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Before I started writing Mold Warriors in 2004, I still had the fanciful idea that there had to be an unknown silver bullet for mold illness. I think I am not alone when I hope for simple answers to complex problems. And mold illness certainly can be incredibly complex. So many people got better with CSM alone, but others needed something in addition, like step two. What were the differences in quick cure and not-cure? Still others, granted a smaller number, needed step three and then fewer needed more, like steps four and five. And sure we had to start with CSM or Welchol, but couldn’t all the rest of the steps be short-circuited? Just add the missing potion. One illness, one drug. Next case. No, trying to skip steps just frustrated all involved, especially me, because that leap-frog approach just didn’t work.

My practice has changed over the years; any more, I don’t get to see many people who just need a dash of CSM. The people I usually see these days are already treated with steps one, two and three, or so it seems. What is that magic potion anyway? Are we bereft of silver bullets?

Now in 2010, mold illness (and all other chronic fatiguing illnesses as well), is revealed to be so complex that each of these disease entities shares a common final pathway, one in which lab abnormalities become eerily so similar from one illness beginning with problem X to the last illness that began with Y (not to mention Z). Yes, I want to know what X and Y are respectively, but more importantly, my job is to fix the problems of a given patient here and now, so the source of the problem, while important, is less important than what they have now.

Some days I almost long for “the good old days,” when all I needed to say for the group of people who were treated successfully in less than one month with CSM, “OK, now stay away from mold.” That was all the advice they needed and the treatment was simple and decidedly not complex. Those days are gone, perhaps due to rapid dissemination of information on the Internet, physician education, patient demand or a combination of factors. And yet the patients who need steps four five and up through nine aren’t being treated as commonly. No surprise, in the patients I usually see, a cohort of persistently ill people for whom we have no Holy Grail of treatment, we need to take them through the steps that last year I didn’t have to offer.

All scientists know to always challenge yesterday’s hypotheses today and today’s tomorrow. What do we know now? I have given up yesterday’s hypothesis that there is a silver bullet. Instead, what we have to do is use good science and disciplined medicine (that means no Ass²) to slog through the inflammatory mechanisms, diverse as they are, to bring us the final Holy Grail: cure.

I know that while CSM helped an initial layer of patients and that was all they needed, other patients had a second layer of illness pasted on top of the CSM layer. This was the coagulase negative staph layer, just chock full of antibiotic resistant, biofilm-forming organisms that silently hurt the host, never let any unfortunate patient know that an illness-perpetuator was sitting on mucus membranes, deep in the back of the nose. But if those bacteria, living in a community of bacteria, protected by a thick layer of impervious “slime” weren’t eradicated then there was no hope for improvement.

As a simple example, imagine having a boat with an anchor rope coated by biofilm after the rope had been in the water a few days. The anchor lifting mechanism is two rubber hubs spinning, and slipping, against the slimy rope. There is no traction; the rope doesn’t get wound up, the anchor stays in place and the boat stays in the same place.

The point here is that if the biofilm-former isn’t eradicated the patient stays ill.

A different problem for patients with low MSH and chronic fatiguing illness was that they never would know about the slime formers that were stabbing them (deep stabs into the very heart of innate immune response) constantly because the bacteria didn’t cause sinus infections or runny nose or anything. And if the physician didn’t do an API-STAPH culture, now done routinely by Cambridge Biomedical, no one in the microbiology lab would be able to report out the very slow growing biofilm makers at all. They simply would be out-competed for space on the culture plate. Ahh, but not so in the nose.

As time passed, high MMP9 was unveiled as the next hurdle. Then all the people with antigliadin antibodies were proven to be an additional layer requiring an additional intervention too. And then there were hormone dysregulation people. My goodness there was the ADH/osmolality crowd and ACTH/cortisol sufferers all mixed in with the low androgen folks. All those hormone abnormalities had to be fixed or forget seeing the final clearance of illness.

