A Discussion About Lyme Disease with Dr. Bruce Hoffman

A Discussion About Lyme Disease with Dr. Bruce Hoffman

The diagnosis and care of a patient with Lyme Disease is multifaceted and can be approached from more than one angle. It likely goes without saying that mainstream medicine is taking a much different approach than those in the functional and integrative space. 

In this video, I discuss the importance of looking at the larger history of said patient and how lab testing plays a role in proper diagnosis of Lyme Disease. 

If you are looking for answers regarding your situation, please contact our office today for more information. 

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A Discussion About Lyme Disease, with Dr. Bruce Hoffman

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Good afternoon everybody. I just finished an interview with the CBC (Canadian Broadcasting Corporation) and they wanted to talk about Lyme disease in Canada. We had a good, 20-minute chat that will probably be aired on some CBC broadcast in the fall. 

I was struck by one of the issues that often arises in my practice when I’m asked to treat complex multi-system, multi-symptom patients. They often come in and say, “I’ve got Lyme disease can you help me?” or “I’ve seen five doctors, naturopaths, et cetera, but I’m not better”.  

One of the biggest frustrations has been people believing that there’s one single trigger for their presentation of symptoms. They have one or two positive antibodies on their lab test, are told that’s a positive Lyme marker, and then are told by their medical provider that they should be on a full treatment program. I think that it’s medical malpractice to jump into the diagnosis and treatment of Lyme disease without a considered approach. 

We do know that there are two schools of thought in the standard of Lyme diagnosis. There are the traditional infectious disease specialists, who have very strict criteria for the diagnosis of Lyme disease, rightfully or wrongfully. Then there is a more broad approach to the understanding, diagnosis, and treatment of Lyme disease, which is purported and put forth by a group called ILADS, to which I happen to belong. 

The two schools of thought do not see eye to eye and that continual friction places the patient in the middle, trying to work out what is the best approach. 

Often patients get a diagnosis of Lyme disease from a provider they’ve seen based on the US test. They then get sent by their family doctor to an infectious disease specialist who reads them the riot act and lets them know that the tests are recording too many false positives, that they are irrelevant, that the lab is just trying to make money, or that the labs aren’t standardized. This battle goes back and forth, causes frustration for everyone, and the poor patient sits in the middle, trying to make sense of it all. 

Our aim is to talk about the differences between the two approaches, address the specifics as to why one group is vehemently certain of their position and the other group contests that position and has their own set of criteria for diagnosing and treating, which, based on the data, can’t be invalidated and has to be taken into account.

So here’s my take on patients who believe Lyme may be a trigger without a thorough health history. Lyme disease and co-infections are based on a very thorough clinical history.

I’m not going to go into the specifics of that clinical history, but the doctor or healthcare professional interviewing you must spend a lot of time taking a very specific history as to what symptoms you’re presenting and how you came to this diagnosis.

Just walking in with a positive lab test, whether it be US based or even Canadian based, isn’t good enough. Although with the Canadian test, if it’s positive, there’s a strong likelihood that Lyme disease is playing a role.

The Canadian test has very strict criteria for false positives and negatives, so if you have a positive test in the Canadian lab, it’s very likely that Lyme is an issue. So, I suggest that your practitioner takes a very thorough history and starts to use certain criteria to make the diagnosis.

One, is there history of a visit to an endemic area? Secondly, is there a history of tick bites?  Third, is there history of rashes? The problem is that many times, in fact most times, that history isn’t obtained. But if the history is there, that guides you in a certain direction. Those questions must be asked. Then a full list of symptoms must be taken, to try and differentiate whether your symptoms are specific to Lyme and related co-infections or whether they cross over with other conflicting or added potential causes for illness.

For instance, we know that in Lyme disease patients, after the first thirty days, the disease is characterized particularly in the later stages by migratory polyarthritis, which is joint pain or muscle pain that goes from joint to joint or muscle to muscle. These sorts of symptoms are very diagnostic. There are other things that cause this, but in the context of exposure to tick-borne illness, if those symptoms exist, you want to dig deeper.   

So migratory polyarthritis or muscle pain, those are very big symptoms for Lyme disease. Now for the co-infections, you want to ask very specific things. Do you have night sweats? Do you have day sweats? These occurrences are very specific for Babesia symptomatology. Do you have shortness of breath or “air hunger”? Do your symptoms come and go? Are there a lot of emotionally based symptoms, particularly anxiety as this has been associated with Babesia. You want to ask these very specific things.

Bartonella tends to be more peripheral so you tend to get a lot of pain syndromes such as Neuritis, which is pain in the peripheral nerves. Painful soles of the feet, particularly when you get out of bed in the morning. This is why the history is so important.

Lyme disease is now considered to be a clinical diagnosis based on history and physical examination, not based on a positive lab test. Why? Because you do get false positives and depending on which tests you run, the interpretation of results is highly complex. Unfortunately, due to cost we have the Canadian tests, which are elementary and introductory at best. 

Infectious disease specialists will say that they’re good enough, however, I disagree. When you want to look further and beyond you do have to look at more advanced testing which is, unfortunately, cost prohibitive. Most people can’t afford what’s really needed. I do try and get as many tests as I can across the spectrum of different testing types, including B-cell antibody testing, T-cell testing, PCR testing, plasma testing, and FISH testing. The more tests you can get, and the more that you correlate those tests with the clinical diagnosis in the symptom profile picture, the more you can hone in on the diagnosis of potential Lyme disease.

In Canada, Lyme disease is rising at a very alarming rate due to the migration of ticks and songbirds to the North. There was a study done showing that there are 32 million South American ticks brought north by South American birds every year. That’s a pretty alarming statistic. We know that songbirds are migrating to the North due to global warming and spreading their tick-borne load further and further North, hence the rise in tick-borne illness in Canada.

So, be cautious. Don’t jump to a diagnosis of Lyme disease because you have a positive test. Make sure that you have a very thorough history taken and make sure that the person who’s interviewing you has experience in the diagnosis and in interpreting lab data. The more lab data you have, the better.

Don’t rush ahead and treat yourself for Lyme disease without due caution. It can lead you into the wrong direction and make your immune system and your gut microbiome quite compromised if you treat inappropriately with some of the drugs out there that are available. Just a word of caution. This was covered in a podcast that you can listen to here.

Podcast: Looking at Lyme: Understanding Symptoms and Treating the Whole Person

Looking at Lyme

I was recently interviewed by Sarah Cormode for an episode of Looking at Lyme, an educational podcast created by the Canadian Lyme Disease Foundation, where I highlight the importance of taking an in-depth patient history to understand and document Lyme disease symptoms.

I also discuss several approaches to treating Lyme disease and explain why such a variety of symptoms amongst patients with Lyme disease exists.

