February 4, 2015

2015 SpiritMed Annual Updates in Environmental Medicine Conference

A report from St Petersburg, Florida
A report from the annual SpiritMed environmental medicine conference, held January 15-18, 2015, in St Petersburg, Florida.
The annual environmental medicine (EM) conference known as SpiritMed was held January 15-18, 2015. SpiritMed is the organizational manifestation of the desire of Walter Crinnion, ND, to educate healthcare providers on EM. He started the organization in 1999 and a year later began offering a 6-month training programs. As the number of graduates who completed this training program increased, it became apparent that some form of update and advanced training was necessary. 
The first SpiritMed update was held in January of 2012 at the Southwest College of Naturopathic Medicine, Tempe, Arizona. That year’s conference theme was “Immunotoxicity,” which was followed in 2013 by the theme “Environmental Impacts on Fertility, Fetal Development and Children’s Health.” In 2014, the conference focused on “Neurotoxicity.” For the 2015 conference, the topic was billed as “Environmental Impact on Stem Cells, Aging and Chronic Illness.”

Conference Details

The 2015 conference was held at the Tradewinds Resort in St Petersburg, Florida, a beachfront location that allowed attendees to get sand between their toes (or in their socks) between lectures. 
The conference was 4 days long, starting early on a Thursday morning and running through lunch Sunday. EM attracts practitioners who are comfortable interpreting statistics, talking about percentiles and quintiles, and noting difficult-to-see associations between very small amounts of material and long-term health outcomes.
During the conference, Crinnion told me, “Since naturopathy holds dear to the principle of tolle causam [remove the cause], it is critical to provide to our colleagues the symptomatic picture of toxicant-induced illness so that we may all properly address the main underlying cause (or causes) of disease.” For much of the conference, Crinnion took turns at the podium with Lyn Patrick, ND. The exception was Friday, when 5 guest speakers presented. 
Crinnion takes a special interest in recruiting speakers and told me, “I always seek to bring in the speakers I would want to sit in a room with and learn from. I also am trying to build a solid EM community and push EM forward. I am always trying to bring new docs up-to-speed in EM with the hope that they will run with it and come back to be one of my teachers. ”
Day 1 of the conference was an overview of how heavy metal treatment has evolved, with a focus on the state of the science. Day 2 brought in the guest speakers, not all of whom were directly focused on EM but who all had interesting things to say nevertheless. Joe Purita, MD, reviewed the use of platelet-rich plasma injections, stem cells, and other cutting-edge therapies. Andrew Campbell, MD, spoke about how environmental factors trigger autoimmunity. He provided somewhat shocking results from years of antibody testing that suggest a fair number of substances that we consider toxic may also be the target of antibody reactions in a subpopulation of patients. Devaki Lindsey Berkson, DC, spoke on endocrine-disrupting chemicals. Paul Anderson, ND, spoke about his experience treating patients with complex problems in methylation, genomics, and chemical sensitivity. He shared his wisdom on how to approach these difficult cases. David Quig, PhD, vice president of Doctors Data, Inc, brought the discussion back to EM when he reviewed the zebras of the heavy metal world, those lesser-known metal toxicities of which we should nonetheless be aware. Crinnion shared his current thoughts on measuring oxidative DNA damage and expanded on the tests he uses to assess damage and measure progress during treatment.
On day 3, Patrick updated us on the current state of affairs with the oil industry’s new techniques for fracking, reviewing the legal loopholes and exemptions from the Clean Water and Clean Air Acts that allow the industry to operate seemingly without regulation, oversight, or legal responsibility. She then examined the range of health effects associated with the different aspects of fracking, from drilling to extraction, and the various pollutants fracking releases into the air and water. She even covered the growing problem caused by open-pit sand mining in Michigan and in particular the increased risks of silicosis brought on by the high demand for fine sand for use in the injection mix. Patrick shared some of her own story about living in Paonia, Colorado, which has become ground zero for high levels of methane pollution caused by fracking.
There is no way to summarize even a fraction of this information here, so I will share just a morsel or 2 from what in total was an overwhelming amount of information.
This lecture was probably the most upsetting and at the same time the most moving lecture of the conference. It wasn’t just that it warned us of a multitude of dangers, but rather because it was in part a personal story of 1 person’s relocation to Paonia only to discover that the town had turned into the toxic epicenter of the fracking activity currently plaguing Colorado. 
Both Crinnion and Patrick teamed up to evaluate current knowledge about how to treat solvent toxicity.
Day 4 focused on environmental cardiology, looking first at the effect of metals on cardiovascular disease (CVD) and then on the role other toxicants have. The conference concluded with a lecture by Woody Merrell, MD, on integrating the concepts of EM into a standard medical setting and then a lecture by Fiona Crawford, PhD, on treating Gulf War illness and the environmental exposures related to the neurodegeneration we see in this patient population.

