GcMAF Immunotherapy Treatment for CFS

The CFS Patient Advocate Blog has covered the recent conference at the new Mt sinai ME/CFS Research and treatment center.he is posting written content, as well as video taken during the conference. Chronic Lyme patients may find the information helpful.

Read : Mt. Sinai ME/CFS conference report – Sunday November 20, 2011

Mt. Sinai ME/CFS conference – De Meirleir lecture

 Six presentations were given at the Mt. Sinai ME/CFS Research and Treatment Center conference on Sunday November 20, 2011. Here is a lecture delivered by Dr. Kenny De Meirleir, who practices medicine in Brussels. Dr. De Meirleir has worked with ME/CFS patients for many years and is seen as one of the foremost ME/CFS Clinician/Researchers. Dr. De Meirleir spoke for a half-hour on the compassionate use of GcMAF in this patient population. Dr. De Meirleir will be associated with this new ME/CFS Center at Mt. Sinai- as a clinical consultant.

 The video and audio was made by Peter and Nicholas Cairns.

Report on the Biotoxin Conference by Scott Forsgren

Scott Forsgren, of BetterHealthGuy.com, posted an excellent blog on his site regarding the Biotoxin Illness Conference hosted by Gordon Medical Associates in Santa Rosa, CA.  Thank you Scott for your hard work in educating patients and doctors regarding this most important health issue.

Biotoxin Illness Conference 2011 – by Scott ForsgrenGordon Medical Associates hosted the “Biotoxin Illness: The Science Behind Accurate Diagnosis and Effective Treatment” October 22-23, 2011 in Santa Rosa, CA.

While this blog post will not cover all of the details of the event, further information can be learned from either the recordings of this event available through Gordon Medical Associates or via several learning opportunities at SurvivingMold.com.

I continue to spend time learning more about Dr. Shoemaker’s work as I have not yet entirely addressed all of the biotoxin illness markers, especially C4a, and am interested in Dr. Shoemaker’s work as I think he’s a rare genius in the field.

The slides from this event are available here.  If your doctor is not already familiar with Dr. Shoemaker’s treatment approach, ask them to get the Physician’s Approach to Biotoxin Illness DVDs or the Surviving Mold book and get educated on the protocol.  The more doctors that learn how to treat biotoxin illnesses, the better off we will all be.

The biggest takeaway for me from the weekend was one that I had already known, but it is also one that I cannot reinforce enough how strongly I feel about it.  In my opinion based on what I have learned from Dr. Shoemaker’s work, everyone with Lyme should have their HLA genetic testing done so that they understand if it is Lyme toxins, mold toxins, or both that they are inefficient in identifying and excreting.  This information may change the course of your treatment.  Additionally, if one is a mold-susceptible type, I think it is critical to have the ERMI testing done to see if your living environment is save.  If one has a mold-susceptible type, an ERMI of < 2 is the goal.  Anything higher than that is potentially unsafe and negatively impacting your health.

Ignoring the mold issue while treating Lyme disease is, in my opinion, much like trying to keep a boat filling up with water from sinking by using a cup to dump the water overboard when the boat itself has several holes in the bottom.  You just can’t win unless we evaluate and address all of the factors involved in our ill-health.  Mold is often a very critical and overlooked factor.

I’m very excited about Dr. Shoemaker’s new web site SurvivingMold.com.  The information there is invaluable.  I highly recommend that you spend some time on the site to better understand how to evaluate and approach biotoxin-related illness (whether it be Lyme, Mold, or other biotoxins).  The Biotoxin Pathway is the best summary of Dr. Shoemaker’s work.

Here are some key points I took away from the weekend.

Dr. Shoemaker

• 92% of people with biotoxin illness have a positive VCS test.  The test can be done online at SurvivingMold.com.  A negative VCS test does not rule out biotoxin illness as there can be false-negative results.
• ADH (anti-diuretic hormone) deficiency is almost universal in biotoxin illness.  When MSH is low, ADH is generally low.  In fact, when MSH is low, many things go wrong in the Biotoxin Pathway.
• When ADH is an issue, you lose water.  Salt then gets dumped onto the skin via the sweat glands.  Dr. Shoemaker did sweat chloride tests and found that when people experienced static shocks, they had high chlorides.
• “Doing air sampling is the stupidest thing I have ever heard in my life,” stated Dr. Shoemaker.
• MSH and VIP are regulatory peptides.  VIP is now available as a nasal spray that can be used after you have followed all of the required steps in his treatment program. It will not work if done without having done the earlier steps.  MSH is not available yet.  ADH is another regulatory peptide.
• When you lose control of inflammation, inflammation goes wild.  If you don’t control inflammation, it will chew you up.
• Uncontrolled inflammation can be evaluated using C4a, MMP-9, and TGF-b1 testing.
• Reduced MSH is a co-factor which can lead to MARCoNS, a nasal staph infection.  MARCoNS activates inflammation.  MARCoNS can also produce biofilms and biotoxins.
• TGF-b1 can be an indicator of autoimmunity.  It can lead to changes in lung tissue and symptoms that are asthma-like.
• The condition that Dr. Shoemaker speaks of is not a “mitochondrial disease” but an oxygen delivery deficiency.

To read the complete blog, please visit BetterHealthGuy.com here…

Mold and Biotoxicity: Part Two – Diagnosis

Mold and Biotoxicity: Part Two – Diagnosis

Read Part One Here: Mold and Biotoxicity – There’s a Fungus Among Us

By Dr. Neil Nathan

Taken from Dr. Nathan’s book On Hope and Healing: For Those Who have Fallen Through the Medical Cracks

Diagnosis

The first order of business is to even consider the diagnosis. Until I had read Dr. Shoemaker’s books and studied with him, I had never thought to ask my patients about their exposure to mold or these other infective agents. Now I routinely inquire about their possible exposures to mold at home or work. Have their homes had any water damage or leakage anywhere? This includes the roof, basement, and walls. Do they notice a musty smell or see any mold? The materials that can be seen are often just the tip of the iceberg. Mold may grow inside of walls and get into the heating-cooling system of the house, sending mold spores over the entire residence. If you are wondering how this happens, be aware that sheet rock paper is made from processed tree bark, which is loaded with mold spores. To bring those spores to life, just add water. How about work? Do co-workers have similar symptoms or complaints? As I explored this area, it is surprising how many of my sick patients do report exposures that they had never suspected as being relevant to their illness. Keep in mind that mold toxins may have occurred in a previous residence (so I have to ask about any exposures) and toxins may still be present in their body, even though they left that home several years ago.

When presented with this information, some physicians dismiss this whole subject by pointing out that in the natural world, we are literally surrounded by molds, thousands of species actually, of every shape and description. In fact, the reason that the mold species make toxins is not to damage us, but to keep other species of mold at bay as the molds try to claim their own piece of real estate in the natural world.  It is a system of checks and balances, with each species holding the ones nearby at arm’s (spores) reach. However, when a species of mold can grow inside of a dampened wall with no competitors, it just grows wild and can make significantly more toxins and many more spores as it reproduces at will. While most of these species are relatively harmless, several of them, including Stachybotris, some types of Penicillium, Fusarium, and Aspegillus, are capable of producing a toxin that can make us quite ill. Stachybotris, or black mold, is the most well known.

MAUREEN’S STORY

Maureen was a twenty-eight year old woman whom I saw for the first time in March of 2006. Her symptoms had begun three years previously when she was working in a building with a very leaky roof. She had also experienced several traumatic events at the same time, including a difficult divorce, which complicated both our evaluation and her perceptions about what may have triggered her illness. In August of 2005, Maureen began to violently throw up on a daily basis, and this went on for months. She saw multiple physicians, including several gastrointestinal specialists, and underwent extensive testing, which showed no obvious cause for her symptoms. She was diagnosed by various physicians as having bipolar disorder, irritable bowel syndrome, and hypochondriasis (meaning it was all in her head or psychosomatic). Since her initial exposure to mold, Maureen had gained thirty-five pounds and had developed sensitivities to all sorts of chemicals and perfumes (which we call multiple chemical sensitivities). This is actually a common event following untreated biotoxin exposure. She continued to experience daily nausea and vomiting, regular headaches, and an inability to think clearly. She described her poor decision making in very simple terms: “It’s like I am inept. “ She also reported blurred vision and bouts of chest tightness with wheezing.

When Maureen came to me, she had just lost her job of fourteen years, at which she had been previously quite competent, and she was trying to live a normal life and raise her three children. But she could hardly function. Her energy level was very low, and she reported difficulty staying asleep and waking up refreshed each morning. She described joint pains in her neck, shoulders, and upper back, and she displayed the classic irritable bowel symptoms of gas, bloating, distension, and diarrhea alternating with constipation.

When I tested her with the Functional Acuity Contrast Test (FACT), which we will describe late, the results strongly suggested biotixin exposure. Her DHEA test was a little low, as was her progesterone level. I started her on natural progesterone cream, ¼ tsp. daily, applied to her skin. I also put her on a small dose of DHEA, and we started cholestyramine in the form of Questran Light, one scoop mixed with water three times daily, which is the best immediate treatment for mold toxicity. (Some may do better with a pure cholestyramine, which is available compounded.)

When Maureen returned in April, just six weeks later, she reported that she was already 80 percent better. Her energy was markedly improved despite the fact she was still living in her home, which had obvious mold exposure. She had a new job, was successfully working again, but noticed when she missed even a single day of Questran, she became lethargic again. She planned to remediate her home to clean up the mold, and she was thrilled that she had her life back; she was no longer plagued by nausea, vomiting, chest pain , and  joint pain.