Don’t forget that some physicians love to use steroid hormones (prednisone and androgens) almost as much as terrorists like to plant road side bombs. If the hormones are truly needed, fine; if they are guessed at (and my goodness do I see incessant and unwarranted guesses here from the fibromyalgia physicians) just forget any decent result over time. The medical results of such misuse of hormones, like the explosions of IEDs, are catastrophic. The “worst hormone patients” were ones that had seen somebody who thought that adrenal fatigue or low testosterone or low thyroid was the problem, even when results from commercial labs (show me the CLIA license please) showed nothing confirming need for hormone therapy. Look out (and run away as fast as you can) when some doc who sees you on occasion and then says you have fibromyalgia and here is some steroid and some thyroid and some kind of testosterone, usually garnished with a cachet of supplements (10-20 isn’t unusual) that are sold by the front door of the physicians’ office. Of course, the supplements you buy there, while perhaps a bit more expensive, are invariably of so much finer quality that the extra value is worth the added price. Give me some time to count to one hundred.

I wish that last scenario weren’t so commonly true.

As time passed, I felt as if treating mold illness (without the unnecessary hormones) was like attacking Medusa. Cut off one head, one layer if you will, and there were a couple more immediately growing out into the light to turn the patient’s life into stone. Even more important, it became pretty clear, pretty fast that the order of correcting these problems mattered a great deal. By 2006, it was “new information” that C3a had to be fixed and only then could we bring C4a levels out of the stratosphere. These are steps seven and eight! After all that, now what’s left to fix? Aren’t there a finite number of things that won’t be screwed up by inflammation?

By 2008, TGF beta-1 was first unveiled as a giant player that hurt mold patients (and others, especially CFSers), and then, after or group was able to show two interventions that lowered TGF beta-1, that previously unknown driver of a “new kind” of immunity (Th-17) surrendered its stranglehold on chronic illness. Soon however, we found out that if the patient was still exposed to a WDB, then whatever we did to TGF beta-1 failed. Stay way from exposure is Rule # 1.

Great, we can fix TGF beta-1, but only if there isn’t ongoing mold exposure. Now what was left? You’d think that after twelve years of unwinding the strings of illness from this amorphous ball of twine called chronic fatiguing illness that all of us (and not just me) were looking at that we’d at least see some of the central core of the ball.

Enter the Missing Piece


Maybe we were. Since 2005 I had seen a constant stream of blood test results that showed a consistent finding of low levels of vasoactive intestinal polypeptide (VIP) showing up in my patients. Sure, VIP deficiency appeared almost in lock step with low MSH. And as we showed, helping VIP, as we could do with tadalafil (Cialis®), also helped MSH in some people. And then there was the role of vasopressin too. Abnormal vasopressin, combined with low VIP and low MSH, was the most commonly seen combo in the worst patients. I called it the “hypothalamic trio” since vasopressin, a hormone we think of being made by the posterior pituitary, actually has important regulatory effects in (the suprachiasmatic nucleus) of the hypothalamus. (Editor’s note: don’t be confused by the fact that there are four names for vasopressin, including antidiuretic hormone, ADH and AVP. We can add arginine vasopressin as garnish to the synthetic form of AVP called DDAVP. They all (i) make the kidney hold on to free water and (ii) regulate the interaction of hypothalamic regulatory hormones MSH and VIP.)

If VIP was a big deal in controlling inflammation (it is), then could it be that even more important was the role of absence of VIP control of inflammation? As I saw it, deficiency of VIP was really no different than deficiency of insulin for a Type I diabetic. Give the Type I diabetic some insulin and he lives as normal person. What happened when people deficient in VIP took VIP? They got better. And just look at what VIP did to regulation of blood flow responses to exercise. Was this compound too good to be true?

As I learned just how important VIP was regarding regulation of inflammation, I also found that VIP could be legally prescribed as a compounded medication for people.