Take a listen below.

I was recently interviewed by Sarah Cormode for an episode of Looking at Lyme, an educational podcast created by the Canadian Lyme Disease Foundation, where I highlight the importance of taking an in-depth patient history to understand and document symptoms.

I also discuss several approaches to treating Lyme disease and explain why such a variety of symptoms amongst patients with Lyme disease exists.

People with Lyme disease have a lot of different symptoms, the bacteria attacks the body in so many different ways. Sometimes it attacks the brain, the heart, the joints, you name it. Today I'm looking at Lyme, we're going to dive into functional medicine, we'll look at the body from a holistic perspective and meet a doctor who treats the whole body and the mind.

Getting treated early for acute Lyme disease is critical. Some people find the attach ticks and others might get a bull's eye rash. But that's not always the case. And without these telltale signs, people might not get diagnosed. The longer that you have the disease, the worse it gets, and the harder it is to treat. That's when we need to go to the doctor. So, let's do that. There are very few medical doctors with the expertise of Dr. Bruce Hoffman. He practices functional medicine, and we'll get him to tell us more about that. We reached him at his Calgary clinic. Good morning, Dr. Hoffman.

Good morning to you.

What's the first thing that you look for in a patient who potentially has Lyme disease?

Your patients present to a doctor's office with many symptoms and many complex, interlocking possible what we call in medicine, differential diagnosis. So, they present with a whole host of symptoms. And it's the task of the doctor taking the history to try and work out what may or may not be Lyme disease. And sometimes patients come in with some Lyme test and say they definitively have Lyme disease, or they have positive biomarkers for Lyme disease on some of the tests they've done. But when a closer history is taken, that may not be the case. So, there's quite a lot to really sift through when you're trying to differentiate whether somebody has Lyme disease or not. The most important thing is the symptomatology. You want to take a very definitive history. In my clinic, we use different types of questionnaires to try and determine whether or not Lyme may be a diagnosis. And we also then start to take a very specific history about whether they visited endemic areas, which is somewhat a moot point because Lyme disease is somewhat, you know, it's specific, it's everywhere. If they visit an endemic area, if they've been bitten by a tick, if they've had the rash, which is very uncommon, by the way. But we start to ask the history of exposure, history of tick bite, history of rashes and in a symptom history, looking over the variable symptoms that present with Lyme disease and/or co-infections that come along with Lyme disease. A lot of questions need to be asked, and you've got to sift through them and try and determine if Lyme disease is the primary presenting feature or are there any other coexisting disorders that interlock, like mold exposure, or heavy metal toxicity or food sensitivities? And there's many of them that may interlock with a symptom presentation. So, there's a lot to ask.

Yeah, it sounds like getting that patient history is just so critical. 

History is everything. You know, you've got to take a good history. You can’t have a patient walk in and say I've got Lyme disease, and I go, okay, let's treat you. No, no, you have to stop and really ask very specific questions.

And it also sounds like you mentioned that most of your patients don't ever remember having a tick attached or getting a rash.

You know, the majority don't. I do have a number of patients who went to college in northeast in the United States, and they were out in the fields and in the forests, have a history of tick bite and rash exposure. But I would say that's probably 5% of my population. My patient population, it's very low.

Guess when we spend time in the outdoors, if we check for ticks and do a tick check and actually found one attached, we have something to at least document or same with a rash. If you found one, it'd be a good idea to get a photo of that to share with your doctor.

Absolutely. It would be lovely if we had that cookie cutter you know, clear cut, walked in the woods, got a tick, notices for within three days a high fever, headache, and then the Lyme disease rash. That's so seldom.

It's never that that clear? Is it?

Never. I wish it was easier.

So how critical is it then for people to get diagnosed and treated early?

Oh, if they've been exposed and there's definitely a tick bite. And the symptomatology of high fever, sore neck, chills and joints. If that occurs, you get them on antibiotics while waiting for lab data or getting the tick, if it's discovered, sent off to the lab for analysis. Definitely, I’ll put them on treatment right away. And there's different standards of Lyme disease treatment, depending on which school of thought you belong to. Some schools of thought say, you just need like a brief dose of doxycycline. And others say at least four to six weeks of treatment. It depends on your approach.

Do you have a preference?

Longer term antibiotics, definitely not a short term

Yeah, that was certainly my experience, I had about 10 days of antibiotics, and then all of my symptoms came back afterwards.

Absolutely. If patients have an acute exposure, and they have symptomatology, we do have a baseline laboratory test. And then we repeat it four to eight weeks later to see if there's any rising titers. And we send the tick off for analysis. I usually cover them with antibiotics for at least six weeks. 

Wow. That's great to hear. And so, what is functional medicine?

Well, functional medicine is this emergent system of approaching a patient from a very different point of view. Like my medical training is what we, I don't mean to be derogatory, but it's called the N2D2 method of diagnosis and treatment; name the disease, name the drug. You know, that's how we learned in medical school, we just look at differential diagnoses, what disease or symptom cluster does this person have, and what drug can I pull out to help them. That's the specific training, highly relevant, nothing wrong with it. But now we have this emerging cohort of patients who have this chronic multi system, multi symptom disease profiles, with many interlocking issues. And that model doesn't work. And I tend to see and many people who are outside of the so-called traditional healthcare system tend to see that cohort of patients. Functional medicine attempts to take an upstream history back to what we call antecedents, mediators, and triggers. We go and look upstream to see, first of all, what's your symptom profile now? But, when did you start to feel unwell? One of the most relevant questions I ask a patient is; when did you last feel well, and then you want to take it from there, backwards and forwards. So functional medicine looks backwards as to the timeline, or the potential triggers and inherited factors which may play a role, the triggers what may have triggered the illness, and then what we call mediators, what may be keeping that symptom cluster alive. In conjunction with that we look at, not so much as pathology and disease laboratory tests, but we look at functional laboratory tests. How is the biochemistry and the metabolomics? How are they functioning? Are they optimized? Or are they deficient within a spectrum? Traditional Medicine has a reference range of, you know, negative or positive. Functional medicine optimizes function based on individual susceptibility and genetics. It's a very elegant form of practicing medicine within chemical principles. Just old school sort of, you know, when did you last feel well; what happened and what may have been playing a role. No longer looking at single factors, instead, looking at multiple causative factors as to what keeps this patient still symptomatic. And I can tell you, from my experience, that there is never one reason why a person is not feeling well. There's usually a whole myriad and host of issues from poor sleep, poor diet, early childhood trauma, dental issues, food and gut sensitivities. It is complex, long list of what made you unwell. 

Yeah, absolutely. Why do the symptoms vary so much from one patient to the other?

You mean with Lyme disease specifically?

