenteric adenitis, gastritis and duodenitis. J Pediatr Gastroenterol Nutr, 2002; 35:3. [Abstract #158.]
Adelson ME, Rao RV, Tilton RC. Prevalence of Borrelia burgdorferi, Bartonella spp., Babesia microti, and Anaplasma phagocytophila in Ixodes scapularis ticks collected in Northern New Jersey. J Clin Microbiol, 2004; 42(6):2799-2801.
Fried MD, Adelson ME, Mordechai E. Simultaneous gastrointestinal infections in children and adolescents. J Practical Gastroenterology, 2004; 78-81. Bartonella rashes:
Stricker RB, Brewer JH, Burrascano JJ, et al. “Cat-scratch disease”-associated arthropathy: don’t forget ticks. Arthritis Rheum, In press.
Seah ABH, Azran MS, Rucker JC. Magnetic resonance imaging abnormalities in cat-scratch disease encephalopathy. Journal of Neuro-Ophthalmology, 2003; 3(1):16-21.
Fleisher AS. Case 14: Headache and unilateral visual changes. Clinical Cases from Johns Hopkins Neurology. Medscape Neurology & Neurosurgery. 2002; 4(2).
Coulter P, Lema C, Flayhart D, et al. Two-year evaluation of Borrelia burgdorferi culture and supplemental tests for definitive diagnosis of Lyme disease. J Clin Microbiol, 2005; 43(10):5080-5084.
Picha D, Moravcova L, Zdarsky E, et al. PCR in Lyme neuroborreliosis: a prospective study. Acta Neurol Scand, 2005; 112(5): 287-92. [Czech Republic].
Medical Diagnostic Laboratories, L.L.C, 2439 Kuser Road, Hamilton, NJ 08690 USA. )
Guarner J, Shieh WJ, Morgan J, et al. Leptospirosis mimicking acute cholecystitis among athletes participating in a triathlon. Hum Pathol, 2001; 32(7):750-752.
Chen W, Li D, Paulus B, et al. High prevalence of Mycoplasma pneumoniae in intestinal mucosal biopsies from patients with inflammatory bowel disease and controls. Dig Dis Sci, 2001; 46(11):2529-2535.
IGeneX, Inc. 795 San Antonio Rd., Palo Alto, CA 94303
Boltri JM, Hash RB, Vogel RL. Patterns of Lyme disease diagnosis and treatment by family physicians in a southeastern state. J Community Health, 2002; 27:395-402.
Association of State and Territorial Public Health Lab Directors (ASTPHLD). Proceedings of the second national conf. on the serological diagnosis of Lyme disease. Dearborn, Michigan USA. 1994; 27-29.
Aguero-Rosenfeld ME, Nowakowski J, McKenna DF, et al. “Evolution of the serologic response to Borrelia burgdorferi in treated patients with culture-confirmed erythema migrans.” J Clin Microbiol, 1996; 34:1-9.
Cameron D, Gaito A, Harris N, et al. Evidence-based Guidelines for the management of Lyme disease. Expert Rev Anti-infect Ther, 2004; 2(1):1-13.
Summary: Evidence-based Guidelines for the management of Lyme disease. Expert Rev Anti-infect Ther, 2004; 2(1):1-13.
Honegr K, Hulínská D, Dostál V. Persistence of Borrelia burgdorferi sensu lato in patients with Lyme borreliosis. Epidemiol Mikrobiol Imunol, 2001; 50(1):10-6.
Lin HC. Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome. JAMA, 2004; 292(7):852- 858.
Singh V, Toskes P. Small bowel bacterial overgrowth: presentation, diagnosis, and treatment. Curr Gastroenterol Rep, 2003; 5(5):365-372.
Genova (Great Smokies) Laboratory:
Doctors’ Data Laboratory
Mormont E, Esselinckx W, De Ronde T, et al. Abdominal wall weakness and lumboabdominal pain revealing neuroborreliosis: a report of three cases) Clin Rheumatol, 2001; 20(6):447-450.
Krishnamurthy KB, Liu GT, Logigian EL. Acute Lyme neuropathy presenting with polyradicular pain, abdominal protrusion, and cranial neuropathy. Muscle Nerve, 1993; 16(11):1261-1264.
Daffner KR, Saver JL, Biber MP. Lyme polyradiculoneuropathy presenting as increasing abdominal girth. Neurology, 1990; 40:373-375.
Pokorny P. Incidence of the spirochete Borrelia burgdorferi in arthropods (Arthropoda) and antibodies in vertebrates (Vertebrata). Cesk Epidemiol Mikrobiol Imunol, 1989; 38(1):52-60.
Savely GR. The Belly Acher: My Most Unusual Patient. Beyond the Textbook, in Clinician News, 2005; 9(9):14-15.
Fried MD, Abel M, Pietrucha D, et al. The spectrum of gastrointestinal manifestations in children and adolescents with Lyme disease. JSTBD, 1999 Fall/Winter; 6.
Rodríguez LA, Gonzales PA, Johansson S. Centro Español de Investigación Farmacoepidemiológica (CEIFE) Aliment Pharmacol Ther, 2005; 22(4):309-315. ©2005 Blackwell Publishing, Mölndal, Sweden.
Molecular self-loathing. The Economist, 2005.
Fetissov SO, Harro J, Jannisk M, et al. Autoantibodies against neuropeptides are associated with psychological traits in eating disorders. PNAS, 2005; 102:14865-14870.
Cone RD. Anatomy and regulation of the central melanocortin system). Nat Neurosci, 2005; 8(5):571-578.
Fallon BA, Nields JA. Lyme disease: a neuropsychiatric illness, Am J Psychiatry, 1994; 151(ll):1571-1583.
Dattwyler RJ, Halperin JJ, Volkman DJ, et al. Treatment of late Lyme borreliosis—randomised comparison of ceftriaxone and penicillin. Lancet, 1988; 1(8596):1191-1194.
Craft JE, Fischer DK, Shimamoto GT, Steere AC. Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness. J Clin Invest, 1986; 78(4):934-939.
Kalish RA, McHugh G, Granquist J, et al. Persistence of immunoglobulin M or immunoglobulin G antibody responses to Borrelia burgdorferi 10–20 years after active Lyme disease. Clin Infect Dis, 2001; 33(6):780-85.
Burrascano JJ. Diagnostic hints and treatment guidelines for Lyme and other tick borne illnesses. 2005. [See “Articles and presentations”].
Lauritano EC, Gabrielli M, Lupascu A, et al. Rifaximin dose-finding study for the treatment of small intestinal bacterial overgrowth. Aliment Pharmacol Ther, 2005; 22(1): 31-35.
Sherr VT. Human babesiosis—an unrecorded reality. Absence of formal registry undermines its detection, diagnosis and treatment, suggesting need for immediate mandatory reporting. Med Hypotheses, 2004; 63(4):609-615.
Zaidel O, Lin HC. Uninvited guests: the impact of small intestinal bacterial overgrowth on nutritional status. Practical Gastroenterology, 2003; 27(7):27.
Parrish CR (Ed), Yoshida CM. Nutrition intervention for the patient with gastroparesis: an update. Pract Gastroenterol—Nutrition issues in gastroenterology. 2005; 29(8):29.
Nichols TW, Faass N. Optimal Digestive Health: A Complete Guide. 2005. Healing Arts Press, Rochester, VT.





