How to Practice Environmental Medicine

Abstract

As the research foundation documenting the major role of toxins in most chronic diseases continues to grow, clinicians are facing the challenge of having to learn how to practice environmental medicine. The great diversity of toxins and their damaging effects, the uniqueness of each person’s biochemistry greatly affecting susceptibility, and inconsistent clinical presentations complicate making sense of this field. Recognizing that there appear to be essentially 3 types of patients suffering environmental damage helps organize how to think about, diagnose, and treat these patients. In this editorial, I propose 3 categories: (1) “Yellow Canaries,” (2) patients with clear toxin exposure, and (3) patients suffering most any chronic disease.

Toxins Now the Primary Drivers of Chronic Disease

The very first class taught at then-named John Bastyr College of Naturopathic Medicine was “Health Effects of Environmental Pollutants.” This was a very challenging class for me to teach, as all available textbooks only covered industrial exposure and very strongly asserted that these toxins affected only highly exposed workers and were not a problem for the public. Having seen many patients in my clinic suffering from metal or chemical toxicity, people I now describe later as “Yellow Canaries,” I knew that these toxins were indeed causing much more human and environmental damage than conventionally accepted. I spent countless hours pre-PubMed walking the journal stacks at the University of Washington School of Medicine searching for population-based research on how these toxins being released into the environment were causing disease. Frustratingly, except for lead, there was virtually no research. This has dramatically changed in the past 20 years.

I have now written many IMCJ editorials documenting step by step that environmental toxicants, endogenous toxins, and what I call “Toxins of Choice” have now become the primary drivers of chronic disease. I am not saying that nutritional deficiencies/excesses are not significant causes of disease. Rather, we have added an even more serious cause of disease, and toxin load is getting worse. After having reviewed several thousand articles, run thousands of laboratory tests to assess toxic load, and treated both directly and indirectly (through corporate wellness programs) thousands of people suffering the effects of toxins, I thought it important to step back to see the big picture. I think a key reason acceptance of environmental medicine has been slow is due to the wide diversity of the clinical presentations, each of which requires fundamentally different understanding, assessment, and intervention. After deeply thinking about this, I believe there are essentially 3 categories of patients suffering the effects of toxicity:

1. The “Yellow Canaries.”

2. Patients with clear toxin exposure.

3. Patients suffering most any chronic disease.

Categories of Patients Suffering the Effects of Toxicity

Yellow Canaries

Presentation

These are the patients who appear to have formed the core population that inspired the practice of environmental medicine. They present as chronically unwell for no apparent reason. Their toxin exposure does not appear unusual but can be elicited with rigorous history. They may be early enough in the pathophysiological process that overt disease may not yet be present. Basically 6 dysfunctions appear—alone or in combination—that explain why these individuals are experiencing much greater damage from toxins than others:

1. Inability to detoxify chemicals in Phase I.

2. High active, or possibly average active, Phase I with inadequate Phase II.

3. Impaired ability to synthesize glutathione.

4. Inability to upregulate glutathione recycling in response to toxins.

5. Inability to effectively excrete metal toxins.

6. Poor non-glutathione-dependent antioxidant defenses.

They may also have multiple unrecognized low-level exposures that alone do not explain their problems, but together overwhelm their ability to detoxify or protect. The key laboratory tests:

RBC glutathione: Low

GTTP: <25 units

The key single nucleotide polymorphisms (SNPs) to evaluate are as follows: glutathione synthesis, glutathione recycling (GGTP), Phase I, Phase II.

Following are the SNP results I found in one such patient. As can be seen, normal Phase I, but poor Phase II and inadequate glutathione function. (These are the reports from the SaluGenecists artificial intelligence system interpretation of SNP results.) This means the patient has elevated levels of the more toxic intermediate metabolites, as Phase II cannot clear them quickly enough. Furthermore, with inadequate glutathione production, this individual is unable to protect against oxidative and other damage.

Intervention

Intervention for all groups starts, of course, with avoidance. However, these patients must be far more careful to ensure as clean as possible air, water, food, cooking, storage, health and beauty aids, and yard and house products—in other words, exposure to toxins from all these potential sources must be aggressively minimized. As discussed previously, a key problem is the buildup of the much more toxic activated intermediates when they are not being conjugated fast enough by Phase II neutralization. Neutralizing the activated intermediates and improving Phase II conjugation are crucial. (Some clinicians also suggest slowing Phase I, but I am not ready to embrace this approach.) In addition, increasing glutathione levels is very important, and effectively absorbed glutathione should be provided preformed (topical or liposomal) as de novo synthesis may be impaired. Most important foods are berries and cabbage-family foods.