Yes. with Lyme disease specifically?

Well, while it depends on a whole host of factors, it depends on the individual immune response of the person, the total toxic load, the infectious load, the expression of the Lyme disease spirochaete, with or without co infections, the metabolic and nutritional strength of the individual, the immune competencies, the presence of natural killer cell functions, whether they can suppress the immune response. The fact that Lyme disease goes from different forms; the cellular form to an intracellular form, to a cystic form to a biofilm form then it comes and goes depending on your immune surveillance. There's a lot of reasons why somebody has waxing and waning of symptoms and feels variations in their symptom profile.

Is it possible for someone to have Lyme but not have any symptoms?

You can have positive laboratory testing for Lyme and be asymptomatic. Absolutely, absolutely. But you don't see those people because they feel good.

Yeah, definitely. Do symptoms flare and go dormant normally for some of your patients?

They do. They wax and wane depending on stressors, diet, travel and multiple factors affect the expression of symptomatology. Treatment or no treatment. Some treatments exacerbate the symptomatology quite dramatically. They get what they call the Jarisch Herxheimer reaction (JHR) where you put in a treatment and the patient's symptoms just go through the roof. And so, there's all these variations as to why people wax and wane and get increased symptoms at times. But yeah, we certainly have people with, with no symptoms, who have positive laboratory tests as well.

Dr. Hoffman, are you seeing a larger increase in the number of patients that you suspect to have Lyme disease and other co infections?

Absolutely. Yeah. As you know that the Lyme disease diagnosis is highly controversial, depending on which school of thought you belong to. Whether you belong to the sort of infectious disease society, the infectious disease group of medicine, or whether you follow the ILADS criteria for the diagnosis and treatment. Those are these two different schools of thought. Now you know, even with that, there's been a tremendous uptake in the Lyme disease diagnosis and co-infections due to global warming. The migration of songbirds further north and the spread of ticks deeper into the north because of global warming. It's been estimated, one study showed that the songbird flight path from South America to North America brought up to 32 million tick species. In the yearly migration just northwards from South America. So, there's a there's a huge increase in the diagnosis. For sure.

Yeah, especially for anyone who's living along any kind of migratory bird path.

Absolutely. Yeah, absolutely. And there’s this great Canadian researcher, John Scott, showing us published papers on this issue.

Yes, hopefully, we'll get him on a future podcast as well. I'd love to hear more about his research

Absolutely. Yeah.

So I was fortunate to go to the ILADS conference last year in Boston, and I learned about mast cell activation. And I was just wondering if you could tell me a little bit about that disorder.

Well, Mast Cell Activation Syndrome (MCAS) is a relatively new diagnosis. It's been around for a while. Dr. Lawrence Afrin is one of the leaders in the diagnosis and treatment. He's just recently published, which I co-authored, a criteria for the diagnosis. And the reason why that has been important is because previously at medical school, we learned about systemic mastocytosis, which is an increase in the number of mast cells that create disease processes. But mast cell activation syndrome is an increase in activity without an increase in number. And there are different criteria for the diagnosis. Mast cell activation syndrome is a very, very important concept to keep in mind when seeing patients with chronic systemic illness because you'll see it a lot. I see it a lot. Mast cells or white cells act as vigilante cells to try and protect you from incoming stressors. Whatever they may be, whether it's mental, chemical, environmental, infections or food, they spew out at least 1000, not 200 as one's thought, but more than 1000 mediators of inflammation. One of them is histamines. Everybody knows the histamine is a sort of allergy hive reaction. There are many other mediators of inflammation. People with mast cell activation syndrome have this heightened inflammatory response to ongoing day to day environmental exposures and present with a multitude of symptoms in multiple organ systems. And they travel from doctor to doctor you know, they go to the allergist and the rheumatologist and to the neurologists, but nobody ties the systemic nature of this condition together. So, it's important again to take a thorough history and elicit whether somebody may be presenting with mast cell activation syndrome. Now, interestingly, mold exposures and Lyme disease trigger mast cell activation syndrome. So you often get a cross mapping of symptomatology.

Well, what would be your best advice for someone who suspects that they might have Lyme disease?

Well, it's a very tricky one. Because here's my experience. People often want to believe in a one diagnosis - one treatment approach when they present with complex illness. And it's really doesn't do them any favors to adopt that attitude. Yes, you may have a classic exposure and symptom profile, no question about that. But when you've got chronic illness, and chronic multi system, multi symptom exposures, and you go into a Lyme test with a naturopath or an MD, they send it to the states or even they send it to the Canadian Winnipeg group. And you come back with a positive test, it doesn't mean that the reason for your symptom profile is Lyme. Lyme may be the trigger, but you may have a whole host of underlying issues that are playing a role in your symptom profile. And one of the great tragedies that I see in my practice is people who come to see me, they've got a positive Lyme test and they've been treated for Lyme. But it's really not the key diagnosis, there are 70 other underlying factors that are far more relevant than that positive laboratory test. So, in response to your question is just be extremely discriminatory, when you jump to the diagnosis of Lyme disease as causing your symptoms, it may not be that. It may be there, you may have a positive test. But it doesn't mean that Lyme disease is at the root of it. It may be that it is. But you can't just take a positive test and treat it as if that's it. And I see that 90-95% of the time. They just go get treated for Lyme, but it's not really Lyme that's causing a symptom profile. Sometimes it is, of course it is, but you've got to discriminate.

So it's that combination of diagnostic testing and patient history,

History, history, history. If you're not taking a two-hour history with your patient, a timeline from conception to present, plus even intergenerational issues because we know that you inherit epigenetically family trauma. It is very well studied and well researched. Now, if you're not taking a thorough history, and following the timeline and symptom presentation of that patient, at least a two-hour history, you can't really discriminate on a history basis, whether this patient is suffering from one illness or 15 possible comorbid conditions. You have to take that history, then you back it up with laboratory data. The more laboratory data, the better, which unfortunately and again, with our healthcare system, that sort of privilege and that sort of luxury of a two-hour interview with extensive lab data. It doesn't exist. You have to go outside the healthcare system to get that service, you know, which is a tragedy, but it's the truth.

I couldn't agree more. Thank you so much for your time, Dr. Hoffman.

Thank you so much.

My key takeaway from that conversation was just how important it is that a doctor gets a full patient history. I know that in my case, I had a lot of symptoms and it was really confusing to understand what was going on in my body. That wraps up another podcast. Thank you so much for listening. Stay safe in the outdoors.

