The 14th Annual International Symposium
on
Man and His Environment in Health and Disease
SPECIAL FOCUS:
 ENVIRONMENTAL ASPECTS OF NEUROLOGICAL
AND
CARDIOVASCULAR FUNCTIONS
February 22-25, 1996
Dallas, Texas

 

 
 
 
 
 
 
 
INTRODUCTION

 

Welcome to the 14th Annual International Symposium on Man and His Environment in Health and Disease. This Symposium is one of the most advanced forums in the world addressing the research and treatment of environmental effects on health and disease.

 

At this year’s Conference, experts from throughout the world will share their extensive experience and specialized knowledge with an audience of physicians, scientists and health professionals.

 

 

GOALS AND OBJECTIVES

 

The 14th Annual International Symposium on Man and His Environment in Health and Disease presents the most current information available in the fields while providing guidelines to identify, diagnose, treat and especially to prevent environmentally triggered responses in the human body.

 

 

 

SPECIAL FOCUS

 

The 1996 Annual International Symposium will focus on the Environmental aspects of neurological and cardiovascular functions. This Conference will explore some of the latest data and provide a forum for discussion as well as case studies to help the professional.

 

 

ACCREDITATION

 

As an organization accredited for Continuing Medical Education, the American Academy of Environmental Medicine certifies that this continuing medical education activity meets the criteria for 23 hours of Category 1 of the physician’s recognition award of the American Medical Association.

 

 
 
1996 Faculty Listing

 

Robert C. Atkins, M.D.

Atkins Center

152 E. 55th Street

New York, NY 10022

`

Miklos L. Boczko, M.D.

Neurology - Biofeedback

280 Mamaroneck Ave., #304

White Plains, NY 10605-1437

 

Joel R. Butler, PhD

Environmental Health Psychologist

P.O. Box 399

Dewey, Ok 74029

 

William E. Connor, M.D.

Department of Medicine

Oregon Health Sciences University

3818 S.W. Jackson Park Road, L465

Portland, OR 97201

 

S. Boyd Eaton, M.D.

School of Medicine

Emory University

Atlanta, Georgia 30327

 

Ronald Finn, M.D.

Royal Liverpool University Hospital

Prescot Street

Liverpool , L7 8XP England

 

Roy A. Fox, M.D.

Environmental Health Center

P.O. Box 2130

Fall River, Nova Scotia B2T 1K6

 

Professor Hartmut Heine

University of Witteh/Herdecke

Department of Anatomy and Clinical Morphology

Alfred-Herrhausen-Strasse 50

D57448 Witten, Germany

 

Satoshi Ishikawa, M.D.

Professor and Chairman

Dept. of Opthalmology

School of Medicine, Kitasato University

Sagamihara, Kanagawa 228 JAPAN

 

Michael Jaumann, M.D.

Orthinolaryngology Environment Medicine

Klinil amEichert, Univ. ULM

Markstr. 25

73033 Geoppingen, Germany

 

Kaye Kilburn, M.D.

Professor of Medicine USC

2250 Alcazar

Los Angeles, CA 90033

 

Allan Lieberman, M.D.

7510 Northforest

North Charleston, SC 29420

 

Jean Monro, M.D. .

Breakspear Hospital

Belswains Lane

Hempel Hempstead, Hertfordshire HP3 9XL, England

 

Doris J. Rapp, M.D.

Environmental Allergy Center

2757 Elmwood Ave.

Buffalo, NY 14217

 

Sherry Rogers, M.D.

Northeast Center for Environmental Medicine

P.O. Box 2716

Syracuse, New York 13220

 

William Sargent, O.D., R.P.H.

114 Village Street

Pikesville, Kentucky 41501

 

 

 

1996 ABSTRACTS
 

The Major Risk Factor Modification System (MRFM) System for Reversing Coronary Heart Disease

Robert C. Atkins, MD

The Atkins Center for Complementary Medicine

152 East 55th St

New York, NY 10022

 

Convincing evidence exists that atherosclerosis is reversible, a fact which should make bypass surgery and angioplasties an inappropriate first therapeutic option. Chelation therapy seems to be a valid approach to reversing atherosclerosis.

 

Creating major changes in recognized risk factors has also been demonstrated to allow for improvements in coronary circulation. The obstacle to universal success has been the belief that there is a single diet, restricting fats and cholesterol, to prescribe to all heart patients.

 

In fact, there are several metabolic imbalances leading to atherosclerosis, and the most prevalent of these is the insulin resistance-hyperinsulinism-prediabetic axis, which is best corrected by a sugar and/or total carbohydrate restriction. Since the low fat diet is high in carbohydrates, choosing between these opposing dietary approaches is mandatory to achieving universal success.

 

Abnormal insulin response to glucose, abnormal glucose tolerance, low HDL cholesterol, elevated lipoprotein(s) are all findings indicative of insulin-based heart disease and are more successfully treated by carbohydrate restriction than by fat restriction.

 

The MRFM system requires the ability to glucose, abnormal glucose tolerance, low HDL cholesterol, elevated triglycerides, hypertension, obesity, and elevated lipoprotein(s) are all findings indicative of insulin-based heart disease and are more successfully treated by carbohydrate restriction than by fat restriction.

 

Nutritional supplements with dramatically beneficial effects on risk factors include essential oils containing EPA and GLA, chromium pantethine, lecithin, niacinates, coenzyme Q10, carnitine, magnesium, ascorbic acid. A special category involves those with homocystine elevations, who are to receive folic acid, B6 and B12. Those with elevated LDL receive antioxidants.

 

 

Panic Disorder: Preliminary Findings of Environmental Triggering

ML Boczko, MD

Neurology—Biofeedback

280 Mamaroneck Ave.

White Plains, NY 10605

 

Consecutive patients with panic disorder diagnosed and treated in my environmentally oriented private practice and in a neurology practice of a multispecialty outpatient setting were investigated. The one diagnostic thread in all of the patients was marked intolerance to simple sugar. In the first category of patients this diagnosis was purely clinical (no glucose tolerance test performed); these patients all had chronic candidiasis in addition to multiple environmental sensitivities. All achieved at least a 95% relief from panic disorder with comprehensive environmental management. In the second group of patients such diagnostic and therapeutic intervention were not possible; however, a 5 hr glucose tolerance test in everyone of them showed reactive hypoglycemia. Except in one case this was accompanied by symptoms similar to those they would experience during an attack. All patients responded to a simple sugar-free diet and limited nutritional supplements with dramatic, immediate improvement.

 

 

Psychoneurocognitive Aspects of Environmental Illness

Joel R. Butler, PhD

Environmental Health Psychologist

P.O. Box 399

Dewey, OK 74029

 

Nancy A. Didriksen, PhD

Health Psychology/Behavioral Medicine Associates

1241 Southridge Court, Suite 105

Hurst, TX 76503

 

Susan F. Franks, PhD

Dept. Of Psychiatry & Human Behavior

University of North Texas Health Science Center

3500 Camp Bowie Blvd.

Fort Worth, TX 76107-2699

 

The toxic effects of environmental contaminants/poisons are widespread, generally diffuse and multiple, often not well understood, and subject to misinterpretation particularly when related to certain specific skill deficits necessary for performance of critical job or task functions.

 

Just as with other manifestations of toxic exposure, the reactions are individualized but still show many common symptoms such as poor memory and low energy. But the toxic responses may also remain subclinical for an extended period of time yet reach the symptom threshold of serious illness with no known additional toxic exposure. The result can mean death—so early evaluation and accurate diagnosis are very important.

 

Psychoneurocognitive symptoms are certainly among the earliest detected. The damaging effects may range from degenerative neuropathology in the CNS and PNS systems to disruption of personality or affective variables. Both primary and secondary symptom results usually occur.

 

There are many difficulties incumbent in psychoneurocognitive evaluation. First, there are very few tests standardized on a population of patients with adverse reactions from exposure to environmental toxins/multiple chemicals. Thus, there are few relevant test norms. Animal analogs have poor generalizability. Premorbid functions are difficult to obtain, etc.

 

However, evaluation of psychoneurocognitive functions or syndromes is useful, available, and should be done whenever the question arises. The authors will address the problems inherent in the evaluation process and the results of studies indicating pathology as well as most prevalent symptoms.

 

Additionally, the most helpful tests to be used for symptom determination will be reviewed, including such measures as the WAIS-R, Harrell-Butler Comprehensive Neuropsychological Screen, CEDA, Trails 1 & II, Benton Visual Retention, Categories Test, etc. Depression and other psychological affective symptoms will be reviewed from the psychogenic to the organic base and the interactions therein.

 

GOALS AND OBJECTIVES

The goals were to highlight the psychoneurocognitive effects of environmental contaminants involving the CNS and PNS as well as personality dysfunctioning. The objectives were to specify appropriate procedures and to point out evaluation problems.

 

CONCLUSIONS AND WHAT IS TO BE LEARNED

Psychoneurocognitive symptoms are likely to be among the first detected from exposure to environmental toxins. There are valid and useful assessment procedures that can and should be utilized to determine the kind and extent of psychoneurocognitive deficits.

 

 

The Nutritional Prevention and Reversal of Coronary Heart Disease

William E. Connor, MD

Professor of Medicine, Section of Clinical Nutrition and Lipid Metabolism

The Oregon Health Sciences University

Portland, OR 97201-3098

 

Ninety years of solid scientific research have shown clearly the causes of our current epidemic of coronary heart disease. Of the important risk factors, the interaction of diet with genetics is the most important.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The onset of the coronary epidemic began after World War I. William Osler, America’s foremost physician, remarked in 1908 that only two or three cases of angina pectoris were seen each year in the large metropolitan hospitals of this country. Americans, at the time of Osler, were not smoking cigarettes, and machine technology had not compromised the need for physical activity to make a living; obesity was less common, and the diet was less fatty and less purified. There is no information about the plasma lipids then, but we presume that cholesterol and triglyceride levels were lower and HDL levels higher.