Patients With Clear Toxin Exposure

Presentation

While technically this includes those industrially exposed, there are many who have nonindustrial exposure and may not appreciate the impact on their health. Examples include people with a mouth full of so-called silver fillings (which are actually 55% mercury); the addicted sushi eater; or the person living or working in a ZIP code with drinking water known to have elevated levels of arsenic (at least 10% of public water supplies), pesticides if in a farming area, and industrial chemicals if the water supply is contaminated, such as seen in fracking or leaking from manufacturing plants into the watershed. Depending upon the duration of exposure, the individual’s ability to detox and ability to protect from damage, while the exposure may be obvious, overt chronic disease or persistent significant symptom may not yet be present. Timelines can be very helpful.

Also, a very significant consideration is that most of the research looking at chronic, low-to-moderate exposure does not show significant clinical indications until around 45 to 50 years of age—a typical example of the body adapting and adapting until the damage to physiological systems and DNA have accumulated to the point adaptation is no longer possible, and the damage starts to quickly manifest.

There may be no symptoms, and the patient may have won the SNP detoxification sweepstakes, but for everyone else, toxin load is real and the time bomb is relentlessly building. If exposure to specific toxins is known, directly measure, first to confirm correct diagnosis and then to monitor intervention efficacy. For current exposure, blood and urine labs are usually effective for most metals and chemicals. However, arsenic needs to be measured in toenails as arsenic’s half-life is only 2 to 4 days. For past exposure, challenge testing may be needed to determine body load. Unfortunately, no accepted gold standard yet exists for body toxic metal load.

Figure 4 shows the results of testing of a 50-year-old Japanese man who smokes heavily and eats sushi almost daily. The first morning urine does not look too bad. But challenge testing (300 mg DMPS + 500 mg DMSA and collecting urine for 6 hours) shows significant toxic metal load. At the time of this test, he was at the early clinical transition stage showing measurable, and increasing, loss of brain function, which he was rationalizing as a “normal part” of aging. Nonetheless, he was astute enough to realize that perhaps there was another perspective.

Figure 4.

First Morning Urine

In addition to assessing toxic metal load, chemical exposure needs to be assessed as well. Measuring persistent organic pollutants (POPs) in the blood will give a reasonable estimate of fat load if adjusted for lipid levels. For the majority of individuals, the ng/mL of a POP in the serum comes directly from lipid turnover.¹

Intervention

Avoidance is much easier with these patients as the toxin and its source are known. The intervention depends, of course, on the toxin. Detailed guidance for each toxin/toxin class is a large topic and beyond the scope of this editorial.

Patients Suffering Most Any Chronic Disease

Presentation

As I have discussed in many of my IMCJ editorials, the research on the substantial contribution of environmental toxins to virtually every chronic disease is growing rapidly. Table 1 shows the diseases most caused by toxins. However, this list may be an artifact of which diseases have been most studied at this early stage of population-toxicity research.

Table 1.

Chronic Disease With Significant Contribution From Toxins (Ordered Alphabetically)

Bone and joint	Gout, osteoarthritis, osteoporosis, rheumatoid arthritis
Cancers	Breast, lung, pancreatic, prostate
Cardiovascular	CVD, hypertension, myocardial infarction, stroke
Endocrine	Adrenal dysfunction, diabetes, infertility, obesity, hypothyroidism
GI/GU	NAFLD, NASH, kidney failure
Immunological	Allergy, autoimmunity, chemical sensitivity, chronic infections
Mitochondrial	Chronic fatigue, early aging
Neurological	ADHD, autism, cognitive loss, dementia, headache, mood disorders, Parkinson’s disease
Respiratory	Asthma, COPD

Chronic exposure to a wide range of toxins undermines physiology; depletes antioxidants; and progressively damages DNA, cells, and tissues. Significant symptoms do not manifest until sufficient damage has accumulated. Table 2 shows which are the most likely damaging toxins for each condition. All of these are drawn from the new textbook I just wrote with Walter Crinnion, ND: Clinical Environmental Medicine. It will be released by Elsevier in June 2018.

Table 2.

