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Hi Everyone,

I truly appreciate all of the prayers and well wishes I received from so many of you. I continue to heal nicely and have been able to work full time now.

So let’s jump back into the mysteries and complexities of healing with today’s newsletter on the important and often overlooked subject of porphyria. As always, comments and questions are welcomed.

Thanks,   Neil 



Another Elephant in the Room?

With gratitude to Steven Rochlitz, PhD, for his extensive work on this subject and helping me to finally grasp the essentials.   Much of the information in this newsletter comes directly from his book which is reviewed below

Porphyria is a very complicated subject, and I will attempt to help us to understand it (admittedly, with simplifications) and help to put our understanding of it into perspective. Over the past 30 years, many medical writers have recognized that porphyria may be more common than usually appreciated, but efforts to diagnose it and treat it have slowly waned, probably due its unique complexity, and to the fact that the treatment of porphyria is completely opposite (in some ways) from the treatment of its causes.

So first of all, what is porphyria? Let me start by reminding you that our bodies can only utilize the red blood cells we make for about 90 days, and then we have to recycle them to make new red blood cells. One of the central components of red blood cells is heme (think hemoglobin). For a wide variety of reasons, if the liver is not working properly, and an individual has a predisposition to a deficiency of certain liver enzymes, the liver may not be able to make adequate enzymes for heme to be recycled, and we get a build-up of some of these break-down products, called porphyrins. There are 8 named porphyrins which we can measure, and when porphyrins accumulate in the body, we get porphyria.

There are a number of rare types of porphyria which are well described in the medical literature, and I can say that I have yet to see a case. Those, I will not be discussing in this newsletter. However, the occurrence of secondary porphyria, meaning a porphyria which is created by an infectious process or toxin, is not rare. In fact, as I shall discuss, I think it is much more common than is generally appreciated.

What are the symptoms of porphyria? They are global, and it will be obvious that they are similar to those of mold toxicity, Lyme and coinfections, mast cell activation, and PANDAS. Like these conditions, porphyria sets off a series of biochemical reactions, inflammatory in nature, which can affect virtually every system of the body.

The symptoms that I find most useful to draw my attention to porphyria as a contributing factor to CIRS-type illnesses are especially psychological in nature, including intense anxiety, depression, and panic; and gastrointestinal, especially severe nausea and vomiting. When these symptoms follow closely on the heels of my patient taking a new supplement or medication, and this reaction lasts longer than 2 or 3 days (a typical Herx-like reaction), this suggests to me that it is possible that we have triggered a porphyric reaction.

Other symptoms include: palpitations, weakness, unusual neurological symptoms as well as paresthesias and peripheral neuropathy, abdominal pain, constipation and/or diarrhea, nausea and/or vomiting, allergic reactions, asthma, shortness of breath, chest pain, insomnia, a wide variety of skin rashes, dizziness, and increasing intolerance to medications, supplements, stress, light, sound, heat, cold, fragrances and electromagnetic frequencies.

In my experience, the basic issue here is that, like mast cell activation, secondary porphyrias are most commonly triggered by mold toxicity and Lyme disease, especially Bartonella, but can also be triggered by viral infections, Chlamydia and Mycoplasma infections, and other toxins.

This means that it is most important to not lose sight of the need to treat the primary trigger or cause of porphyria, while also not ignoring the biochemical effects of porphyria which may need to be addressed to quiet the intense reaction. Treatment of the underlying cause may not be able to be addressed unless the porphyria (the excessive amounts of porphyrins in the body) are treated first, or concurrently. Unlike the other conditions we may be working with here, like mold or Lyme or mast cell activation, the chemistry of porphyria is distinctly different and may be at odds with the treatment of those other conditions.

What this means for me, personally, is that I often find myself struggling to find the correct balance of what to treat, in what order, and how. The most obvious example is this, with porphyria, is that treatment requires a higher carbohydrate intake. When we treat mold or candida, we typically limit carbohydrate intake to 60 gm or less daily. It is fascinating that some patients find that they feel “awful” until they get their carbohydrate intake up to 80-100 gm and I wonder if these patients have a mild degree of porphyria. I have not yet studied this, specifically, but I think this may be worthy of research.

An acute flare up of porphyria, which looks to me like a prolonged Herx reaction (lasting from 1-3 weeks or more) may respond well, in this context, to the use of intravenous dextrose in a 10% concentration (D10W) using 500cc daily. This often will produce a significant improvement in symptoms, greatly shortening the porphyric reaction. Since it is not always easy for my patients to obtain this intravenous treatment, they can also try taking dextrose (glucose) tablets to see if their reaction can be aborted. The mechanism of this appears to be that the IV dextrose affects the liver by stopping the production of heme, (and therefore of its breakdown products) and the effects of a chemical made by the stomach called PGC-1 alpha, thus stopping the production of excess toxic porphyrins.