 

Hyperlipidemia results from a composite of two factors:

1. Overproduction of cholesterol, triglyceride, and VLDL by the liver.

2. Defective removal of lipids and lipoproteins by the liver. The classic example is impaired removal of LDL, the chief transport modality for cholesterol, by the LDL receptor in the liver.

 

Atherogenicity of lipoproteins (relative ranking):

Chylomicrons 0

VLDL (triglyceride and cholesterol) 2+

Remnants (IDL) of VLDL and chylomicrons

(Triglyceride and cholesterol) 3+

LDL (cholesterol) 4+

Lp(a) 2+

HDL -4

 

Lp(a) acts to inhibit fibrinolysis. LDL is more pathogenic when oxidized.

 

DIETARY FACTORS GREATLY AFFECT THESE LIPOPROTEINS.

Evidence from population studies, animal experiments, molecular biology, and human metabolic and clinical trials has indicated that some dietary factors are pathogenic for coronary atherosclerosis and myocardial infarction and other dietary factors are protective.

 

Pathogenic dietary factors that increase plasma cholesterol, LDL, and triglyceride levels include the following:

1. Saturated fat;

2. Cholesterol (contained only in animal foods); and

3. Excessive calories with associated visceral obesity.

 

Protective dietary factors against the development of atherosclerosis include the following:

1. Fish and fish oil (omega-3 fatty acids),

2. Fruits, vegetables, grains, and beans,

3. Fiber, soluble and insoluble,

4. Saponins that inhibit cholesterol absorption,

5. Antioxidants (vitamins C and E, beta-carotene, flavonoids, etc.), and

6. Reduced calories and increased physical activity to avoid obesity.

 

The molecular biological effects of dietary factors is as follows:

1. Both dietary saturated fat and cholesterol decrease the messenger RNA (mRNA) for the synthesis of the LDL receptor. With fewer LDL receptors there is less removal of LDL from the plasma, thereby increasing the concentration of LDL and total cholesterol in the plasma. 2. Excessive calories stimulate the liver to produce more triglyceride, cholesterol, and VLDL.

3. Saturated fat in the diet, in addition, is thrombogenic.

4. Fish and fish oil are protective because they stimulate endothelial-derived relaxing factor, inhibit platelet-derived growth factor, retard monocyte migration, block thromboxane A-2 production in platelets, reduce the plasma VLDL by inhibiting its hepatic synthesis, promote chylomicron clearance and inhibit the growth of the atherosclerotic plaque.

5. Fruits, vegetables, grains, and beans contain fiber, saponins, and antioxidants, which are likewise protective against atherosclerosis and thrombosis. Oxidized LDL is more atherogenic.

 

PREVENTION OF CORONARY DISEASE

Four populations with a very low coronary heart disease rate provide possible guidance for our own efforts to prevent coronary heart disease. These include the following: Mediterranean peoples, the Eskimos, the Japanese, and the Tarahumara Indians. Note their dietary similarities and differences.

 

The evidence is strong that coronary heart disease can certainly be prevented by the application of current knowledge. That knowledge has also been applied to reversing coronary heart disease in both experimental animals and humans. The keys to reversibility consist of profound cholesterol and LDL lowering in the plasma along with the omega-3 fatty acids from fish. In experimental animals, the regression of lesions is relatively rapid. In humans, the rate of change of improvement in coronary anatomy is about 1-2% per year of study. The turnover of cholesterol in the plaque of coronary atherosclerosis is about 400 days compared to 30 days in normal arteries. When it is considered that the disease inevitably advances at the rate of 2-3% per year, this reversibility is, indeed, remarkable.

 

As a result of dietary changes in the United States, along with smoking cessation and better treatment of hypertension, the coronary epidemic is now waning, but it is far from overcome. Our national diet has less cholesterol and fat. Smoking has virtually disappeared in some population groups (such as physicians), and is at the level of 25% in the population at large versus 70% in many countries. However, the national statistics about obesity and physical activity are still dismal.

 

In contrast to the relatively hopeful signs in the United States, Canada, Australia, and New Zealand, the burden of coronary heart disease in the developing world is taxing health care facilities that could be better devoted to other health needs. What happens as developing populations change their diets is illustrated by an 8-week study of the Tarahumara Indians, in which their customary low fat diet of corn and beans was replaced by eggs, butter, lard, sugar, and flour, with a resulting weight gain of 8 lbs and over 30% increase in cholesterol and LDL in the plasma. Advancing technology should not mean the turning away from traditional food practices and the adoption en mass of the bad food habits of the Western World.

 

 

The Plasma Lipids, Lipoproteins, and Diet of the Tarahumara Indians of Mexico1-3

William Connor, MD; Maria T. Cerqueira, MS; Rodney W. Connor, MD; Robert B. Wallace, MD; M René Malinow, MD; and H. Richard Casdorph, PhD

 

The Tarahumaras are unacculturated Indians of the Sierra Madre Occidental Mountains renowned for their running in competitive races. Over a 4-year period at different locations, 523 healthy Tarahumaras (ages 5 to 70 years) were surveyed for plasma lipids and lipoproteins. We determined also the nutrient intakes of a sub sample (174 adults). Mean plasma cholesterol was 125 ± 25 (SD) mg/dl and triglyceride 120 ± 52. Men and nonpregnant women had similar values. Pregnant women were higher. Children were similar, cholesterol of 116 ± 22 and triglyceride of 115 ± 50. For all ages, lipoprotein cholesterol was 87 mg/dl low density lipoproteins, 21 very low density lipoproteins, and 25 high density lipoproteins. Lipoprotein triglyceride was 40 mg/dl low density lipoproteins, 84 very low density lipoproteins, and 24 high and the low density lipoproteins and high density lipoproteins cholesterol. Plasma triglyceride, very low density lipoproteins triglyceride, and cholesterol of Tarahumaras were somewhat higher but not abnormal. The diet of the Tarahumaras (versus the diet of Iowans) was low in cholesterol (71 mg/day), in fat (12% of calories), and in saturated fat (2% of calories). Protein was adequate (13% of calories). The carbohydrate (75% of calories) and fiber (19 mg/day) were high. Corn and beans were the chief caloric sources. The total plasma cholesterol correlated positively with dietary cholesterol intake (r=0.874), the first time in man such a correlation has been found. Particularly notable was the virtual absence of the hypertension, obesity, and the usual age rise of the serum cholesterol in adults. Thus, the customary diet of the Tarahumaras is adequate in all nutrients, is hypolipidemic, and is presumably antiatherogenic. Am. J. Clin. Nutr. 31: 1131-1142, 1978.

 

 

Cardiovascular Disease in Evolutionary Context

S. Boyd Eaton, MD

Northwest Radiology Consultants

2887 Howell Mill Rd., NW

Atlanta, GA 30327

 

This symposium’s attendees are apt to think of themselves as sophisticated, established, and successful members of 20th Century Western society, but that’s only how our minds interpret the situation. Our genes, which determine human physiology and metabolism, don’t know about the 20th Century. From their point of view, each of us is still a Stone Ager displaced through time to an environment that’s foreign and, in many ways, hostile.

 

Humans today are only 0.005% different, genetically, from our preagricultural ancestors of 10,000 years ago; our genes are still adapted for the life circumstances of that time, but we now function amid biocultural circumstances that place our ancient biology at a significant disadvantage. The resulting mismatch between our genes and our lifestyles fosters the "afflictions of affluence," of which coronary heart disease is a particularly instructive example. Medical giants like Olser, White, and Burkitt personally observed and commented on the beginnings of the heart attack epidemic, which is now waning. Both its rise and its decline illustrate the ill effects of deviation from our Paleolithic precedent and the benefits of readopting the essentials of life as our ancestors enjoyed it.

 

 

The Concept of Environmental Disease—Cancer and Dementia

Ronald Finn, MD, FRCP

Royal Liverpool University Hospital

Prescot St.

Liverpool, L7 8XP England

 

THE CONCEPT OF ENVIRONMENTAL DISEASE

There are only three basic causes of disease: (1) genetic, (2) degenerative, (3) environmental. Effective therapy is necessarily limited for genetic and degenerative disease, but removal of an environmental cause will prevent a disease such as tobacco-induced lung cancer or control an already established disease. The environmental physician should, therefore, be concerned with the identification and neutralization of environmental triggers of disease. The environmental physician should, therefore, have a wide knowledge of the various environmental causes of disease in those conditions in which environmental triggers are important or in combination with other standard treatments. This paper gives examples of an environmental approach to two intractable medical problems.

 

SENILE DEMENTIA

Senile dementia is becoming a major problem in advance societies associated with greater longevity. No specific therapy is available, and patient care is extremely expensive. We investigated 25 classical cases from a psychogeriatric unit. The investigation comprised a very detailed life history obtained by a trained environmental physician. The cases were selected so that each had a close family caretaker who was fully aware of the patient’s life history. Three major risk factors were identified: (1) a genetic factor; (2) heavy tobacco consumption; (3) chronic ingestion of aluminum containing antacid. Fifty percent of the cases did not have a family history, and the implication of this study is that avoidance of the two environmental components could possibly reduce the incidence of Senile Dementia by about 50%, which would have major clinical and cost benefits.

 

BREAST CANCER

Breast cancer is the most common female cancer and despite breast screening and modern therapy, there has been no major reduction in mortality. It is, therefore, suggested that an alternative environmental approach should be explored. There is almost certainly an, as yet unidentified, major environmental component, as the incidence of breast cancer varies widely in different countries. Environmental chemicals could be important as the disease is most common in advanced Western societies.