She was so impressed with her improvement in just a short period of time, that she bought a copy of Mold Warriors to give to her family physician, who had essentially told her she was a hypochondriac. Her physician refused to even look at the book or to take Maureen’s story seriously.

It has been my experience that most of our mold-toxic patients have had a similar experience to Maureen’s. Their symptoms are usually misunderstood as representing psychological imbalances, particularly depression, but they do not respond well to antidepressant and anti-anxiety medications. That should be a tip-off that we need to look deeper for the cause of these symptoms. Recalling that only 25 percent of patients are genetically unable to make the antibodies they need to these toxins, these patients may live in a home with others who have no symptoms or work in a mold laden environment where others are not sick. Family and co-workers therefore assume that since only one person is sick, that it is in his head. These patients feel like no one is listening to them, including their physicians. The trouble is that no one is listening. This adds even more to their burden of suffering, often tearing up families and friendships which makes them even sicker. Now they are sick and depressed, but we can see clearly which came first. It is difficult to try to fight a biotixin illness, and even more difficult when no one believes you are sick.

The good news, however, is that we are now beginning to understand these symptoms, and there are treatments available. While no precise test exists yet for any specific toxin, we can measure the effects of toxins in several ways.

The simplest is a visual screening test called the Functional Acuity Contrast Test (FACT) or the Visual Contrast Sensitivity test (VCS). This is a well established analysis used by ophthalmologists for many years, in which the patient looks at a series of grayish lines of decreasing clarity. If the patient is unable to see the lighter lines that normal people can, this indicates poor retinal function, and has been closely linked to biotoxicity. Maureen was unable to see any of the lines in the last two columns, which is strongly suggestive of biotixin illness. If you are interested in this process, you can go to Dr. Shoemaker’s website to take this test online.

Dr. Shoemaker has discovered a whole series of biochemical tests that show the patient is experiencing an inflammatory reaction to toxin. He has clearly demonstrated that a treated patient , when placed in a moldy environment, will have noticeably elevated levels of these inflammatory markers ( measured in blood tests), which then come back to normal when the patient is removed from the moldy environment and treatment has been resumed. Once the diagnosis of biotoxicity has been entertained, we can begin treatment. In fact, the response to treatment confirms the diagnosis, as in Maureen’s case.

Dr. Neil Nathan was one of the speakers at the October 22-23th weekend on Biotoxin Illness. An audio recording of this weekend will be available soon.If you are interested in the recording, check back here to find when it is available, or get on the waiting list.

Dr. Nathan is a gifted physician who is passionate about healing. Since he loves to learn, he considers himself  “always a student’, and gets fired up about learning new approaches that might work for his patients. Never satisfied to just learn superficially, when something grabs Neil’s attention, he will research and study with the person who really KNOWS how to do it, so he can maximize its clinical benefits. He is the author of On Hope and Healing: For Those Who Have Fallen Through the Medical Cracks, and a contributor to  Insider Secrets For Treating Fibromyalgia: 12 Top Experts. You can find Dr. Nathan at Gordon Medical Associates in both Santa Rosa and Fort Bragg.

Mold and Biotoxicity

Mold and Biotoxicity

There’s a Fungus Among Us

Taken from Dr. Nathan’s book On Hope and Healing: For Those Who have Fallen Through the Medical Cracks

When it comes to understanding the different components of chronic illness, the concept of toxicity has received a good deal of attention. With the publication of Dr. Ritchie Shoemaker’s brilliant book Mold Warriors, we now have some new tools to both evaluate and treat toxicity in its different forms.

A toxin is simply a poison. Microbes in our bodies produce these poisons that make us sick, then sicker, a phenomenon referred to as biotoxicity. It is fairly obvious that a microbe (bacteria, virus, fungus, parasite, or other infectious agent) makes us sick by infecting us, and it is equally clear that treating these disease-causing microbes will make us better. But what is just becoming clear to us is that not only do these microbes make us sick by causing an infection, but some of these microbes can, in the process of being killed by our immune system, release toxins into our bodies that make us even sicker. Because these toxins are made by microbes, which are living biological systems, we call them biotoxins. This term distinguishes these materials from other types of toxins such as heavy metal toxins or synthetic toxins, which are not made by living systems.

Doctors are beginning to appreciate that some of these toxins remain in the body and cannot be excreted or destroyed. Thus, they actually accumulate within our bodies. The body’s natural method for processing toxins is to concentrate them in the body’s main organ of detoxification: the liver. Once the biotoxins congregate in the liver, they bind to the body’s bile and are sent out into the gastrointestinal tract for release in the stool. However, as the liver binds the toxin to bile and sends it into the intestines, the body’s natural recycling system, which we call enterohepatic circulation, recirculates the bile when it reaches the small intestine. So the toxin, still attached to that bile secreted by the gall bladder, goes back to the liver rather than leaving the intestinal system, and thus accumulates within our body.

Hence, even when we kill the invading microbes with our immune system, the remaining toxins continue to plague us with their harmful effects. Not everyone is subject to this problem, however. For most, the immune system recognizes these toxins and uses its defense mechanisms to destroy them. Unfortunately, about 25 percent of people are genetically unable to make an antibody to these toxins, and those patients may get progressively sicker as the toxins accumulate within their bodies.

What specific microbes are we talking about? The most common offenders are molds, especially the black mold Stachybotris, but several other mold species such as Cladosporium and Fusarium can play a role in toxin formation. Harmful toxins can also be produced by certain viruses, especially those in the Herpes family, such as Epstein-Barr virus, which is the agent of mononucleosis; Cytomegalovirus; and Human Herpes Virus 6 (HHV-6), which is the agent of roseola infection. A new and particularly toxic strain of HHV-6 has recently been discovered and has now been linked to chronic fatigue and fibromyalgia. Lyme bacteria can also produce these toxins, as can infections with the mycoplasmas, which are infective particles between viruses and bacteria in size. The atypical pneumonias (walking pneumonia) and Gulf War Syndrome are examples of these infective agents.

Dr. Shoemaker is the physician who first demonstrated the presence of toxins in our environment with his pioneering work on the Pfisteria outbreak in Chesapeake Bay in 1997. He later found similar microbes in algae-borne lakes in Florida and in long standing cases of Ciguatera poisoning (which occurs from eating certain seafood.) We suspect that other microbes will be implicated as our understanding of the problem deepens.

Symptoms

So what are the symptoms of biotoxicity? Patients with this problem may experience a surprisingly wide range of symptoms related to different organ systems. When this confusing array of symptoms is taken out of context or not understood as representing the many manifestations of biotoxicity, it is easy to see how both patients and physicians might mistakenly think that this is “all in their heads.” The list below outlines these symptoms:

• Fatigue
• Muscle cramps and aches
• Unusual pains (“ice pick” or “lightening bolt”)
• Sensitivity to bright light, tearing, blurred vision
• Cough, chest pain, shortness of breath
• Cognitive impairment
• Appetite swings and weight gain
• Numbness and tingling, often in unusual patterns
• Frequent urination
• Sensitivity to static electrical shocks
• Excessive thirst
• Menorrhagia (abnormal vaginal bleeding)
• Weakness
• Headaches
• Abdominal pain, nausea, diarrhea
• Chronic sinus congestion
• Joint pain with morning stiffness
• Skin sensitivity to light touch
• Mood swings
• Night sweats
• Temperature dysregulation
• Metallic taste in the mouth
• Impotence

These symptoms sound a lot like fibromyalgia or chronic fatigue or depression. In children, it might appear like ADHD. In fact, many patients with these particular diagnoses may have unrecognized biotoxicity as either a component of their illness or the direct cause, and most of them would benefit greatly from an evaluation for mold toxicity and treatment if appropriate.

In the next post: Diagnosis and Treatment

Dr. Neil Nathan will be one of the speakers at the October 22-23th weekend on Biotoxin Illness. He is a gifted physician who is passionate about healing. Since he loves to learn, he considers himself  “always a student’, and gets fired up about learning new approaches that might work for his patients. Never satisfied to just learn superficially, when something grabs Neil’s attention, he will research and study with the person who really KNOWS how to do it, so he can maximize its clinical benefits. He is the author of On Hope and Healing: For Those Who Have Fallen Through the Medical Cracks, and a contributor to  Insider Secrets For Treating Fibromyalgia: 12 Top Experts. You can find Dr. Nathan at Gordon Medical Associates in both Santa Rosa and Fort Bragg.

Dysauntonomia, Biotoxins, and Lyme

Question:

I have a long term lyme patient who has recovered from most of her lyme symptoms with the exception of intermittent hypo tension 80/40 with  pulse in the 40′s known as autonomic insufficiency or pots or dysautonomia.  For years when she has a lyme flare she will experience strabismus.  I am convinced that ocular damage is from the lyme and is part of the etiology for her flares as well as the  dysautonomia. None the less researching this subject quickly makes one realize that it is complex with many suspected etiologies.  I have started her on florinef .1 mg for now.  So anyone have any other pearls of wisdom?  She has been on cortef for years low dose.  Her endocrinologist did not check with me and also put her on cortef so she got a 30 mg dose for a month or so, of course she felt great.   I have had her consult with a cardiologist, endocrinologist as well as neurologist.  They just kind of threw up their hands especially with a ” lyme dx” in the mixture.  I will consult next week again with her neurologist in an effort  to co-manage this case but may get left holding the bag as I usually do in  trying to treat lyme patients.   Anyway I would appreciate tips on treating this common problem with our lyme patients.

Answer from Dr. Eric Gordon:

Have her check her VCS (visual  contrast sensitivity) at Surviving Mold at a time when n she is well and again when she is symptomatic.