Here was another concern. The worst of the VIP deficient patients (and they always were mold patients first) were the multiple chemical sensitivity (MCS) people. Would VIP replacement fix most (even an optimist like me can’t realistically dream for all) people with chemical sensitivity, since VIP controlled the inputs of olfactory nerves in the master gland part of the brain, the hypothalamus? Let’s face it, while no one knows the cause of chemical sensitivity, every one of the chemically sensitive people I saw was dead low in VIP. Would fixing VIP fix the MCS?

As it turned out, yes. I think someone invented the “OMG” acronym of test message fame for this finding. But the benefits of the VIP didn’t accrue to those who still had exposure to WDB and/or untreated inflammatory problems. No magic potion there: the steps to correction of the illness had to be taken in order. No exceptions. Don’t say the drug didn’t work if you skipped steps.

Actually, the problem with patients with such complex illnesses that I see rarely can wait for one step at a time. Here is a real problem: patients who frequently have limited control of mood and limited ability to concentrate and limited ability to assimilate new knowledge have to be disciplined in their approach to a scientific aspect of medical intervention. Good luck.

For those who can adopt a scientific approach (as deep down I think those who don’t know they must), there is a transparent documentation of what is wrong physiologically; what happened with intervention; and what was done next. Follow this protocol through nine steps or ten steps or eleven steps and out comes a healed person.

But you’ve got to be out of exposure.

I have to tell you that there are people I see who say “I’m not better any more. CSM didn’t fix me like those people in the book.” My response is usually: “Did you have the ERMI test done?” No. “Did you remove yourself from exposure?” No.

Yikes. Am I being too aggressive here to say WHY NOT? And then if you don’t permit my use of a why question, then may I ask what in the world are you thinking?

This next item was a big one for me. Actually, the idea of reducing MASP2 activity underlies Surviving Mold. Stop the reactivity caused by autoactivation of MASP2 and the illness can go away. The idea is key for all those with C4a that went nuts after just a 5-10 minute exposure to a WDB (like mine used to). Would people become less reactive following exposure to WDB? This idea is crucial to everything I wanted to achieve in this 12 year odyssey of mold illness! Save the survivors from relapse! Can you imagine my excitement when C4a responses didn’t rise, telling us indirectly that MASP2 was sleeping, when a series of my initial VIP patients didn’t get sick with re-exposure?

Less reactive means no more “sicker, quicker,” after even trivial exposure. Instead, for the same exposure that hurt people so badly when their MASP2 was going on auto-pilot and they were exposed for just a lunch at a WDB restaurant (one open for business; who knew about the flood in the women’s bathroom three months ago), we would see a “tiny bit sick over a long enough time” and a trivial rise in C4a after the same exposure. If the inflammatory forces driving the illness were blunted, then the therapy needed to permit people to recover from the exposure to the WDB would be much less intense and much shorter in duration.

Here was a big concern. Years ago, my brother, Wells, a Stanford-trained pediatrician and now a consultant to a number of national health care reform think tanks, cautioned me to never be the first or last to use new ideas in medicine. I wasn’t the first to use VIP but for chronic fatiguing illness treatment with VIP was new. Did I know I was going to cause “No Harm,” as Hippocrates would have us swear to Apollo and Aeskepalus (not to mention Hygeia and Panacea)? Would treated people die immediately, grow three heads or become manic depressive or demented? Nope to all of those. In fact, so-called adverse events just didn’t happen with any rate over 2%. Would VIP cause antibody formation against the normal human form of the compound? Nope. How about exercise tolerance? Would people be able to do more, show less fatigue and suffer less delayed recovery from normal activity? Right, right, and right.

It all sounded too good to be true.

Was VIP replacement my panacea for those at the top of the “pyramid” of persistent illness?

Think about it: If I just knew the physiologic philosopher’s stone, I could stop the abnormal innate immune activation, restore regulatory control to a damaged system and provide a mechanism to correct all the damaged secondary phenomena found in chronic systemic inflammatory response syndromes (that would work for so many and not just for those ill due to mold).