Toxins Most Important for Common Chronic Diseases (Ordered Alphabetically)

ADHD	Lead, DDT, Hg, organophosphate pesticides, PAHs, PCBs
Adrenal dysfunction	Alcohol, cigarette smoke, drugs, chlorophenols, organochlorine pesticides, organophosphate pesticides, air pollution, PCBs, pyrethroid pesticides, salt, Pb, Cd, Hg
Autism	Insecticides, phthalates, air pollution
Cancer, bladder	As, Cd, PCBs
Cancer, breast	Cd, PCBs
Cancer, lung	As, Cd, DDT, PAHs
Cancer, pancreatic	As, DDT, PAHs
Cancer, prostate	As, PAHs
Cognitive loss	Vehicular exhaust, phthalates, organophosphate pesticides, metals, PCBs
CVD	Vehicular exhaust, PAHs (tobacco smoke), PCBs, BPA, phthalates, Pb, Hg, Cd, Hg
Dementia	Air pollution, mercury, pesticides
Diabetes	As, POPs (as a class), phthalates, polycyclic aromatic hydrocarbons, BPA, PCBs, dioxins, organochlorine pesticides
Gout	As, Pb
Hypertension	PCBs, Pb, Hg, As
Hypothyroidism	Organochlorine compounds (PCBs, DDT, dioxins), pesticides (chlorinated, organophosphate), Hg, Cd, perchlorates, PBDE, perchlorate, phthalates
Infertility, female	Chlorinated pesticides, PCBs, organophosphate pesticides, BPA, herbicides, solvents, Hg, Cd, trihalomethanes, PFOS
Infertility, male	Phthalates, PFOS, PBDE, PCBs
Mood disorders	Vehicular exhaust, phthalates, organophosphate pesticides, metals
Myocardial infarction	Vehicular exhaust, PM2.5, PCBs, PAHs, BPA, Hg
Osteoarthritis	General toxic load
Osteoporosis	Cd, salt, wheat, prescription drugs
Parkinson’s disease	Pesticides, lead
Rheumatoid arthritis	PCBs
Stroke	PM2.5 (and the other toxins noted above that damage the cardiovascular system)

Several conventional lab tests are helpful in determining which patients have the heaviest toxin load. The most useful according to current research are listed in Table 3. These tests are elevated within the normal range in proportion to toxin load. They reflect either adaptation to toxin (GGTP recycles glutathione to help with detoxification and neutralization of free radicals) or physiological damage (8-OHdG is a measure of DNA damage).

Table 3.

Conventional Laboratory Tests Showing Elevation in Proportion to Toxic Load^2,3,4,5

GGTP	Alcohol, lead, mercury, smoking, OCPs, PAHs
ALT	Cd, Pb, Hg, PCBs, PAHs and PFOAs
Uric acid	Perfluorinated hydrocarbons
8-OHdG	DNA damage

GGTP is especially of interest as it increases in proportion to almost all toxins and oxidative stress. Alcohol, lead, mercury, smoking, OCPs, PAHs, and others induce GGT in proportion to exposure. It is important to watch for false negatives in the approximately 10% that genetically do not upregulate GGT in response to toxins and oxidative load. (I suspect that these, however, are most likely in the Yellow Canary category.) I think it is not surprising that GGT levels correlate with risk of death.⁶

Measuring POPs in the blood will give a reasonable estimate of fat load if adjusted for lipid levels. For the majority of individuals, the ng/mL of a POP in the serum comes directly from lipid turnover.

Intervention

While intervention always starts with avoidance, the intervention can be optimized by first measuring the toxins most associated with the presenting chronic disease and then designing an elimination protocol for those found to be elevated.

As POPs play a significant role in many diseases, clinicians must ensure their patients realize that elimination is slow (half-lives measured in years and even decades), meaning clinical improvement will take months of detoxification work.

Of great importance, while some toxins will be identified as being at the highest level or the most serious for the person’s unique biochemistry, these patients typically have a substantial body load of many toxins. With my patients, I first prepare their elimination systems for toxin breakdown and elimination before doing anything that will increase release of toxins from the tissues. This means gut, liver, and kidneys must all be functioning well and not being overloaded by any controllable toxin. Examples include chronic antibiotics disrupting the gut, causing loss of permeability control; heavy alcohol consumption depleting glutathione in the liver; and NSAIDs causing oxidative damage to the kidneys.

Conclusion

I have tried to step back and think about the big picture of how toxic damage is manifesting in the population. I am extremely interested in the thoughts of the heroic, pioneering clinicians who for decades have worked, despite many challenges, to develop and practice this emerging field of environmental medicine.