Changes in the results may indicate exposure she may be having a mold exposure, or exposure to a multitude of antigens which are triggering her innate immune response ,  no longer self correcting since her Lyme disease caused dysregulation. It would be good to also check her C4a (Complement 4 anaphylatoxin), MMP-9 (Matrix metallopeptidase 9), VEGF (Vascular endothelial growth factor), TGF beta-1 (Transforming growth factor beta-1) when she is symptomatic. Run that group again when she is asymptomatic, and add VIP (Vasoactive intestinal polypeptide) and MSH (Alpha melanocyte stimulating hormone). You can find information about these tests at Lab Tests and information about how to order them, and where at Lab Orders.

This is Ritchie Shoemaker’s work and it can be confusing because it has lots of acronyms for uncommon and multifunctional immune modulators. There are other parts of his protocol but just the VCS online, and MMP-9, TGFbeta-1, and VIP (all of these from Labcorp) will let you know if further work up will be useful.

I have been using Dr Grubb’s protocols for dysautonomia for years, they are good band aids but don’t address the core problem. Ritchie’s protocols don’t work for every patient but they do help us better treat our “post Lyme” patients and a lot of the active Lyme patients who “herx”   yet never improve.

Ritchie will be presenting his latest work in Santa Rosa on Oct 22nd and 23rd, and we will be helping him to give people an explanation of the fundamental concepts and terminology he uses.

I have struggled for years to apply his approach. Like many original thinkers there are steps in his process that are like air to him, leaving the rest of us stumbling in the dark. We have worked with him to address this issue, so that he can better teach people how to really use his work. Dr. Neil Nathan from our offices will be at the conference with  a “Shoemaker for Dummies” talk to provide a foundation for understanding what Ritchie is doing. Other practitioners from our offices who also use Shoemaker protocols will be present to answer questions.

Learning to use Ritchie’s approach has improved the lives of many of my patients. Better understanding of persistent immune activation allows me to make better choices for my patients care.

The October 22-23 Biotoxin Illness conference, with Dr. Ritchie Shoemaker is open to the public on Saturday, the 22nd, and to medical professionals on both Saturday and Sunday, the 22-23rd. For more information, look HERE.

Dr. Eric Gordon is the founder of  Gordon Medical Associates. What Dr. Gordon emphasizes is listening to his patients. “I believe my patients. Their description of what is going on in their body is the most accurate way we have to assess what is going on with them. I interpret the information they present, and blend it with laboratory results and imaging and other tests to determine a protocol that is customized to their condition.”

Biotoxin Illness: Mold, CFIDS, Fibromyalgia, Lyme, and Inflammation – Ritchie Shoemaker MD and Neil Nathan MD

You are invited to Gordon Medical’s next event,  a weekend seminar offered on October 22-23, 2011 in Santa Rosa, CA. Our speaker,  Ritchie Shoemaker MD, a well known mold and biotoxin illness expert, will be making a rare appearance in the Bay Area.  Both medical professionals and the interested public will find this weekend  filled with essential  information. You will learn to understand, diagnose, and treat biotoxin illnesses caused by mold, Lyme bacteria, and other triggers.  In addition to Dr. Shoemaker, Neil Nathan MD will guide you through the basics of biotoxin issues, and Alan McDaniel MD will address problems with mold and inflammation that are NOT biotoxin associated.

The first day, open to the public, will provide a solid foundation in the principles of how biotoxins damage the body, and what can be done about it. The second day, open to medical professionals only, will provide the tools necessary for practitioners to use these principles in their practice.

Saturday and Sunday October 22-23, 2011

Ritchie Shoemaker MD

Author of Surviving Mold and Mold Warriors

and Neil Nathan MD

Author of On Hope and Healing: For Those Who Have Fallen Through the Medical Cracks

and

Alan McDaniel MD speaking on Non IgE Mold Allergy and Inflammation

The Hyatt Vineyard Creek

Santa Rosa, CA

To learn more, to see the schedule for the talks, or to register, use the links  below.

Get more information

Register Now!

 If you have more questions, please call Gordon Medical Associates at the number listed below. You can also find more information about speakers at www.survivingmold.com and www.gordonmedical.com .

Thank you for your interest in our events! In the next year, we expect to continue to present cutting edge researchers and clinicians with exciting ideas on how to improve patient’s health.
Gordon Medical Associates
3471 Regional Parkway
Santa Rosa, CA 95403

(707) 575-5180

Conversations with Eric Gordon, MD – Tracking Treatment, Rheumatoid Arthritis, and Lyme

Continuing the phone conversation with Eric Gordon, MD from August 16, 2011.

DR. GORDON:

Okay.  So, where were we?

Interviewer:

You were talking about having those high inflammation levels and how those impact how to decide what to treat.

DR. GORDON:

Ah, how to decide….yes.  At least for me what makes treatment so difficult is the noise. I mean in the sense of, when you start someone on a therapeutic trial, if you’re moving somewhere with them when they start antibiotics, and they begin to respond partially, and then they have some problems, which you fix, and then there is more partial response, and they have more problems.  After a while you’re doing a lot of fixing the problems, trying to do a lot of symptomatic therapy.

At the same time using the antibiotic, it can be difficult to know whether the antibiotic is helping, or whether it is causing some of the symptoms. You have to constantly be going back and looking at what is really happening. It’s so important for the patient to keep really clear records, the calendar of when their treatments start, and responses to them, that simple thing I find very useful in deciding how treatment is going.

Interviewer:

I haven’t seen Wayne’s (Anderson) calendar.  It might be interesting to have a copy of that, but what do you look for when you’re looking at that calendar.

DR. GORDON:

It is a pattern of response that we look for.  What we ask people to do is just, the simplest level is just keep a calendar and write down a plus for a good day, a minus for a bad day, and a zero for a regular day; also a zero goes for any day you really have to think about it.

If you’re not sure if it’s a good day, then put a zero.  A good day is a good day.  And now some people like to analyze that a lot, they break it down to, “Was my energy good?” “Was my pain good?” Those kind of categories.

But I encourage them to keep a simple one to start with because it’s simple and they will actually do it.  The symptoms tend to run together if they don’t somehow keep track of how they are doing, especially in response to treatments.  If the active infection is giving most of the symptoms, that’s another hint that we ought to be looking elsewhere for the cause other than just Lyme, look for a lot more bugs if the symptoms really diverge a lot.

We’re looking for patterns, you know, Joe’s (Burrascano) thing about Lyme symptoms coming in 3 to 4 week cycles.  I’ve seen it be shorter than that.  But it does tend to run in a pattern, symptoms will be worse every 3-4 weeks and with the correct treatment you’ll start to see good days.  That’s how you’ll know you’re getting somewhere.

This response to treatment often isn’t a linear response. You’ll see that when you have acute Lyme or Lyme for less than a year then they’ll often get better in that more linear fashion.  I mean it’s really kind of dramatic. You’ll give them the antibiotic and they just get better.  I see that in a lot of the people around here who have had recurrent episodes of Lyme but have never gotten really, really sick—they tend to get a joint pain or fatigue or joint pain, fatigue, and headache.  But they’ll do okay.  They never have to stop functioning.

Those folks, you give them the antibiotic and it’s like flipping a switch.  You know, even if they’ve had Lyme for 20 years, we see some of the farmers, some of the grape growers, they respond. And what I’m doing with them now, the ones who keep getting re-infected is just to put them on antibiotics 1 week a month.

Interviewer:

Oh, interesting.

DR. GORDON:

And it seems to work.  You know, 1 week a month of Minocin or doxycycline and Zithromax and it seems to keep them ahead of the infection, they feel fine.  And if they stop they’ll often feel fine for 2 months or 3 months, and then their symptoms start to come back.  Now Joe Burrascano and Ray Stricker would probably say that these people have never been completely treated, and they might be right. I don’t know if they’ve been treated completely, but they keep getting reinfected because they keep being outside. This is better than leaving them on the antibiotics all of the time.

It seems to work.  The problem that we have is the chronic Lyme patient, someone who has symptoms that interfere with their life even when they’re on antibiotics, is more challenging.  There’s still a subset of them who will get better if we get the right antibiotic into them.

But I don’t know again….  The problem we suffer from is we don’t know our denominators.  It’s not like you get 100 people who come into the hospital with a heart attack and we’ve  all agreed on the standards of care, EKG changes and troponins and the biochemical change, and you can kind of ignore the individual patient more or less, and we do that, use “X” therapy, and we see how we do.

In chronic Lyme we don’t have that.  We don’t have clear standards on how to treat someone to best be sure they will get well. So what we’re left with is unending anecdotal medicine, and that is the great weakness of what we do. The only way it’s going to change is if we actually empower patients to keep better records of what they’re doing and what are their outcomes.

Interviewer:

Okay.  So that’s what I was going to ask you:  How would you set it up?  Are you still talking about that simple procedure of better/worse or a more complex system of tracking things so that you’d really get useful data.

DR. GORDON:

If you are going to have a real answer, I’d like to see a more complex system of really tracking things.  You know, the real way to go is if someday we could get Syd Baker’s software, but in the meantime if we can just get Joe Burrascano’s program online. If he actually gets his thing together where it’s not as robust, but at least it would be a relatively simple online questionnaire because it’s branching questions, so you don’t have to look at a thousand questions.

Interviewer:

Right.  Not unless it’s pertinent to you.