A major chemical exposure in advanced societies is regular therapeutic medication. Modern drugs are highly reactive chemicals, and it is, therefore, possible that multiple drug therapy over prolonged periods could have toxic effects that could destabilize cellular control mechanisms and predispose an individual to cancer. We have, therefore, investigated eighty patients with biopsy-proven breast cancer and ascertained whether they were taking regular medication over prolonged periods prior to the diagnosis of the breast cancer. The results of this survey support the hypothesis that prolonged medication is a risk factor for breast cancer.

 

GENERAL CONCLUSION

Modern pharmacological agents have enabled us to control many diseases and are an essential part of multiple long-term drug therapy for conditions in which their effectiveness is either marginal or doubtful. This practice could lead to long-term toxic effects. It is, therefore, suggested that conditions for which there is no effective drug therapy should be treated with nonpharmacological alternative methods.

 

 

Dysfunctional Vascular Endothelium

Roy Fox, MD

Nova Scotia Environmental Health Clinic

Dalhousie University

 

The vascular endothelium has long been regarded as a necessary but inert lining of the vasculature. This view has had to be revised. The endothelium is a selectively permeable barrier, and when healthy, it is a deterrent to intravascular coagulation. The healthy endothelium also has major endocrine, paracrine, and autoregulatory functions.

 

ROLE AND FUNCTION OF ENDOTHELIUM

Blood vessels consist of a lumen surrounded by endothelium, underneath which are the subendothelial tissues—media and adventitia.

 

Endothelium functions as a specialized regulatory organ, covering an area of 1,000 sq meters (six tennis courts), for an average 70 kg man. The cells form a continuous layer of flattened, elongated polygonal cells (long axes oriented in direction of flow) that is covered by a dense carpet of glycocalyx (hydrophilic side chains of membrane proteins and oligosaccharide groups esterified with membrane lipids). This determines the external environment of the cell wall and provides an external pool of calcium for intracellular activities.

 

Endothelial cells contain a variety of plasma membrane receptors—e.g., histamine—plus charged areas that may bind proteins—e.g., lipoprotein lipase.

 

1. PERMEABILITY

Endothelium is permeable to all plasma proteins. Macromolecules travel via transcytosis and through intercellular junctions.

Permeability is controlled by:

 

2. HEMOSTASIS

Clotting does not occur under normal circumstances.

Hemostatic properties include the following:

 

3. VASCULAR TONE

Endothelial cells regulate vascular tone and contraction by the production of relaxing and constricting factors in response to physiological stimuli. Relaxation from release of:

(A) Prostacyclin—stimulates production of CAMP

(B) Endothelium-derived relaxing factor (EDRF)—stimulates production of CGMP

Constriction from release of endothelia—opens voltage-dependent calcium channels.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Vascular tone is a balance of competing effects, the endothelial cell acts as the pivot.

 

Platelet release substances that promote release of EDRF—negative feedback on platelet aggregation.

 

Platelets also release other substances that promote constriction—serotonin and thromboxane.

 

Net effect of intact endothelium is to promote relaxation of platelet and thrombin-free vessel wall.

 

4. EDRF

Acetyl-choline acts as a vasoconstrictor in vitro.

Acetyl-choline dilates when given in vivo—an intact endothelium in needed for this effect (Furchgott and Zawadaski, 1980).

 

Other stimuli that release EDRF include hypoxia, increase in flow and electrical stimulation.

 

EDRF is Nitric Oxide—NO—accounts for the biological properties of EDRF.

Short half life. Acts locally.

NO is generated by NO synthase (NOS)—3 isoenzymes

i. Neuronal and epithelial cells

ii. Macrophages and smooth muscle

iii. Endothelial cells

 

L-arginine is usual precursor, NO released from guanidino nitrogen by NOS in presence of oxygen and cofactors (ionized calcium, tetrahydrobiopterin). Arginine is not rate limiting, but production can be increased by excess arginine.

 

Inhibited by arginine analogues (L-NMMA, monomethylarginine). Efficacy reduced by superoxide.

Inhibition can be reversed by excess substrate—arginine.

 

Actions of NO—diffuses from site of production to lumen and wall. In lumen, increases GMPc production in platelet, thus reducing platelet adhesion. In wall, GMPc causes smooth muscle relaxation.

NO is a major regulator of vascular tone—inactivation of NOS produces a potent vasoconstrictor effect. NOS also present in autonomic nerve fibers of the adventitial layer.

Activation of nerves causes release of NO and relaxation of smooth muscle. NO has neuroinhibitory role in cerebral arteries.

NO also acts in CNS—role in memory, learning, and vision. NO centrally decreases sympathetic output, decreases blood pressure. Inhibit NO output and produce rise in blood pressure by central effect.

NO production or action can be inhibited at a number of sites (Figure 1).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

5. DYSFUNCTION

Endothelial dysfunction may lead to atherosclerosis, associated with hypercholesterolemia. In essential hypertension ACH appears to have less effect on blood flow in the forearm of hypertensives. Basal NO-mediated dilatation is reduced in essential hypertension. Endothelial dysfunction appears to pay an important role in essential hypertension as a contributor to increased peripheral resistance. There is a deficiency in the release of NO. Dysfunction is important in the early stages of atherosclerosis. Dysfunction is directly proportional to risk factors—smoking, hyperlipidemia, diabetes.

 

6. IMPLICATIONS FOR ENVIRONMENTAL ILLNESS

Environmental illness is characterized by the induction of dysfunction in one or more of the body systems. It has long been recognized that function of the cardiovascular system is often perturbed.

 

Typical problems that occur and suggest vascular dysfunction include the following:

 

I conclude that endothelial dysfunction contributes to the symptomatology of EI. Vasoconstriction can be produced in a number of ways, for example, by increasing intracellular calcium or by activation of the sympathetic nervous system. Endothelial dysfunction and the loss of the dilator effect appear to be another important mechanism.

 

The pathophysiology of fatigue in EI is not well understood. Endothelial dysfunction has been studied in heart failure patients, and blood flow enhancement of NO is blunted. It is postulated that impaired vasodilator capacity of the peripheral circulation during exercise accounts for fatigue and inability to exercise in such patients. Similar mechanisms might be important in environmentally triggered fatigue, weakness, and inability to exercise.

 

Synthesis and release of NO can be blocked by various chemicals—specifically, those with active amine groups, which are arginine analogues and block NOS activity.

 

NO is a very active molecule and interaction with superoxide will inactivate. Free radicals will inhibit NO activity. In the experimental animal, increasing SOD will protect NO and allow it to act (Wei et al., Circulation Research, 1985, 57:781). Increasing superoxide dismutase in humans with hypertension does not appear to reverse endothelial dysfunction (Grunfiled et al., Hypertension, 1995, 26:854), and increased breakdown by superoxide does not appear to be the mechanism for dysfunction in hypercholesterolemia (Garcia et al., Amer J Cardiol, 1995, 76:1157).

 

Peroxynitrite formation by the interaction of NO with superoxide can lead to formation of nitrosamines in the presence of nitrates or nitrate donors, like amines. Vitamin C can reduce nitrosamine formation. Vitamin E has also been investigated for its effect on endothelial dysfunction.

 

7. TREATMENT OF DYSFUNCTION

The most important aspect of treatment in hypertension, atherosclerosis, and hypercholesterolemia is reversal of "risk" factors. Thus, lifestyle changes as practiced in the treatment of EI should improve endothelial function—removal of inhibitors, etc. Angiotensin converting enzyme inhibitors block endothelial function. Exogenous nitrates act as an external source of EDRF and thus supply a dysfunctional endothelium. Arginine has been used to upregulate NOS, but this only appears to be effective with direct arterial perfusion in forearm plethysmographic studies. Glutamate has been used as a source of arginine and given to patients without toxic effects. The dose required is large.

 

8. CONCLUSION

The vascular endothelium is an important organ that is vulnerable to toxic damage. Endothelium dysfunction is likely to be important in the etiology and pathophysiology of environmental illness. This presentation introduces some of the current research that is taking place. It is clear that study of nitric oxide and its role in the various control mechanisms of the body is likely to help us in our understanding of EI. Some of the insights gathered from this provide a better understanding of various empirical observations that have been made in the treatment of patients and begin to provide explanations for the production of various clinical features.

 

9. REFERENCES

Boor, PJ, et al. "Chemical-induced Vasculature Injury." Toxicology and Applied Pharmacology. 132: 177-195. (1995)

Domiiniczak, AF, and DF Bohr. "Nitric Oxide and Its Putative Role in Hypertension." Hypertension 25:1202-1211. (1995)

Dupuis, J. "The Endothelium and the Paradoxes of Heart Disease." Can J CME Dec. 1995.

Elliott, TG, et al. "Effects of Vitamin E on Endothelial Function in Men after Myocardial Infarction." Ameri J Cardio 76:1188-1190. (1995)

Moncada, S, et al. "Nitric Oxide: Physiology, Pathophysiology, and Pharmacology." Pharmacol Rev 43:109-142. (1991)

 

 

Chronic Toxic Encephalopathy from Sick Buildings

Roy Fox, MD

Nova Scotia Environmental Health Clinic

Dalhousie University

 

The neurotoxic effects of volatile organic substances found in indoor air remain a subject of some debate. The evidence is strong that poor indoor air quality can have an adverse effect on brain and nervous system function. The purpose of this presentation is to summarize some of the information that has become available from the "ecological" disaster, which occurred within one of the major teaching hospitals of Dalhousie University in the City of Halifax. This information is used to develop a hypothesis for the pathophysiology of the neurocognitive effects and to help in our understanding of the nature of chemical sensitivity.