Another simple treatment of an attack of porphyria (and a way to quiet it) is to increase the blood level of carbon dioxide. There is good evidence that a low carbon dioxide level (hypocapnia) prevents the body from utilizing oxygen properly by depleting glutathione, which then depletes 2,3 DPG (diphosphoglycerate) in red blood cells as first hypothesized by Dr. Rochlitz. This appears to be able to be reversed, to a certain extent, by rebreathing techniques such as breathing into a paper bag, or using shallow breathing techniques developed by Dr. Konstantin Buteyko. I referred to these breathing techniques in my newsletter #4 when I reviewed the book The Oxygen Advantage and outlined some of these techniques.

Low sodium levels, or hyponatremia, is common with porphyria and taking a small amount of salt under the tongue may help with an attack. However, in some patients, this can trigger an attack so the patient must approach this carefully. Drinking lots of good water is very important and may help to dilute the porphyrins, mitigating, to a certain extent, their effect.

Since the function of liver enzymes is essential to improving porphyria, supplements which assist this process, such as milk thistle, and charcoal, which can adsorb excess porphyrins, may be helpful. Steven Rochlitz has, in his book “Porphyria” set out a more extensive list of supplements which are of potential specific value in this treatment.

I think of the interventions described above as fairly simple and basic, and would encourage patients who have porphyria to try them to see what works to quiet their inflamed systems. Parenthetically, since resurrecting my interest in porphyria, I have checked ten of my most sensitive patients with a Labcorp urine porphyrin test, and 7 have come back positive. This would seem to confirm the assertion that porphyria, in patients with CIRS, may be far more prevalent than we have realized. Admittedly, this is a small sample, but hopefully others will start looking at this as well. For those who are collecting a urine porphyrin sample, be sure to wrap the urine specimen in aluminum foil as soon as it collected, and put it in the refrigerator until it can be brought to the laboratory for analysis. Remember, also, that porphyrins can be fleeting or transitory in the body, so the results will be more accurate if the patient can collect their urine during a severe flare-up or when they feel their absolute worst.

I am still attempting to integrate the treatment strategies for porphyria into my treatment strategies for patients with mold toxicity, Lyme, Bartonella, and mast cell activation and I find this to be quite a challenge. Each patient needs to be treated individually, and I don’t have any clear “rules” or any kind of algorithm to follow. The patients we are discussing tend to be extremely sensitive and toxic, so each treatment modality needs to be assessed separately so that we can be reassured that it is safe and helpful for our patient, before moving on to the next component of treatment.

What I hope I have conveyed, in this short discussion, is that considering the diagnosis of porphyria, and treating it, may be of great benefit for some of our most sensitive patients. I would welcome feedback from those practitioners who have experience in this area.




Porphyria: The Ultimate Cause of Common,
Chronic & Environmental Illnesses
With Breakthroughs in Diet, Supplements
and Energy Balancing
by Steven Rochlitz, PhD
(obtain through

Since today’s discussion centers around porphyria, I want to credit Steven Rochlitz, PhD, for this fascinating and extensive discussion of this subject. I have read many books and scientific articles over the years, but I feel this book clarified this complicated subject better than any others. Each chapter is devoted to either an aspect of porphyria or of another condition it is related to. The treatment suggestions are the most comprehensive I have come across, and could be practically pursued by patients or health care providers. In addition to the ones I described in my article, above, there is material on vagus nerve imbalances (which appear to be quite common in the chronically ill patients were are treating) and the hiatial hernia syndrome. The possible connection to patent foramen ovale (which Dr. Paul Cheney has confirmed as an important and overlooked component to Chronic Fatigue Syndrome), multiple chemical sensitivities, candidiasis, parasites, Chlamydia (and other infections), mast cell activation syndrome is explored in some detail. In fact, Dr. Rochlitz (in an earlier book on Porphyria) outlined a mechanism based around the P450 enzymes which describes how porphyria directly and inevitably causes mast cell activation. Thus the two disorders are much more closely linked (and common) than is generally appreciated.

While the casual reader or patient may be initially overwhelmed by the wealth of information here, if they can take a step backwards and try to put this information in perspective with the totality of their symptoms, I think they will find this information to be of great benefit.

I strongly encourage my readers to obtain this book and study it, as I believe it contains answers for many of you, especially those who have been ill for many years and not had a clear diagnosis.