DR. GORDON:

Exactly.  You look at like maybe 10 questions, and you go down the pathways that are pertinent to you. And that will help.  See, that’s just the point that these people can’t deal with the complex questionnaires. We’re treating people who have multiple things wrong with them. One of them happens to be Lyme or a coinfection, but the people who just have Lyme or a coinfection, I think by and large get better with the antibiotics relatively quickly.

And then we have the people who don’t get well quickly and some not at all. The thing that makes that not necessarily true is that you have the other people that Lyme doctors treated who got well, we have to remember they treated them predominantly with antibiotics for years and years and years and years. And a lot of them got better.

But then you look at (Dr. Richard) Horowitz, you know, Horowitz might be a better reporter, when you think about it, because Horowitz had a lot of patients who didn’t get better. And that’s why he started using the alternative stuff. It could be that some of the people who didn’t get well when working with other doctors just didn’t keep seeing them, so they didn’t get reported.

Interviewer:

This brings up an important point. I think Dr. Burrascano is great, and I think he’s done a tremendous amount of good, but also sometimes the patients listen to him and they feel like failures because they either couldn’t do what he said, or they did it and it didn’t work.

DR. GORDON:

Something to remember when you see different providers is; you just have to remember their therapy still has to fit your situation. It doesn’t matter what doctor you go to.  If their story is that this is an infectious disease that can be treated predominantly by use of antibiotics, it will fail if what you have is a genetic tendency to hypercoagulability and mold sensitivity and have had a mold exposure. If you go to a doctor who thinks that things are predominantly mold exposures and your problem is predominantly a chronic Babesia infection which happens to have symptoms that are almost identical to the neurotoxic response to mold.

And you just have to be willing to not feel bad because you don’t respond to their therapy.  Their therapies are very, very good and effective, but they often have to be done at either the right time or more importantly in the right patient.

Interviewer:

Exactly.  It’s not about the doctor or the patient being wrong.

DR. GORDON:

No.

Interviewer:

Sometimes it’s just a matter of you  have to find a doctor that you can actually communicate well enough with and feel like what they’re doing is good enough, whether or not it’s the absolutely optimum thing, but if you can work with them you’re going to do a lot better.

DR. GORDON:

Yes.  I think one of the things we can say is that many of the leaders in new therapy tend to be people who are very bright, very strong willed, and able to really look beyond what we know. And push the envelope. That very strength of character which allows them to do that can often make them intimidating when you’re sick and you’re not responding the way their theory says you should.

And it’s just the price that we pay.  We are all mortals, and we all have our pluses and minuses, and the plus is that those people are going to lead us to new visions of how to know people.  A minus is that if you don’t happen to respond to their therapy they might not pay much attention to you, and not because they’re bad people, it’s just the nature of being a human being.

Interviewer:

Exactly.  And when patients can get clear….  I find when they get clear about what they can get from a doctor and what the doctor has to give, instead of being angry at the doctor for not giving them something, they can just see that doctor doesn’t have it to give. If you need it you go somewhere else, but you get from the doctor what they have, what they’re good at.

DR. GORDON:

Right.  That’s the whole point of the clinic is that hopefully we’re going to put together enough doctors who are good at different things but they can at least see the whole picture.

But the difficulty is that we all want to be everything.  But it’s just the looking at possibilities that’s important. You have to encourage patients to remember that 20 years ago almost everybody was only treating Lyme, and then 15 years ago they realized, oh, maybe we should be treating more of these coinfections.  And then they came up with, well we should treat the coinfections first.

But, is that always true?  I don’t know.  You know, I kind of wonder about that, if it’s always true.

Interviewer:

Well how can that be always true, if at the beginning when they didn’t know about coinfections, and they treated people later for the coinfections because they didn’t know about it, and people still got well?

DR. GORDON:

Yes, exactly.

My point is that we don’t know, and I would like to just assume that….  It depends on what the symptoms are and how people are feeling, what you treat.

Interviewer:

Yes.

So either we can do some more of this later, or you could go into this one section here that can kind of feed off of this.  It’s just 2 questions.  One is:  If Lyme turns into CFS or arthritis, do you stop the Lyme treatment and just treatment the arthritis?

DR. GORDON:

No.  That’s an absolute no.  No, no, no, no.

I mean that’s something I think is important, I can just say for myself I first began to treat rheumatologic diseases with antibiotics before I knew that Lyme was such a major player, that people have been treating rheumatologic diseases, especially rheumatoid arthritis, with antibiotics since the late 1940s.  Thomas Brown started that and we have to remember that when wondering about rheumatic disease. So, you really need to keep treating the Lyme aggressively if you have symptoms from it. And there are people, I have patients who develop what looks like rheumatoid arthritis by all the lab tests.

Rheumatoid factor is elevated, the whole nine yards, but they keep responding to the antibiotics.  And their joints stay preserved as long as we keep them on the antibiotics, so something else is happening.  And it doesn’t necessarily need to be the anti-inflammatory antibiotics, which I think is the important point, is that we’re treating the bug.  For some reason we’re not eradicating the bug, and that’s where alternative therapies I think come in, maybe using more neural therapy.  I mean this is something that I’m interested in, is if you listen to Dietrich Klinghardt, the concept that if we have a joint that remains inflamed and it doesn’t keep moving around, that’s where we should be treating the joint:  inject the antibiotics right into the joint, inject ozone right into the joint.

Interviewer:

Oh, okay.  Interesting.  So—there’s another question here, it says:  Discuss post-Lyme, specifically autoimmune which presents as rheumatoid arthritis, and is this especially nonresponsive to antibiotics?  So would you….?

DR. GORDON:

Well if it’s especially nonresponsive to antibiotics then I would be looking to what else is going on.  Are there heavy metals?  Are there other toxins?

Interviewer:

But do you feel like this thing that you’re talking about with Dietrich might also be a useful way to approach that?

DR. GORDON:

That would be an interesting concept is to consider, you know, more local treatment because what happens is that when you have inflammation you have poor blood flow to the area, so the drugs you’re giving don’t get there.

Interviewer:

Right.  You also have patients who are immobile.  They’re not moving around, they’re not active.

DR. GORDON:

Right, just like the infection will limit blood flow.  I mean that’s what bugs do. They shut off the blood flow and they shut off the drainage, and so by bringing the antibiotics or other therapies directly locally, injecting into the joint and around the joint, you can open up blood flow as well as the delivery of medication to the area that needs it, so that’s something that we think about.  But again you always have to look at heavy metals and toxins when people aren’t responding.  You know, what else is inflaming your immune system, because you have to remind people that autoimmune disease merely means that you have a dysfunctional immune system but we don’t know why.

Okay?  It doesn’t tell you anything else other than that.  People think autoimmune disease is a diagnosis like Lyme, and it’s not.  Autoimmune disease is more like being told you have chronic fatigue.

Interviewer:

Yes, it’s a syndrome, more like.

DR. GORDON:

Yes, it’s a collection of symptoms hung together….  There’s specific testing and there’s changes to the cells blah blah blah, but we know practically, I don’t want to say nothing, but we know practically nothing as to the etiology because that….people don’t pay attention to that as they should, and so what we see clinically is that when we either treat heavy metals, treat other toxins that are affecting the immune system or kill the bugs, these autoimmune diseases get better.  Not always but sometimes.

They should also often be checking for Chlamydia with a rheumatologic disease and Mycoplasma, but sometimes it’s not going to work, and I think that’s what they have to understand is that at some point we just keep trying.

Dr. Eric Gordon is the founder of  Gordon Medical Associates. What Dr. Gordon emphasizes is listening to his patients. “I believe my patients. Their description of what is going on in their body is the most accurate way we have to assess what is going on with them. I interpret the information they present, and blend it with laboratory results and imaging and other tests to determine a protocol that is customized to their condition.”

Conversation with Eric Gordon, M.D. on Transmission and Treatment Issues

Dr. Gordon spent some time in conversation to cover some of the remaining patient questions from the conference with Dr. Burrascano. The following is a transcript from that conversation. The second part of the talk will be posted later this week.

Initial questions:

Can Lyme or co-infections be transmitted thru sex or kissing?

 Please address whether Lyme is an STD?

 Can it be transmitted from an adult to young children during normal care giving?

 What do you think about the possibility of sexual transmission or other TBD?

DR. GORDON: 

Can Lyme disease be transmitted through sex or kissing? The answer is through sex, probably; through kissing is much harder. I don’t believe anybody has found Lyme bugs in saliva. Usually you don’t get it from saliva. You might be able get it because there is a cut, there is a little bleeding….

INTERVIEWER:

An opening to the bloodstream.

DR. GORDON:

….gums that bleed or something.

INTERVIEWER:

Eric, have you heard anything in any of the conferences about what it takes to actually be able to transmit the infection. For example, with sexual transmission, men’s sperm actually suppress women’s immune system so they can impregnate the egg.

So they think that’s why, or it’s part of why, it might be easier to transmit Lyme disease from males to females, but is there anything else that you’ve heard in terms of what it takes to transmit the bacteria, like if it got on your arm could it crawl through the skin….?

DR. GORDON:

No, I wouldn’t believe so. I mean, most bugs don’t do that very effectively.

It takes usually a broken area…. The skin has to be broken. If you had an open cut or an open sore, that would be theoretically possible. But so far, there is no evidence to show that it happens in reality.

INTERVIEWER:

Yes.

DR. GORDON:

These are just guesses. I mean, yes, I’m sure it can happen, but if you look at something like Hepatitis C and AIDS, they are good examples. Hepatitis C is definitely contagious and transmissible through sexual contact, but it still happens to be relatively difficult to do so, and does not happen often.