 

1. SITE OF AIR QUALITY PROBLEMS

Camp Hill Medical Centre is a collection of teaching hospitals within the city of Halifax. There are three buildings of various ages on one site. The oldest part was opened in 1917 and contains over 200 beds. It is passively ventilated and heated by piped steam. A second building is about thirty years old and contains an HVAC system. The third building (VMB) was completed in 1987 and is a sealed building with HVAC systems. The latter two buildings are heated by steam. All steam is generated in a central boiler plant. Excess steam was used to humidify the buildings in the winter time.

 

In 1988 the majority of kitchen workers (VMB) became ill with skin complaints, respiratory problems and cognitive deficits. The latter were not recognized at the time. From 1991 to 1993 over 700 workers became ill. At the present time over 100 remain disabled. This presentation will focus on the cognitive problems that have been identified.

 

2. IDENTIFICATION OF THE PROBLEM

In 1991, during the peak of the IAQ problems, 134 of the workers volunteered to complete questionnaires. This represented 96% of the workforce of two floors of the VMB, thought to be the major problem area. A control group (57 subjects) was taken from the workers in another hospital building on another site, about one mile away. The two groups were comparable for age, sex, and home environment. The VMB group had a slightly higher educational level. The group from the VMB had a lot more work-related complaints predominantly cognitive problems, skin rashes, respiratory difficulties, and mucous membrane irritation. The control group only reported back problems in relationship to work. It was concluded that the workers’ complaints were work-related and a result of IAQ problems (Marchant et al. 1991).

 

Twenty patients had neuropsychological screening, including completing a solvent questionnaire. Seventy percent of the workers endorsed five or more of the questions. Family members reported that memory and concentration problems were the most significant. The major deficits noted were in immediate recall of information, poor visuoconstruction abilities, and impaired executive functioning (Hayes 1992).

3. EXTENT OF COGNITIVE PROBLEMS

Most of the volunteers proceeded to more detailed neuropsychological testing by a number of psychologists. Twenty of 39 workers who completed detailed testing had abnormal neuropsychological profiles. One individual had severe deficits, and twelve were considered moderate. This represents a conservative estimate as there was no attempt to assess premorbid levels of intelligence. The domains primarily affected were problem solving and memory. Depression was identified as significant in 44%.

 

Despite these findings the link with the workplace has not been generally accepted. A control study was completed by two psychologists—L.R. Marsh-Knickle and C. Hayes. Twenty staff members from CHMC who had been recently exposed and were symptomatic were compared with twenty previously exposed workers from CHMC and with 22 comparable staff members from a general hospital in another part of the province. There were no differences in age, sex, and educational level. There were marked differences between the CHMC groups and the control group—the CHMC workers endorsed more positives in the solvent questionnaire than the control, and this was correlated with more symptoms in the cognitive failures questionnaire. Controls were able to perceive more missing details in pictures than the exposed groups. Digit symbol was more impaired in the CHMC groups, and fewer digits could be recalled in these groups. There were significant differences in performance intelligence quotient differences. There were other differences, but, in summary, the control group had higher mean scores in over 50% of the tests as compared with the CHMC groups. Those subjects who were working or who had been off work for less than six weeks had lower scores on various objective measures. This information clearly supports the contention that the neurocognitive problems experienced by the workers at CHMC were related to IAQ problems.

 

4. RECOVERY FROM COGNITIVE IMPAIRMENT

Workers continue to complain of cognitive problems five years after leaving work. In a follow-up of 39 cases, 31 had shown meaningful improvement—this means 20% failed to show any improvement. Studies of patients with persisting cognitive deficits are continuing, and cognitive retraining has been undertaken in some with good results. No further data is available at this time.

 

5. ETIOLOGY

No specific hypothesis has been developed as to the pathophysiology of the cognitive problems—except that it is clearly linked to indoor air quality problems. One of the important "toxic" components of the air at CHMC was a high concentration of amines, which were used to prevent corrosion from steam in the boiler and the pipes. The major ingredients appear to be morpholine, cyclohexylamine and various primary and secondary amines. These substances are likely to have a variety of effects, including an effect on Nitric Oxide production and action.

 

Two site of possible action are the following:

1. Interference in the generation of NO, by blocking the interaction of arginine with NO synthase.

2. Rapid removal of NO by the production of nitrosamines. Cyclohexylamine is easily nitrosated.

 

NO is important in memory and learning as well as vascular function. It has also been postulated that it functions as the retrograde messenger in neurones. Study of this model may help in our understanding of the various clinical features of environmental illness.

 

6. CHEMICAL SENSITIVITY

The patients at Camp Hill Hospital, in common with many other patients with environmental illness, became chemically sensitive. This phenomenon appears to be only one of many changes that result in increased sensitivity. The author categorizes environmental triggers into six groups, which include the following:

1. Biologicals—pollens, dust, dander, mold

2. Foods

3. Chemicals

4. Medications

5. Electromagnetic

6. Physical—light, sound, vibration, touch

The sensitivity is mediated by a variety of mechanisms that have been studied:

1. Altered immune reactions including the development of allergy

2. Impaired biotransformation

3. Saturation or loss of receptors

These mechanisms do not explain the "sensitivity" that many patients experience. It appears that thresholds for neuronal excitation are lowered, thus all senses may at times be more responsive to stimuli. Physical arousal to various stimuli is well-documented, but many patients become much more sensitive to emotional stimuli and less resistant to stress of any kind. A review of the classical models of neuronal function and a look at more recent models show that apparently in the chemically sensitive individual there is widespread disturbance of neuronal function wherein neurones are more easily fired and lose their ability to prevent arousal. The interaction of the Camp Hill "amines" with the nervous system need to be studied as a model to increase our understanding of neuronal function.

 

7. CONCLUSION

Cognitive dysfunction may occur as a result of poor indoor air quality within sick buildings. It is important to recognize that this is so and to ensure that only air of good quality without toxic substances is available for human use. The Camp Hill experience provides much useful information but also suggests that some of the damage that occurs may be permanent. Great care needs to be taken in the use of contaminated steam or other materials in occupied buildings without careful assessment of possible effects.

 

8. REFERENCES

Baker, EL. "A Review of Recent Research on Health Effects of Human Occupational Exposure to Organic Solvents." JOM 36, 1079.

Marsh-Knickle, LR. "The Effect of a ‘sick building’ on neuropsychological functioning." Master’s Dissertation in Applied Psychology, St. Mary’s University, Halifax.

Marchant, R, K Yosida, and D Figley. 1990. "Investigation of the Camp Hill Medical Centre."

Hayes, C. 1991. In Marchant, R, et al. 1992. Investigation of the Camp Hill Medical Centre.

Marchant, R. "Chemical Hyper-responsiveness." In Chemical, Microbiological, Health and Comfort Aspects of Indoor Air Quality—State of the Art in SBS, eds. H. Knoppel and P. Wolkoff, 1992, pp. 201-229.

 

 

Neurotoxicity of Silicone Formulations: Preliminary Neuropsychological Data

Susan F. Franks, PhD

Dept. Of Psychiatry & Human Behavior

University of North Texas Health Science Center

3500 Camp Bowie Blvd.

Fort Worth, TX 76107-2699

 

Joel R. Butler, PhD

Environmental Health Psychologists

P.O. Box 399

Dewey, OK 74029

 

The purpose of the present study was to determine the neurocognitive effects associated with silicone breast implants and to verify the extent of a causative relationship between silicone breast implants and neurocognitive deficits as well as theoretical brain involvement.

 

The value of neuropsychological assessment techniques for determining subclinical neurotoxic conditions has recently been acknowledged by a number of well-recognized agencies including the Environmental Protection Agency, World Health Organization, National Institute of Occupational Safety and Health, as well as various other national and state organizations—yet controversy has resulted withen silicone breast implants have been implicated as causal agents for neurotoxicity. The American College of Rheumatology has reported that silicone breast implants do not cause serious disease and that little or no increased health risks have been found, and they have cited studies supporting this position.

 

In contrast, the Food and Drug Administration has cited evidence considered sufficient to ban implant use, except for women needing breast reconstruction. The present authors reported at last year’s symposium that women with silicone breast implants were consistent with the profile of patients with environmental illness/chemical sensitivities as determined by valid tests designed to differentiate environmental illness from other disease syndromes. The results of neuropsychological screening on those patients with silicone breast implants clearly indicated that they had a significant level of neurocognitive impairment.

 

The present study represents a more detailed investigation of brain function in patients with breast implants. Comprehensive neuropsychological evaluations were performed on twenty of these patients. Results are consistent with screening data, indicating that silicone formulations have neurotoxic potential. Specific patterns of neurocognitive dysfunction (executive function, attention/concentration, language, memory, perception, emotion) will be presented and discussed, with implications for assessment/identification of general subclinical neutrotoxic conditions.

 

GOALS AND OBJECTIVES

The goals were to determine the association between silicone breast implants and neurocognitive functioning, as well as the implication of causality. The objectives were to verify (by use of a comprehensive neuropsychological test battery) consistency with neurocognitive screening data found in a previous study, and additionally to find specific neurocognitive deficits.

 

CONCLUSIONS OF WHAT IS TO BE LEARNED

Results support a strong association between silicone breast implants and neurocognitive dysfunctioning suggesting that the silicone implants act as an environmental contaminant to which the patient has reacted adversely.

 

 

Introducing a Functional Cell Cycle

Bertie Griffiths, PhD

Environmental Health Center—Dallas

8345 Walnut Hill Ln, Suite 205

Dallas, TX 75231

 

The cell cycle offers a "snap shot" of the status of one’s immune system. However, only static values can be obtained from a single cell cycle profile, which does not indicate the functional capability of these lymphocytes. The proper functioning of one’s lymphocytes may be compromised by varied factors.

 

This presentation describes a flow—cytometric method of assessing cellular function of relatively pure lymphocyte subsets to selected stimuli, thus providing a functional cell cycle as an aid to clinical evaluation.