Kryptopyrroluria (aka Hemopyrrollactamuria) 2017: A Major Piece of the Puzzle in Overcoming Chronic Lyme Disease

Dietrich Klinghardt, MD, PhD, is a practicing physician in Woodinville, Washington with a focus on the treatment of chronic neurological conditions such as Lyme disease, autism, and CFIDS. In the years that he has treated patients with chronic infections, he has observed that, for many, recovery is often elusive. Patients may plateau or find that their recovery is stalled. In other cases, patients may not succeed in their attempts to rid the body of a particular toxic or infectious burden, such as in patients with longstanding or therapy-resistant, late-stage Lyme disease.

In looking for possible explanations as to why some patients struggle more than others to regain their health, coauthor Klinghardt has found a high correlation between patients with chronic Lyme disease and those with kryptopyrroluria (KPU), or more precisely hemopyrrollactamuria (HPU). The condition is alternatively known as the “mauve factor” or “malvaria.”

KPU may be an inherited condition, but it can also be induced by psychological trauma or chronic infections. Epigenetic influences such as intrauterine, birth, childhood, or transgenerational trauma may trigger KPU; other triggers may include a car accident, divorce or emotional trauma, and physical or sexual abuse. Chronic infections, such as Lyme disease, may themselves serve as a trigger for the condition.

The HPU complex is a biochemical marker and neurotoxic substance frequently identified in the urine of patients with autism, learning disabilities, alcoholism, substance abuse, schizophrenia, ADHD, Down syndrome, depression, bipolar disorders, and even criminal behavior. Some estimate the incidence of KPU to be 40-70% in schizophrenia, 50% in autism, 30% in ADHD, and 40-80% in alcoholism and substance abuse.

Based on testing with Klinisch Ecologisches Allergie Centrum (KEAC; http://www.hputest.nl) in Holland,
Klinghardt has found the incidence of KPU in Lyme disease to be 80% or higher; in patients with heavy metal toxicity (lead, mercury, aluminum, cadmium, and others) over 75%; and in children with autism over 80%. These are very significant percentages of the patient population with chronic illness that may benefit from a treatment program that addresses KPU. Healthy controls do not test positive for KPU.


In 1958, a psychiatric research program in Saskatchewan, Canada, led by Abram Hoffer, MD, PhD, the father of orthomolecular psychiatry, was looking for the possible biochemical origin of schizophrenia and a lab marker that would make it easier to identify affected individuals. One study involved evaluating the urine for certain chemical fractions and evaluating those of schizophrenic patients and those of normal controls. The effort yielded “the mauve factor,” a specific substance that reliably allowed the examiners to identify the schizophrenic
patients, as it was not found in the normal controls.

Early on, the substance was known as “the mauve factor” due to the mauve color that was observed on the stained paper. It was then termed “kryptopyrrole”, later identified as hydroxyhemopyrrolin-2-one (HPL). The researchers first called the disease associated with this condition “malvaria,” but it was renamed by Dr. Carl Pfeiffer, MD, PhD to “pyrolleuria” which was, for no obvious reason, consistently spelled “pyrroluria” in later publications. Today, the condition is generally referred to as “pyroluria.” In the 1970s, Dr. Pfeiffer created an assay for the condition and was able to show clinical improvement in positive patients with high doses of zinc and vitamin B6 (between 400 mg and 3,000 mg B6).

Associated Conditions

A partial list of conditions where KPU may be a factor includes ADHD, alcoholism, autism, bipolar disorders, criminal behavior, depression, Down syndrome, epilepsy, heavy metal toxicity, learning disabilities, Lyme disease, multiple sclerosis, Parkinson’s disease, schizophrenia, and, substance abuse. The items listed in bold are those in which Klinghardt has observed a connection to KPU in his patient population.


The KPU condition results in a significant loss of zinc, vitamin B6, biotin, manganese, arachidonic acid, and other nutrients from the body via the kidneys. There are many symptoms of KPU, which may result from deficiencies of these nutrients. Those in bold are tell-tale signs of the condition. Klinghardt finds that depression is often a leading symptom of the condition. Symptoms may include the following:

  • Abdominal tenderness
  • Abnormal fat distribution
  • Acne, allergy
  • Amenorrhea, irregular periods
  • Anxiety / Nervousness
  • Attention Deficit / ADHD
  • Autism
  • B6-responsive anemia
  • Cold hands or feet
  • Constipation
  • Course eyebrows
  • Crime and Delinquency
  • Delayed puberty, impotence
  • Depression
  • Emotional liability
  • Eosinophilia
  • Explosive or episodic anger
  • Familial
  • Hypoglycemia, glucose intolerance
  • Knee and joint pain
  • Light, sound, odor intolerance
  • Mood swings
  • Nail spots (Leukodynia)
  • Obesity
  • Pale skin, poor tanning
  • Paranoia / Hallucinations
  • Perceptual disorganization
  • Pessimism
  • Poor breakfast appetite
  • Poor Dream Recall
  • Poor short-term memory
  • Stress intolerance
  • Stretch marks (striae)
  • Substance abuse
  • Tremor, shaking, spasms
  • Withdrawal

Impact of Nutrient Loss

Elevated levels of HPL found in urine are the result of an abnormality in heme synthesis. Hemoglobin is the substance that holds iron in the red blood cells. Heme is also the principal building block of many enzymes involved in detoxification (cytochromes), enzymes involved in healthy methylation (MSR and CBS), and NOS – a significant enzyme in the urea/BH4-cycle. HPL is a byproduct of dysfunctional heme synthesis and can be identified in the urine. HPL binds to zinc, vitamin B6, biotin, manganese, arachidonic acid (omega-6), and other important compounds that, as a result, are excreted via the urine.

This leads to a significant depletion of these nutrients throughout the body and to the synthesis of non-functioning or poorly functioning enzymes. Turning to the importance of zinc, vitamin B6, biotin, manganese, and arachidonic acid in the body, it becomes clear how widespread the problems may be that are created by this condition.

Zinc deficiency may result in emotional disorders, food allergies, insulin resistance, delayed puberty, rough skin, delayed wound healing, growth retardation, hypogonadism, hypochlorhydria, mental lethargy, short stature, diarrhea, stretch marks or striae (which may be misinterpreted as Bartonella in some patients with Lyme disease), white spots on the fingernails, reduction in collagen, macular degeneration, dandruff, skin lesions such as acne, hyperactivity, loss of appetite, reduced fertility and libido, transverse lines on the fingernails, defective mineralization of the bones leading to osteoporosis, and many others.

Zinc is a powerful antioxidant, and lower levels lead to an increase in oxidative stress. Lower levels are correlated with lowered glutathione, an important part of the detoxification system. Zinc is required to support proper immune function. “White blood cells without zinc are like an army without bullets,” says Klinghardt.