I knew that Paul Cheney MD was seeing people with long-standing Chronic Fatigue Syndrome get better with stem cell replacements obtained out of the country (talk about being the first to try something!). I was seeing the same results from simple correction of the inflammatory pyramid and then adding the final touch of VIP. I knew that VIP was safe; was readily available through standard medical processes and didn’t cost arms and legs. Surely this was the Golden Age of treatment!

These are qualities for what the ideal mold survival drug would be that I dreamed about.

1. Available
2. Affordable
3. Effective
4. Safe

The ideal drug would

1. Stop excessive reactivity
2. Reduce inflammatory changes, especially C4a
3. Restore neuropeptide control to inflammation
4. Provide correction of secondary hormone problems involving vitamin D and androgens.

What I didn’t know to ask for in my dreams was that the same drug that would also

1. Lower TGF Beta-1
2. Raise VEGF
3. Raise MSH

VIP was all of those. Too good to be true!

After reading just about everything that Drs. Doina Ganea and Mario Delgado had written on VIP (and others too), I knew that VIP could restore neuropeptide control of inflammatory responses and thereby should bottle up the inflammation genie that was wreaking havoc on my patients.

Then I read that VIP deficiency affected just about every cell in the body by its role in regulating a vital cellular communication system tied to cyclic AMP (cAMP). This compound, called the second messenger, takes the signal coming from outside the cell to the guardian of the cell, the cell membrane, and then transfers the message to structures deeper in the cell, including the nucleus. If there were a receptor for VIP on the cell (and there are several kinds of VIP receptors), then cell function would be affected by lack of VIP.

Basically, messages from the “outside world” arrive at the outer membrane of a cell constantly. Some messages simply fail to be received; others are greeted as important and are ushered directly to the command center of the cell, the nucleus. The vast majority of chemicals are subjected to further processing using the “second messenger” system. The idea is that cell-to-cell signaling must be reinterpreted with a built-in delay mechanism. Events inside the cell contribute to signal-processing with cAMP having a key role. Since VIP regulated cAMP, then VIP had a key role in communications.

Having intracellular regulation and therefore, intracellular function depending on extracellular regulation (VIP) is a phenomenal concept. Can you just imagine correlates of human behavior if a whole person were like an individual cell: here is some Big Brother (VIP) basically deciding what outside messages will be successfully processed inside and therefore controlling what the cell does, by controlling the inside message system. We aren’t looking at outside control from some monolith; we are looking at cells freed to do what they are supposed to do. VIP jacks up cAMP such that those messages that involve cAMP are preferentially efficiently transmitted to the nucleus.

Hey, what about individual cell freedom? Forget about it. And what about freedom of choice? None. Poor cell; it is just a pawn in the game of life!

Just imagine if our enemies were able to disrupt each and every cell in our body by disrupting VIP physiology. Horrors! Frankly, this part of the VIP story is a bit scary because biotoxins do that every day to everyone who is genetically susceptible.

But the reality is that it isn’t our enemies that tears apart systemic regulation of systemic inflammation, not to mention cell communication for so many innocent people. It is our homes, our schools and our workplaces. Take it one step further, it is the people responsible for detection of indoor microbial growth in those buildings who are responsible. It is those people with the duty to clean up and repair properly in those buildings when the alarm is sent off saying there is microbial growth. Let us not forget the ultimate responsibility rests on those vested interests whose cash runs those moldy buildings. When they don’t order the maintenance or the correction and they run the cover-up, well, would you say that they are the real domestic terrorists?

Not everyone becomes ill from a moldy building, but when enough people lose VIP regulation from unopposed inflammation, we might have as well been attacked by some foreign terrorist using a handful of Aspergillus penicilloides with some Actinomycetes thrown in as an accelerant. At least if a foreign terrorist did the dirty deed we could have someone to blame besides the US Chamber of Commerce and State Farm (among other insurance companies) like we do now. But so far it isn’t a foreigner who is hurting so may people every day in so many buildings. Walt Kelly, creator of Pogo had his character tell us: “We have met the enemy and he is us.”