 

 

The Ground System (GRS) of the Human Body

Hartmut Heine, PhD, Professor

University of Witten/Herdecke

Dept. Of Anatomy and Clinical Morphology

Alfred-Herrhausen-Strasse 50

D-58448 Witten, Germany

 

The GRS computes all interactions between cells, extracellular matrix, microcirculation, and the autonomic nervous system. Thus, it influences all regulative processes of the body. The GRS is an energetically open system in continuous exchange with its environment.

 

The GRS, as an open system, is objective oriented, the objective being the maintenance of the individual homeostasis. This requires the maintenance of a certain energetic difference to the environment. Accordingly, the GRS is able to reduce complexity: the data concerning the organism are changed into biochemical messenger substances. However, this also means a continuous risk of incompatibilities in the processing of data.

 

Like any other system, the GRS has certain structures that determine relationships between elements of the system. These structures form subsystems that, to some extent, perform independently. This leads to a relief in the total system control.

 

The main subsystem in the GRS is the extracellular matrix with its cellular and humoral components, the microcirculation, and vegetative nerves.

 

For individual subsystems in the GRS, all other elements of the system form the "environment," i.e., "internal environment." This differs from the "external environment" insofar as it has a higher degree of order and a lower degree of complexity.

 

Complexity enforces the development of structures that are subject to selection. Consequently, the GRS registers.

 

 

Cholinergic and Noncholinergic Toxicity of Organophosphorus Pesticide

Satoshi Ishikawa, MD

Professor and Chairman

Dept. Of Ophtamology

School of Medicine, Kitasato University

1-15-1 Kitasato, Sagamihara City

Kanagawa 228 Japan

 

It has been known that a certain organophosphorus pesticide (OP) when chronically exposed produces sensory and/or motor neuropathy. At the first part, we will introduce how to establish the diagnosis of chronic intoxication is not easy. But it may be made asking history of contamination with OP. Thereafter, clinical improvement due to therapeutic trial by anticholinergic drugs is helpful. The measurement of erythrocyte cholinesteras (ChE) activity may be available in about _ of the cases. We have been using neuro-ophthalmological examinations in order to obtain objective findings to establish the diagnosis. The measurements are as follows:

1. Contrast sensitivity of visual function

2. Visual field measurement

3. Vertical smooth pursuit of the eyeball

4. Pupil reaction to the light

 

In this presentation, we will introduce the results of these tests done to the farmers to find out chronic intoxication with neuropathy of the nervous system. In the second part, noncholinergic action of OP examined by cultured retinal neurons after the administration of low dosages of OP will be introduced by viewing Ca ion and free radicals.

 

 

Chemical Encephalopathy: Evidence of the Human Nervous System is Most Sensitive to Toxic Chemicals

This study reviews the results of testing 145 subject exposed to chemicals considered as one group and six populations exposed to trichloroethylene, toluene, arsenic, chlordane, chlorine, and hydrochloric acid using a battery of neurobehavioral tests. These tests showed that "incident" brief single exposures to formaldehyde, diesel exhaust, methyl bromide, gasoline, indoor air, and other mixtures produced neurobehavioral impairment. In the patients and all six groups balance, simple and choice reaction time, blink reflex latency, color discrimination and recall, cognitive function, and perceptual motor speed were impaired compared to unexposed referent subjects recruited from voter registration rolls in three sections of the country to adjust for age, age squared, and education level, which were the principal modifiers of performance before considering chemical exposure. To define patterns the test profiles for subjects exposed to various chemicals were compared, and both similarities and differences were found. Single chemicals and mixtures in single brief exposures and during years of residence adjoining industry or its waste disposal cause widespread neurobehavioral impairment of such severity that their use and disposal should be interdicted.

 

 

Olfactory and Trigeminal Hypersensitivity to Perfume and/or Chemicals in Multiple Chemical Sensitivity (MCS)

Dr. Med. Michael P. Jaumann

Artz fur Hals-Nasen-Ohrenheilkunde

Stimm-und Sprachstorungen

73033 Goppingen, Marktstr. 25, Germany

 

The importance of smell and taste for life is underestimated as long as they are functioning well. Smell and taste, together with mechano-, thermo-, and nociception, are the "lower" senses. They directly influence the limbic system, which is a part of the Archaeo-cortex and is responsible for affective behavior and moods.

 

Neurotoxicity in humans encompasses a vast variety of effects, ranging from cognitive, sensory, and motor impairments to immune system deficits. Interactions between chemicals and the neuroanatomy and neurophysiology of the olfactory and limbic system have been shown in animals and men. Inhaled or injected chemicals (solvents, pesticides) accumulate in the olfactory mucosa. This mucosa has its own P450-system and contains many neurotransmitters (GABA, glutamat, dopamine, neuropeptides). Through this mucosa, inhaled molecules are absorbed and transported via axon and transneural to the bulbus olfactorius, the limbic system and the brain. In this way molecules of substances influence the olfactory bulb, starting a cascade of biochemical reactions in the olfactory and limbic system, the hippocampus, hypothalamus and formatio reticularis. Scientific data show that repeated low-level exposure creates an augmentation in central nervous system (CNS) excitability, which is called "kindling." Therefore, many neurologic diseases can be understood as the result of one or more disturbed systems of neurotransmitters.

 

Clinical observations in many cases worldwide suggest this illness (MCS, hypersensitivity) involves a two-step process: (1) Priming (sensitization) and (2) triggering.

 

Olfactory (chemosensory) event-related potentials (CSERPs) were first obtained in 1965 as a response to odorants. In the meantime many medical doctors realize that an objective assessment of the sense of smell is needed. The sophisticated stimulators developed by KOBAL facilitate the measuring of the function of the N. Olfactorius and N. Trigeminus. This is of special importance in patients with olfactory dysfunction, M. Parkinson and M. Alzheimer.

 

For two years we have applied this CSERPs in about forty patients with MCS. In many cases a hypersensitivity to odors and chemicals could be proven. These findings support the ideas about the "chemical kindling" of the limbic system due to neurotoxic and neurochemical damage.

 

LITERATURE

Ashford, NA, and CS Miller. (1991). Chemical Exposures: Low Levels and High Stakes. New York: Van Nostrand Reinhold.

Ghanthous, H., et al. (1990). "Accumulation and Turnover of Metabolites of Toluene and Xylene in Nasal Mucosa and Olfactory Bulb in the Mouse." Pharm Toxicol 66:87-92.

Gilbert, ME. (1994). "Phenomenology of Limbic Kindling." Toxicol and Industrial Health 10(4/5):343-358.

Jaumann, M.P., W. Eckrich, and G. Schwinger. (1991). "Early Detection of Neurotoxic Effects of Organo-Halogen Compounds by Auditory Evoked Potentials (AEP)." Organohalogen Compounds 7(2):407.

Kobal, G. Elektrophysiologische Untersuchungen des Menschlichen Geruchssinnes. Thieme: Stuttgart, 1981.

Kobal, G. Process for Measuring Sensory Qualities and Apparatus Therefore. United States Patent Number 4, 681, 121.

Meggs, WJ. "Neurogenic Inflammation . . . ." Environmental Health ProSpectives 101(3):234-238.

Walsh, T., and D. Ermerich. (1988). "The Hippocampus as a Common Target of Neurotoxic Agents." Toxicology 49:137-140.

 

 

Neurotoxicity in Otolaryngology: Early Detection of Neurotoxicity by Evoked Response Audiometry (ERA)

Dr. Med. Michael P. Jaumann

HNO-Belegabteilung

Klinik am Eichert

73035 Goppingen, Germany

 

Neurotoxicity of the human organism and the diseases following are an outstanding problem in medicine nowadays. Public heath politics and the public are not aware of this problem yet. Most of our medical knowledge about neurotoxicity derives from severe intoxications: mercury in Minimata, TOCP and PCBs in oil, lead in the Roman Empire. Many substances not only have additive but also synergistic effects. The increasing understanding and definition of "subclinic neurotoxicity" shows the new dimension of threat in our "chemical environment."

 

Along with sensible and motoric dysfunction, the complete failure of sensory systems—like sudden hearing loss or the "retrobulbar neuritis"—is a symptom of neurotoxicity. The inhalative uptake of toxic substances is, compared to the oral ingestion, severely underestimated: molecules inhaled pass the 0,6 ;um thin air-blood-barrier of the alveolar region and are instantly transported to the brain; the same via the pharyngeal and nasal mucosa (Shipley 1985). Prime targets are the temporal lobes, the hypothalamus, and hippocampus (NAS 1990; Walsh 1988).

 

Disturbed systems include the most important neuronal pathways and intersections, the autonomic nervous system, and the hormonal regulation of the pituitary gland (Corwin 1987). No part of our brain is further than 50 um from brain capillaries.

 

The situation with many disturbances of cerebral nerves and the nowadays available modern diagnostic procedures in Otorhinolaryngology (ORL) enable the early detection of neurotoxic disease.

 

Altered ERA-potentials in patients were highly significant correlated with an intoxication of hexachlorbenzene (HCB), DDT, DDD, DDE, and/or polychlorinated biphenyls (PCBs) compared to controls (Jaumann 1991).

 

Besides a thorough history, the ORL-examination includes standard examinations with endoscopy, audiology including ERA and P300, ENG and otoneurological tests, functioning of the visual system (VEP), taste, smell, and trigeminal nerve (computed multi-channel olfactometry, SSEP, CSEP). All these tools of applied physiology and medicine enable the detection of peripheral or central "nerve dysfunction."

 

There is more and more proof that there is no safe level (NOEL) with many chemicals and toxic substances. The delicacy and complexity of our nervous system and the brain, the information transported by molecules and neurohormones, make our nervous system and brain most vulnerable to changes of the chemical environment.