“Bullseye” Low Dose Naltrexone & Lyme Disease Documentary

Very informative documentary put out by the LDN Research Trust on Lyme/MSIDS.  Dr. Horowitz, Dr. Toups, Dr. Schweig, Dr. Windham, Dr. Holtorf, & Dr. Schwarzback, speak on everything from testing, to diet, to inflammation, and how LDN can help patients. (Video found here)  Approx 1 Hour


For more on LDN:




Overview of Anti-Inflammatory Diets

Overview of Anti-Inflammatory Diets

by Kate Raines, May 13, 2018

The following is the second half of a two-part article on nutrition that addresses chronic inflammation. Click here to read the first half of the article.  

Most anti-inflammatory diets agree on many of the foods to include, however, the “not allowed” foods may differ, sometimes dramatically.

For example, the Autoimmune Protocol nixes nightshade vegetables, nuts, seeds and eggs. The Paleo diet is fine with grass-fed meats, eggs and seeds but rules out grains, as well as dairy and legumes such as chickpeas, lentils, beans and peanuts. The Zone allows some low-fat dairy and an occasional egg white, but discourages all refined grains. And Dr. Weil’s anti-inflammatory diet echoes the nod given to leafy greens and salmon, but encourages whole grains and adds the importance of anti-inflammatory spices like turmeric and ginger.

Dr. Joseph Mercola warns that refined sugars, processed fructose, trans fats and grains encourage inflammation, while fermented vegetables, traditionally cultured foods, leafy greens, animal-based Omega3-fat and nutrient rick green teas are anti-inflammatory, as are garlic, blueberries, shiitake mushrooms, cloves, ginger, rosemary, turmeric, cinnamon, oregano, sage, and thyme.1  

Following is a bare-bones summary of the basics of a few of the more popular anti-inflammatory diets, along with current medical opinions about them. Anti-inflammatory diets as a whole differ significantly from the current recommended “choose my plate” recommendations of the United States Department of Agriculture.2

The Anti-inflammatory Diet3 4  

Based on both the Dietary Approaches to Stop Hypertension (DASH) and the Mediterranean diets, Dr. Weil’s anti-inflammatory diet suggestions offer a few revisions and additions, including the addition of green tea, omega-3 fatty acids and natural anti-inflammatory spices, such as turmeric and ginger.  Dr. Weil emphasizes that his approach to eating is aimed at supporting a healthy life and reducing chronic inflammation in the body, which he agrees is at the base of many chronic diseases today. He recommends that approximately 40 to 50 percent of daily calories should come from carbohydrates, 30 per cent from fat, and 20 to 30 per cent from protein.

Atkins5 6

If the Mediterranean Diet could be considered the mother of the anti-inflammatory diet movement, then Atkins may be the father of it. Quoting from the Atkins website, “The ‘Atkins Diet’ started as a fad, but quickly became a counter-conventional movement that reset people’s understanding of nutrition and weight loss, and its link to health.”

Developed in the 1960s by cardiologist Robert Atkins, MD, the new low-carb approach to eating was embraced by a population sick of fat-shunning, calorie-counting diets that left them hungry and did nothing to curb the growing epidemic of obesity in the U.S. Although his early followers may have delighted in the diet’s permission to fill up on bacon, butter and heavy cream, the diet has evolved and been modified since then.

The Atkins diet is divided into four phases, beginning with near-total abstinence from carbohydrates and gradually incorporating healthy and nutrient-rich carbs from vegetables, nuts, seeds and, eventually, starchy vegetables, fruits and grains as tolerated.

Research does support health benefits for the Atkins and other so-called ketogenic diets, which restrict carbohydrates in an effort to encourage the body to shift from using glucose as the main fuel source of energy and instead burn fat stores and produce ketones for energy.7    

Some ketogenic diets have been used to successfully reduce the numbers of seizures suffered by children who have seizure disorders.

In addition, there is evidence that high-fat, low-carb eating can modify symptoms of other neuro-immune disorders, such as Parkinson’s, Alzheimer’s, multiple sclerosis, sleep disorders, and autism, as well as some types of cancer and diabetes. In his new book Fat for Fuel, Dr. Mercola highlights the importance of diet in helping the body to use fat instead of glucose for fuel in the prevention and healing from cancer and other diseases marked by inflammation in the body.8  

Most of the scientific evidence for ketogenic diet benefits is focused on short-term use of the diet, and research is ongoing to evaluate and produce more scientific evidence for the health benefits of long-term use of different types of modified ketogenic diets.

Autoimmune Protocol (AIP) Diet9 10  

Similar to the Paleo diet but more restrictive, the Autoimmune Protocol (AIP) diet is aimed specifically at healing leaky gut in order to treat inflammatory bowel syndrome and other autoimmune or immune-mediated diseases. Leaky gut occurs when the gastrointestinal wall becomes increasingly permeable and absorbs toxins, bacteria, fungi, and parasites, which leads to gastrointestinal dysfunction and can lead to allergy and autoimmunity.11  

Adhering to Hippocrates’ 200-year-old admonishment that “all disease begins in the gut,” the AIP diet eliminates all grains, legumes, dairy, nuts, seeds, eggs, nightshade vegetables, almost all oils, processed foods, alcohol, non-steroidal anti inflammatory drugs, sugars, starches, most fruit, yeasts, gums, seed herbs and tapioca. Whew!

