Zhang's mice. And, where have all he patients gone? The cure!

Lyme cured! Or is it. Dr. Zhang and (Jie Feng) are heroes in the Lyme story and their work will be of great import in the history of medicine.

Dr. Zhang and colleagues have been very busy building the case for chronic Lyme disease or persistent Lyme disease. Their publication March 28, 2018 support previous in-vitro (test tube) studies in a mouse, called a “murine model.” He has previously demonstrated that Borrelia burgdorferi strains, bacteria responsible for Lyme disease subdivide into different morphological forms. The means the same bacteria, with the same DNA, can alter their appearance and function dramatically. We associate a thin spiral, elongated form with Lyme, a spirochete. But the long thin forms of Lyme can change shape and appear round. Alternatively, the spirochetes can aggregate in a community protected by strong mucopolysaccharide substance, a microcolony or biofilm.

Three forms:  spirochetes, round forms and microcolonies (biofilm colonies).

The bacteria can be free floating in the blood referred to as planktonic forms. The term contrasts bacteria safely guarded in the biofilm (microcolony) form. I have always thought of planktonic bacteria as free swimmers. They are demonstrated to be primarily round form and non-motile in the studies.

Test tube finding (in-vitro) support the mouse study.

The different forms, morphologies Lyme takes on are best killed by different antibiotics. Only a specific combination of three antibiotics eradicates Lyme spirochetes in mice infected with microcolonies.

Posttreatment Lyme or persistent/recurrent symptoms may occur in 20% of patients treated by standard protocols, generally with doxycycline. (This is from the CDC). A study from 2015 indicates that 36-63% of patients may have persistent symptoms.

The term PTLDS, posttreatment Lyme disease syndrome is popular but not helpful.  I believe its use is primarily political, used in deference to the powers that be.

PTLDS ostensibly describes a group of patients with early diagnosis and treatment who nonetheless develop chronic symptoms.

The authors brilliantly point out that there exists a large population that never receive early diagnosis or treatment which he refers to as type 2 patients.  In my experience most patients are type 2.

Experimentally, spirochetes were divided into the three forms through laboratory procedures. 

Mice were inoculated with either spirochete or persister forms.

Pathologists examined tissues for inflammation. The  greatest was observed in mice infected with persister forms, especially biofilm forms.

Mice infected only with spirochetes could be cured with doxycycline and other antibiotics.

Mice infected with stationary forms were only cured with the specific combinations of: Daptomycin, Ceftriaxone and doxycycline. Negative cultures were obtained from  ear biopsy and bladder tissues.

The authors suggest that different forms of Lyme are delivered through the tick bite. Biofilm colonies may be introduced in tick saliva and then seed other tissues.

This is contrary to what I know about the bacteria.  Lyme bacteria are highly motile, extracellular and possess ligands which facilitate adhesion to the matrix between cells. The bacteria are polytropic or pantropic and quickly infect many tissues and organs. There is no known mechanism by which biofilms can directly seed other tissues. The standard model is that organisms within a biofilm communicate by molecular signaling, quorum sensing-- and that individual, planktonic spirochetes are released under the right conditions to seed new tissues and create new biofilm colonies.  The spirochetes may be protected by special compartments in the body, for example they readily cross the blood brain barrier and live in the brain, an immune privileged area. Biofilms have been demonstrated in the brain. I think only individual spirochetes with their lipophilic outer membrane can get through the blood brain barrier.

There is ample evidence that spirochete rapidly convert to round forms when attacked by antibiotics. In-vitro colonies of spirochetes morph into other forms, persister forms, the 5% doxycycline does not kill.

If biofilm colonies are truly injected into skin by ticks at the outset, standard therapy, doxycycline and others is doomed to fail.  Very plausible. Frightening. 

The currently recommended therapy for early, stage 1 Lyme disease is a failure. It might be argued that other regimens should not be experimented with. These new therapies have no scientific basis. But there is compelling scientific evidence that standard therapy is a failure.  