 

Many doctors are not aware of this upcoming challenge. Intensive education is needed as many neurotoxic diseases are "mislabeled" today. Public Health Care has to understand that only prevention of pollution will pay.

 

LITERATURE

Corwin, A. (1978) "A Chemist Looks at Health and Disease." Proceedings of the Society for Clinical Ecology, 12th Advanced Seminar, Key Biscayne, FL.

Jaumann, MP, W Eckrich, and G Schwinger. (1991) Early Detection of Neurotoxic Effects of Organo-halogen compounds by auditory evoked potentials (AEP)." Orhanohalogen Compounds 7(2): 407.

Shipley, M. (1985) "Transport of Molecules from Nose to Brain: Transneuronal Antigrade and Retrograde Labeling in the Rat Olfactory System by Wheat Germ Agglutirrin—Horseradish Peroxidane Applied to Nasal Epithelium." Brain Research Bulletin 15:129-124.

Walsh, T, and D Emerich. (1988) "The Hiippocampus as a Common Target of Neurtoxic Agents." 49:137-140.

 

 

Doors and Windows of the Blood-Brain Barrier (BBB): Mechanisms for Transport of Immunoglobulins and Albumins into the Brain

Gerald P. Kozlowski, PhD

Dept. Of Physiology

The University of Texas

Southwestern Medical Center

5323 Harry Hines Blvd.

Dallas, TX 75235-9040

 

The BBB differentially excludes serum v-globulins and albumin. The mean concentration of IgG (24 mg/L) in cerebrospinal fluid (CSF) of adult humans is about eight times lower than albumin (204 mg/L). One of our goals was to compare immunostaining for IgG and albumin in brain sections in order to determine if there were relative differences in the patterns of intracellular vs extracellular staining.

 

Brains of male, Long-Evans rats were perfusion-fixed with Zamboni’s fluid and 40 um Vibratome sections were used in a modified immunocytochemical (ICC) procedure employing the avidinbiotinylated peroxidase complex (Vectastain Elite ABC kit). We screened several primary antisera against either IgG (rabbit, sheep or goat antirat IgG) or albumin (rabbit antirat, rabit antihuman, rabbit antibovine) in our staining protocol. Biotinylated forms of either Proteins A (BPA, Vector Labs) or G (BPG) were used as bridging molecules. Protein G was bioengineered by Genex Corp to improve its IgG binding capabilities and eliminate possible cross-reaction with albumin found in native Protein G. Additional brains were removed from animals treated 24 hours earlier with 100 ug of colchicine.

 

In both cases of ICC and colchicine-treated animals, staining for IgG was eliminated. For most animals, selective staining for albumin was far more prevalent than for IgG in the hippocampus, hypothalamus, and cortex. Patterns of staining included either dark or clear cells on a dark background; or dark cells on a clear background. In the median eminence and organum vasculosum lamina terminalis, the neuropil was dark indicating diffusion of proteins from fenestrated vessels. Dark staining neurons on a dark background were particularly evident in the arcuate nucleus, presumably because they project to areas outside the BBB and take up serum proteins by endocytosis and transport them retrogradely to their perikarya. Supraoptic and paraventricular neurons also project outside the BBB and likewise take up proteins by endocytosis.

 

However, unlike the circumventricular organ areas, they appear as dark ce*p-1X1s on a clear background because they reside beyond regions of protein diffusion. In areas such as the lateral septum, there were clear (unstained) neurons on a dark background possibly due to diffusion of CSF-borne proteins into the neuropil yet no uptake by lateral septal neurons. In cases like the hippocampus, where dark cells appear on a clear background, proteins may be passed from neuron to neuron via transcytosis. Therefore, it can be concluded that the pattern of staining for serum proteins in the brain can suggest various possible sites of origin.

 

Of great interest to practitioners of environmental health is the discovery of a nose-brain pathway that allows the free entry of substances directly into the brain. Also, newer findings of immune agents such as cytokines and their receptors endogenous to neurons, glial cells, and blood vessels suggest that the central nervous system may play a vital protective role independent of the peripheral nervous system.

 

OUTLINE OF TALK

I. Introduction

A. Normally the only places to find IgG and albumen was around the circumventricular organs (CVO).

1. Now using ICC with specific antibodies, more IgG was visualized.

2. Zlokovic’s work showed IgGs crossed the BBB

3. Recently, Ellison showed IL-2 transported IgG across blood vessels.

4. Kozlowski and Nilavers studies demonstrate albumen in arcuate neurons.

 

II. Materials and Methods

A. Rat brains

B. Antisera when used with biotinylated pA or pG and ABC kit stain:

1. IgG: rabb anti-rat, goat anti-rat, and sheep anti-rat

2. Albumin: rabb anti-rat stained. Rabb anti-rat.

3. Biotinylated prot A or prot G by itself does not stain. Why?

Bio pG is better than bio pA as a second reagent because pG stained more intensely.

4. Controls—normal vs injured, SCID, and nude mice.

C. Primary tissue culture of CNS block.

D. Colchicine studies by Gaj Nilaver.

E. Blocking experiments where IgG was added to anti-IgG got enhanced staining of myelin structures (autoimmune complexes) at higher concentrations. Stock solution was 1 mg rat IgG added to 1 ml of PBS. Working dilutions of 500 ul/5 ml (1:10), 250 ul/5ml (1:20), and 1:100 stained. When 1:500 was used to stain, so used soluble complexes.

F. Blocking experiments where bovine serum albumin was added to rabb anti-bovine albumin. Stock solution = 5 mg added to 5 ml of stock was added to 1:500 of rabb anti-BSA. No staining so completely blocked.

1. 100 ul of rat plasma from same animal used for brain histology was added to 5 ml of PBS to give 1:50 dilution. Then to that solution was added 10 ul of undiluted rabb anti at alb. The final dilution of 1:500 stained very little.
2. Precoated tubes by BSA and gelatin—no difference for IgG complexes.

 

III. Results

A. IgG

1. Technical differences between antiseras but same structures stained.

2. If BBB is damaged, everything stains. Selective staining at first but after long time everything stains. Depends on site of injury.

3. If BBB is undamaged, localization in CVOs—for median minence dark neurons on a white background, around IIIv get white neurons on black background. A few in ctx under dura mater having fenestrated bvs, in hippocampus where ILs allow IgG through.

4. If look at primary culture after 24 hours, no IgG staining in neurons or medium eminence.

B. Alubmin

1. Different from IgG. Diffuse staining almost everywhere, except for frontal structures like triangularis septi, medial septum. In m.e., get dark cells on white background.

 

IV. References

 

 

The Neurotoxicity of the Organophosphates

Dr. Christopher Heard

Jean Monro, MD

Breakspear Hospital

Belswains Lain, Hempel Hempstead

Hertfordshire HP3 9XL, England

 

AIMS AND OBJECTIVES

This presentation aims to present information on the neurotoxic and neuropsychological effects of the organophosphate compounds, including those used as pesticides.

 

ABSTRACT

The gradual realization of the neurotoxic potential of the organophosphates used as pesticides since the 1930s continues even today. There are three distinct neuropathic patterns, through the immediate type of neuropathy seen in animals has yet to be confirmed in humans. Recent research has highlighted the existence of long-term neuropsychological effects that may be subtle and therefore be overlooked. An overview of the neurotoxicity of the organophosphates is presented.

 

CONCLUSION OF WHAT IS TO BE LEARNED

1. The organophophates have uses other than as pesticides

2. There are three distinct patterns of neuropathy—immediate, intermediate, and delayed.

3. There is an emerging pattern of neuropsychological dysfunction that persists long after exposure has ceased.

4. The organophosphates, in common with the organochlorines, are capable of amygdala kindling, one of the proposed mechanisms of multiple chemical sensitivity.

5. Since the compounds are also immunotoxic, they may trigger or exacerbate multiple chemical sensitivity disorder.

6. There are complex interactions between members of this class of compound and between organophosphates and other chemicals, including standard medications.

 

 

Vitamin B6 Deficiency in Multiple Chemical Sensitivity Neurological Consequences and Possible Mechanisms

Dr. Christopher Heard

Dr. Jean Mongo

 

AIMS AND OBJECTIVES:

To present information about the function, biochemistry, and deficiency of vitamin B6 and its possible relevance to MCS.

 

ABSTRACT:

Seventy percent of patients with multiple chemical sensitivity attending Breakspear Hospital have a functional deficiency of vitamin B6. The vitamin is required for the metabolism of neurotransmitters, hormones, and sulphur amino-acids. The potential relevance of impairment in these metabolic steps to the symptomatology of MCS will be presented and discussed.

 

CONCLUSION OF WHAT IS TO BE LEARNED:

1. Vitamin B6 is deficient in approximately 70% of MCS patients attending Breakspear Hospital in the UK.

2. Absorption is impaired when jejunal ph is elevated as a result of reduction in gastric acidity from ulcer medications and normal aging.

3. The vitamin has a pivotal role in sulphur amino-acid metabolism, which is more frequently impaired in patients with food sensitivity and MCS.

4. B6 is implicated in oestrogen and androgen metabolism, which may be impaired in patients with MCS. 5. Deficiency states have been associated with neurological impairment, hyperactivity, convulsions, and confusion; these are

 

 

Phytochemicals: A New Era in Preventative and Therapeutic Nutrition

H. Reginald McDaniel, MD

Scientific Consultant

Director of Research Fisher Institute for Medical Research

2010 N. Highway 360

Grand Prairie, TX 75050

 

For survival animal-life has always migrated to a more tolerant environment, if available. A plant has the choice to adapt or die. The adaptation mechanism for plants is production of countless free-radical and anti-oxidant molecules in its cells (phytochemicals) to protect life processes, seeds or plant tissue essential for the next generation. These labile molecules are maximally stored in plant-ripened, seeds, fruits, and vegetables. Economics and social customs have created mass phytochemical dietary deficiencies leading to a myriad of chronic human diseases that are poorly managed by drugs and standard modalities. Flash-freeze-dried phytochemicals from mature plant tissues can restore normal cellular physiology that includes immunity and anti-cancer activity.