What’s left are primarily animal proteins, vegetables other than the nightshades, and limited fruit. Admitting it can be a difficult diet for many to follow long term, Dr. Sara Gottfried says, “The AIP is very difficult for many people to follow, but sometimes it’s temporarily necessary to fully heal a very leaky gut.”

GAPS12 13  

The GAPS (Gut and Psychology Syndrome) Nutritional Program was created by Dr. Natasha Campbell-McBride as a refinement of Dr. Sidney Valentine Haas’s Specific Carbohydrate Diet (SCD), originally designed to naturally treat chronic inflammatory conditions in the digestive tract as a result of a damaged gut lining.” The GAPS diet is individually tailored for each patient and focuses on “healing and sealing” the gut lining, and optimizing the gastrointestinal ecosystem to better support the immune system and bran function. Although few studies have shown a consistent benefit from diets like GAPS in healing disorders with an inflammatory component, the principals have shown promise in some children.  The mainstays of the GAPS diet are introduced in a specific order in the six-stage initiation stage and continued in the full GAPS protocol.  The detailed list of allowed foods—and the even more exhaustive list of prohibited foods—focuses heavily on bone broth, animal fats and fermented foods, with an emphasis on using the healthiest choices available and avoiding additives. The GAPS diet is extremely restrictive, especially at first, but personal testimonials abound from parents suggesting it may be beneficial for some children with autism spectrum disorder.

Mediterranean14 15  

Probably the mother of all the well-publicized anti-inflammatory diets, the Mediterranean diet, is based on the common eating habits of people living in Spain, Italy, France, Greece and the Middle East. The diet was introduced to the U.S. in the early 1990s and featured a reprisal of the standardized food pyramid.  The foundation of the Mediterranean pyramid includes fruits and vegetables, whole grains, seeds and nuts, beans and legumes and olive oil to replace animal fats. An important difference is that meat is grouped at the top with sweets in the “rarely or never” category, instead of being grouped with fish and poultry.  Long-standing research supports the principals of eating the Mediterranean way, showing a clear benefit in terms of reducing risk for cardiovascular disease as well as cancer, Parkinson’s, and Alzheimer’s. Although it may not be as interesting as some of the newer diets, proponents point out that it represents a traditional healthy way of eating for life, rather than a short term diet to be kept until a specific goal has been reached.

Paleo16 17 18  

Designed on the concept that modern humans could be healthier if we ate like our “pre-agricultural, hunter-gatherer ancestors” did, the Paleo diet focuses on “whole, unprocessed foods that resemble what they look like in nature.” The diet is based on seasonal and regional availability, with an emphasis on pasture-raised and grass-fed animal proteins and fats.  Permitted foods include meat, fish, eggs, vegetables, fruits, nuts, seeds, herbs, spices, animal fats and oils. Foods to avoid include all processed foods, sugar, soft drinks, grains, most dairy products, legumes, artificial sweeteners, vegetable oils, margarine and trans fats.

Raw Food19 20  

Taking the idea of eating like our ancestors did to its extreme, the Raw Food Movement holds that, “our biological and physiological requirements were in place long before the practice of cooking food began [and so]…the closer we can get to those ideals in our modern lives, the higher the level of health we will enjoy.”

Emphasizing the cumulative damage caused by the chemical changes that occur when food is cooked, “raw foodists” subsist on a diet that looks much like that of a wild primate: The emphasis is on consumption of fruit (75 to 80 percent of the daily intake), and all types of fruit are encouraged, as well as green, leafy vegetables (10 to 20 per cent) and small amounts of nuts and seeds (5 percent). Unlike other diets that eschew the nightshade vegetables, tomatoes and peppers are considered “optimal foods” in a raw food diet.

Other followers of a raw food diet add unpasteurized dairy foods, raw eggs, meat, and fish, as long as the temperature of the foods never exceeds 118 degrees. Followers claim a raw food diet can help cure inflammatory conditions such as headaches, allergies, arthritis and diabetes and can improve memory and support the immune system. Medical authorities tend to agree that the focus on high-fiber, low-salt, low-fat foods may provide a benefit in terms of risk for stroke, osteoporosis, stomach cancer, kidney disease and diabetes, primarily because it promotes weight loss. There is also considerable debate over the need to compensate for the diet’s limited supply of nutrients such as protein, vitamin B12, iron and calcium.

Whole30 21 22  

Based on the assumption that eating specific food groups such as sugars, grains, dairy and legumes creates an environment conducive to the development of such conditions as skin issues, digestive troubles, allergies, and chronic pain, the Whole30 diet proposes to reset the body in 30 days. The diet does not involve measuring or counting calories but encourages eating moderate portions of whole, unprocessed foods: meat, seafood, eggs, vegetables, some fruit and natural fats. It is basically an elimination plan and totally prohibits all sugars, alcohol, grains, legumes, dairy, baked goods and processed foods. For 30 days. After the initial period, food groups are added back in gradually, one at a time, with the expectation that newly acquired awareness of how foods can affect one’s health will allow for healthier choices moving forward.

Some nutritionists have misgivings about the Whole30 plan, questioning its lack of independent scientific study and alleging that it is based instead on general anecdotal anti-inflammatory theories. The diet also has been criticized for allowing high levels of sodium and processed meats like cured pork (read, bacon) while prohibiting nutrient-rich foods like legumes and dairy. The biggest criticism seems to be that a temporary plan tends to lead to temporary results.

The Zone 23 24  

Developed over 30 years ago by Dr. Barry Sears, the Zone diet was designed not as a weight-loss tool but as a “a life-long dietary program based on strong science to reduce diet-induced inflammation.” The basic tenets of the Zone diet can be put simply: Every meal and every snack follows the ratio of one third protein (egg whites, fish, poultry, lean beef or low-fat dairy); two thirds carbohydrates (in the form of non-starchy vegetables and a little low-sugar fruit), with a little monounsaturated fat such as olive oil, avocado, or almonds).

The Zone food pyramid looks a little different from the Mediterranean diet, with vegetables in the primary foundation tier and grains relegated to the top of the pyramid, to be consumed only rarely. The Zone also recommends the addition of supplements including Omega-3 fatty acids (fish oil) and polyphenols.