Oral therapies with combinations that showed some promise invitro might have a better chance, for example, doxycycline, rifampin and artemisinin.

The curative therapy described is problematic. Ceftriaxone and doxycycline are standard, generic fare but not daptomycin. Daptomycin is a relatively new, powerful antibiotic currently held in reserve for multi-resistant bacteria such as MRSA.  It’s non-generic cost of $400.00 per dose/day-- not covered by insurance may be prohibitive. A thirty-day course costs $12,000. Generic available, $150.00 per dose. Cost lowered to about $4000.00 monthly.

Experimental treatment based on scientific plausibility and clinical experience for late stage Lyme has helped many, many patients.

The paradigm that Lyme disease present with: an observed tick bite, a bull’s eye rash, Bell’s palsy, a swollen knee, meningitis, heart block and other well described acute manifestation is wrong.

Ticks go unseen, rashes are the exception not the rule and most patients present with -- fatigue, pain, neurological symptoms and cognitive dysfunction – the bones of Lyme disease. The meat is filled with symptoms referable to nearly every organ system. Most patients go misdiagnosed for months, years or decades. This is the tragedy of the Lyme epidemic.

Patients are belittled, diagnosed with chronic fatigue syndrome, fibromyalgia, depression and/or the aches of pains of daily living.

Doctors who take chronic Lyme seriously are ridiculed by peers and medical licenses are censured.

There is math problem

Of 300,00 type 1 Lyme cases yearly in the U.S. 60,000 become chronically ill.  The number is at least doubled when you add in type 2 cases.

This means there must be hundreds of thousands of patients, more likely  not millions of patients suffering with chronic Lyme disease.

Despite this patient are nearly universally told it’s not Lyme, can’t be Lyme, no known disease acts like that, etc.

This leaves a simple question: Where are all the missing patients?

Einstein warned scientist lack imagination. Everything doctors do today with be laughable to future counterparts. Phages which kill only specific bacteria or other technologies will surely make antibiotics obsolete in the not too distant future.

Antibiotics and Germs

Its still complicated but I am trying to explain some basic concepts for the lay person.

Antibiotics only kill germs called bacteria.  Germ is not a medical term but a colloquial substitute for pathogen, a microorganism of one sort or another that causes human illness.

Disease causing germs are representatives of various families in the animal kingdom of microbes, including:  bacteria, viruses, fungi, yeast, protozoans and worms .

With few exceptions, antibiotics kill only bacteria so that is what we will discuss.

Bacteria are one cells prokaryotic microbes, so named because they lack an organized nucleus.

Please keep in mind that the vast, vast majority of bacteria are friendly or harmless, including the 2-6 pounds of normal “flora” we carry around, necessary for immune functions and detoxification.

Bacteria present as a menagerie of forms and shapes: comma, spiral (spirochete), cocci (round), rod (elongated), chains, grape-like groupings, filamentous etc.

THE SHAPE OF A  BACTERIA DOES NOT DETERMINE WHETHER IT IS A PATHOGEN, A GERM.  ONE SPIROCHETE MAY BE NORMAL FLORA, HARMLESS, AND ANOTHER MAY BE LYME.

Families of antibiotics may contain similar members. Members of the same family may perform different.

In general, specific antibiotics target bacterial germs which possess certain characteristics.

For example, an antibiotic may target bacteria with cell walls constructed  somewhat differently --  gram negative or gram positive. Antibiotics may target gram positive bacteria, gram negative or others such as intracellular bacteria etc.

Intracellular bacteria may only survive in host cells: some have no cell wall e.g. mycoplasma.

Bacteria (think Lyme) may lack a cell wall but rather have a double outer membrane.

Antibiotic classes include penicillins and cephalosporins which are considered cousins because both share a  ring structure (beta lactam). The drugs are divided into generations. First generation, second and third.

With progressive generation more types of bacteria are killed (broad spectrum versus narrow spectrum.  


Antibiotic classes include tetracycline, macrolide, sulfa, rifamycin, quinolone, antiparasitic, e.g. (Flagyl (nitroimidazole) etc.