INTERVIEWER:

Yes. Well that’s what I keep trying to say to people when they say, “Well I can get Lyme from mosquitoes,” or “I can get it this way.” Ticks have a very unique transmission process, that suppresses the immune system enough to allow the bacteria a chance to be established.

DR. GORDON:

Yes. Lyme, you probably cannot get from mosquitoes. You can probably get Ehrlichia and any of the Rickettsial things from mosquito bites. And Bartonella may be transmitted through other vectors, but Lyme, I don’t know if it is possible, I don’t think so.

INTERVIEWER:

They haven’t been able to prove it yet in transmission studies, so, you know, it seems like when they ask, “Can it be transmitted from an adult to a young child in your daily care taking?” Again, it seems unlikely except….

DR. GORDON:

With Lyme it would be very, very unlikely.

INTERVIEWER:

Except, you know that there is a possibility with breastfeeding. Borrelia has been found in breast milk.

DR. GORDON:

Yes, again, could be, but unlikely, because the mother should have some immune globulins going at the same time. So if the breastfeeding is passing the infection, it is also passing protection from the infection. Other than that, you just have to say, what people don’t understand, is that this disease has not been studied.

And people are making these statements based on evidence that could have other interpretations. Like, we know in utero transmission has happened, but we really only have maybe one or two documented cases. Everything else is a guess.

So I have always been uncomfortable about this whole thing. I think you just have to say that it is possible, yes, but likelihood is very low, yes; just like yes, it is possible to win the lottery.

INTERVIEWER:

Right, right. But I think the thing that people are asking you, Eric, is do they need to do anything different? Do they need to be concerned in their sexual relationships? Do they need to be concerned when taking care of their children? That’s of course the bottom line about these questions.

DR. GORDON:

The bottom line is that we don’t know, and I think there’s probably a better chance that you can do more harm to your child by worrying about it than by doing it.

INTERVIEWER:

Well, there you go.

DR. GORDON:

And as far as relationship, it is the same thing. If you’re in a committed relationship, it’s not something I would worry about. If you are really worried then, get yourself tested! Because you have to remind people that most people who get Lyme can be treated relatively easily.

They’re not all going to be chronically infected. The IDSA is not all wrong.

INTERVIEWER:

So talk a little bit more about that, Eric…

DR. GORDON:

Back to my statement—my basic statement to the world is that the reason we’re in this terrible political battle is because the IDSA (Infectious Disease Society of America) people really do see folks respond to short-term antibiotics, and get well, and they don’t go on to get recurrent illness. I forget…. The rate in Connecticut is like, what, 10% or 15% of the people have had Lyme disease?

INTERVIEWER:

Yes, something like that.

DR. GORDON:

It’s some huge number, and they are not all having chronic joint pain and brain fog and difficulty functioning.

INTERVIEWER:

Right. Ten percent of their population is not disabled.

DR. GORDON:

Exactly! This is a disease that does disable people and do terrible things, but it takes a combination of events, and a combination of genetics, and other infections before this will lay you low, and that’s why it has been so difficult to convince so many doctors that chronic Lyme does exist. Because the IDSA looks at their regular patient population, and then they have somebody who thinks they have chronic Lyme come in. They have people come to them who have diagnosed themselves on the internet, because they read about what Lyme symptoms are, and the problem with that is if you read the symptoms, they fit multiple diseases.

So yes, this is a clinical diagnosis, but it is a clinical diagnosis where you have to listen to lots of people to make it. When patients have the symptoms, and read a lot about Lyme, they don’t always know the difference between the achiness that might come from something else, and the level of disability that Lyme can bring, unless they have seen a lot of patients. So sometimes the IDSA doctors can be right when they tell a patient they don’t have Lyme disease, or that it is not the cause of their symptoms.

Another big part is that the IDSA usually doesn’t pay any attention to the kind of symptoms that those of us who treat Lyme recognize as more Lyme-specific symptoms. So they miss some of the people who do have Lyme.

INTERVIEWER:

Okay.

DR. GORDON:

So, a lot of what are really neuropathic pain symptoms, like the deep burning pain that moves around, the joint pains, like one day your shoulder hurts; the next day your knee hurts…. Those are the things that they tend to just  ignore.

INTERVIEWER:

Or they think it’s something psychological.

DR. GORDON:

Exactly, when you have symptoms that move around they think you’re kind of crazy, so that just adds to their impression that what they’re dealing with is a psychologically over-stimulated population who has some minor illness that a little therapy would help.

INTERVIEWER:

Exactly. Are there some other symptoms that you feel like you look at carefully that they disregard?

DR. GORDON:

Well, it would be…. The type of pains, I guess: It’s burning pains, the sense of muscle fasciculations, a sense of what they call not fasciculation but formication – the sense that ants are crawling on your skin. That’s a common Lyme symptom, but not common in regular medical practice. People in medicine think it’s a psychological problem.

Also, sharp, stabbing pain that once they work you up, they don’t find anything really wrong on the regular tests, that also goes into the realm of probably psychological.

INTERVIEWER:

Right, because they can’t find a physiological cause.

DR. GORDON:

Right, right. So if  you’re an average Lyme patient who does not have a swollen joint, but merely achy joints, okay, and painful, tender muscles, has brain fog and has lots of muscle fasciculations and the joint pain moves around, has headaches and sleep disturbance, they go to an infectious disease doctor, that doesn’t add up to any infectious disease they recognize. The symptoms have been there for a year or two and their tests show you are normal.

Those guys, they see this person who they think is no big deal, and then they get that same kind of patient show up who has been on IV antibiotics for two years, and isn’t getting better, and they just go, “Oh my God, this is malpractice! This is terrible medicine. So they rightfully decide that the doctors who treat chronic Lyme disease are really just enablers, and dangerous enablers.

Because that’s what they see. And on top of that, all they need to see is one patient once a month, or once every 6 months who comes in with these kind of symptoms, and had been diagnosed with Lyme disease, and it turns out that they actually have sleep apnea.

INTERVIEWER:

Right, something that was missed.

DR. GORDON:

Right. And they think, oh, let’s treat the sleep apnea, and the body pain gets a lot better, and the doctor ignores the parts that don’t get better, and they think, “Oh my God, well it was just sloppy diagnosis.”

Or the patient sees somebody like Richie Shoemaker, who notices that they’ve got mold toxicity, and so therefore all their Babesia symptoms are meaningless, because they can both look the same as far as symptoms. Not all doctors think about whether you might have both, and need to be treated for both.

INTERVIEWER:

So, Eric, what other kinds of things do you see? This is another thing that I feel like people with Lyme, they have this tendency to think everything they have is Lyme. They are always asking, “Do Lyme patients have this? Is this because of Lyme?” And it’s so possible to have multiple issues going on.

DR. GORDON:

Well, what I think we have to say is that the other good example is  celiac disease, but you don’t have to have celiac disease in the classic sense. You could just have milder forms of gluten intolerance or GI inflammation.

INTERVIEWER:

Yes, yes. And do you find that in people with Lyme that because of the inflammation levels that they are more likely to have that?

DR. GORDON:

Absolutely. Any inflammatory process makes the others easier. Because if you’re stuck in inflammation, your body’s ability to modulate inflammation goes down because if it didn’t you would not be stuck there. Usually the ongoing inflammatory response is no longer effectively killing the bug, okay? It’s no longer self regulating.

INTERVIEWER:

So what besides celiac or gluten intolerance, or sleep apnea, what other kinds of things do you see most often are missed?

DR. GORDON:

Oh,  the chronic biotoxin issues Dr. Shoemaker talks about. Insulin resistance, which increases the inflammation in the body. Shoemaker’s Actos treatment helps a lot of people by lowering the constant inflammation from insulin and leptin resistance.

If you also put them on a high protein, low glycemic diet, their inflammation might go down also. Because insulin is very pro-inflammatory, and so if you have insulin resistance and you eat, but you’re sick and you’re tired and the only thing that lets you get through the day is a little bit of ice cream now and then, or just peanut butter and jelly, or whatever high carb snack works for you, and if you have the genetics, which a lot of people do, or just start to gain a little weight without the genetics, you begin to have higher and higher levels of insulin being released all the time, and that drives inflammation. That turns on a lot of the inflammatory cascades. It also will suppress your adrenals.

This goes back to the whole naturopathic concept….and why a lot of naturopaths have been late to the game of treating Lyme is because they, in their training, they think that if they fix the gut and balance the hormones and supplement the hormones, help resuscitate the adrenals and the hypothalamus and pituitary gland, get that functioning better, get the ovaries and testicles working better, restore basic nutrition and deal with some of the allergic foods, you’re going to get people well. And you will help them. But if their main trigger is a Lyme or Bartonella or Babesia or Chlamydia or Mycoplasma infection, you’re not going to get them well. You might improve them, but if they’re really sick you don’t even do much for them—until you begin to remove the bug. And you don’t have to necessarily cure the infection. Suppression of the infection and allowing the immune system’s self regulatory pathways to function again,  will then keep the bug in a dormant state. Similar to having a chronic herpes virus which stays dormant as long as the immune system is healthy. And the problem is that  the  Lyme world has been so focused on killing the bug, and that does work with some people. But what I would love to know with some of the Lyme doctors is, they talk about the number of patients that they treated and claim are well. I wonder what was their dropout rate, though? One of the problems with the use of long tern antibiotics by many physicians is that they may be seeing their successes and forgetting about those people who had to drop out because they couldn’t tolerate the long term antibiotics. This doesn’y invalidate long term antibiotic therapy, it just means that we have to remember to tailor the therapy to the patients.