Again linking back to the idea of returning to evolutionary roots in terms of dietary habits, the Zone was designed specifically to reduce diet-induced inflammation by avoiding inflammation-producing processed carbohydrates and keeping specific physiologic markers in balance. Some medical doctors have questioned the Zone’s restrictions on certain fruits and vegetables and the difficulty of adapting the Zone diet for vegetarians.


1 Mercola J. The Anti-Inflammatory Foods, Herbs and SpicesMercola Newsletter Feb. 3, 2015.

2 USDA. Choose My Plate. Choose My 2018.

3 What Is The Anti-Inflammatory Diet And Food Pyramid? Dr.

4 Dr. Weil’s Anti-Inflammatory Diet. Dr.

5 The Benefits of a Low Carb Diet: How Does Atkins Work?

6 Atkins Diet: What’s Behind the Claims? Mayo Clinic. Aug. 16, 2017.

7 McIntosh J. Ketosis: What is ketosis?Medical News Today Mar. 21. 2017.

8 Mercola J. Fat for Fuel: A Revolutionary Diet to Combat Cancer, Boost Brain Power and Increase Your Energy. Hay House 2017.

9 Gottfried S. Is the Autoimmune Protocol Necessary?10 Flanigan J. What is Autoimmune Paleo or AIP Diet?AIP Lifestyle. C 2018.

11 Barbara G, Zecchi L et al. Mucosal permeability and immune activation as potential targets of probiotics in irritable bowel syndromeJ Clin Gastroenterol 2012.

12 West H. The GAPS Diet: An Evidence-Based Review. HealthLine. July 23, 2017.

13The GAPS Diet. c 2018.

14What Is the Mediterranean Diet? America’s Test Kitchen. C 2018.

15Mediterranean diet: A Heart-Healthy Eating Plan. Mayo Clinic. Nov. 3, 2017.

16 Cordain L. The Paleo Diet Premise. 2018.

17Paleo Diet 101. Paleo Leap. 2018.

18 Gunnars K. The Paleo Diet – A Beginner’s Guide Plus Meal Plan. Health Line. June 16, 2017.

19 Lenz, N.  Basic Raw Food FAQ. Raw School. C 2018.

20 Robinson KM. Raw Foods Diet. WebMD. Nov. 21, 2016.

21 Hartwig M. The Whole30 Program. Thrity & Co. C 2018.

22 London J. 6 Things You Need to Know Before Trying Whole30Good Housekeeping. Jan. 4, 2018.

23What Is the Zone Diet? Zone Labs. C 2018.

24 Nordqvist C. The Zone Diet and Inflammation: All You Need to Know. Medical News Today. July 14, 2017.


Many Lyme/MSIDS patients suffer with both environmental and food sensitivities and even allergies.  Getting to the bottom of that will help their healing process dramatically.

For more:  The many benefits of MSM – including allergy symptoms:
*Reduces cytokines & inflammation (in vitro studies show MSM reduces IL-6 (a marker implicated in chronic inflammation as well as suppressing NO and prostanoids) *antioxidant *free radical scavenger *kills gastrointestinal, liver, and colon cancer cells *restored normal cellular metabolism in mouse breast cancer and melanoma cells *helps wounds heal *increases blood flow *reduces muscle spasms *antiparasitic properties (especially for giardia) *normalizes the immune system *cholinesterase inhibitor *alleviates allergy symptoms *increases energy *improves condition of hair, nails, and skin  Lyn-Genet Recitas, author of “The Plan,” calls MSM the wonder supplement for your gut. It can alleviate allergy symptoms, helps with detoxification, eliminates free radicals, and improves cell permeability. She states that with given time, MSM will start to actually repair damage caused by leaky gut – a common problem with Lyme/MSIDS patients. It can also help the body’s ability to absorb nutrients from food. Many Lyme patients struggle with paralysis of the gut where the muscles of the stomach and intestines stop being efficient. MSM helps this muscle tone as well.  In this talk Cyndi O’Meara discusses challenges with wheat. Diagnosed with MS, Dr. Terry Wahls received the best standard medicine had to offer. After declining to the point of being in a wheel chair, she took matters into her own hands and learned how to properly fuel her body. Using the lessons she learned at the subcellular level, she used diet to cure her MS and get out of her wheelchair.

Neurological Lyme Disease: What You Need to Know Lyme Disease: What You Need to Know

Neurological Lyme Disease: What You Need to Know

by Dr. Bill Rawls
Posted 4/20/18

Lyme disease can manifest in a seemingly endless number of ways. While the spectrum of symptoms is similar for most sufferers, the worst of the bunch varies from person to person. And for those who have a predominance of neurological symptoms, the disease can feel especially debilitating and difficult to overcome.

That’s in large part because neurological Lyme — also referred to as Lyme neuroborreliosis (LNB) — is often confused with other serious neurological conditions such as multiple sclerosis and Parkinson’s Disease, which can be scary and overwhelming. And because most doctors lack an understanding of Lyme disease in general, and especially of Lyme associated with a predominance of neurological symptoms, LNB often goes unrecognized.

So how to know if the symptoms you’re experiencing do signify LNB, and where do you go from there to find relief? Keep reading for information that could provide the turning point in your recovery.

Understanding Symptoms of Neurological Lyme

Lyme neuroborreliosis is thought to occur in about 15% of Lyme disease cases — but a definite percentage is impossible to pin down. Everyone with Lyme disease experiences some neurological symptoms, but a specific composit of symptoms that constitute neurological Lyme is not well defined. Making matters worse, the Centers for Disease Control (CDC), does not recognize LNB as a separate entity, and it doesn’t acknowledge the existence of a chronic form of Lyme disease.

The most common initial symptom is neurogenic (nerve) pain that starts in the back and radiates down the legs. With that comes weakness, numbness, and tingling in the lower extremities.

Another common presenting symptom of LNB is facial nerve palsy (Bell’s palsy), which is characterized by temporary paralysis on one side of the face. Some people also experience sound sensitivity and discomfort in the ear on the paralyzed side, and if you’re unable to close that eye, dry eye can occur. Most people recover fully from Bell’s palsy, with improvement in the first few weeks and continuing for three to six months, but a minority of people have symptoms for life.