We use principals of pharmacology to decide which antibiotic(s) to use for a particular infection.  Deciding factors may include the severity and location of the infection.

We consider MIC, minimal inhibitory concentration and MBC, minimal bactericidal concentration.  This means the amount of antibiotic to inhibit growth or to kill the bacteria.

We must consider the risk of side effects and complications, like C. diff colitis.

We have to make sure the antibiotic can get to the source of trouble, for example the brain, with ability to transverse the special BBB) blood brain barrier.

There are a lot of very complex factors that influence antibiotic decision making.

Treating chronic Lyme disease is a vary complex process.  As  with a patient I saw this afternoon, Lyme  triggered a cascade of problems, including: dysautonomia (POTS), MCAS, mast cell activation syndrome. 

She also suffers with a very stubborn case of babesiosis.


There are a lot of balls in the air to juggle.

 A recent live Facebook event was successful.
I hope we will soon cut through some of the confusion.

I will be scheduling another live Facebook presentation: Treating Lyme with Q&A in the near future. My Facebook coordinator Brittany Goff will be setting this up.

Lyme, evidenced based medicine, Fallon and the Institute of Medicine

I recently gave a talk about Lyme and EMB, evidenced medicine.  I had no idea that Brittany, who runs my Facebook page, live-streamed and posted the talk on Facebook.

The Institute of Medicine holds a lot of sway in the medical community.  Something called “patient centered medicine” is said to be enshrined.  There are many facets to patient centered care -- the one of interest to me here is that patient preferences are given credence.  In fact, the IOM states not to consider patient preferences is morally wrong, a violation of patient rights.  Vocal critics say this ignores EBM, evidence-based medicine. Not true. EBM is part of the consideration, not the only consideration.

Evidenced based medicine doesn’t require consideration of scientific plausibility.  If the results of a study contradict accepted science or reality, then it is likely the study if flawed. 

This is about where we are with Lyme disease, I think.

All clinical trials are flawed and biased in many ways. The interpretation of results is frequently fraught. Text books of statistics  are full of complex mathematical equations and show innumerable ways of crunching the same data and numbers.   If an investigator does not like the conclusions, other statistical models can be tried until he finds the one meets the objective: support preexistent beliefs.  It is like trying on new shoes. This is particularly true when subjective questionnaires are used for endpoint analysis.

To avoid bias: Methods of statistical analysis is a variable which must be controlled, delineated before the start of the trial and strictly adhered to.  Appropriate clinical questions need be determined  at the outset. 

For medical studies THE statistical question is: did the treatment benefit the treated cohort in a manner that cannot be explained by chance alone?  Or with 95% certainty.

In the Fallon study:  Did treated patients have cognitive improvements 12 weeks after therapy compared to the group given placebo, by statistical analysis?  In the treatment group were improvements in fatigue durable after 24 weeks? The answer in each case is yes.  As Dr. Fallon later states, the study shows efficacy: the treatment works.

Those who claim the study was negative are looking at the wrong question.

The study showed:  IV Rocephin 10 weeks caused cognitive improvements at 12 weeks which later, without further treatment reversed, whereas--improvements of physical symptoms like pain, fatigue and function were maintained at 24 weeks.  

The study conclusion stated the treatment was not effective for PTLDS.

This never sat right with me.  The conclusion is not reflective of what the study shows.  Do University internal politics had something to do with crafting the wording. This process is certainly not transparent.

The terms efficacy and effectiveness sound the same but are different.  Efficacy is the demonstration of A positive clinical response to treatment.   Effectiveness refers to successful clinical use of a treatment as a whole.

The second standard had the same chance of being proved as threading a camel through the eye of a needle.  The first standard shows proof of concept and that is huge. The conclusion does not reflect the paradigm shattering enormity of the study.

The favored null hypothesis of mainstream medicine in 2007 (and now?) was:  Persistent symptoms after Lyme treatment is a post treatment Lyme syndrome, an autoimmune affect, all the (clinically significant) spirochetes (Borrelia burgdorferi) have been eliminated.  