Vitamin B6 deficiency is thought to be a rare occurrence. However, in those with KPU, this is not the case. B6 deficiency may lead to nervousness, insomnia, irritability, seizures, muscle weakness,
poor absorption of nutrients, decrease of key enzymes and cofactors involved in amino acid metabolism, impairment in the synthesis of neurotransmitters, impairment in the synthesis of hemoglobin, seborrheic dermatological eruptions, confusion, and neuropathy. Like zinc, B6 is an antioxidant and correlates to levels of glutathione.

Biotin deficiency may be evidenced by rashes, dry skin, seborrheic dermatitis, brittle nails, fine or brittle hair, and hair loss. More importantly, however, it may be associated with depression, lethargy, hearing loss, fungal infections, muscle pain, and abnormal skin sensations such as tingling. Biotin is an important co- factor in the production of energy in the mitochondria. Biotin is essential for a healthy brain and nervous system. Biotin deficiency is associated with many aspects of the aging process.

Manganese deficiency may be associated with joint pain, inflammation, and arthritis. Deficiency may result in a change in hair pigment or a slowing of hair growth. It is essential for normal growth, glucose utilization, lipid metabolism, and production of thyroid hormone. It may be associated with diseases such as diabetes, dyslipidemia, Parkinson’s disease, osteoporosis, and epilepsy.

Arachidonic acid (from omega-6) deficiency may lead to the impairment of white blood cell function, primarily the leukocytes, which may lead to one being more vulnerable to infection. It may lead to neuropathy, neural and vascular complications in preterm babies, skin eruptions, behavior changes, sterility in males, arthritic conditions, dry eyes, growth retardation, dry skin and hair, slow wound healing, hair loss, kidney dysfunction, heart beat abnormalities, and miscarriages.

When one considers the magnitude of potential health problems that may be present when a single condition leads to a deficiency in zinc, vitamin B6, biotin, manganese, arachidonic acid, and other nutrients simultaneously, the negative implications on health are almost endless.

KPU and Lyme Disease

Three possible origins of KPU are discussed in the literature: genetics, trauma, and chronic infections. The connection between KPU and many of the illnesses previously discussed has been known for quite some time. However, prior to Klinghardt’s early work in treating Lyme disease, never before had a connection been observed or published between KPU and Lyme disease. This discovery has been a key for Klinghardt to return his patients to an improved state of health and wellness, and the changes he has observed have been profound.

Klinghardt has found that 4 of 5 patients with chronic or persistent Lyme disease test highly positive for this condition (when tested with KEAC). That suggests that 80% or more of patients with symptoms of chronic Lyme disease may benefit from a treatment protocol that addresses KPU.

Klinghardt finds that it is rare for a patient to have chronic symptomatic Lyme disease as an adult without the patient having developed KPU. He postulates that the biotoxins from microbes block one or more of the eight enzymes of heme synthesis. This leads to a significant loss of key minerals in the white blood cells, which effectively disarms cellular immunity.

In those where KPU was triggered by infection with Lyme organisms, Klinghardt has observed that the KPU is often an unstable form of the condition where there are times of higher levels of pyrroles being excreted and times when this is not observed. If a person has episodes of depression, these episodes generally correlate to times when pyrroles are being released in higher levels in the urine.

One young adult female struggling with Lyme for several years had severe multiple chemical sensitivities (MCS) that were not improved by any previous treatment. After starting the KPU protocol, she noticed improvements in her MCS for the first time since she became ill. Other patients with intractable chronic infections have experienced significant improvements in immune function and a resulting lowering of total microbial burden.

Klinghardt has observed numerous patients that have struggled to rid the body of parasitic infestations. In these patients, regardless of the interventions used, the patient continues to expel these parasites on an ongoing basis. Therapy-resistant infections are a hallmark sign of KPU. Klinghardt has found that once the KPU protocol is put in place, there is often a swift resolution of long-standing infections and infestations. This includes patients who have failed years of antibiotic therapy for chronic or late-stage Lyme disease.

Sandeep Gupta, MD, from Australia has stated that parasites and pyroluria almost always go together. He has observed that almost every chronically unwell individual seems to have both; one opens the door to the other. Chronically low levels of zinc allow parasites to invade the mucosal layer of the gut. Parasites may then move to the liver and gallbladder. They interfere with mood, energy levels, and sleep. Addressing the parasites while restoring zinc and B6 often makes a tremendous difference in his patients.

Chronic Lyme disease patients often suffer from severe jawbone infections that may require cavitation surgery, which often tends to fail in this population. When the clients are pretreated for KPU, the outcome of the surgical procedure is generally much better. In some mild cases, ozone treatment of the jaw may be sufficient to turn things around.

Klinghardt has followed the interest in HLA-DR genetic typing in regards to biotoxin illnesses such as Lyme disease and mold. Prior to KPU, patients with certain haplotypes were considered more difficult to treat as the body could not properly and effectively respond to and remove biotoxins from Lyme disease, molds, or in the worst cases, both. In his experience, once the KPU issue is addressed, these HLA types become far less of a concern in most patients and no longer hold them back on their road to regaining health.

Once bodily systems are back online and functioning properly, a few months after introducing the KPU protocol, patients become less vulnerable to Lyme disease, to mold, and even to heavy metals. Their bodies are now much better equipped to deal with these conditions when they have appropriate levels of zinc, vitamin B6, biotin, manganese, and arachidonic acid to support optimal functioning of numerous bodily processes.

KPU and Methylation

In Klinghardt’s work, if a patient has KPU, treating the KPU condition first is a foundational intervention before pursuing more specific methylation support. Specific enzyme blockages are discussed earlier in this article.

In people with cancer and active EBV infection, EBV triggers a hypermethylation inside the cancer cells that may accelerate cancer cell growth. If methylation support is introduced based on genetic SNPs or other lab testing but the patient has an untreated, active EBV infection (such as is common in chronic fatigue syndrome, Lyme disease, and other related conditions) or an EBV-related cancer such as throat, stomach, breast, prostate, or Hodgkin lymphoma, supporting methylation may lead the patient to an increased risk of cancer or accelerated rate of cancer growth.

This potential makes treating KPU first even more important as balancing the zinc and B6-dependent enzymes indirectly
without the addition of methyl groups is generally a safer way to restore healthy methylation on all fronts as opposed to directly supporting methylation with methyl donors.

When people begin to explore methylation, KPU should always be evaluated and addressed first. Several enzymes in or adjacent to the methylation cycle use the heme molecule which utilize zinc and vitamin B6 as primary building blocks. By supporting KPU, the methylation cycle works more smoothly, both in its ability to methylate and demethylate, and at a lower risk to the patient.