Having the chance to use VIP brought out some thoughts of free will and failed attempts to restore immune regulation form the past. Teach of these concepts would serve me well in taking the next step of use of VIP in an IRB approved clinical trial.

The Holy Grail

Still, VIP as a Big Brother concerned me. Command and control is needed for every military operation, every business operation and every family operation. And that’s the way it should be for a single entity too, as a person is the organized sum of a trillion (or so cells) acting as a coordinated unit and not just as a trillion independently acting units. The individual cell is out of luck. If it wanted to be free, like one-celled bacteria, one-celled fungi and one-celled dinoflagellates, it should have picked different parents!

Imagine if we had a regulatory behavioral system for each entity in a human population. We would lose diversity of response to external methods acting as clone instead. George Orwell and Aldous Huxley worried about loss of individual freedom, as have countless Sci-Fi writers. But an individual must act as a sum of cloned cells because we ARE! Every one of our cells starts with the exact same genetic information. We must have our big brothers, regulatory hormones such as VIP, or we die.

What a curious spin on the idea “Do as I say, not as I do,” for we talk about individual freedom but live as a tightly message-controlled compilation of individual automatons.

Just look at the free-swimming bacteria, an idyllic one-celled creature, swimming in a planktonic pool of life. No controlling Big Brothers, no limit to what its DNA can do-and no limit to how quickly the helpless little fellow can be killed in the hard life that is reality for such small “primitive” creatures. Imagine having to breed every twenty minutes just to keep your DNA flowing to offspring. Maybe Big Brother doesn’t sound so bad. If one or two bacteria had Chronic Fatigue and was too tired to reproduce, they would die.

Or consider one way the planktonic bacteria can rest a bit in the struggle for life. Imagine if individual cells traded individual freedom to live in a community-one that provided safety and security as the struggle to find food, drink and places to reproduce and raise young was assured. Sound like a good plan?

Bacteria live just this way in biofilm. Each individual cell sacrifices freedom for security. Each is a clone of its neighbor but doesn’t necessarily act like a clone because DNA messaging, the response to extracellular messaging, has another layer of regulation built in. Differential gene activity means some DNA is activated, open for business-and some isn’t. Such differences in gene activation provide the biofilm bacteria with an extra margin of diversity that in turn adds safety, enhanced productivity and reduces the demand for constant reproduction to ensure survival. Biofilm communities are still a collection of single cells and aren’t a multi-cellular organism.

This fundamental biological difference between a single cell pulling one oar versus a multi-celled creature pulling multiple oars simultaneously is associated with a change from no Big Brother to presence of a Big Brother. If we want our oared trireme vessel to perform better in the seas of life, we could add more levels of rowers, more kinds of oars and more ways to row. All of these activities demand more command and control-more Big Brother.

A simple question follows: did the fundamental leap from a single-celled creature to a multi-celled creature only occur after Big Brother arrived?


MSH is just such a Big Brother. It is long been known to be part of the primordial innate immune system. MSH is manufactured deep in the hypothalamus (among other areas) in some of the evolutionarily oldest pathways of control of hormone activity, inflammation activity and nerve functioning pathways. If MSH production is impaired and it usually is in mold illness patients, patients don’t have an important Big Brother. Without command and control, individuals lose coordinated responses of hormones, inflammation chemicals and nerve response. And yet, despite such foul-ups we don’t die. We need MSH for a good life but absence isn’t fatal.

Restoring MSH production should lead to better control of hormonal function (it does); better control of inflammation (it does) and nerve function (it does that too). Simple examples of the importance of MSH deficiency are the hypothalamic symptoms of mood swings, appetite swings, sweats (especially night sweats) and loss of control of regulation of body temperature (always hot; always cold; fluctuating from hot to cold). Given the importance of MSH deficiency, having access to replacement MSH should be followed by new life with green grasses replacing dusty, fallow fields and fullness of command and control creating a biologically unified entity, thriving with Big Brother at the helm.