Fallon’s study proves the alternative hypothesis: Post treatment symptoms are associated with persistent infection and respond to additional antibiotics.

The IDSA makes the classic type I mistake of failing to discard the incorrect null hypothesis.

EBM -- IDSA guidelines were written on the basis of a glaring mistake of logic and statistics.

Biological plausibility, although not a necessary consideration here, was not looked at.  The fact that Lyme had not been eradicated in animal models then (and now) suggested that persistence of Lyme in human cases is highly likely.  The results should not have been surprising. 

In the IOM approach, EBM is decided by a closed panel, opinion driven, and at best provides narrow endpoints lacking generalization. The two other key elements of patient oriented medicine are medical judgement and experience – the art of medicine and patient preferences.

The IOM argues that clinical experience is necessary to fill in gaps or gaping holes left with only the EBM approach.  The IOM brilliantly exposes the inherent weakness of EBM.  Within this framework doctors are healers in the traditional sense and allowed to figure out the puzzle each patient is. This is critical when the disease is extremely complex and multisystem.  

My next talk will be about treating Lyme.  I want to get into some specifics.  I hope to tease out the roles of science, EBM, clinical experience, patient preferences, and the principal of first do no harm.

.

Lyme and the plague

A perfect storm.  It was a perfect storm which led to the spread of the bubonic plague endemic which hit Europe in waves over more than 5 centuries.  The plague is a vector borne zoonotic disease and, in this way, similar to Lyme disease. The reservoir for the disease is rats who travelled in the bowels of trading ships making new homes in heavily populated port cities and other population centers. The vector was not a tick but rather an unsuspected rat flea which carried the deadly bacteria, Y. pestis.  The infection led to gruesome deaths killing half the population of Europe and decimating much of Asia, killing a third of the global population. Plague doctors suspected the disease was carried by a miasma, bad air, perhaps carried by birds. They donned scary beaked costumes and bled patients to rectify an imbalance of the 4 bodily humours. Some of their patients lived; the mortality rate was somewhere between 40-90%. When patients recovered, they claimed success. It was a perfect storm because populations became increasingly concentrated in cities like London, trade was active amongst Europe and Asia and the rat hitchhikers found wonderful new homes with food and shelter and because at the height of the plague, around 1360, the germ theory of disease would not be discovered for another 500 years. 

Today, Lyme, and some consider a silent plague has much in common with the black death.  Lyme disables rather kill and the subtle manifestations, or not so subtle if you look carefully, go unseen by the Medical community, writ large.  In this case birds really do transmit the disease increasing tick habitat over years and decades.  Rather than staying close in cities where one can walk everywhere, the car led to populations spreading out, suburbs abutting wooded areas and habitat for animals including Lyme requisite mice and deer.  Deer became increasingly plentiful. Predators, like mountain lions were scarce.   Mice thrive because potential predators: fox, raptors, owls and others moved away as well.  Deer, mice and ticks increased dramatically in number.  Over time, tickborne pathogens flourished and more and more ticks became infected, now most ticks (deer ticks and lone star ticks), with Lyme and other nasties. 

Betty was reading a book, enjoying a glorious late spring day, lounging in her chair next to the garden she planted in her back yard, a yard shared with so many beautiful white tail deer. Her husband Bob, sweating in the sun, smiled at her, enjoying the task of clearing brush in the wild back of the property. 

Betty developed fatigue, malaise, diffuse muscle pains, night sweats, brain fog, depression and irritability.  She visited her GP who even did a Lyme test (just to be thorough) and diagnosed depression, sending her off with a bottle of Prozac. 

Bob developed strange rashes, headaches and numbness and tingling in his feet.  His doctor suspected neuropathy and this was confirmed by an EMG.  His blood sugar has been borderline and his father has diabetes. He was sent home with a diagnosis of diabetic neuropathy and a bottle of Neurontin, gabapentin. 