…and I think again we need a common denominator to use, because to be fair to the doctors who only use antibiotics, you know, they help a lot of people by just keeping them on antibiotics forever, but they don’t stop to go back and go, okay, what else do people need? Maybe the infection has been knocked down but the patients are still sick and look the same.

INTERVIEWER:

It’s unfortunate because some don’t tend to look very much in sort of the more conventional issues other than Lyme.

DR. GORDON:

Right. You know, what makes this difficult and I think we have to emphasize is why this is so individual because,  I have one patient who sticks in my mind. She was somebody who saw a doctor for like 5 years, and he did a good job, he really did; she was a very, very sick young lady. She came to see me—I was lucky. I had just started supervising one of his patients, okay, and she had some severe headaches and was so sick and had been on tons of Rocephin for a year and all kinds of antibiotics, you know, and she has been on a ton of Mepron. And it hadn’t helped. She still had positive Babesia tests.

So I put her on  IV clindamycin? But not in the way Dr. Jemsek uses.  Rather, I put her on it daily for one month.  I was only going to do it for a month, but she improved so much she stayed on it for a few months, and then we did vancomycin. She eventually lost about a hundred pounds that she had gained and is  now symptom free.

INTERVIEWER:

Oh my gosh!

DR. GORDON:

And she’s now back to functioning normally. I mean she really got well after being totally disabled and on high doses of narcotics for six years.

INTERVIEWER:

Wow!

DR. GORDON:

I mean, she’s young. She’s only in her mid 30s, but she got well. This is somebody who when you found the right antibiotic and the right antibiotic combinations, it worked.  We have to remember is that we don’t want to say never do that, but we need some parameters while we’re treating to make sure that the thyroid and the adrenals are being looked at, sort of like checking, sort of like cooking, like, “Is it done?”

INTERVIEWER:

Yes. And what else does it need now?

DR. GORDON:

Yes.

.……… This interview will continue later this week.

Dr. Eric Gordon is the founder of  Gordon Medical Associates. What Dr. Gordon emphasizes is listening to his patients. “I believe my patients. Their description of what is going on in their body is the most accurate way we have to assess what is going on with them. I interpret the information they present, and blend it with laboratory results and imaging and other tests to determine a protocol that is customized to their condition.”

Will Surviving Mold Mean Surviving Lyme?

The following is the most recent article from Dr. Ritchie Shoemaker, a specialist in biotoxin caused illness. This article was originally published in Public Health Alert, and is republished here with the permission of Dr. Shoemaker. Plans are under way to bring Dr. Shoemaker to the San Francisco Bay Area in October of 2011 to speak with professionals and the public. If you are interested in attending events offered at that time, please contact us at Putting Lyme Behind You.

NOTES FROM THE MOLD FRONTIER

Ritchie C. Shoemaker MD
With Laura Mark, MD

Will Surviving Mold Mean Surviving Lyme?

 Take out a microscope and look under the in the kitchen cabinet right underneath the pinhole leak in the water supply line.  Is there something growing in the water-damaged area?  You bet: You’ll surely see some filamentous fungi (AKA molds), but look too at the bacteria and actinomycetes.  They are feasting on the simple food stuffs created by the extracellular digestive enzymes of the fungi.  Free food!  This habitat is a nice warm 65-72 degrees all day, every day, year round.  Microbe paradise!  Plenty of food, plenty of moisture and plenty of places to breed safely means plenty of microbial growth and plenty of secondary products of microbial metabolism.  Call the products toxins, inflammagens, cell wall fragments and beta glucans; they are all foreign antigens as far as our immune response is concerned.  And they all cause intense inflammatory responses that are well-demonstrated in tests of innate immunity.

If you put those compounds in the nose or lung of someone with “increased susceptibility,” you will see innate immune functions going nuts trying to defend against the invasion of these foreign antigens.  The excessive host inflammatory response can become the enemy if levels of melanocyte stimulating hormone (MSH) are low or if there is a particular collection of immune response genes present.  As it turns out about 25% of the general population have these specific immune response genes (HLA DR).

Add to this example of health hazards created by a leaky pipe some other sources of water intrusion that beget microbial growth like musty basements, crawlspaces with sagging flexible duct work, leaky roofs and slid-shod construction in schools, homes and workplaces.  You will see why in 2011 NIOSH says that 50% of our buildings in the US are water-damaged.

Do you think that people with chronic illnesses are helped by being subjected to inflammatory stressors from within?  No, they aren’t.  Don’t forget, those chronic illnesses are altered in presentation and therapy by such exposure to toxigenic microbes.

This entire mold problem hasn’t gone unnoticed.  There are numerous reports from US agencies (some are just downright deceptive, however, don’t believe it when you hear that mold is a nice warm fuzzy co-habitant that doesn’t make people sick unless they eat it), the Government Accountability Office and the World Health Organization all describe how moldy buildings sicken people.  There are hundreds of academic papers published showing the diversity and intensity of the inflammatory responses found in people sickened by exposure to the interior environment of water-damaged buildings (WDB) even without other illnesses. We have accurate diagnostic tests and our meticulous research has defined the abnormal physiology carefully. Such delineation led to published treatments that detail the step by step protocols used successfully by our group (and countless others) in thousands of patients.  We aren’t done; these illnesses continually show us that there is still much to learn.

Paralleling the march of science in the “mold” community has been a similar call in the Lyme community: to (1) establish better diagnostic tests, (2) identify accurate physiologic markers that define the illness; and then, (3) publish case control data on protocols (not anecdotes!) that work.  We have these three defining parameters in the mold world but they are not yet in the world of Lyme.  Indeed, some practitioners who focus on Lyme still don’t acknowledge the devastating effect of exposure to the interior environment of WDB has on their patients.  Lyme isn’t just Lyme when a patient is moldy too.  And to secure the diagnosis of Lyme, the illness must pass intact and unchallenged through the sieve of all other CIRS, including mold.

Mold illness is essentially identical to Lyme in symptoms and chronicity.  This observation is critical to understanding why some Lyme patients just don’t get better with antibiotics.  There can be no “clinical diagnosis” of Lyme simply based on the geography at the time of onset of illness or symptoms until mold has been considered and ruled out by careful environmental evaluation and sampling that includes DNA sampling.  Mold illness doesn’t get better with antibiotics.

Maybe some perspective will help bring understanding to treatment of the many patients suffering needlessly who are taking antibiotics for Lyme that haven’t worked.  The answers start with genetics, move on to loss of regulation of inflammation and then to the effects of unregulated inflammation (including silent colonization by commensal bacteria living in biofilms). Finally, correction of T regulatory cell (T regs) abnormalities must occur before return to normal health can be claimed. In the end, if the inflammatory elements that are invariably abnormal in Lyme and mold, specifically C4a, TGF beta-1 and MMP9, aren’t identified and corrected the patients won’t get better.  Said bluntly: If these parameters aren’t improving with a given therapy, the therapy isn’t correct.  Clearly, what many physicians who treat mold illness use for therapy has direct application to the management of illnesses collectively called Post-Lyme Syndrome.

The reader may find complete discussions and up to date information on mold illness at www.survivingmold.com and by reading Surviving Mold: Life in the Era of Dangerous Buildings, by Ritchie C. Shoemaker MD, published 12/2010. Another useful resource is the peer-reviewed consensus statement, “The Expert Mold Treating Physicians Report,” hosted by Policyholders of America (see www.survivingmold.com or www.policyholdersofamerica.com) and published in 7/2010.  This consensus statement has the most compete set of references of any of the current mold reports.  Additional information is found at www.globalindoorhealthnetwork.com.

So what is “Mold Illness?”

Long answer: The acute and chronic health conditions caused by exposure to the interior environment of a building with a history of, or ongoing, water intrusion in which there is amplified growth of microbes, including but not limited to fungi, bacteria, mycobacteria and actinomycetes; and presence of inflammagens in air and dust, including but not limited to beta-glucans, endotoxins, mycotoxins, mannans, proteinases, hemolysins, microbial volatile organic compounds (mVOCs) and spirocyclic drimanes.  The illness is readily identified by a combination of health symptoms, visual contrast sensitivity (VCS) deficits and abnormalities shown in blood tests performed by high complexity, CLIA-approved laboratories.  These tests are eligible for insurance coverage and are all available to practicing physicians (see  the laboratory section).

Short answer: this is an incredibly common Chronic Inflammatory Response Syndrome from Water-Damaged Buildings (CIRS-WDB).  The lesson for the Lyme community is that Post-Lyme is a CIRS too.

The US Government Accountability Office (US GAO) conducted and published its own review of governmental agency efforts to look at CIRS-WDB.  What they found wasn’t pretty:  no rigorous science, no coordination of research efforts and no involvement sought by agencies of people who actually treated the illness.  At least the GAO provided an overview of the inflammatory basis of the illness and a case definition.  That definition superseded the one published by our group in 2003.  The GAO looked for three elements: (1) similarity of symptoms of a given individual to those published (see roster of symptoms in Table 1) and a (2) similarity of lab abnormalities seen in published studies involving experimental animals and people (see roster of lab abnormalities in Table 2).  Finally, the (3) GAO wanted to see improvement with treatments.  The GAO reserved special criticism for a paper published in 2006 from the American Academy of Allergy, Asthma and Immunology (AAAAI) that is routinely used by defense interests in mold litigation.

In July 2009, the World Health Organization (WHO) weighed in with a far more comprehensive assessment of the inflammatory basis for mold illness, with recognition of the diverse potential sources of inflammation found inside WDB.

