New GMA Blog Coming Soon

It has been over a year now since Gordon Medical agreed to post the answers to patient questions on this blog, following a local presentation by Joseph J. Burrascano, MD and the GMA doctors. In that time, we have tried to work our way through the questions asked, and to bring you other information of interest.

The doctors at Gordon Medical, in addition to treating many patients with Lyme disease, also treat many other patients with acute and chronic illness, including Fibromyagia, mold illness, Chronic Fatigue and Immune Dysfunction, as well as many who have illness that doesn’t fit a specific category, other than chronic inflammatory illness. We have decided to expand our blog to one that addresses the full range of what we do. As we work to make the shift to the new blog, please forgive us if our attention is not fully on this one. It will be worth it in the end, as we hope to make it a resource for all patients in need of new thinking in treating their illness.

 

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.

Dr. Eric GordonAnswer 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.”

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.”

A New Model for Understanding – And Treating – Depression and Chronic Pain

There has been a great deal of interest in the cross over of emotional issues and chronic illness. We wanted to repost this information from Dr. Neil Nathan, originally published on his blog for Et Alia Press.

Dr. Neil NathanFrom Dr. Nathan:

At last: the times, they are a changin’. For the past 25 years, the medical profession has viewed clinical depression as a “simple” imbalance or deficiency of serotonin and dopamine, two of the brain’s basic neurotransmitters. This misguided view has reduced the treatment of depression almost exclusively to anti-depressant medications.

Despite hundreds of published studies showing that these drugs are only partially effective, the pharmaceutical industry has persuaded my colleagues that they are the best tool available, and we have bought into this paradigm hook, line, and sinker.

As a result, a majority of psychiatrists now limit their practice to the prescription of medications, while the “talking cure” of psychotherapy has been left largely to psychologists. This has created fragmented care that does not adequately address the needs of large numbers of patients who continue to suffer and show limited ability to cope in their daily lives.

Our preoccupation with medications as the savior of the depressed has kept us from taking a deeper look at the problem and, thus, at finding better solutions.

Last month (November 2010) , I attended a seminar hosted by the Stanford University School of Medicine in San Francisco, titled “Breakthroughs in Neurological Therapies: Restoring Function to the Nervous System,” and I am pleased to note that a new model, a new understanding, of depression is emerging, which will allow us to make some new progress in this arena.

Typically, depression is defined by its general symptoms (mood swings, low self-esteem, loss of pleasure in life, etc.) rather than its causes. But Dr. Brent Solvason began his talk with a definition that, while daunting to the layperson, shows a real paradigm-shift: as he described it, depression is a systems-level disorder affecting integrated pathways linking select cortical, subcortical, and limbic areas and their related neurotransmitter and molecular mediators.

What does this mean? As neuroscientists are beginning to realize, it means that depression is created by complicated interactions among different parts of the brain that are not communicating with each other in a “normal” or functional way.

This new definition arises out of recent research with “deep brain” stimulation for the treatment of depression, obsessive compulsive disorders (OCD), and movement disorders. At academic centers such as Stanford, neurosurgeons are implanting electrodes into specific brain centers that can be stimulated with electricity to produce improvement and cures. We have long known that electroshock therapy can be effective in some patients whose severe depression has not responded to medication, and yet some patients who did not respond well to electroshock are benefitting from this new approach.

In addition to the implanted electrodes, new studies show that transcranial magnetic stimulation (which reaches only to the surface of the brain) is almost equally effective in treatment.

The essential concept here is brain circuitry and its “pathways.” Depression, OCD, and other disorders represent some kind of neurological “stuck place” or “loop.” Somehow, often by injury, emotional overload, chemical / heavy metal exposures, or a combination of these, the nervous system creates (or stumbles upon) a dysfunctional pathway or circuit. And once such malfunctioning circuits are created, some individuals can’t seem to break out of the neurological loops that result. They get mired, as it were, in a neuro-electrical bog.

The same model underlies our emerging understanding of chronic pain. For some time, we have suspected that chronic pain results from a “reverbating loop,” in which a pain-impulse, upon reaching the spinal cord, starts to stimulate neighboring neurons; these then turn back on themselves, producing an electrical loop. The loop becomes self-stimulating and self-perpetuating: once in place—even when the original source of pain has long since resolved—the electrical stimulation keeps going on, and on, and on.

What we need, in order to restore the normal electrical system of the brain, is to find a way to “reboot” it. In the same way that we reboot our computers when they freeze or get “stuck” in a malfunctioning loop, we are discovering ways of doing the same with our nervous system.

While offering exciting new prospects, the research presented at Stanford University is still based on invasive neurosurgery, and I cannot imagine that this is the ultimate solution to the problems of depression and chronic pain. In fact, several newer technologies bring hope that solutions are right around the corner.