KPU and Heavy Metal Toxicity

When KPU is present and zinc and vitamin B6 are depleted, the detoxification pathways are overwhelmed and ineffective as the heme molecule is an integral part of many detoxification enzymes. Both zinc and vitamin B6 deficiencies, which are important cofactors in the methylationcycle, reduce levels of glutathione in the body. Glutathione is important for the detoxification of heavy metals and other toxins.

Replacing missing zinc and vitamin B6 increases glutathione. This, in turn, increases the rate of detoxification of heavy metals and other body burdening
toxins. Once KPU treatment is introduced with zinc and B6, reducing the metal burden no longer requires heroic measures.

However, it is also the case that incorporating the KPU protocol will liberate additional heavy metals within the body. This aspect of the KPU protocol is discussed later in this article and is important for the practitioner to understand before beginning to treat patients for the condition as additional detoxification support is generally needed. This protocol is intended to be done only with the guidance of a knowledgeable practitioner.

KPU and Porphyrin Disorders

There is a group of disorders related to pyroluria called porphyrias. KPU is one of a group of conditions known as porphyrin diseases. In 100% of porphyrin diseases, the HPL compound is found in the urine.

Porphyrin testing is readily available and is a reliable tool. Klinghardt prefers to send a urine sample to Laboratorie Philippe Auguste (http://labbio.net) in France for testing. Other options are also available in the US, such as through Genova Diagnostics, Doctor’s Data, and Great Plains Laboratory.

In the US, pyroluria and porphyria are viewed as separate conditions. However, in collaboration with the Dutch lab KEAC, it has been established that everyone with elevated porphyrins has pyroluria. When pyroluria is addressed, the porphyrins go down.

In porphyrin testing, uroporphyrin is an indicator for aluminum, coproporphyrin for lead, and precoproporphyrin for mercury. Klinghardt has not seen a case with elevated porphyrins that did not have KPU, and when the KPU was corrected, aluminum, lead, and mercury are excreted
from the body, and the porphyrins go down.

This is, in part, due to the fact that when the body has been deficient in zinc for a long period of time, it may retain heavy metals much more readily. When zinc is missing from the body, it is replaced in our bones with lead. If zinc is supplemented, lead is expelled. Secondly, the enzymes needed to detoxify these metals are heme-dependent enzymes,
and these metals accumulate when heme synthesis is abnormal.

Klinghardt notes that discussions on the topic of porphyria are much more widely accepted than those on pyroluria. In his experience, he finds that almost all of his patients have elevated porphyrins, and that pyroluria is the deeper core issue.

KPU and Histamine

When a KPU patient is having a good day, low histamine levels are observed; on a bad day, higher histamine levels are observed. It is the relative elevation of histamine in response to foods, inhalants, allergens, emotional stressors, and electrosmog that is problematic and causes the allergic phenomena, not the absolute histamine level. When histamine levels rise from a low level to a moderate level, the reactions are often severe. Learn how to control your histamine levels in my guide located here.

When exploring histamine levels in a KPU patient at a time when they are experiencing hives or asthma, the histamine levels are elevated, but not to levels that would create a problem for others. The relative rise in histamine, however, in KPU patients is experienced in a far more significant way.

Klinghardt has worked with biochemists in Germany that are beginning to link KPU with mastocytosis or mast cell activation syndrome (MCAS). They have observed that KPU treatment repairs the heme molecule, which notably stabilizes the mast cells and lowers the response to these relative rises in histamine.

KPU and Multiple Sclerosis

Klinghardt has treated many patients with multiple sclerosis. The MS patients that he has tested have been highly positive for KPU. Over time, he has
concluded that KPU is a frequent cofactor in MS. He has found that patients with MS respond favorably to KPU treatment.

In patients with KPU, absolute histamine levels are almost always low. The treatment for MS patients with KPU may include histamine in addition to the KPU protocol outlined in this article. Treatment with histamine may be either with oral or transdermal products. Prokarin is a transdermal patch which delivers histamine and has been used by some practitioners in the treatment of MS.

Evaluation and Testing

Klinghardt recommends that people start with the HPU Questionnaire (http://www.hputest.nl/evraag.htm). Once the questionnaire is completed, a score is calculated to provide a probability that a person may have KPU. If the score is 10-14, Klinghardt will often recommend proceeding with treatment without the need for confirmatory testing as the treatment itself is generally well-tolerated.

If the score is 0-9, he may suggest testing for the condition using additional lab work.

Pyrroles are impacted by light, temperature, oxygen, and time; and they readily break down. Once they begin to break down, the likelihood of detection is significantly lowered. Ideally, testing would be performed within eight hours after the collection, though this is not practical and rarely possible.

Within the United States, two of the available labs for testing include the following:

  • DHA Laboratory (https://www.pyroluriatesting.com) uses a frozen one-time collection at a cost of $80. They recommend the collection be the second urination of the day. They suggest avoiding all supplements, vitamins, and minerals for 12-24 hours prior to the specimen collection. The lab is testing for hydroxyhemopyrrolin-2-one (HPL).
  • Health Diagnostics and Research Institute (http://www.hdri-usa.com) charges $140 for a 24-hour collection and $90 for a random collection. HDRI suggests stopping zinc and B6 as well as antidepressant medications for 48 hours prior to the collection. They suggest not smoking or consuming caffeine for 24 hours prior. While there is no additional cost for testing the hydroxyhemopyrrolin-2-one (HPL) compound, this must be specifically ordered on the requisition form as it is not part of their KPU assay by default. If you do not specify HPL as an add-on, you will get kryptopyrrole (2,4 dimethyl-3-ethyl pyrrole) only.
  • In Europe, Klinghardt uses the Dutch Lab KEAC (http://hputest.nl) for HPU testing. The lab is guided by microbiologist Dr. John Kamsteeg, a world leader in HPU. The results of HPU testing with this lab align closely with the percentages of patients with chronic Lyme and other conditions that Klinghardt identifies with the HPU condition.
  • In Australia, KPU testing is available through SAFE Analytical Laboratories (http://safelabs.com.au) and Applied Analytical Laboratories Pty Ltd (http://www.apanlabs.com).

Each lab has their own very specific instructions for performing the test. This includes information such as shielding the specimen from light as well as how to handle and ship the specimen. It is important that the recommendations be closely followed to optimize the sensitivity of the test result.

To further maximize the sensitivity of testing, it may be best for the patient to be under stress at the time the test is being performed as HPL excretion is known to increase during times of stress.

In some circumstances, however, patients may still test negative even when the condition is suspected. In those cases, it may be best to repeat the test. In many cases, the result will be positive on the second or third test. In some patients, an empiric trial of the KPU protocol may be indicated despite repeated negative KPU tests, and this often leads the patient to
higher ground. WBC (not RBC) intracellular zinc may be a useful tool for exploring the potential for zinc deficiency where it matters most – in the white blood cells.