The transition from acute to chronic neurological symptoms is not well defined, and it varies widely from person to person. Many people don’t remember a tick bite and experience minimal acute symptoms. The range of symptoms includes both motor and sensory nerve deficits. On the list: headache, memory loss, brain fog, cognitive impairment, learning disability, anxiety, depression, limb pain, muscle weakness, and paresthesias (sensory loss and odd sensations on the skin).

Symptoms of LNB are thought to occur from infiltration of white blood cells — immune cells like lymphocytes and plasmocytes — into the white matter of the brain and the spinal cord, otherwise known as the central nervous system (CNS). This is associated with an increase in inflammatory immune messengers, called cytokines, in cerebrospinal fluid.

Loss of sensory and motor nerve function is thought to be related to demyelination of nerve fibers. Found in the brain and peripheral nervous system, nerve fibers are coated with a fatty substance called myelin. Myelin acts much like the plastic coating on a copper wire: it wraps around nerve fibers, thus preventing the nerve fibers from touching each other and “shorting out” when an electrical current passes through. If demyelination is severe enough, it can result in abnormal nerve conduction tests, similar to multiple sclerosis.

Treatment for neurological Lyme is highly controversial. The CDC recommends antibiotic therapy using doxycycline, cefuroxime, or amoxicillin, limited to 10-21 days for formally diagnosed Lyme disease only. Remember, they don’t define LNB as separate from Lyme disease, and so specific treatment recommendations are not provided. Notably, the CDC website also cites numerous scientific articles showing that long-term antibiotic treatment for Lyme disease is not efficacious.

Among physicians who do recognize and treat LNB, there is no absolute consensus on therapy. Some physicians recommend 1-3 months of combined intravenous antibiotic therapy, and some continue to treat patients as long as symptoms are present. Confusing matters more, some studies that suggest oral antibiotic therapy is as efficacious as intravenous antibiotics, but long term follow up for any therapy is limited.

Central to the confusion is the fact that understanding of LNB and Lyme disease in general is clouded by reductionist science — studying one variable in a vacuum, while ignoring all other potential influencing variables. The variable in this case: the microbe Borrelia burgdorferi, the primary pathogen behind Lyme.

An Alternative View of Neurological Lyme

Anyone struggling with Lyme knows that the disease isn’t caused by borrelia alone. Indeed, having coinfections with microbes other than borrelia is more common than not. The most common coinfections include mycoplasma, bartonella, chlamydia, babesia, anaplasma, ehrlichia, and rickettsia. And all of these pathogens have the potential to cause neuroinflammatory symptoms that are characteristic of LNB.

Though all of these microbes can be transmitted by ticks, they can also be transmitted by other routes. For instance, bartonella is most commonly spread by scratches and bites from dogs and cats. Babesia can be transmitted by ticks and mosquitos. And mycoplasma and chlamydia are most commonly spread by respiratory or sexual route.

Often called stealth microbes, these microbes share similar characteristics:

  • They often don’t cause significant symptoms at initial infection.
  • They infect white blood cells and quietly spread to all tissues throughout the body, including brain and nerve tissues.
  • They are able to generate inflammation to break down tissues and gain access to nutrients.
  • They are masters at manipulating the immune system.
  • They grow very slowly.
  • They occur in low concentrations in the body, allowing them to blend in with other microbes.

The stealth microbes we know about may be just scratching the surface — science uncovers new ones on a regular basis. Ticks and other biting insects can spread an enormous variety of microbes beyond the classic coinfections. Microbes can also be spread by oral routes, inhalation, intimate contact with other people, breaks in skin, and blood transfusions or contact with contaminated blood.

Some of these microbes are more concerning than others, but if your immune system functions are strong, you’ll never know they’re there. In other words, the chances that you’ve encountered and picked up a variety of stealth-type microbes at some point in your life are much higher than you might think. And you’ve likely carried them without even knowing it, because they can remain dormant in tissues for years without causing harm.

This is true even with borrelia: People suffering from chronic Lyme disease typically don’t become chronically ill immediately after a tick bite. Onset of illness can happen months or even years later — it is typically surrounded by a perfect storm of stress factors that come together to disrupt immune system functions.

I’ve often related it to a pot boiling over on the stove. If immune system functions are healthy, microbes can be present in tissues, but suppressed and not causing symptoms — the equivalent of a pot of water on the stove being kept at a low simmer. But if immune system functions become disrupted, the pot of water starts to boil.

Immune disruption is most often caused by a combination of chronic stress factors such as poor diet, exposure to toxic substances like mold toxins, and emotional or physical stress. Sometimes, the tipping point is the infection caused by microbes that are acquired from a tick bite. But most often, the microbes are already present in the host, and they only become ill when other stress factors accumulate in their lives.

No matter what the initiating cause, however, when the pot reaches a full boil, it’s no longer an infection with one microbe or even a few microbes. Instead, it’s a disruption of the entire microbiome.

Once microbes start becoming active, inflammation increases and immune functions are further compromised, establishing what I call Chronic Immune Dysfunction (CID). In its weakened state, the immune system allows reactivation of viruses such as Epstein Barr virus (EBV), Cytomegalovirus (CMV), and other similar viruses — all of which most people harbor in their tissues. These viruses are commonly associated with neuroinflammation, and they tend to complicate the picture of LNB.

Chronic Immune Dysfunction also allows opportunistic pathogens to flourish in the gut and elsewhere in the body. The inflammation they generate compromises the gut barrier, allowing microbes along with foreign proteins from food to pass into the bloodstream. This heightens systemic inflammation and can compromise the blood brain barrier, allowing microbes to pass into the brain and nervous system.

Making Connections to Clarify Diagnosis

Chronic Lyme disease shares many symptoms with other chronic illnesses. This is especially true of Lyme neuroborreliosis and chronic neuroinflammatory illnesses such as multiple sclerosis, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), Parkinson’s disease, and traumatic brain injury.

Not surprisingly, new sophisticated methods of microbial detection are showing potential links between these neuroinflammatory illnesses and many of the microbes associated with chronic Lyme disease.

For instance, both mycoplasma and chlamydia have been closely linked to multiple sclerosis. Mycoplasma, borrelia, and chlamydia have been associated with demyelination. Parkinson’s and ALS have been linked to borrelia and other microbes commonly associated with Lyme disease. Borrelia and other stealth pathogens have been found in the brains of patients who died of Alzheimer’s disease.