The idea was developed by Pasteur in the 1850s and further worked out by Koch in the 1860s-1870s. The germ theory was born. Poor Semmelweis, an Austrian obstetrician in the 1840s went mad asking only that colleagues wash their hands, to prevent so many childbed fevers and deaths of newborns and their mothers, but no one listened. 

Penicillin, the wonder drug of the 20^th century was discovered in 1929 and mass produced in the middle of the second world war. 

Medical knowledge and science have exploded exponentially. The entire human genome has been sequenced.  HIV/AIDS has been conquered.  People no longer die from small pox, syphilis, tuberculosis or the plague.

So why I ask, do the modern-day doctors caring for these two souls afflicted with disabling if not deadly illness, treat them with the same level of knowledge, expertise and self-confidence as bird costumed plague doctors of 1360 bleeding patients to correct bodily humours?  Of course, we know.  But nothing can justify the horrific sentence of misery imposed on these unknowing and trusting patients.  Before long, Betty will have lost her mind, become confused and suicidal and admitted to a psychiatric hospital for electroconvulsive shock therapy.  Bob will have become progressively weaker confined to a wheelchair with the diagnosis of autoimmune CIDP, crying every night, trying to comprehend what has happened to his beautiful, wonderful wife.  

It feels like Semmelweis all over again. 

Note: case presentations fictional. 

Babesia confusion

Babesia is a protozoan, a higher life form than bacteria. Both are single cell organisms.  The primary difference is protozoa have an organized nucleus containing DNA. It is a member of the phylum Apicomplexa.  This is a relatively small group of organisms. Its closest relative is Malaria; only Babesia and Malaria (Plasmodium spp.) are intraerythrocytic, meaning live inside red blood cells. Because of this, many therapies against malaria are also effective against Babesia.  Mainstream medicine offers two therapies only: quinine/clindamycin and Zithromax/Mepron (atovaquone). These approaches frequently fail and additional approaches are required. 

Historically, Babesia was first described in the 1950s as a cattle disease.  The first human cases, B. microti were described around Nantucket Island in the 1960s.  Many physicians have stubbornly, erroneously clung to the belief that human babesiosis on the east coast, is virtually always caused by B. microti.  Although B. duncani was first described on the West Coast, it currently accounts for the majority of speciated cases diagnosed on the East Coast as well.  More often than not the diagnosis is made without speciation. (the species of Babesia causing the illness is not identified).  There are more than 100 species of Babesia known.  Other species, MO1, CA1 are recognized human pathogens in the US.  B. divergens, a bovine species, is known to have jumped species, cow to human.

Most Lyme doctors make the diagnosis empirically, based on symptoms.  Underused diagnostic tools include Giemsa stains and FISH tests.  Many Babesia symptoms are nonspecific.  In my practice I especially pay attention to a triad:  night sweats +/- feeling feverish, air hunger and change in emotional state – especially random bouts of tearfulness. 

For many patients the two “standard” therapies, as stated above, proves ineffective or only partially effective.  Other therapies may be effective and medically necessary.  Therapies must be science based and rational. The term evidence based refers to mainstream treatment vetted through a peer reviewed process and frequently, not always FDA approved.  Second tier drugs and therapies are used when “evidence based” treatments have failed.  Science based approaches require biological plausibility, e.g. med works well against malaria and/or their use is supported by body of empirical evidence, e.g. traditional herb has been used for a century to treat malaria.  Doctors prescribing these therapies need to be knowledgeable about the disease.  

One approach/theory must be debunked.  This is the idea that 4 months of treatment is all that is required.  The basis for this thinking is that red blood cells only live 120 days. Therefore, after 4 months every infected red blood cell will have been replaced. It may sound plausible, but the reasoning is not sound. Every red blood cell (RBC) has a different birthday and at a different point in its lifecycle.  Cells are destroyed and made every day.  Infected senescent cells may transfer merozoites (infecting stage of parasite) to new born cells on any given day.  There is no specific duration that will always be effective. A short course of therapy, e.g. 3 weeks of quinine/clindamycin could at times achieve compete remission. 