My Conference Takeaways

There is no way to summarize even a fraction of this information here, so I will share just a morsel or 2 from what in total was an overwhelming amount of information. These few ideas stood out.


The conference really drove home the importance of using the correct terminology when diagnosing and treating patients with problems associated with unusual toxic metal burdens. Metal toxicity is defined as high levels of metal in the blood. Finding elevated levels of metals in the urine, particularly in urine postprovocation with a chelating agent, has nothing to do with this standard definition, so we cannot employ that terminology in charting or billing. Practitioners and patients should not be told that urine tests diagnose toxic levels of metals. Doing so can lead to disagreements between practitioners and regulatory boards. Retention and accumulation of toxic metals is not toxicity. The latter is defined by signs and symptoms caused by this burden. If this sounds like splitting hairs, it is because there has been some pushback in recent years from some medical groups about what we have been doing and saying. 
Speaking about careful wording, what we do with these patients no longer has much to do with metal chelating; rather, it is more correctly referred to as “metal decorporation therapy.” This brings up the fact that the worldview held by most naturopathic physicians—and in particular those doctors involved in this specialty of EM—differs in many ways from mainstream practicing toxicologists. The American College of Toxicology would appear to be waging a serious public relations campaign against many of the ideas espoused at this conference. 

8-hydroxy-deoxyguanosine test

The second takeaway that really stood out for me is a specific laboratory test that Crinnion was excited about. During the course of several lectures, he mentioned a screening test I had never heard of previously, a urine test for 8-hydroxy-deoxyguanosine (better known as 8-OH-dG). This chemical results from oxidative damage to DNA and so reflects current reactive oxygen damage. It is quite sensitive, offering a way to assess both general damage but also track improvements in response to interventions. 
A quarter of a century ago, researchers reported that smoking 2 cigarettes was enough to increase baseline levels of 8-OH-dG from 3.3 to 5.1.1Levels rise significantly with exposure to solvent fumes,2 cigarette smoke,3 heavy metals such as mercury,4 arsenic,5 cadmium,6 lead,7 and organophosphate pesticides.8 This test quickly started to look like an easy screening test for environmental factors that impact health. The test is also an excellent reflection of exposure to ultrafine airborne particles produced by motor vehicle exhaust,9-11 especially diesel exhaust,12 making it a valuable measure of CVD risk and effectiveness of pollution controls and air filtration systems.
Increased blood levels of 8-OH-dG are associated with risk for or prognosis in cancers of the breast (particularly BRCA+),13,14 prostate,15 cervix , ovary,16 lung,17 nasopharynx,18 stomach,19 and bladder.20 This test may be useful in assessing prognosis for cancer occurrence, aggression, metastasis, and recurrence, any of which would be valuable. As an aside, while it seems likely that these test results would skyrocket after radiation treatment, they don’t necessarily do so and thus may be useful to assess cancer patients even after they have been treated for cancer with radiation.21
The test is also predictive of CVD. It is positively associated with increasing carotid artery intima media thickness, a marker of atherosclerosis22 and with the presence and severity of coronary artery disease.23 Levels go up after myocardial infarction (MI)24 and with chronic heart failure; this test provides a measure of disease severity25,26 and measures the benefit of therapy.27 Higher levels are also found in stroke patients and can be used as a predictor of extent of recovery.28
To have such a simple predictor of CVD risk and cancer is exciting, as many of the lifestyle changes we want patients to adopt change the test’s results measurably. Adhering to a Mediterranean diet lowers 8-OH-dG levels,29 probably because the diet increases consumption of polyphenol rich foods.30 Tai chi, green tea,31 and quercetin32 also do the same. Typically, 8-OH-dG levels go up due to the oxidative damage caused in diabetes33 and metabolic syndrome34 and so may also prove useful in monitoring this patient population. 
This test seems like it would have potential value in a range of practices. Exposure to fine particulates caused by motor vehicle exhaust and air pollution also increases levels of 8-OH-dG, and this led Crinnion to another important topic, the relationship between these fine particulates and CVD.
Carotid intima media thickness (CIMT) is a good way to assess atherosclerosis. Each standard deviation increase in CIMT increases risk of stroke or MI by about a third. Increasing levels of particulate matter in the air quickly increases CIMT. Curiously, this increase is almost tripled in patients taking statin drugs.35
CVD is now strongly associated with the particulates from motor vehicle exhaust.36 For women, simply living within 50 m (150 ft) of a major roadway increases risk of a sudden death from heart attack by nearly 60%.37 For people who have suffered MI, living less than 100 m from a major roadway is associated with a 27% increase in mortality over a 10-year period.38
Air pollution, particularly in the home, is something that people can alleviate. While it’s a rare patient who will pick up and sell a home based on a practitioner’s suggestion, we should be able to convince our patients to use a home air filter and to consider wearing facemasks when they are exposed to extreme levels of pollutants. Using a dust mask can cut levels of inhaled fine particulates by 90%.39
A study conducted in Smithers, British Columbia, provides a measure of the impact using a home air filter has. Smithers, a lovely rural community, has certain peculiarities of topography that combine with the common use of wood heat to create periodic high levels of airborne particulate pollution. Using indoor air filters for just 7 days reduced c-reactive protein levels in the 45 participants of a study by almost 33%.40

SpiritMed Conference Lectures

Access the lectures from this year’s SpiritMed update here. Learn about SpritMed’s next 6-month course on EM here