So when I asked the FDA for permission to use MSH in people, I thought of the benefits of giving insulin to those with Type I diabetes and giving thyroid hormone to those without it. My Holy Grail became MSH, for with restoration of MSH restoration of functional life would follow. The solution to nearly all chronic fatiguing illnesses was just around the corner. I only forgot one thing.

The FDA hadn’t approved MSH approved MSH for human use. Oops. The FDA was perfectly willing to let me use MSH once I submitted the animal data they needed complete with toxicology studies, cardiovascular studies and more. I could have my Grail and use my Big Brother for the benefit of so many millions who needed it just as soon as I satisfied a real Big Brother-the FDA-that my idea passed their regulatory requirements.

So my naïve ideas fell flat. No wonder the big drug companies had to spend so many millions of dollars to bring drugs to the market. Surely there would be an answer to the MSH problem.

MSH deficiency
Wandering in the Wilderness

Back in 1999, fixing MSH deficiency became a new purpose. If I couldn’t just overwhelm the inflammation resulting from MSH deficiency with armies of replacement MSH, the first step was to stop the process that destroyed the MSH production process. That idea makes sense but what are the destroying factors? Inflammatory cytokines that bound to leptin receptors in the brain would block production of MSH, so fix the inflammation.

But correcting inflammation didn’t always result in MSH production. MSH is vulnerable to attack from exotoxins too. Made by unusual, biofilm forming coagulase-negative Staph species, exotoxins are proteins that cleave MSH, effectively destroying it. The MSH/exotoxin battle was epic, if biological warfare on a cellular basis can be called epic. If MSH is present, the biofilm is destroyed and the Staph species vanish from their sanctuaries on mucus membrane surfaces deep in the nose. Without MSH, the Staphs quietly thrive, protected by their igloo-like biofilms from other mucus membrane defenses. So the strategy was straightforward: Compounds released by MARCoNS could destroy MSH, so get rid of the MARCoNS.

But what about the sources of the inflammation, namely exposure to the interior environment of WDB? As it turns out, this step must be the first. Use Welchol or CSM, without fail.

As it turned out, way back then, finding the source of MSH destruction unveiled basic mechanisms of the innate immune inflammatory responses that kept patients chronically fatigued. Their cognitive symptoms that others assumed to some sort of mental illness were no different. Fix the inflammation and the cognitive aspects cleared. MSH controlled inflammation until inflammatory responses overwhelmed the MSH production mechanism. Like wolves caged to protect the cage-keeper from being supper, once freed from control, the inflammatory process turned on its controller providing more freedom from control. Inflammatory anarchy, if you will. No big Brother.

By 2002 we knew that MSH deficiencies didn’t guarantee a terrible clinical prognosis, just a tremendous risk for development of illness if and when another exposure occurred. Having no MSH was an open invitation for unchecked inflammation in lung, GI tract, skin and anywhere blood circulated.

By 2004, we knew that a group of patients especially didn’t show the expected improvement in MSH. The people had the now infamous HLA of 4-3-53 or 11-3-52B (less commonly 13-3-52A and 12-3-52B as well). There was just something awful about those HLA haplotypes; I called them the dreaded, as I dreaded seeing them. Just why these haplotypes are dreaded still isn’t clear though TGF beta-1 is woven into the answer (see chapter 3)

And yet, even allowing for ongoing exposure, ongoing inflammation, colonization with MSH-splitting biofilm-formers and genetics there was another missing factor-there has to be something else had to be keeping MSH low. The answer didn’t come until 2005: VIP.