Other laboratory indicators that may be suggestive of KPU include the following:

  • WBC < 5000/mcL (due to low levels of zinc)
  • High LDL / Low HDL
  • Low normal alkaline phosphatase (<60U/L)
  • Low omega-6 fatty acids in red cell membrane test
  • Low taurine in amino acid profile
  • High MCV
  • Low glutathione
  • Low ATP
  • WBC and RBC zinc and manganese levels may be normal while biopsies from bone and CNS are completely deficient.
  • Bone biopsies are a reliable predictor of KPU. Severe deficiencies of zinc, manganese, lithium, calcium, magnesium, and molybdenum are often found.

Alkaline phosphatase (ALP) is a zinc and magnesium dependent enzyme. When someone is consuming adequate magnesium and is still presenting with low ALP, zinc deficiency is a likely consideration, and this may represent another indication for KPU. When ALP is below 55, zinc deficiency can be suspected; when below 40, it is likely.

A consequence of KPU is low glutathione and low ATP. In the realm of chronic illnesses, low reduced glutathione and low ATP are common and should alone trigger the suspicion that KPU may be a factor.


KPU is a severe but reversible deficiency of zinc, vitamin B6 (or P5P), biotin, manganese, arachidonic acid, and other co-factors. It is important to recognize, however, that treatment with zinc and vitamin B6 does not result in fewer pyrroles being excreted in the urine. KPU orthomolecular treatment does not fix the underlying condition; it substitutes what is being lost as a result of the condition such that the person is no longer deficient in key nutrients needed by the body to move towards health.

The general KPU substitution treatment that Klinghardt uses in his practice is as follows (dosages for 160 lb.) adult and should be adjusted based on weight; may be customized for specific patient needs):

With Breakfast

  • Zinc 25-30 mg (as picolinate, gluconate,sulfate, or zinc l-carnosine). Nausea after zinc supplementation may be a sign of hypochlorhydria or low stomach acid; this often resolves after a few months on treatment.
  • Vitamin B6 50-100 mg (split between pyridoxine HCl and P5P, with P5P being the predominant form)
  • Biotin 3-5 mg for brain, skin, hair, and nails
  • Magnesium 100 mg (glycinate, bisglycinate, or malate) – or titrate to bowel tolerance.
  • Arachidonic acid from omega-6 oils (Ghee such as Mt. Capra Goat Milk Ghee, Evening Primrose Oil, Hemp Seed Oil, Black Currant Oil, Borage Oil, Pumpkin Seed Oil; 4-6 capsules of Evening Primrose Oil per day is commonly used.)

With Dinner

  • Zinc 25-30 mg
  • Vitamin B6 50-100 mg
  • Biotin 3-5 mg
  • Magnesium 100 mg
  • Omega-6 Oils

This is the core treatment Klinghardt utilizes for KPU.

Additional Support

  • Vitamin A 1,500-3,000 IU per day to improve the absorption of zinc in the gut
  • Niacin 40-50 mg per day for psychiatric symptoms. (Abram Hoffer used up to 3000 mg per day.)
  • Taurine 100 mg twice per day (up to 2,000 mg at bedtime) for brain-related symptoms such as seizures, brain fog, and memory loss. Supports elimination of neurotoxins, improves bile quality, increases glutathione, and normalize brain rhythms.
  • Lithium 5-10 mg per day (Orotate or Aspartate); lithium is lost in the urine in some patients with KPU.
  • Manganese 2-5 mg per day (Patients with joint problems may require additional manganese above the dosages recommended here; see additional considerations later in this article on manganese for patients with Lyme disease.)
  • Chromium 250-500 mcg per day
  • Molybdenum 100-500 mcg per day
  • Boron 1-3 mg per day
  • Trace Minerals – As more is learned about KPU, additional elements are found to be lower in those with the condition. Thus, supplementing trace minerals may be a supportive strategy. BioPure MicroMinerals, Quinton Isotonic, or similar mineral products may be helpful

As compared to the first version of this article which was published in 2009, Klinghardt has found that many of hispatients do quite well with lower dosagesof some of these key nutrients than were originally utilized.

In Europe, Depyrrol is one product which provides support for KPU. Additionally, and in the United States, BioPure CORE and CORE-S are available to support those dealing with the condition. Another product in this realm is Mensah Medical’s Pyrrole Pak. These products serve as a solid foundation for KPU treatment; though additional co- factors may be needed for a given patient.

Some patients may not tolerate both vitamin B6 and P5P as contained in some products and may find it necessary to take each component of the KPU program separately.

In terms of BioPure’s CORE and CORE-S, CORE-S is a recent reformulation of the CORE product which has been available for many years. While either may be an appropriate option, CORE-S generally results in less nausea, better absorption, and is often better tolerated by those patients with Lyme disease as it does not contain manganese. While many with pyroluria may benefit from manganese, it may act as a growth factor for untreated Lyme disease, and thus, some may prefer to avoid its use in this patient population. The reformulated CORE-S contains horsetail as people with KPU excrete higher levels of silica in the urine, which leads to higher levels of aluminum toxicity. With either CORE or CORE-S, two capsules twice daily are a common target dose for a 160 lb. adult.

When first starting to introduce products in support of KPU, it is best to start with lower dosages and to take them towards the end of a meal and to gradually work up to the target dosage. Levels of B6, taurine, or biotin may be additionally and individually titrated upwards depending on the patient’s symptoms and needs. With the introduction of zinc, it is best to monitor copper levels after a few months on the protocol as copper replacement may also be needed. Zinc, vitamin B6, and manganese are copper antagonists. Thus, monitoring levels of copper and supplementing where needed is an important part of the treatment protocol.

Copper deficiency can lead to hemorrhoids, varicose veins, fatigue, edema, hair loss, anorexia, skin problems, osteoporosis, cardiovascular disease, aneurisms, and many other undesired conditions. Current nutritional teachings are misinformed on the topic of copper toxicity. The immune system uses copper and iron to fight infections associated with Lyme disease. As a result, oxidized copper is displaced in the connective tissue and may appear as though the patient is copper toxic by some testing methods when in fact copper supplementation may be appropriate. High dose Vitamin C has the effect of reducing oxidized copper to a form that can be reused by the body.

Detoxification and Course of Treatment

As treatment for KPU is implemented, this often can result in toxin mobilization as the body begins to release heavy metals. Symptoms may include muscle aches, bowel problems, or those normally associated with cleansing or detoxification reactions. Additionally, the immune system begins to become more active which can result in a Herxheimer-like reaction as the immune system begins to better respond to the backlog of microbes that it was previously unable to adequately address.