The connections go well beyond Lyme disease microbes. Two recent studies are shedding new light on how closely disruptions in the microbiome are linked to neuroinflammation. One, published in Frontiers of Aging Neuroscience, evaluated the presence of microbes in the autopsied brains of deceased Alzheimer’s patients. The other, published in Scientific Reports, evaluated the presence of microbes in the autopsied brains of people who had died of multiple sclerosis.

Both studies used a new type of microbial testing called 16S ribosomal RNA gene sequencing, which enabled scientists to separate human cells from microbial ones, and positively identify microbes. They found that not only were microbes present in diseased brains in both studies, but the magnitude of their presence was astounding: The entire microbiome, with a full spectrum of microbes from the gut, mouth, and skin, were represented.

Equally interesting, the control brains from people who had died of other causes also had a full spectrum of microbes present. The main difference? Diseased brains had a much higher concentration of microbes, and a greater prevalence of microbes with higher potential to cause inflammation.

I believe these studies are landmark, because they illustrate the close ties between disruption of the microbiome and chronic neuroinflammatory illnesses. Considered in this light, they also highlight the potential connection between Lyme neuroborreliosis and other neuroinflammatory diseases. This would suggest that Chronic Immune Dysfunction is central to the equation, allowing opportunistic pathogens of many varieties (not just those from ticks) to flourish, cause system inflammation, and create a vicious cycle of unending misery.

Ultimately, the type of illness a person might end up with depends on three key things: how the immune-disrupting factors come together; the types of pathogens they accumulated through life; and genetics (some people are more genetically at risk than others for these types of illnesses). Therefore, targeting individual microbes with antibiotic therapy alone is unlikely to restore normal health.

So what does restore well-being? Therapy that comprehensively addresses chronic immune dysfunction and widespread disruption of the microbiome.

How to Recover from Neurological Lyme

When you’re suffering from debilitating symptoms of neurological Lyme, it’s tempting to seek out medications that promise fast relief. Unfortunately, the place for drug therapy in chronic neuroinflammatory illnesses is limited. In fact, because neuroinflammation is so complex, targeted synthetic drug therapy often disrupts the healing process.

Many medications suppress or disrupt immune system functions and inhibit deep sleep, which is absolutely essential for recovery. Anti-inflammatory drugs, including steroids and nonsteroidal anti-inflammatory agents like ibuprofen and naproxen, disrupt immune functions and inhibit healing.

These drugs have also been shown to inhibit clearance of beta amyloid, a proteinaceous substance associated with neuroinflammatory disorders that is the hallmark identifying factor of Alzheimer’s disease. Though short-term use of antibiotic therapy has shown limited benefit in some cases of dementia and MS, tolerance to therapy and relapse are inevitable with long term use of synthetic antibiotics.

This makes sense when you consider that LNB and other neuroinflammatory conditions are primarily associated with disruptions in the balance of the entire microbiome and chronic immune dysfunction — as opposed to infections with specific pathogens. So while antibiotics initially suppress microbes in general, with extended use, pathogens arise in the gut and skin, gut and brain barriers are further compromised, and immune functions are further depressed, thus enhancing illness.

Instead, to overcome Lyme neuroborreliosis, you must approach it like you would another neuroinflammatory condition. The key components of recovery from any type of neuroinflammatory condition include:

  • Reducing both systemic and nervous system inflammation
  • Promoting optimal blood flow and vascular function
  • Restorating normal sleep
  • Supporting the immune system and restoring homeostasis
  • Enhancing healing and restoration of normal gut and brain barriers
  • Restoring balance to the microbiome of the gut and the entire body

That might sound like a lot, but in fact, finding lasting relief from neurological Lyme calls for a more measured, lifestyle approach — one that’s supportive of your immune system so that you’re enabling your body to fight its own battles. Here, the five steps for putting this approach into motion.

1. Nourish your body

Optimal nourishment is essential for reducing neuroinflammation. An anti-inflammatory diet is especially rich in fresh vegetables, healthful fats, and anti-inflammatory protein sources:

  • Vegetables provide essential nutrients and antioxidants for healing, and fiber for balancing the gut microbiome.
  • Healthy fats reduce brain inflammation. These include the monounsaturated fatty acids in natural sources like olive oil and avocados, and omega-3 fatty acids from fish.
  • Inflammatory foods, such as food products derived from corn and wheat, and corn-fed beef and pork, should be strictly avoided.
  • Optimal sources of protein include fish, eggs, and poultry. Eggs in particular are rich in choline and other essential brain nutrients. If you’re seeking vegan protein sources, quinoa, peas, and hemp are good alternatives.
  • Following a strict ketogenic diet has been shown to benefit recovery from neuroinflammatory conditions. That means keeping your carbohydrate intake low enough to cause brain cells and other tissues to switch from burning glucose to burning ketones. Admittedly, however, strict ketogenic diets are challenging to stick to consistently.

Beyond eating fresh fish regularly, supplementing with omega-3 fatty acids has been widely studied for reducing inflammation in both acute and chronic neuroinflammatory illnessKrill oil and fish oil are optimal sources of the DHA and EPA omega-3 fatty acids necessary for brain health. To determine your optimal dosing levels, consider doing periodic blood testing for omega fatty acid balance; test kits can be bought online for approximately $100.

Herbs are ideal for reducing systemic and neuroinflammation. They work by balancing your immune response instead of suppressing it, and directly inhibit tissue inflammation in the brain and nervous system. Anti-inflammatory herbs also promote optimal blood flow to the brain and tissues by enhancing vascular system function. Some of the best choices include turmeric, boswellia, resveratrol from Japanese knotweed, and French maritime pine bark.

Cannabidiol (CBD), a cannabinoid found in the hemp variety of cannabis, has shown great promise for reducing neuroinflammation and calming nerve irritability, reducing pain, enhancing mood, and promoting normal sleep. Cannabinoids also balance immune functions.

CBD from hemp is legal in all fifty states and can be shipped across state lines. It does not contain THC, the psychoactive substance in marijuana. CBD oil is the optimal form for delivery and absorption. Average dose is 20-50mg of CBD with mixed cannabinoids; look for products with 1500 mg per fluid oz.