The mold world is dominated by litigation, with outcomes of personal injury cases resting on decisions made by judges across the country that have a marked diversity of interests in the science involved in mold illness.  The defense in these cases can only cite one or two papers that purport to show that mold illness can’t possibly exist, especially the 2002 (and now 2011) consensus statement from the American College of Occupational and Environmental Medicine (ACOEM).  This trivial contrivance has no data, no science and nothing even close to facts in it, and the newer version added no new information and no new references despite the passage of nine years (see ACOEM: Ploys and Lies), yet there it is at every mold case, portrayed as the best science in the world.  Unfortunately for the defense, however, the collusion and bastardization of science that underlies ACOEM was exposed by Dr. James Craner in 2008 and the Wall Street Journal in 1/2007 in an expose` written by David Armstrong.

These battles sound eerily similar to what goes on in the Lyme world: the basic battle of patients and their physicians versus entrenched university types with their numerous conflicts of interest goes on, though I haven’t heard of $22 million judgments against the deer and mouse community for fomenting tick borne disease like I see in construction defect mold cases.  Not surprisingly, the same strategies manipulated by Big Tobacco for years (see the Tobacco Legacy Library documents at UCSF) involved a tightly coordinated use of well paid physicians who would opine that cigarette smoking never hurt a fly.  In fact, the same docs who so often opine that mold won’t hurt a fly either are the same ones whose opinions were used by Big Tobacco to hide the truth about health risks associated with using tobacco.

Actually, few of the physicians involved with mold cases are “insurance company whores.” The research interests in the mold community are broad-based with good science being published constantly.  International meetings help researchers share peer-reviewed papers on a regular basis.  Physicians affiliated with our group, for example, use the same template to collate and share data in an organized fashion.

Until the Lyme community can attain the same research collaboration from treating physicians, with many clinicians involved in publishing peer-reviewed papers based on hard data and solid statistics, the argument against Post Lyme Syndrome will continue to be a one-sided battle of university physicians with academic reputations (and an agenda) versus anecdote (but also with their own agenda).  Organized data collection would end the arguments but even though I hear of attempts to bring such organization to the variety of Lyme docs out there, there is no position paper with authoritative references in favor of long-term antibiotics in Lyme patients not healed by three weeks of antibiotics. Even the studies of long-term antibiotics in Lyme don’t sort the benefit of antibiotics alone by HLA haplotype (see below for why this lack of recognition is a major oversight). I recently looked over some of the opinions I wrote in 1999 and 2000 for  Dr. Bransfield’s list serve about microbes and mental illness (mmi) calling for organized data collection; nothing has changed.  No organized data collection is ongoing that has led to publication of multiple data-driven papers.

So what is a CIRS-WDB? 

(And what implications does this entity hold for Post-Lyme patients?)

 The innate immune system directs inflammatory responses seen in both mold illness and Lyme disease.  The host defenses are constantly prepared for battle with foreign antigens.  Antigen detection is performed by specialized cell membrane-based receptors (Toll, c-linked lectin, dectin, mannose and many more) that when activated set off inflammatory responses characterized by release of pre-formed cytokines and complement.  Such inflammatory responses lead to differential gene activation and suppression such that the exact time course of acute exposure/illness acquisition can be identified as a sequence of activation of innate immune elements (SAIIE). These changes are easily seen in mold illness with re-exposure and in cyanobacterial illness (blue green algae syndromes), also with re-exposure.

The exact time course has been delineated by our published research.  What we see is complement activation with enhanced production of C4a on day 1; leptin rising on day 2 as cytokine responses block the activity of the leptin receptor in the hypothalamus creating temporary leptin resistance; MMP9 rising on day 2 to day 3 as endothelial cells are producing MMP14 from gene activation by cytokines and then MMP14 is cleaved to MMP9.  VEGF rises on day 1 as cytokine responses create capillary hypoperfusion, generating tissue hypoxia.  As VEGF rises, enhanced production of TGF beta-1 down-regulates VEGF, a well-documented feature of the day 3 labs.  Factor VIII, an acute phase reactant, falls on day 1, recovering to baseline by day 3.  Von Willebrand’s antigen and ristocetin associated co-factor fall by day 3, with such a nadir often associated with bleeding from lung or nose.  Interestingly, TGF beta-1 will rise later in day 1 and is well established by day 2.  TGF beta-1 will initially cause a rise of T regs. This rise is difficult to catch unless there are two blood draws on day 1, as by the time the blood is drawn on day 2 the T reg levels are falling (!) as they are bound in tissue with many apparently are being converted to pathogenic T cells.

I only have a few acute Lyme patients who waited three days to start antibiotics specifically so that they could participate in clinical care by testing our research models.  Their lab parameters demonstrated the exact same pattern as those seen in our mold patients, understanding that I have hundreds of mold patients recorded in acute exposure data sets.

The inflammatory response following antigen detection also activates immature dendritic cells (professional antigen-presenting cells) to then engulf (phagocytose) the antigen/receptor complex into a “bubble” inside the cell called an endosome.  This endosome, if acidified, will fuse with a lysosome where a specific molecule of HLA DR will be attached.  Further processing of the antigen/HLA complex occurs when the antigen complex is processed in the endoplasmic reticulum, finally leading to presentation of the finished antigen/HLA complex at the cell surface to a naïve T lymphocyte.  If there are no blocking cells, activation of the T cell leads to presentation of the HLA-labeled antigen to a B cell.  From then on, antibody production occurs.  (See Figure 1, the Biotoxin Pathway.)

Click picture to download larger image

Here’s the bottom line of the findings that both mold and Lyme communities must acknowledge:  there are individual differences in response to Lyme and mold solely based on the immune response genes found on chromosome 6, HLA DR.  Specific haplotypes are associated with a marked increase in incidence in cases of mold illness and Post-Lyme patients.  The haplotypes overlap, with several being “multisusceptible,” and in that group there are two types that (while uncommon) are wildly over-represented in those with the worst clinical illness.  These are the “dreaded haplotypes,” of 11-3-52B and 4-3-53, with the subtypes of 0401, 0402 and 0404 being the worst of the 12 identified subtypes of 4-3-53.  Elegant research has shown why these HLA structures don’t do well in antigen presentation.

Data on HLA DR haplotypes in over 7000 patients confirm that there are six separate haplotypes conferring increased relative risk (incidence in cases divided by incidence in controls) for mold illness and four haplotypes for Post-Lyme.  For those with Lyme (don’t guess!) who don’t improve with antibiotics, expect to find one of these four haplotypes.  Similarly, in those who become ill following exposure to the interior environment of a WDB, expect to find one of the six mold susceptible haplotypes.  Understanding that essentially nothing in biology is guaranteed, there are some moldy patients without one of the six mold haplotypes and there are a few Post-Lyme people without one of the Lyme susceptible types.  In the general population, the incidence of these mold susceptible haplotypes is 25% and for Post-Lyme susceptible is 21%.

The key point here is that when a patient continues to experience illness symptoms and is shown to have genetic susceptibility, it is mandatory to understand that defective antigen presentation is ongoing and that production of a protective antibody (ies) is NOT happening.  The problem must then be re-defined- persistent antigen stimulation of production of cytokines, TGF-beta-1 and complement factors have become the illness, with all of the SAIIE activity ongoing.  Now that we know that there are inflammatory parameters that must be corrected in order for mold patients and Lyme patients alike to return to health, physicians and their patients need to be educated about fixing what is shown objectively to be wrong. Don’t guess!

 Differential diagnosis is never ending.

 Since the clinical diagnosis of Post Lyme and mold illness are the same, how can one say the illness is one or the other?  Without exposure, diagnosing neither illness would be supported, but with exposure, each illness could be present (and many times both are!).  What evidence could be used to convince a skeptic that mold illness could be present?

First, look for the moisture.  There are many sources of water intrusion commonly seen in construction, both brand new and old.  Crawl spaces and basements are the biggest offenders.  Look for water coming through concrete walls (block and poured concrete are porous wicks for water).  Check for in-ground water pressure against a subterranean wall, especially if the wall is at the bottom of a hill.  When you hear about a sump pump or dehumidifier being used in the basement look out: water intrusion already confirmed!  Musty smells should not be ignored.  “Dry” soils in crawlspaces are always releasing water through transpiration and evaporation:  that dry soil isn’t benign!  Whenever you see fiberglass ductwork in a crawlspace of basement, be very wary as it won’t be long before the joints between sections of those ducts loosen and permit entry of air full of bioaerosols made by the crawlspace microbes into the universal distributor, the HVAC system.  That means the “dry soils” in the crawlspace just contaminated the whole house.

Bathrooms surprisingly aren’t the common source of moisture most people think.  Sure pinhole leaks in plumbing will contaminate wall cavities but the black fungal growth you see on grout lines and along condensation areas of windows usually isn’t from the big-time illness causers.  Always test: never guess.

Common disasters from construction defects include lack of flashing around doors and windows, venting exhaust pipes into the attic, failure to seal around roof boots and over-flowing condensation pans. This isn’t an exhaustive list.

As it turns out, it makes no difference in determining the potential for exposure if we use DNA testing (ERMI, environmental relative mold index), observe mold growth or simply smell musty odors. Each of these indicators of impacted building health is correlated with human illness.  What ERMI does is to provide a clear indicator of what organisms are present, something that air sample never can do thoroughly, and that make-up of the fungi tells us what levels of water saturation are going to be found. That information in turn tells us where to look to (1) fix the moisture; (2) tear out the wet building materials and clean reservoirs in air, possession and floor/wall/ceiling.  Cleaning the reservoirs of microbial products is maddeningly demanding of attention to detail.