Categorized Under


  1. Kiyosawa H, Suko M, Okudaira H, et al. Cigarette smoking induces formation of 8-hydroxydeoxyguanosine, one of the oxidative DNA damages in human peripheral leukocytes. Free Radic Res Commun. 1990;11(1-3):23-27.
  2. Chang FK, Mao IF, Chen ML, Cheng SF. Urinary 8-hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to ethylbenzene. Ann Occup Hyg. 2011;55(5):519-525. 
  3. Yano T, Shoji F, Baba H, et al. Significance of the urinary 8-OHdG level as an oxidative stress marker in lung cancer patients. Lung Cancer. 2009;63(1):111-114. 
  4. Chen C, Qu L, Li B, et al. Increased oxidative DNA damage, as assessed by urinary 8-hydroxy-2'-deoxyguanosine concentrations, and serum redox status in persons exposed to mercury. Clin Chem. 2005;51(4):759-767. 
  5. Lin TS, Wu CC, Wu JD, Wei CH. Oxidative DNA damage estimated by urinary 8-hydroxy-2'-deoxyguanosine and arsenic in glass production workers. Toxicol Ind Health. 2012;28(6):513-521. 
  6. Huang M, Choi SJ, Kim DW, et al. Risk assessment of low-level cadmium and arsenic on the kidney. J Toxicol Environ Health A. 2009;72(21-22):1493-1498. 
  7. Hong YC, Oh SY, Kwon SO, et al. Blood lead level modifies the association between dietary antioxidants and oxidative stress in an urban adult population. Br J Nutr. 2013;109(1):148-154. 
  8. Ding G, Han S, Wang P, et al. Increased levels of 8-hydroxy-2'-deoxyguanosine are attributable to organophosphate pesticide exposure among young children. Environ Pollut. 2012;167:110-114. 
  9. Kim JY, Mukherjee S, Ngo LC, Christiani DC. Urinary 8-hydroxy-2'-deoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to fine particulates. Environ Health Perspect. 2004;112(6):666-671.
  10. Song S, Paek D, Park C, Lee C, Lee JH, Yu SD. Exposure to ambient ultrafine particles and urinary 8-hydroxyl-2-deoxyguanosine in children with and without eczema. Sci Total Environ. 2013 Aug 1;458-460:408-413. 
  11. Lai CH, Liou SH, Lin HC, et al. Exposure to traffic exhausts and oxidative DNA damage. Occup Environ Med. 2005;62(4):216-222.
  12. Harri M, Svoboda P, Mori T, Mutanen P, Kasai H, Savela K. Analysis of 8-hydroxydeoxyguanosine among workers exposed to diesel particulate exhaust: comparison with urinary metabolites and PAH air monitoring. Free Radic Res. 2005;39(9):963-972.
  13. Dziaman T, Huzarski T, Gackowski D, et al. Elevated level of 8-oxo-7,8-dihydro-2'-deoxyguanosine in leukocytes of BRCA1 mutation carriers compared to healthy controls. Int J Cancer. 2009;125(9):2209-2213.
  14. Loft S, Olsen A, Møller P, Poulsen HE, Tjønneland A. Association between 8-oxo-7,8-dihydro-2'-deoxyguanosine excretion and risk of postmenopausal breast cancer: nested case-control study. Cancer Epidemiol Biomarkers Prev. 2013;22(7):1289-1296. 