In This Issue

As the United States struggles with the continuing health care crisis, associate editor, David Riley, MD, asks us to think more broadly about the problem. Specifically, the many nonprofessionals providing daily care to family members with disabilities. The price they pay in loss of their own health is a huge issue that requires more attention.

Another associate editor, Jeffrey Bland, PhD, discusses chronic fatigue syndrome and how it is a good example of how functional medicine provides a strong model for understanding and helping patients suffering this enigmatic condition. I especially appreciate his comments on the important roles of Paul Cheney, MD, PhD, and Scott Rigden, MD, in developing functional medicine. I know I learned a lot following their work as they identified and then unraveled this challenging condition.

John Weeks covers several emerging stories on how nonpharmacological approaches are being very seriously considered as a solution to the opioid abuse epidemic. I join John in mourning the loss of our friend and natural health product pioneer, Bill Brevoort. He and his wife, Peggy, through East Earth Herbs, played a major role in bringing Chinese herbal medicines to practitioners and the public. Rest in peace my friend.

Managing editor, Craig Gustafson, interviewed David Rakel, MD, about his ideas on how technology will affect the practice of medicine. I fully concur with his message that the huge inundation of research and data is impossible for a clinician to handle, let alone understand, without access to the right information systems and decision support tools.

Very interesting original research by Prashanth Shetty, BNYS, MSc, PhD; Kiran Kumar Reddy B, BNYS, MD; D R Lakshmeesha, BNYS, MD; Shiva Prasad Shetty, BNYS, MSc; Selva Kumar G, BNYS; and Ryan Bradley, ND, MPH, on the impact of teaching yoga breathing and posture exercises to patients with elevated blood pressure. I doubt any reader of IMCJ will be surprised to learn they demonstrated statistically significant improvement on all measures of hypertension.

Long-time readers of IMCJ know that we have published many articles and editorials on natural health product quality control. Michael D. Levin contributed our very first article on this important topic over 15 years ago. In this issue, he joins colleagues Carolyn A. Lammersfeld, MS, RD; Paul Reilly, ND; Joseph W. Coyne, RPh; Timothy C. Birdsall, ND; and Maurie Markman, MD, in describing their work in developing a formulary for cancer patients. Hard to think of any group more susceptible to poor quality or contaminated therapeutic health products. A must-read article on a topic critical for the advancement of this medicine.

We publish the seventh part of our ongoing series on probiotics in this issue. Jessica M. Pizano, MS, CNS; Christy B. Williamson, MS, CNS; Keren E. Dolan, MS; Crystal M. Gossard, MS, CNS; Cathleen M. Burns, MS, RD; Margaret G. Gasta, MS, RDN, CCN; Heather J. Finley, MS, RD, LD, CEDRD; Emily C. Parker, MS, RD; and Elizabeth A. Lipski, PhD, CNS, CCN, BCHN, IFMCP, review the research on probiotics and immune disorders.

Megan Vissing, MD; Chase Wilson, MD; Nico Mousdicas, MD, MBCHB; and Stefanie Ali, MD, provide us a case report on using comprehensive integrative medicine for treating a patient suffering from recalcitrant rosacea. I think a key takeaway is recognizing the patients we see are complex and likely suffering more than the most apparent problems. To paraphrase one of the deep insights of functional medicine pioneer associate editor, Sid Baker, MD, “When a patient is sitting on 2 tacks, removing 1 does not make them feel 50% better.”

Managing editor, Craig Gustafson, also interviewed assistant editor, Patrick Hanaway, MD, 2017 Institute for Functional Medicine Linus Pauling Award recipient. The story of his progression to functional medicine is fascinating, and, I suspect, will resonate with many subscribers to IMCJ. His work at the Cleveland Clinic is pioneering and will eventually revolutionize medicine.

Associate editor, Bill Benda, MD, finishes the issue with the other side of computers in medicine. Mr Dylan had it right.

Finally, congratulations to Dugald Seely, ND, MSc, winner of the Hecht Foundation Dr. Rogers Prize for Excellence in Complementary and Alternative Medicine. I believe this is the first time in North America a naturopathic doctor has won such a major award.

Joseph Pizzorno, ND, Editor in Chief

drpizzorno@innovisionhm.com

http://twitter.com/drpizzorno

Figure 1.

Normal Phase I SNPs

Figure 2.

Slow Phase II SNPs

Figure 3.

Problems With Glutathione SNPs

Figure 5.

Challenge Test Results

Biography