The two that have captured my interest are Frequency Specific Microcurrent (FSM) and Low Energy Neurotherapy System (LENS).

FSM uses a microcurrent (one thousandth of an ampere) at specific frequencies to break electrical and chemical patterns in the body. LENS utilizes brain-mapping technology to determine which areas are either over- or under-stimulated and then applies an almost homeopathic electrical microcurrent to move electrical energy through the blocked areas. Both of these technologies accomplish healing that I had previously thought impossible.

With FSM, I have seen patients who have suffered with fibromyalgia for years receive an hour of gentle microcurrent stimulation and get off the treatment table with an 80% reduction in their pain. With repeated treatments, I have seen these patients get lasting results!

With LENS, I have seen patients with severe neurological impairments (due to a variety of causes: traumatic brain injury, Lyme disease, etc.) show marked improvement within 4-8 treatments.

While we are not certain exactly how these micro-miracles work, our current understanding is that both therapies somehow “reboot” the nervous system, so that it can return to normal functioning, even after years of illness. This accords with our current understanding that the nervous system has “plasticity,” meaning that it is capable of creating new circuit-pathways and being healed. Our older understanding (though never embraced by the entire medical profession) was that, once the nervous system had been damaged, healing was unlikely, and that nerves healed so slowly that it would take 2-3 years if it happened at all.

That these therapies work in hours or days or weeks means that the very notion of a “damaged” nervous system might not be correct in all cases: it might have been stunned, or stuck, or irritated, or inflamed, but the nervous system was not damaged. This gives us renewed hope that we are on the verge of offering healing to thousands.

Dr. Neil 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.

Can Treatment Damage Hearing?

Question:

Could you speak to Ototoxicity (toxicity to the auditory nerves) of the antibiotics used to treat Lyme?  My neurologist cannot tell if hearing loss is caused by Lyme or antibiotic use.

Dr. Eric GordonAnswer from Dr. Eric Gordon:

If ototoxicity is present, I do not know how to be sure if it is due to antibiotics versus infection of the 8th cranial nerve.  Not all antibiotics are considered ototoxic, and even those that are will not cause problems for every patient. The toxicity from antibiotics is probably mediated by oxidant stress, and this may also be the cause of some of the damage by infection, as well.  Individuals have varying ability to manage oxidative stress. With that in mind, checking glutathione adequacy, methylation pathway tests  from Vitamin Diagnostics Labs (special testing, have your physician contact the lab), as well as evaluating the other detox pathways and your heavy metal burden would be helpful.  All of these problems will make ototoxicity more likely whatever the stressor of the system.  Treatment of these metabolic problems will often improve ototoxicity.

I would also get a good evaluation by a cranial osteopath.  Occasionally osteopathic cranial manipulation will mitigate some of the tinnitus.

Consult your physician for a more complete workup of your toxic load in order to support your ability to deal with any toxicity, as well as the infection.

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.”

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.

Dr. Alan McDanielAnswer 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.

Neurologic Lyme Disease

The following question and answer are from two Lyme researchers who represent points of view in a Point/Counterpoint discussion. To read the complete article click on the links provided.

Question:

How will research on neurologic Lyme disease need to change to to identify better treatments?

Dr. John HalperinAnswer from Dr. John Halperin:

Distinguish Between Clinical Constructs

Four clinical constructs are commonly attributed to nervous system Lyme disease, but only one of these represents nervous system infection with Borrelia burgdorferi, also known as neuroborrelliosis. However, there are legitimate and important research questions regarding each of the four.

Neuroborrelliosis manifests as lymphocytic meningitis, multifocal inflammation of nerves and nerve roots, and – very rarely- multifocal inflammation of the central nervous system. …

to read the complete article click here

Dr. Halperin is a professor of neurology at Mount Sinai School of Medicine, New York, and is chair of the department of neurosciences at Overlook Hospital in Summit, New Jersey.  He has served as expert witness defending physicians accused of failure to diagnose nervous system Lyme disease.

How will research on neurologic Lyme disease need to change to to identify better treatments?

Dr. Brian FallonAnswer from Dr. Brian Fallon:

Although progress has been made in our  understanding of  neurologic Lyme disease, important questions and unmet needs remain, particularly with respect to diagnostic tests and the cause and treatment of chronic sequale.

The following five steps will further advance our understanding:

  • Conduct a large prospective study of neurologic Lyme disease, which may clarify the incidence of chronic symptoms after standard treatment and identify risk factors that influence relapse vs. recovery.
  • Apply newly developed technologies to identify better diagnostics and biomarkers …

to read the complete article click here

Dr. Brian Fallon is director of the Lyme and Tick Borne Disease Research Center and professor of clinical psychiatry at Columbia University,  New York. The center received a small grant last year from the Lyme Disease Association toward developing a repository for Lyme specimens.