2005: Enter VIP

The name, vasoactive intestinal polypeptide, doesn’t give one much more than a few clues that VIP was a big deal in the body’s inflammation regulation business. Who would think such a non-descript protein would become so “magical” in restoring life to those with ongoing chronic fatiguing illnesses and lack of regulatory control of innate immune responses.

That VIP deficiency turned out to be really common in those with mold illness shouldn’t now be much of a surprise. People who weren’t sick, those without chronic fatigue and without a multisystem, multisymptom illness had normal levels of VIP. As the work of researchers like Drs. Ganea and Delgado made clear, global beneficial effects of VIP replacement on inflammation and cell physiology followed its use in the test tube and in animals. There was a developing literature of studies done in animals that when taken as a whole supported the entire idea that VIP was a master controlling peptide, similar in overall magnitude to the importance of MSH.

Question: Was VIP the missing link to refractory MSH?

Answer: You bet!

By 2006 we knew that VIP MSH and mutually regulated each other and that improvement in levels of one of the two peptides improved the other. When the additional role of antidiuretic hormone (ADH, also called vasopressin) became clear as the third member of the hypothalamic regulatory triangle, we knew that with improvement of any one of the three helping with deficiency of the other two, we had a “system” approach to regulation. Looking at either MSH or VIP as an integral part of a systemic whole was exactly correct.

As we can now predict, the ongoing model of lack of regulation of systemic responses failed if we only looked at one regulatory element. When we look at all three (VIP,MSH, ADH), the model worked precisely. I started calling this hypothalamic triumvirate the “three-legged stool,” as cutting one of the three legs resulted in the fall of the chair. Similarly, if the lack of inflammatory regulation was due to lack of repair of any one of the three key hormones regulators, the risk of rapid reacquisition of illness with re-exposure increased rapidly.

The scientific literature provided guideposts for me in this research but the only solid human data that I could rely on came from my patient practice. It didn’t take data sets from 2000 patients to see the simple patterns of MSH, VIP and ADH, yet the strength of my data sets came from the countless repeat examples of what I write here. The systems approach, also called a landscape approach, gave intelligible answers to complex questions. I insist to this day that no clinical intervention be a multiple: do one thing at a time. Yet I also insist that each result of any single intervention be analyzed systemically.


VIP as part of systems analysis


If inflammatory responses were going wild in mold illness (they were) and lack of regulation of inflammation let those inflammatory responses go wild (they did), then systems analysis predicted that (1) correction of the source of inflammation followed by (2) correction of the excess of “downstream” inflammatory compounds, followed by (3) maximal normalization of MSH and ADH/osmolality would lead to a single targeted therapy using VIP. “It will work,” said the all-encompassing model. If I had the right to use VIP (I did) and I knew the dose of VIP to use (I did) then restoration of regulation should work rapidly.

It did.

Too Good to be true

We began before Thanksgiving, 2008. We could give VIP by nasal spray. VIP is broken down quickly so the risk of over-dosage is basically non-existent. If we gave the drug four times a day, as the Europeans had done, we should see improvement in inflammation, reduce exercise tolerance and improved joint symptoms almost overnight.

We were wrong. The beneficial effects, including reduction of cognitive problems appeared in 15-minutes.

Side effects? Nothing occurred in more than 2% of our first hundred patients.

Benefits? At least 95% had dramatic improvement in essentially all modalities.

Reducing inflammation? Yes, C4a and TGF beta-1 fell.

Adding control? Yes, ADH/osmolality improved, as did MSH.

How about vitamin D, the new buzzword compound in chronic fatigue? For the relatively small number with problems, benefits accrued that vitamin D replacement (and its specific compounds, especially vitamin D3) hadn’t corrected.

How about androgen problems? The enzyme aromatase, one that converts testosterone to estradiol, is blocked; androgens rise, estrogens return to normal but we don’t see too much androgen or too little estrogen.

Over time, patients decreased the dose of VIP to two sprays a day and then to one a day. A few no longer use VIP, except as an urgent drug for acute exposure or one used in preparation for exposure or exceptional exertion.