Finally, essential oils are excellent for reducing brain inflammation. They contain primarily fat soluble phytochemicals of herbs — ideal for penetrating brain and nerve tissue, which is 60% fat. Good essential oil choices for neuroinflammation include rosemary, oregano, frankincense, lavender, and lemon balm — the latter three also support normal sleep. Aromatherapy (olfactory delivery) is the most direct way to administer the phytochemicals of essential oils to the brain and nervous system.

2. Purify your system of toxins

A toxic environment impedes recovery from any illness. And unfortunately, chronic systemic inflammation and neurological inflammation can compromise detoxification and waste removal processes in the brain and body even further.

Toxic substances can enter the body by three routes — oral, respiration, and skin — so step one is minimizing the inflow. To reduce oral toxins, avoid processed food products, and eat a fresh, whole food diet weighted toward vegetables (the fiber in veggies enhances detoxification). Clean water is also key, and is as simple as installing a water filter.

Regularly changing your HVAC air filters and placing free-standing HEPA filters in rooms where you spend the majority of your time can go a long way toward improving indoor air quality. Breathing fresh air in natural places as often as possible can also promote healing.

As for your skin, adopting a practice of using only natural skin care products allows you to avoid a surprising number of toxic substances commonly found in commercial skin care products. The same goes for household cleaning supplies. The Environmental Working Group is a great resource for finding toxin-free consumer products.

Supplements that support detoxification in the body include activated B vitamins for enhanced methylation (a metabolic process that’s vital to cellular health), and glutathioneNAC, and alpha lipoic acid to support cellular functions and detoxification. Dandelion and milk thistle protect the liver and stimulate bile flow, which is essential for removing toxic substances from the body.

Optimal levels of vitamin D are also important for recovery, as are zinc and magnesium. Magnesium is best taken as magnesium glycinate, which is calming and easy on the digestive tract.

You might also consider hyperbaric oxygen therapy, a treatment that involves breathing 100% oxygen inside a body chamber with low and controlled atmospheric pressure. This therapy was found to be valuable in the Sears-Bailes protocol for overcoming traumatic brain injury, and has also been shown to be beneficial for Lyme disease recovery.

3. Invite more calm into your life

Since stress is a powerful immune system disruptor, finding more calm is key to restoring immune health and resolving symptoms of neurological Lyme. One of the best tools to fight stress is getting optimal sleep. Without it, your immune functions are disrupted, and healing is compromised.

Sleep is especially important for recovery from neuroinflammatory illnesses. Studies have shown that even one night of compromised sleep in healthy people is associated with accumulation of beta amyloid in the brain, a hallmark of Alzheimer’s disease.

Your goal: At least 8 hours of good sleep a night, including 4 hours of deep sleep. Practicing good sleep hygiene can help you hit the mark; that includes keeping a regular bedtime, and limiting light, computer screens, and stimulation in the evening.

What happens during the day is also key to drifting off at night. Finding additional ways to de-stress, getting regular low-intensity exercise, and practicing meditation a couple of times during the day promotes good sleep onset and better quality sleep at night.

Early on, when neuroinflammation is pronounced and the nervous system is very agitated, sleep medications may be indicated. But use them intermittently, and stick to the lowest dose possible.

If you’re still battling stress and occasional sleeplessness, herbs can help. Some with calming, neuroprotective properties include ashwagandhabacopa, gotu kola, kudzu, and milky oat seed. Nervine herbs also promote calm during the day and help improve sleep at night; these include passionflowermotherwort, lemon balm, and chamomile.

Melatonin, an important antioxidant in the brain that initiates sleep, is reduced in neuroinflammation. Supplemental melatonin at bedtime (1-3 mg) can help rebalance disrupted sleep pathways. Tart cherry juice is an excellent natural source of melatonin, as is Chinese skullcap, an herb providing both antimicrobial properties and immune balancing properties.

Acupuncture can be beneficial for reducing pain and restoring normal energy pathways in the body. It is also helpful for restoring normal sleep.

4. Get active

Healthy blood flow is essential for recovery. Increased blood flow flushes out toxic substances that have accumulated from inflammation, and stimulates healing systems in the body.

The best way to increase blood flow is by moving your body. Increased activity is associated with increased endorphins. Best known as the “feel good” substances that improve mood and wellbeing, endorphins also stimulate natural killer cells, the most important white blood cells for taking out cells infected with microbes.

That being said, movement must be balanced so as to not generate more inflammation. For this purpose, low intensity exercise such as walking, yoga, and tai chi is the best choice. If exercise is not practical, far infrared sauna is an ideal way to increase blood flow and promote removal of toxins from the body.

5. Balance the microbiome

Restoring normal immune function and balancing the microbiome of the body is the most important part of overcoming neuroinflammatory conditions. It includes suppressing opportunistic microbes while also allowing normal flora to flourish so that immune systems can rebound.

For this purpose, herbal therapy is a natural fit. Herbs with antimicrobial properties selectively suppress opportunistic and stealth microbes without disturbing normal flora. Herbs also help boost parts of the immune system that have been suppressed by the microbes. Many of the chemical components of herbs cross the blood-brain barrier and provide neuroprotective benefits. By restoring balance in the gut microbiome and the extended microbiome of the body, the gut-blood and blood-brain barriers are allowed to heal.

There are many herbs with antimicrobial properties that can provide benefit for neuroinflammation associated with microbiome disruption. Some of the more common ones used in Lyme disease include andrographiscat’s claw, Japanese knotweed, cryptolepis, and neemMonolaurin is a fatty extract from coconut that provides antimicrobial properties, and because it is fat soluble, it easily crosses the blood-brain barrier and penetrates into brain tissues.

Berberine and berberine-containing herbs, including coptis, goldenseal, and barberry, are ideal for balancing the gut microbiome and restoring a normal gut-blood barrier. Sarsaparilla is another antimicrobial herb that is particularly good for balancing the gut microbiome.

Herbs that boost the immune system’s ability to control stealth microbes and restore normal immune system functions, but at the same time reduce inflammation, are called immunomodulating herbs. Immunomodulating herbs that also provide neuroprotective benefits include cordycepsreishirhodiola, and eleuthero. These herbs are also adaptogens, herbs that improve stamina and resistance to stress without having drug-like effects.