 

 

Aloe Polymannose: An Essential Phytochemical for Optimal Health

H. Reginald McDaniel, MD

Scientific Consultant

Director of Research, Fisher Institute for Medical Research

2010 N. Nighway 360

Grand Prairie, TX 75050

 

Aloe Vera has been used for over 5,000 years as a medicinal agent. Recent research has determined for molecular biology for this unbroken chain of use. Polymannose units synthesized in the aloe plant activate macrophages to produce numerous cytokines and colony growth factors that facilitate the normal physiology of body defense, repair, and healing. The breakdown product of processed Polymannose is mannose-6-PO4. This is a nutrient essential for cell membrane and lysosomal enzyme synthesis. A bonus is the virtual lack of toxicity in animal and human testing. Polymannose is a phytochemical that supports synthesis of gene dictated molecules responsible for the biochemistry that supports synthesis of gene dictated molecules responsible for the biochemistry of cellular and organ function. Dietary use results in an unparalleled spectrum of benefits for supporting optimal health and healing.

 

 

Are Your Patients Sick and Tired of Being Sick and Tired?

Doris J. Rapp, MD, FAAA, FAAP

Environmental Allergy Center

2575 Elmwood Avenue

Buffalo, New York 14217

Phone: 716-875-5578

 

UNUSUAL PATIENTS—CHRISTINA AND AMIE

Two young, teenage women will be presented who have very similar complaints. Both have had daily severe fatigue, intestinal pain, cephalgia, myalgia, and obvious chemical sensitivities. Both have high IQs with poor school performance and major problems with visual perception. Printed letters twirl around, drop out, and are upside down. They can both read upside down, as well as in a normal manner. Both youngsters have a positive personal and family history of allergy, evidence of fetal allergy, infant symptoms, allergic rhinorrhea, allergic tubotymapnitis, gastrointestinal symptoms, probable hypoglycemia, PMS, candidiasis, allergic conjunctivitis, asthma, eczema, urticaria, and extreme fatigue associated with the allergic-tension-fatigue syndrome. Amie had been suicidal. Christina could read writing from a blue magic marker, but could not read writing made with a green, black, or red marker. Their response within three days to provocation/neutralization allergy testing and treatment was remarkable.

 

SPECIFICS ON CHRISTINA

When Christina was tested for molds, her reaction was similar to the type that caused her to be rushed to the emergency room on several occasions. She developed severe left lower quadrant pain, which radiated to her back. She had a severe headache; she was doubled up and crying in a corner in the hall. Within less than a minute after the correct dilution of the mold mix, she felt the best she had in years. Her PMS symptoms subsided quickly with a correct dilution of progesterone. She definitely had left lymph node swelling with certain skin tests, and this has been a recurrent problem in the past.

 

During provocation/neutralization testing, we found the following:

1. Christina’s intestinal complaints were caused by molds, chocolate, epithelials, and progesterone;

2. Her headaches were caused by epithelials, molds, and chocolate.

3. Her muscle aches were caused by molds and progesterone.

4. Her lymph node swelling was caused by mold, mites, and ragweed.

5. Her cystitis symptoms were caused by molds and chocolate.

6. Her drowsiness was caused by dust, chocolate, and wheat.

7. Her dizziness was caused by wheat, milk, and epithelials.

 

SPECIFICS ON AMIE

Six weeks prior to coming to our office, Amie developed red vision (macular edema), and subsequent to that, she could only read upside down. It is of interest to note that when we tested Amie for alternaria, she suddenly could not read at all. When we found the correct neutralizing dose, she could read in her normal manner, upside down. The next day, however, we tested her for fermented soy, and, much to our surprise, we found that she could read right side up again, as well as upside down. The letters no longer twirled and disappeared as they had done previously. Her depression markedly diminished.

 

Amie’s extreme fatigue began when she started in a new school in September 1994. At about that time, they had also installed a new carpet in her home. She was so tired that she spent one entire week, at one point, in bed. She was too tired to throw a basketball, until the family had her placed on a four-day rotational diet.

Because of her many medical complaints, pains, and fatigue, she was so depressed at one point that she tried to slash her arm in an attempt to kill herself. At the present time, she is very positive about her future.

 

At one point, she was playing ball on a lawn sprayed with pesticides and lost consciousness. At that point, no one knew what had caused that difficulty.

 

During provocation/neutralization testing, we found the following:

1. Amie’s headaches were caused by dust, milk, wheat, and molds;

2. Her extreme fatigue was caused by mites;

3. Her reading problems were caused by molds and soy;

4. Her intestinal complaints were caused by molds and grass; and

5. Her cold hands and feet were caused by rice, flu, and molds.

 

Both of these girls have claimed that they had never had a day in their lives when they had felt entirely well. We have to ask how many other Christina’s and Amie’s there are out there who have no idea what is wrong or what to do about it.

 

 

The Environmental Aspects of Neurological Disease

William J. Rea, MD, FACS, FAAEM

Environmental Health Center—Dallas

8345 Walnut Hill Ln, Suite 205

Dallas, Texas 75231

 

Jaqin Pan, MD

Yoshiaki Ichibe, MD

Bolin Chen (PhD candidate)

 

Many toxic environmental exposures, especially pesticides and solvents are attracted to, and cause damage to, the nervous system. The autonomic, peripheral, or central nervous system can be involved alone or in combination. Central nervous system involvement has been difficult to document in the early stages until recently as the development of neuropsychological profiles, computerized balance tests, and SPECT brain scans have become available. Now one can correlate these brain function tests with blood levels of toxic, immune tests, and intradermal, oral, and inhaled challenges. Not all chemically sensitive patients have central nervous system involvement; however, a large segment of the chemically sensitive population does. Now a modern technology for diagnosis and therapy can be carried out on a long-term basis, using a sound scientific foundation.

 

The Environmental Aspects of Cardiovascular Disease

William J. Rea, MD, FACS, FAAEM

Environmental Health Center—Dallas

8345 Walnut Hill Ln, Suite 205

Dallas, Texas 75231

 

Jaqin Pan, MD

Yoshiaki Ichibe, MD

Bolin Chen (PhD candidate)

 

It has become clear that most cardiovascular disease along with hereditary tendencies are triggered by some aspect of environmental pollutants. These triggering agents are multifactorial and probably disturb the ground regulation system of the extracellular matrix and secondarily disturb the endocrine, immune, and neurological systems. The neurovascular connections appear to deregulate blood vessels along with local injury. We have now studied over 5,000 patients with vascular dysfunction and arteriosclerosis. The clinical entities include general and specific organ arterosclerotic occlusive and disease and vasospastic phenomena (i.e., coronary spasm) and microcirculation disturbances. It is clear now that the triggering agents of vascular disease can be defined and that prevention is possible.

 

 

Molecular Basis for Diet and Lifestyle Changes in Healing Recalcitrant Cardiovascular and Neurologic Diseases

Sherry A. Rogers, MD

Northeast Center for Environmental Medicine

P.O. Box 2716

Syracuse, NY 13220

 

The mainstay for treatment of most cardiovascular and neurological diseases is phramacologic intervention. The pharmaceutical industry progressively discovers new biochemical ways to ignore or poison biochemical pathways that no longer function, in order to relieve symptoms temporarily. The problem is that by overriding the damage and deficiencies that underlie dysfunctional pathways the patient is pushed to develop new symptoms and diseases faster. Then more specialists are consulted and more medications are prescribed.

 

But because of the artificial division into specialties, it assumed that the development of seemingly unrelated symptoms has no bearing. Using medications to ignore the basic biochemical defect deprives the patient of the opportunity of finding and fixing what is broken. This also allows the disease process to continue, and in fact accelerate, as well. Hence, further drugs and surgery are required.

 

The reason many of these pathways have become damaged in the first place is because of diet and lifestyle transgressions that can be remedied. And once remedied, these can cause reversal of symptoms that, when treated with the current medication/surgery protocols, reach an impasse.

 

As one example, calcium channel blockers are widely used for angina, arrhythmia, and hypertension. But the initial damage to the calcium pump has multiple dietary and lifestyle causes, like pesticides and other xenobiotic exposures, transfatty acids, and nutritional deficiencies. Studies confirm that mere poisoning of the calcium channel with calcium channel blockers leads to an accelerated rate of cancers and other diseases, as it should, for to ignore repairing the cell membrane allows other membrane functions to deteriorate as well.

 

Take, as an example, one membrane constituent, phosphatidyl choline, crucial for membrane function and calcium channel physiology. It is ripped from the endoplasmic reticular membranes during the work of xenobiotic detoxication, and it is lost forever. PC can be lost from the cell membrane as pesticides and other xenobiotics damage gap junctional proteins, cell hormone receptors, and mitochondrial membranes.

 

PC normally proceeds to form choline on its way to forming the primary brain neutrotransmitter, acetyl choline. But choline also forms glycine, glutathione, and methyl groups, all of which are lost in the work of daily environmental detoxification. This can severely compromise the amount of choline available to make acetyl choline for recent memory, optimum mood chemistry, and neurological function.

 

Another membrane disease that feeds this vicious cycle and causes some patients never to get completely well is hyperpermeability of the intestinal wall. This, in turn, fosters the development of food and chemical sensitivity, autoimmunity, poor nutrient absorption, and resultant cardiovascular and neurological disease.

 

This dramatically points out how pervasively important the principles of total load and environmental controls that ecologists have singularly taught for decades are for any physician who endeavors to treat any disease. And it explains why and how with the current treatment protocols (practice guideline), the sick get inevitably sicker more quickly. Neurological disease can progress to cardiovascular disease and vice versa, or to cancer.