  15. Kosova F, Temelta? G, Ar? Z, Lekili M. Possible relations between oxidative damage and apoptosis in benign prostate hyperplasia and prostate cancer patients. Tumour Biol. 2014;35(5):4295-4299. 
  16. Pylväs M, Puistola U, Laatio L, Kauppila S, Karihtala P. Elevated serum 8-OHdG is associated with poor prognosis in epithelial ovarian cancer. Anticancer Res. 2011;31(4):1411-1415.
  17. Peddireddy V, Siva Prasad B, Gundimeda SD, Penagaluru PR, Mundluru HP. Assessment of 8-oxo-7, 8-dihydro-2'-deoxyguanosine and malondialdehyde levels as oxidative stress markers and antioxidant status in non-small cell lung cancer. Biomarkers. 2012;17(3):261-268. 
  18. Huang YJ, Zhang BB, Ma N, Murata M, Tang AZ, Huang GW. Nitrative and oxidative DNA damage as potential survival biomarkers for nasopharyngeal carcinoma. Med Oncol. 2011;28(1):377-384. 
  19. Chang CS, Chen WN, Lin HH, Wu CC, Wang CJ. Increased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor kappaB expression and enhanced antiapoptosis-related proteins in Helicobacter pylori-infected non-cardiac gastric adenocarcinoma. World J Gastroenterol. 2004;10(15):2232-2240.
  20. Soini Y, Haapasaari KM, Vaarala MH, Turpeenniemi-Hujanen T, Kärjä V, Karihtala P. 8-hydroxydeguanosine and nitrotyrosine are prognostic factors in urinary bladder carcinoma. Int J Clin Exp Pathol. 2011;4(3):267-275.
  21. Yamazaki H, Inoue T, Koizumi M, et al. Urinary 8-hydroxy-2'-deoxyguanosine excretion as a biomarker for estimating DNA oxidation in patients undergoing external radiotherapy and/or brachytherapy. Oncol Rep. 2005;13(5):847-851.
  22. Ari E, Kaya Y, Demir H, et al. Oxidative DNA damage correlates with carotid artery atherosclerosis in hemodialysis patients. Hemodial Int. 2011;15(4):453-459. 
  23. Xiang F, Shuanglun X, Jingfeng W, et al. Association of serum 8-hydroxy-2'-deoxyguanosine levels with the presence and severity of coronary artery disease. Coron Artery Dis. 2011;22(4):223-227. 
  24. Ho HY, Cheng ML, Chen CM, et al. Oxidative damage markers and antioxidants in patients with acute myocardial infarction and their clinical significance. Biofactors. 2008;34(2):135-145.
  25. Kobayashi S, Susa T, Tanaka T, et al. symptomatic status and severity of systolic dysfunction in patients with chronic heart failure. Eur J Heart Fail. 2011;13(1):29-36. 
  26. Watanabe E, Matsuda N, Shiga T, et al. Significance of 8-hydroxy-2'-deoxyguanosine levels in patients with idiopathic dilated cardiomyopathy. J Card Fail. 2006;12(7):527-532.