Because the toxicity of most commonly used herbs is so low, herbs can be taken for extended periods of time without harmful effects. In fact, that’s exactly what it takes to wear down stealth microbes and other opportunists, and allow normal flora to flourish.

The neurological system takes a long time to heal — it’s not a game that’s won in weeks or even months. Patience and persistence for the long haul is required to regain wellness. Many people have found, however, that persistence pays off: A comprehensive, natural approach to recovery is the most secure way to win.

 Dr. Rawls is a physician who overcame Lyme disease through natural herbal therapy. You can learn more about Lyme disease and recovery in Dr. Rawls’ best-selling book, Unlocking Lyme.

You can also learn about Dr. Rawls’ personal journey in overcoming Lyme disease and fibromyalgia in his popular blog post, My Chronic Lyme Journey.

2. Geeta Ramesh et. al. Inflammation in the Pathogenesis of Lyme Neuroborreliosis. Am J Pathol. 2015 May; 185(5): 1344–1360.
3. Forrester JD et. al. No Geographic Correlation between Lyme Disease and Death Due to 4 Neurodegenerative Disorders. Emerg Infect Dis. 2015 Nov;21(11):2036-9.
4. Clark K et. al. Lyme borreliosis in human patients in Florida and Georgia. Int J Med Sci. 2013 May 23;10(7):915-31.
5. Batinac T et. al. Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma. Med Hypotheses. 2007 Jan 2;69(1):117-9.
6. Tsiodras S et. al.Central nervous system manifestations of Mycoplasma pneumoniae infections. J Infect. 2005 Dec;51(5):343-54.
7. Tsai CS et. al. The association between Mycoplasma pneumoniae infection and speech and language impairment: A nationwide population-based study in Taiwan. PLoS One. 2017 Jul 3;12(7).
8. Panagariya A et al. Reversible neurological syndromes with atypical pneumonia. Ann Indian Acad Neurol. 2011 Apr;14(2):127-9.
9. Kaufman DL et. al. Neurological and immunological dysfunction in two patients with Bartonella henselae bacteremia. Clin Case Rep. 2017 Apr;5(6):931-935.
10. Mayne PJ. Clinical determinants of Lyme borreliosis, babesiosis, bartonellosis, anaplasmosis, and ehrlichiosis in an Australian cohort. Int J Gen Med. 2014 Dec 23;8:15-26.
11. Breitschwerdt EB et. al. Bartonella vinsonii subsp. berkhoffii and Bartonella henselae bacteremia in a father and daughter with neurological disease. Parasit Vectors. 2010 Apr 8;3(1):29.
12. Usmani-Brown S et. al. Neurological manifestations of human babesiosis. Handb Clin Neurol. 2013;114:199-203.
13. Salva I et. al. Rickettsial meningitis. BMJ Case Rep. 2014 Mar 10.
14. Hongo I et. al. Ehrlichia infection of the central nervous system. Curr Treat Options Neurol. 2006 May;8(3):179-84.
15. Hassani A et. al. Epstein-Barr virus is present in the brain of most cases of multiple sclerosis and may engage more than just B cells. PLoS One. 2018 Feb 2;13(2).
16. Leibovitch E et. al. Viruses in chronic progressive neurologic disease. Mult Scler. 2018 Jan;24(1):48-52.
17. Emery DC et. al. 16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain. Front Aging Neurosci. 2017 Jun 20;9:195.
18. Branton W et. al. Brain microbiota disruption within inflammatory demyelinating lesions in multiple sclerosis. Sci Rep. 2016 Nov 28;6:37344.
19. Cadavid D et. al. Antibiotics for the neurological complications of Lyme disease. Cochrane Database Syst Rev. 2016 Dec 8.
20. Halperin JJ. Chronic Lyme disease: misconceptions and challenges for patient management. Infect Drug Resist. 2015 May 15;8:119-28.
21. Shokri-Kojori E et. al. β-Amyloid accumulation in the human brain after one night of sleep deprivation. PNAS. 2018 Apr 9.
22. Sugeno N et. al. A case with anti-galactocerebroside antibody-positive Mycoplasma pneumoniae meningoencephalitis presenting secondary hypersomnia. Neurol Sci. 2012 Dec;33(6):1473-6.
23. Neal W et. al. The role of primary infection of Schwann cells in the aetiology of infective inflammatory neuropathies. J Infect. 2016 Nov;73(5):402-418.
24. Colonna M et. el. Microglia Function in the Central Nervous System During Health and Neurodegeneration. Annu Rev Immunol. 2017 Apr 26;35:441-468.
25. Obermeier B et. al. The blood-brain barrier. Handb Clin Neurol. 2016;133:39-59.
26. Fung TC et. al. Interactions between the microbiota, immune and nervous systems in health and disease.
Nat Neurosci. 2017 Feb;20(2):145-155.
27. Layé S et. al. Anti-Inflammatory Effects of Omega-3 Fatty Acids in the Brain: Physiological Mechanisms and Relevance to Pharmacology. Pharmacol Rev. 2018 Jan;70(1):12-38.
28. Devassy JG et al. Omega-3 Polyunsaturated Fatty Acids and Oxylipins in Neuroinflammation and Management of Alzheimer Disease. Adv Nutr. 2016 Sep 15;7(5):905-16.
29. McDougle DR et. al. Anti-inflammatory ω-3 endocannabinoid epoxides. Proc Natl Acad Sci. 2017 Jul 25;114(30):E6034-E6043. doi: 10.1073/pnas.1610325114. Epub 2017 Jul 7.
30. Rudroff T et. al. Cannabidiol to Improve Mobility in People with Multiple Sclerosis. Front Neurol. 2018 Mar 22;9:183.
31. Petrosino S et. al. Anti-inflammatory properties of cannabidiol, a non-psychotropic cannabinoid, in experimental allergic contact dermatitis. J Pharmacol Exp Ther. 2018 Apr 9.
32. Mori MA et. al. Cannabidiol reduces neuroinflammation and promotes neuroplasticity and functional recovery after brain ischemia. Prog Neuropsychopharmacol Biol Psychiatry. 2017 Apr 3;75:94-105.
33. Richer A. Functional Medicine Approach to Traumatic Brain Injury. Med Acupunct. 2017 Aug 1; 29(4): 206–214.