One approach for minimizing these reactions is to start slowly with introduction of the KPU nutrients and work up over time. In most cases, there is no reason that the treatment course must be an aggressive one. Nonetheless, this treatment should always be guided by a knowledgeable practitioner. In addition to the KPU treatment discussed earlier, consideration should be given to detoxification support and to protection of the red blood cells as the treatment is initiated.

According to Klinghardt, many of our metabolic enzymes use zinc as part of their molecular makeup. However, in patients with KPU, there is not enough zinc available to satisfy the need. In these cases, lead, mercury, and other 2-valent metals bind to these sites instead in a poor attempt to fulfill the role of zinc.

Once zinc is reintroduced into the body, 2-valent metals such as mercury, cadmium, aluminum, and lead are liberated. The patient may now have dislodged heavy metals circulating throughout the body.

These may be competing for the already overtaxed detoxification pathways or may be redistributed to places where they may be more problematic. Lead moves back into the blood, which can cause problems including damage to red blood cells. To protect the red blood cells, freeze-dried garlic and Vitamin E are often used.

Incorporation of known toxin binders further supports the detoxification process. Some of the binders that Klinghardt uses in his practice include chlorella, Ecklonia cava, zeolite, and
chitosan. Silica from horsetail supports binding of aluminum, and thus, the use of a high-silica zeolite such as BioPure ZeoBind is often utilized. It is critical to support the kidneys with specific drainage and organ support remedies in order to optimize the removal of heavy metals and to avoid stressing the kidneys.

An interesting observation has been that patients with KPU often get worse when an attempt is made to incorporate detoxification agents or antimicrobial agents prior to having first addressed the KPU condition. Once KPU has been addressed, other treatment options are often much more effective and better tolerated.

Additional Considerations

Many patients with chronic Lyme disease have issues with sulfur intolerance. This leads to a patient being unable to effectively utilize a number of detoxification agents such as alpha-lipoic acid, DMSA, DMPS, and glutathione; as well as supplements such as garlic. This may be related to genetic predisposition, but some of the enzymes involved in sulfur metabolism (CBS and others) are heme and B6 dependent; both of which are depleted in KPU. As patients are treated for KPU, these sulfur tolerance issues may resolve. Klinghardt has found that molybdenum at a dose of 100-500 mcg per day may correct sulfur intolerance in patients with KPU, as molybdenum may also be lost in these patients.

Ammonia is generally high in patients with KPU. As KPU is treated, high levels of ammonia tend to normalize. To bind and excrete ammonia, zeolite may be used.

Resolution of KPU

For most with the condition, supplementation will be required for life. However, Klinghardt has seen complete resolution of the condition after having addressed epigenetic influences, trauma, or unresolved conflicts using tools such as mental field therapy, family constellation work, or EMDR. By resolving trauma in the ancestry, the epigenetics are influenced in a positive way and the condition resolves.

Klinghardt has also observed complete resolution of Lyme-induced KPU when the infection is managed successfully with biological interventions.

Final Thoughts

Once patients are on the KPU protocol and mobilized metals have been addressed, the body begins to respond to backlogged infections and significant improvements in the patient’s condition
are often observed. Hormonal status often improves. Some patients who have been on thyroid medication for years may even become hyperthyroid as the body begins to function more optimally. Other patients may lose weight. Symptoms directly related to low levels of zinc, vitamin B6, biotin, manganese, and arachidonic acid often resolve.

Just as homes are built by first laying a solid foundation, addressing KPU and the deficiencies in zinc, vitamin B6, biotin, manganese, and arachidonic acid are key pieces of the puzzle in addressing the complexities of chronic Lyme disease and many other conditions.

Evaluation for KPU is one of the first things that Klinghardt pursues in working with patients with chronic illnesses. Implementing the KPU protocol often yields progress that had not previously been possible, and patient recovery is accelerated in a very deep and profound way.


This article is not intended to provide personalized treatment recommendations or to facilitate self-treatment. Treatment should be done only under the care and supervision of a licensed medical authority. Attempts to self-treat the condition may result in unintended negative consequences.


Useful Resources

Scott Forsgren, FDN-P, is the founder of BetterHealthGuy.com, a health coach, blogger, podcaster, health writer, advocate, support group facilitator, and LymeLight Foundation board member. He recovered his own health after a 20-year journey through Lyme disease and mold illness. Today, Scott is grateful for his current state of health and all that he has learned on this life-changing journey. Dr. Klinghardt served as a powerful mentor, teacher, and guide as Scott worked to understand the disease which had previously taken so much of his life and moved toward a place of health and wellness. Scott continues to utilize a maintenance pyroluria protocol which he started almost a decade ago. To follow Scott’s work, visit http://www.betterhealthguy.com. His podcast “BetterHealthGuy Blogcasts” is available on his web site and on YouTube, iTunes, Google Play, and Stitcher.

Dietrich Klinghardt, MD, PhD, studied medicine and psychology in Freiburg, Germany, completing his PhD on the involvement of the autonomic nervous system in autoimmune disorders. Early in his career, he became interested in the sequelae of chronic toxicity (especially lead, mercury, environmental pollutants, and electromagnetic fields) and its impact on chronic illness. Dr. Klinghardt has contributed significantly to the understanding of metal toxicity and its connection with chronic infections, illness, and pain. He has developed Autonomic Response Testing, a comprehensive evaluation system that has helped many practitioners to become accomplished holistic practitioners. He founded Sophia Health Institute (http://www.sophiaha.com) in 2012, and is actively involved in patient care at his clinic outside of Seattle. More information on his educational seminars can be found through the Klinghardt Academy (http://www.klinghardtacademy.com; US) and the Klinghardt Institute (http://www.klinghardtinstitute.com; UK).[/vc_column_text][vc_empty_space][vc_row_inner][vc_column_inner width=”1/2″][dt_default_button bg_hover_color=”#dd3333″ border_radius=”6px” border_width=”0px” button_padding=”12px 18px 11px 18px” default_btn_bg_color=”#1e73be” font_size=”16″ icon=”JTNDaSUyMGNsYXNzJTNEJTIyZmElMjBmYS1maWxlLXBkZi1vJTIyJTIwYXJpYS1oaWRkZW4lM0QlMjJ0cnVlJTIyJTNFJTNDJTJGaSUzRQ==” icon_size=”16″ link=”url:http%3A%2F%2Fhoofa.wpengine.com%2Fwp-content%2Fuploads%2F2017%2F08%2FKryptopyrroluria-aka-Hemopyrrollacramuria.pdf||target:%20_blank|” size=”custom” text_color=”#ffffff” text_hover_color=”#ffffff”]Download PDF of this Article[/dt_default_button][/vc_column_inner][vc_column_inner width=”1/2″][/vc_column_inner][/vc_row_inner][/vc_column][/vc_row]