If one is considering a Lyme diagnosis, take a minute or two (that is all it takes) to ask the questions about water intrusion.  If you have a problem, and NIOSH says over 50% of US buildings do, then the illness might not be Lyme.  Or if Lyme really is there, it might be both Lyme and mold illness! Treating with antibiotics alone in the face of mold illness is illogical and potentially disastrous for the patient.

Tip-offs to presence of mold illness and not Lyme will be absence of elevated C3a at any time, especially after treatment for mold illness is completed.  C4a will be high in both illnesses as will TGF beta-1.  Sorting illness presentation by HLA DR is wonderfully instructive. When one sees a mis-match of HLA DR and illness, we need to re-consider the differential diagnosis. In fact, always challenge today’s diagnosis tomorrow.

Each step along the sequential path of therapy includes an assessment of outcome from what the prior intervention. Treatment should be transparent, logical and plodding with one step at a time the rule.  Repeated evaluations of the response to therapy help narrow the diagnostic process.  Please remember that a sudden worsening of illness or a recurrence of prior symptoms will usually mean re-exposure to a WDB or there might be a new colonization of a MRCoNS.

Genomics

We have entered the world of genomics testing.  This diagnostic advance, using microRNA and mRNA, has given a preliminary fingerprint to the genomic differences between controls and those with mold illness; between controls and Lyme patients defined before and after antibiotics; and between mold and Lyme.  The genomics of ciguatera has been established previously.  We are working on defining the role of commensals, such as biofilm-forming, methicillin resistant coagulase negative staphylococci (MRCoNS), as agents that influence genomic changes in affected hosts. We know that eradication of such organisms is absolutely mandatory as one of the steps in therapy for both mold illness and Lyme, but now we are seeing just why that observation is correct.  The future of this research is bright!

For those physicians interested in learning more about genomics, please contact the Surviving Mold website. Specialized testing tubes are used in phlebotomy for genomics assays; cost of these tubes is about $15 each.  After the tubes are filled with blood (we will provide instructions on specimen handling) and frozen the stabilized RNA can be analyzed electively.  The website also offers the new seven-hour instructional videos in mold illness and Lyme, as well as the Physicians’ Section where treating docs can share information, ask questions and comment on what they have seen in their practices.  The potential for cooperative interaction here is expanding rapidly, as new docs are being trained in protocols and collation of research data every day.  Learning how to use an evidence-based and sequentially organized approach to diagnose and treat biotoxin illnesses opens a world to improve the health and lives of our patients.

This brief discussion is just an overview of the research basis of modern mold illness practice.  Given the commonality of findings in mold illness and Lyme, clinicians need to consider if their data base is current.  If not, we truly hope they will ask what can be done to bring their practice into the exciting new era of management of CIRS.  Successful patient outcome depends on it.

We don’t have to guess any more about complex illnesses.  Use of physiologic and genomic parameters will bring order to the arguments that continue in the Lyme community, just as it has for mold illness.

Ritchie Shoemaker, M. D., is a recognized leader in patient care, research and education pioneer in the field of biotoxin related illness.  While illness acquired following exposure to the interior environment of water-damaged buildings (WDB) comprises the bulk of Shoemaker’s daily practice, other illnesses caused by exposure to biologically produced toxins are quite similar in their “final common pathway.”  What this means is that while the illness might begin acutely with exposure to fungi, spirochetes, apicomplexans, dinoflagellates and cyanobacteria, for example, in its chronic form, each of these illnesses has similar symptoms, lab findings and Visual Contrast Sensitivity findings.

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Still Have Symptoms After Treatment for Babesia

Question:

With a history of dysnomia related to babesia, although the babesia may be gone, I still have Neurally Mediated Hypotension, high BP (blood pressure), POTS (postural orthostatic tachycardia), temperature problems, sleep off and on, it often takes until 5 AM to fall asleep, 8 years post-function adrenal collapse.  Please explain the physiological dynamics of what is going wrong with the autonomic nervous system and the hypo-pituitary adrenal system.

Answer from Dr. Alan McDaniel:

This question is certainly appropriate to follow my previous answer to questions on hypersensitivity from June 14, 2011.  In that, I have written about factors predisposing to infection, the “total load” and the cycle of maladaptive responses that can follow Lyme and tick-borne diseases.  In fact, these problems also are common among chronic fatigue (syndrome or not) patients, people suffering from long-term stress and others who are chronically-ill.

Our writer comments that after the infection has been treated, his (let’s assume) adrenal, autonomic, and other symptoms persist.  There are several possibilities we should acknowledge: First, the infection may still be active, just “underground.”  Please, though, do not assume that freedom from all symptoms is the only sign of cure!  Secondly, the patient’s infection, and the many stresses it caused in his life, may well have weakened his “constitution” and produced these symptoms in the spiral of consequences I earlier addressed.  Thirdly, these same problems could have been latent in the patient before the infection – could have been the reason the infection became rooted and caused him trouble in the first place.  That “8 years post-adrenal collapse” is tantalizing; we don’t know if that was before or after his infection had started.

Neurally Mediated Hypotension (NMH) is an interesting diagnosis.  I’ve written a lot about this in the adrenal chapter of my book.  First described at Johns Hopkins, it has been widely accepted.  Researchers have shown patients’ blood pressure drops excessively when they are passively tipped from lying down to an upright position (called the “tilt-table test”).  But is the problem really “autonomic?”  I have not read any convincing proof that autonomic nervous system dysfunction causes the problem.

In fact, all the symptoms of NMH are identical to those of adrenal insufficiency.  What’s more, successful treatments of NMH specifically cover for adrenal problems.  Indeed, a synthetic adrenal steroid (Florinef or fludrocortisone) is the first-line treatment used – in addition to a high-salt diet, which also compensates for low adrenal function.  Researchers say their patients’ adrenals are normal, but never specify on what test(s) they base this assertion.  I feel quite strongly they have missed the true cause of the problem in many or even most of their patients.

Remember, conventional Endocrinologists don’t believe there is any such thing as “adrenal fatigue” or in this case, “functional adrenal collapse.”  However, my experience indicates the condition indeed exists and this is supported by Drs. Jonathan Wright, James Wilson and many other practitioners.  Before I will believe my “NMH” patient has anything other than adrenal fatigue, I’d need to see his 24-hour adrenal steroid profile performed with GC-Mass Spect.

Do his temperature problems support the hypothesis that his autonomic nervous system is weak?  I believe it would be far more successful to ask instead whether this patient is capable of activating his thyroid pre-hormone T4.  You know why?  Not only is such an issue, called “Non-Thyroidal Illness,” quite well defined and rather common, we can easily test it.  We have but to draw blood for total T3 and total Reverse-T3 and calculate their ratio (put ‘em in the same units, OK?).  Oh, sure – we ought to test the whole panel of thyroid hormones if that’s not been done already.  Most docs, though, test only a standard panel, which omits both tT3 and RT3.  Yes, I talk about this a lot in my lectures.

Here’s what happens: Our body adapts to stress by slowing down the metabolism – the rate at which we produce and use up energy.  This is a defense designed to keep us alive longer when we are hurt, as by infections (like Lyme and Babesia).  This is partly mediated by the hypothalamic-pituitary axis, as our questioner points out.  Another aspect of the stress response occurs in the cells of our body.  They “choose” to not activate the pre-hormone T4 into the active form, T3.  Instead, our cells make T4 into RT3, which is known to further block T3 production and can have anti-thyroid effects.  I expect that Lyme and tick-borne disease (TBD) victims will have a persistently low ratio of T3 to RT3.  If so, they are “stuck” in a maladaptive response resulting in “functional” hypothyroidism (NTI).  Fortunately, this can be corrected with biologically simple treatment.  I am eagerly looking forward to seeing the results of these tests – and of treatment, as indicated – in my medical practice.

Let me be the first to agree that basal body temperature is not exclusively a test of thyroid function.  Nope; low body temps show a lower metabolic rate and many factors put-in on that.  While the thyroid gland is (as Dr. DeGroot famously wrote) the “thermostat” of the metabolism, the adrenals are the furnace.  Low adrenals will result in low body temperature as well.  Your levels of steroid sex hormones influence your body temperature, too (remember birth control using a thermometer?).  Of course, illness and nutritional deficiencies can also lower the metabolism and cause low body temps.

The complex condition of Lyme disease may aggravate other latent health problems.  For example, 40% of Americans carry the genetic program for insulin resistance (IR).  Lyme and TBD patients often have to stop their exercise routine, which makes trouble for those with IR.  An elegantly simple Swedish research project showed reduced activity significantly worsens insulin sensitivity – after only 3 weeks, they needed twice the insulin to keep their blood sugar the same as it had been when they were exercising.  Insulin resistance can cause lots of the same symptoms we associate with TBD.

There now; with these few issues we might be able to explain all of the symptoms bothering the writer of this question.  If this were not the case, we’d have to act like clinicians: Listen to our patient, ask questions, examine him, use the laboratory skillfully, and assess our data.  Discuss options with the patient and fix what we’ve found.  Then, we need to re-assess and find out what else needs to be fixed!  It is an on-going project.  When patiently pursued – and both the patient and the practitioner are included here – good results usually crown the effort.

Alan McDaniel, MD is a Board-certified Ear, Nose & Throat specialist with two sub-specialties.  His work with dizziness and allergy in the 1980s led him to seek solutions for Chronic Fatigue Syndrome.  Since 2003, Dr. McDaniel has taught physicians practicing on five continents to effectively employ nutrition and hormones for this and other issues in his two-day course titled “The New Endocrinology.”  Dr. McDaniel has been a visiting physician at Gordon Medical Associates in Santa Rosa.