  27. Susa T, Kobayashi S, Tanaka T, et al. Urinary 8-hydroxy-2'-deoxyguanosine as a novel biomarker for predicting cardiac events and evaluating the effectiveness of carvedilol treatment in patients with chronic systolic heart failure. Circ J. 2012;76(1):117-126. 
  28. Hsieh YW, Lin KC, Korivi M, Lee TH, Wu CY, Wu KY. The reliability and predictive ability of a biomarker of oxidative DNA damage on functional outcomes after stroke rehabilitation. Int J Mol Sci. 2014;15(4):6504-6516. 
  29. Mitjavila MT, Fandos M, Salas-Salvadó J, et al. The Mediterranean diet improves the systemic lipid and DNA oxidative damage in metabolic syndrome individuals. A randomized, controlled, trial. Clin Nutr. 2013;32(2):172-178. 
  30. Pedret A, Valls RM, Fernández-Castillejo S, et al. Polyphenol-rich foods exhibit DNA antioxidative properties and protect the glutathione system in healthy subjects. Mol Nutr Food Res. 2012;56(7):1025-1033. 
  31. Qian G, Xue K, Tang L, et al. Mitigation of oxidative damage by green tea polyphenols and Tai Chi exercise in postmenopausal women with osteopenia. PLoS One. 2012;7(10):e48090. 
  32. Barcelos GR, Angeli JP, Serpeloni JM, et al. Quercetin protects human-derived liver cells against mercury-induced DNA-damage and alterations of the redox status. Mutat Res. 2011;726(2):109-115. 
  33. Chang CM, Hsieh CJ, Huang JC, Huang IC. Acute and chronic fluctuations in blood glucose levels can increase oxidative stress in type 2 diabetes mellitus. Acta Diabetol. 2012 Dec;49 Suppl 1:S171-S177. 
  34. Cangemi R, Angelico F, Loffredo L, et al. Oxidative stress-mediated arterial dysfunction in patients with metabolic syndrome: Effect of ascorbic acid. Free Radic Biol Med. 2007;43(5):853-859. 
  35. Vedal S, Campen MJ, McDonald JD, et al. National Particle Component Toxicity (NPACT) initiative report on cardiovascular effects. Res Rep Health Eff Inst. 2013 Oct;(178):5-8.
  36. Erdogmus B, Yazici B, Annakkaya AN, et al. Intima-media thickness of the common carotid artery in highway toll collectors. J Clin Ultrasound. 2006;34(9):430-433.
  37. Hart JE, Chiuve SE, Laden F, Albert CM. Roadway proximity and risk of sudden cardiac death in women. Circulation. 2014;130(17):1474-1482. 
  38. Rosenbloom JI, Wilker EH, Mukamal KJ, Schwartz J, Mittleman MA. Residential proximity to major roadway and 10-year all-cause mortality after myocardial infarction. Circulation. 2012;125(18):2197-2203. 
  39. Palmberg L, Larsson BM, Sundblad BM, Larsson K. Partial protection by respirators on airways responses following exposure in a swine house. Am J Ind Med. 2004;46(4):363-370.
  40. Allen RW, Carlsten C, Karlen B, et al. An air filter intervention study of endothelial function among healthy adults in a woodsmoke-impacted community. Am J Respir Crit Care Med. 2011;183(9):1222-1230.