Antimalaria drugs make work well but not all antiprotozoal drugs kill Babesia. This seems to be a common misconception.  Some drugs used to treat toxoplasmosis (like Mepron) may be effective against Babesia.  Drugs active against, Giardia, Amoeba, Leishmaniasis and other protozoans will likely not be effective.  Flagyl is a broad-spectrum drug with activity against Giardia and Amoeba. It is also an effective anti-Lyme drug. It has no activity against Babesia. 

Anti-worm drugs, such as ivermectin, is active against microfilaria, and has no antibabesia properties.  If the drug provides relief of symptoms it is doing something else.

Unless you are a scientist -- reading about complex cellular biology, biochemistry, etc. is likely only to confuse. A patient copied and pasted something from the internet which claims that Babesia infection suppresses the production of nitric oxide.  The truth is that Babesia infection activates macrophages and stimulates the production of nitric oxide (NO).  Nitric oxide is an extremely complex signaling molecule and an entire science journal is dedicated to this one compound. Reading about cytokines and metabolic pathways, killer T cells, Th1, Th2 etc. and trying to apply it to your illness is an example of how a little knowledge can be dangerous.

The Mepron/ Zithromax combinations is the most widely used initial approach.  The higher dose, Zithromax 500-600 mg and Mepron 2 tsp twice daily is more likely to be effective.  Medication doses are within FDA recommended levels.  This is generally the best place to start. 

Quinine/clindamycin is too toxic for most to tolerate but is very effective. 

Malarone has been used in lieu of Mepron but the dose of the active ingredient, atovaquone is quite low. 

The traditional herb artemisinin has a long track record and is a very helpful adjunct to treatment.  Combining active artemisinin with the whole plant (artemisia) may enhance adsorption and bioavailability.

The FDA approved Coartem contains artemether, a more active derivative of artemisinin and is very effective. 

Liposomal artemisinin available through a compounding pharmacy is a potent alternative. 

Artesunate is another artemisinin derivate, available in other countries; it may also be highly active.  An oral version of the agent is also available through TCM (Traditional Chinese Medicine) sources. 

There are many traditional herbs, this is a partial list.   Cryptolepis can be very effective at times, sold as a single agent through a compounding pharmacy.  

Herbal combination therapy, described by Buhner: cryptolepis, sida acuta and alchornea may be an effective option. 

Daraprim (with leucovorin) folic acid antagonist, a drug typically used to treat toxoplasmosis and has some anti-Babesia properties.  It may be helpful adjunctively. 

Larium, related to quinine (with doxycycline) is very effective but its use has been limited because the side effect depression. 

Antibiotics, generally not effective as single agents.  IV clindamycin can be effective in stubborn cases. 

Bactrim touted to have anti-babesia properties is typically ineffective. 

Other, novel approaches have been used in patients with very resistant disease.  For example, the anticoagulant heparin coats merozoites and inhibits RBC penetration. (works in mice, some human data).

Babesia can be associated with numerous symptoms: fever, feeling flulike, malaise, fatigue, chills, sweats, headache, air hunger, cough, joint pain, muscle pain, cough, abdominal pain, nausea, depression, changes in emotional state and many others.

Clinically, Babesia is usually seen as a coinfection with Lyme and other tickborne pathogens and symptoms may be more confused.  Babesia is the second most common tickborne infection after Lyme. Long term remission is attainable in the vast majority of patients, time frame unpredictable.

Lyme ADD

Attention deficit disorder, ADD/ADHD brains operate in much the same way.  For purposes of this piece I will only discuss ADD. ADD is common, perhaps much more than appreciated. It may affect 20% of the general population. Symptoms vary tremendously in degree  and severity from one person to the next. 