“I had a hit yesterday so I went back on my VIP for a while. I know how to use it now. For me, its like Tylenol and a headache. I will never be cured of all headaches, but if I get one, I take a Tylenol and go on with my life.”

Can you imagine VIP as “Tylenol”?
Just ask Sisyphus

Basically, VIP brought me to even consider a four letter word for chronic fatiguing illnesses, especially mold illness. The word is one I haven’t used in my life for this illness until now: Cure.

Here has been my medical mountain: cure. How I labored (as do many others) as Sisyphus. We pushed our interventions up the mountain as did the tortured mythological Greek figure, only to see the results of our labors dashed as the boulder of Sisyphus bounds back done the hill. Like Sisyphus, however, we as treating physicians don’t have the luxury of NOT pushing the boulder back on the mountain.

And this time the boulder stayed up! Imagine my joy, my utter ecstasy seeing VIP do what it can do! I felt like a proud parent whose child was marching at the head of the parade.

Oh, I needed to tell my friends and my colleagues.

“What is VIP”? The boulder was again on my back.

“Great, I’ll just use VIP first, before all those other steps are finished. My patient has been so sick for so long, we can’t wait. Besides, I really am uncomfortable doing all the things you say I have to do.” Boulder #2 is on my back.

“I’m going to dose the drug differently, because I think so and I don’t care about mold exposure.”

Boulders 3-10 now loading on Sisyphus’ back. And the mountain just got higher.

“I used VIP twice a day, and not only didn’t I get a cure, I felt even worse.” Here’s the rest of the mountain of boulders on my back. We know that mold exposure, hidden or obvious, MUST be cleared before using the drug. In fact a rise in TGF beta-1 and/or C4a after a test dose of VIP is warning to look for hidden exposure. And don’t skip the diagnostic test dose either.

“Oh, I use VIP for headache; and I use it for menstrual cramps; and I use it for my androgen deficiency; and I use it for…” I guess it is human nature to abuse whatever good new thing comes along. And I guess it is human nature to be creative and independent about exciting new therapies, so I really shouldn’t be complaining about misuse of VIP by fellow physicians. Still, I worked so hard for nearly five years to bring this golden goose to life that I don’t want to see someone cut off the head of the golden goose just because he thought it might be a good idea.

What would you do?

When the Alaska Gold Rush Boys (Juneau, Harris and Chief Keowa) announced their Bonanza find, the four letter word spread like Oklahoma wild fire: Gold. Soon there would be an endless string of men climbing Chittook Pass in the snow, waiting for the ice to melt to let them into the Yukon Gold fields.

How was this overwhelming wave of human demand going to be different for my four-letter word: Cure.

So our group decided to wait. Deficiency of VIP had to published. It had to be studied (it is) and it had to be controlled. We had to do a double blinded study and we had to publish those data. Hiding Juneau’s find of the yellow riches wasn’t easy; enforcing another four-letter word (wait) wasn’t easy either.

People stole the gold. They killed others in the hope of having the gold. More gold became a yellow fever that gripped a nation’s poor, the desperate and the shrewd. Was my fear of the dead golden goose historically incorrect?

Our study will be finished soon, with collaborating physicians in several places in place. We will have our good science and our good studies, all approved and in order. There is no room for error, as when used exactly as our protocols require, we shown the restoration of life to those with VIP deficiency and metabolic inflammatory disasters. They change from being the walking dead to what they were, though with a loss of time and a host of scars to show for their journeys.

We will continue to look at the top of the pyramid, for biology is an unforgiving discipline. Just when I think we have reached the top of the therapy mountain, we will find some other unexplored rocky height above us that was hidden by perpetual clouds, but was there all the time.

So, we’ll just try to figure out how to get up the next cliff, even if the way isn’t clear at first.

And in the end, I’ll trust science in its purest form to show me the way.

RShoemaker, MD
Pocomoke, Maryland