ADD is closely associated with “executive function” disorder. Brain housekeeping functions controlled by the frontal lobe are askew.  Patients have problems with focus, attention and staying on task.  Minds wander. Patients are impatient and interrupt. They don’t follow conversations; their minds are elsewhere. Their memories are full of holes. They lose their keys, wallets and misplace important papers. They forget where they parked their car at the mall. Routine tasks don’t get done, like washing dishes or filing tax forms. If something interests the ADD brain the person may hyper-focus: play a video game for hours on end, stay up all night reading a book despite predictable exhaustion the next day.  It is not all bad. People with ADD can be extremely creative, interpret the world in unique ways.  For example, only an ADD Einstein could imagine what it is like to travel next to a beam of light and discover relativity.  The same Einstein never learned to drive a car, he lacked the required focus. (Einstein’s brain was unique in other ways as well). ADD people are risk takers, which may be good or bad. They have other unique personality traits/quirks. 

These are the symptoms I hear every day from Lyme patients. They have ADD. Adult ADD. Or do they?

Adult ADD is a misnomer.  ADD is a genetic brain glitch. You are born with it. Symptoms should be present in elementary school or before.  Preexisting ADD may be discovered at any age.  Once it was believed that ADD, a pediatric disorder resolved over time. Perhaps the hyperactivity component resolves in many cases; the important frontal lobe executive dysfunction does not. 

The important question for a Lyme patients is: were you like that before?  If the answer is: no, I was precise, organized and orderly. Then the diagnosis is not ADD.  It is Lyme masquerading as ADD, or “Lyme ADD.”  Findings on functional brain scans, like SPECT may be similar to those seen with ADD.  Patients with preexisting ADD are afflicted the most. They experience ADD on steroids. 

Of course, Lyme, Lyme brain, Lyme encephalopathy, neuroborreliosis (synonyms) are treated with antibiotics etc.  But “Lyme ADD” patients can also be effectively treated, if only temporarily with classic ADD drugs and experience much improvement. 

Stimulants tend to be the most effective agents and may be multipurpose since most patients are suffering with severe fatigue as well.  Drugs like Nuvigil work only for wakefulness, not for ADD.  The principal drugs are Ritalin and Adderall and there are multiple variants. 

Proper dosing, side effect are other clinical details are outside the scope of this discussion. 

Appropriate treatment may drastically improve quality of life for many suffering with "Lyme brain."

Lyme and Hashimoto's.

It has been reported by “Lyme doctors” that Lyme infection is associated with endocrinopathies (disorders of the endocrine system). The most frequent is thyroid disease, generally autoimmune hypothyroidism AKA Hashimoto’s disease.  When looking at Lyme associated endocrine disorders, we need to take them one at a time.  A patient I saw today gained 70 pounds and was first diagnosed with hypothyroidism prior to Lyme. Thyroid supplementation helped him loose the weight. Thyroid disease, particularly autoimmune Hashimoto’s disease is very common. Lyme is very common. But do Lyme patients have hypothyroidism more frequently than would be expected on the basis of chance? Is there is a causal relationship? Hypothyroidism is almost entirely autoimmune. Anti-TPO and other anti-thyroid autoantibodies are invariably present. First off, we know that Hashimoto’s is a familiar disorder, e.g. mom and 2 daughters all suffer with it.  It has been well established that there is genetic predisposition, i.e. HLA DR3, DR5 mutations. 

Autoimmune disease likely is caused by several different mechanisms, one is called molecular mimicry. It has been reported that Bb shares certain amino acid sequences with thyroid proteins.  Antibodies directed against Lyme, in genetically predisposed individuals, may precipitate the productions of self-directed antibodies.  In other words, Lyme antibodies accidentally trigger anti-thyroid antibodies in some cases. 

It appears there may be a causal relationship.  I don’t think there is anything published confirming this suspicion. 

Most endocrine disorders are not autoimmune, including: hypothalamic, pituitary, adrenal disorders, sex hormones and (? POTS -- angiotensin 1 receptor).  If relationships exist, other factors are in play. 

All of my Lyme patients, who invariably complain of fatigue, have their thyroid functions checked.  Most doctors just screen with TSH.  T3 and T4 may be helpful but anti-thyroid antibodies are essential.  If these antibodies are present the patient will need thyroid supplementation sooner or later. If they have exhaustion – sooner, irrespective of the other numbers (except with hyperthyroidism or Grave’s disease).