 

We will explore the use of some interesting orphan nutrients like phosphatidyl choline arid choline, case examples, and the literature behind them, and most importantly, how to arrest and reverse this chain of events that can lead to multiple "dead-end" illnesses, which have become recalcitrant to current therapies.

 

Diet and lifestyle (or what we call environmental controls) have been a mainstay of environmental medicine since its inception. Yet this combination of factors is low, if not nonexistent in terms of current medical therapeutic priorities. It pales in excitement when compared with high-tech medications and procedures and seems too simple to be true. And this is in spite of studies proving the benefits, even when all else that medicine has to offer has failed (Ornish, Lancet, 1990; Carter, Am. J. Clin. Nutr., 1993).

 

With the current knowledge of xenobiotic detoxification, however, this demonstrates that diet and lifestyle change should be the foundation of ethical medical treatments, and especially when all else has failed.

 

For over 1,000 references, see the following:

SA Rogers
Depression Cured at Last!
Sand Key Pub.
Box 40101
Sarasota, FL 34242

For diet and lifestyle directions, see the following:

SA Rogers
Wellness against All Odds
Sand Key Pub.
Box 40101
Sarasota, FL 34242

For further back-up, see the following:

SA Rogers

The Scientific Basis of Selected Environmental Medicine Techniques

Sand Key Pub.

Box 40101

Sarasota, FL 34242

 

 

Environmentally Induced Neuropathic Symptoms—A Review of the Symptoms, Types of Exposures and Chemical Contamination Found among Patients with Peripheral Neuropathy at the Environmental Health Center-Dallas

Gerald H. Ross, MD

Environmental Health Center—Dallas

Dallas, TX

 

Peripheral neuropathies can generally be categorized on the basis of the affected tissue, whether it be axonal degeneration or demyelination. Neuropathies can be associated with inherited conditions (such as Friedreich’s ataxia and porphyria); systemic and metabolic disorders (such as diabetes, uremia, and alcoholism); nutritional deficiencies; infections and inflammatory diseases (such as leprosy, AIDS, sarcoidosis, and rheumatoid arthritis). Neuropathies may also be associated with malignant diseases and Guillain-Barre Syndrome. From an environmental point of view, they may also be connected to toxic exposures, especially to hydrocarbon solvents, metals, certain medications, organophosphate compounds, including pesticides, and others.1

 

A computerized search for the diagnosis of neuropathy was conducted among patients presenting at the EHC-Dallas over a two-year period ending October 28, 1995.

 

There were 114 patients identified in this manner, and, of these, fifty were chosen at random for chart review. Four patients were found to have inadequate data or had been lost to follow up, leaving 46 patients in the study group. There were 15 men and 31 women, and their average age was 45.3 years.

 

Symptom frequencies will be presented for the categories of (1) numbness or tingling, (2) fatigue, (3) joint swelling or pain, (4) muscle pain or weakness, (5) headache, (6) myalgia, (7) dizziness or lack of coordination, (8) cold extremities, (9) blurred vision, and (10) presence or absence of Rombergism (for example, 29 of these 47 patients had positive Rombergism, which, in our experience, can be a valuable clue to neurotoxic effects). The type of chemical exposure associated with the condition will be characterized, along with the numbers and types of chlorinated, aromatic, and aliphatic solvents, PCBs, and chlorinated pesticides detected in the blood of these patients.

 

For those cases in which brain metabolic SPECT scans were conducted, a breakdown of these findings will also be presented. The incidence and characterization of abnormal function of the autonomic neurological system, as measured by pupillography, will be shown. Finally, the degree of chemical sensitivity was high in these patients, as seen by intradermal testing, and this data will also be presented.

 

In summary, there appears to be a high incidence of chemical contamination in these patients with peripheral neuropathy, especially from xenobiotics that are known to have neurotoxic effects.

 

GOALS AND OBJECTIVES

To review some of the common environmentally triggered causes of neuropathy, specifically to identify symptoms and findings in neuropathy patients presenting to an Environmental Medicine practice, and to identify factors associated with and contributing to the symptoms to help educate physicians on the need to consider environmental inducers of neuropathy.

 

CONCLUSION OF WHAT IS TO BE LEARNED

Commonly encountered chemicals have the potential for significant neurological effects, and neurotoxic xenobiotics are frequently found in patients with neuropathic symptoms. Options for investigation and characterization are available.

 

REFERENCES

1. Aminoff MJ. Nervous System, Chap. 23, in Current Medical Diagnosis and Treatment—1994, Tierney LM, McPhee SJ, and Papadakis MA (Eds.), Appleton and Lang, Norwalk, CT, 1994, pp. 798-854. 2. Rea WJ. Chemical Sensitivity, Vols. 1-3, Lewis Publishers, Boca Raton, FL, 1992, 1993, 1995. 3. Baker, EL. A Review of Recent Research on Health Effects of Human Occupational Exposure to Organic Solvents—A Central Review, Jour. Occ. Med., 36 (10), Oct. 1994, pp. 1079-1092.

 

 

Gastric Acid Secretion Regulated by the Nervous System

William G. Sargent, OD, RPH

Vision Care Specialist/Self Practice

(Optometrist, Pharmacist, Teacher)

30 Village St.

Pikeville, KY 41501

 

Brain stem malfunctions are the etiologies of most systemic disease. Cardiovascular functions are regulated in the brain stem by the vagus nerve and the autonomic nervous system. Gastrointestinal functions are regulated by the vagus nerve, hypothalamus, humoral secretion, and the enteric nervous system in the alimentary canal.

 

Hormones and neurotransmitter chemicals are synthesized and released by many reflex responses among the suprachiasmatic nucleus, located in the hypothalamus and the endocrine system. Interactions of all systems are possible by reflexes and responses.

 

The stress of holding both eyes on the point of fixation for binocular vision appears to cause malfunctions of the brain stem. When the source of electrical impulses are depleted or reduced, malfunction of the brain stem manifests. The brain stem sorts afferent impulses and processes certain impulses and inhibits others, reducing the demand for electrical impulses with relieving prism restores normal function of the brain stem.

 

Specific reflexes involved with brain stem malfunction are investigated in this paper. Monocular loss of a blink reflex, loss of micturition reflex in the brain stem, loss of resreflex while asleep, and loss of flexor reflexes in the leges are researched for etiology.

 

INTRODUCTION

The purposes of the alimentary canal are digestive and absorptive properties of proteins, fats, and complex carbohydrates. The products of digestion and vitamins, minerals, and water cross the mucosa and enter the lymph or blood. Digestion of the major foodstuffs is an orderly procedure involving the action of many digestive enzymes. These enzymes are found in the secretions of salivary glands, the stomach, and the exocrine portion of the cells lining the small intestine. Actions of enzymes are aided by hydrochloric acid secreted by the stomach and the bile secreted by the liver.

 

Mucosal cells in the small intestine have a brush border made up of many microvilli lining their apical surface. This border is rich in enzymes. It is lined on the luminal side by a layer rich in neutral and amino sugars. The alimentary canal is equipped to obtain small units absorbed into the transport systems

 

Gastric secretion and motility are regulated by neural and humoral mechanisms. Stimulation of the vagus nerve in the chest and neck increases acid pain and pepsin secretion. However, vagotomy does not abolish the secretory response to local stimuli. Compression of the vagus in the brain stem may increase gastric acid secretion. Nerves in the intestinal wall constitute a complex enteric nervous system considered a third branch of the autonomic nervous system. Local reflexes release neurotransmitters as serotonin and several peptides from gland cells in the mucosa. Local feedback responses inhibit many different hormones used in the digestive system. All activities of secreting peptides are not yet clear.

 

All gastrointestinal functions are regulated and controlled by the brain stem.

 

 

Scintigraphic Insights on the Brain

Theodore R. Simon, MD

Nuclear Medicine Consultants of Texas

4429 Southern Ave.

Dallas, TX 75205

 

David C. Hickey, MD

Audrey Stein Goldings, MD

 

Scintigraphy has allowed us to probe into the function of the brain by examining the dynamic and static distribution of a radiotracer that is altered by detoxifying reductases such as glutathione. Vasculitis has been raised as an alternative explanation for the phenomenon. We have applied this technique to normal controls and to patients with a history of solvent exposure, breast implants, or pesticide exposure as well as to veterans of Desert Storm/Desert Shield.

 

This technique is not extended to Lyme Disease, which may affect the brain by including a vasculitis or by inciting a neurotoxic process through cytokines. Nine consecutive patients were analyzed. The six women and three men ranged in age from 28 to 76 years. All had abnormal examinations.

 

We conclude that Lyme Disease can cause abnormalities in a brain scintigram that closely mimic or are identical to the pattern seen in other neurotoxic disease processes.

 

 

Cardiovascular Scintigraphy and the Environment

Theodore R. Simon, MD

Nuclear Medicine Consultants of Texas

4429 Southern Ave.

Dallas, TX 75205

 

David C. Hickey, MD

 

Emission Computed Tomography and Transmission Computed Tomography used to provide complementary information: functional vs. anatomic. Recent developments in Electron Beam Transmission Tomography have dramatically increased energy resolution and decreased imaging time. These enhancements allow functional information to be obtained using both techniques. This powerful new tool can rapidly screen large numbers of people inexpensively and noninvasively. Diagnostic information of sufficient quality is often immediately available to resolve clinical questions or to accurately guide the remainder of the diagnostic algorithm.
The application of these techniques to the environmental patient is actively underway. Preliminary work investigating the effect of chelation therapy has shown short-term increases in the calcium burden of the coronary arteries with therapy.

The combination of cardiovascular scintigraphy and electron beam transmission tomography offers the environmental patient new options in investigating the effect of the environment on health. The efficient use of this combination is an area of active exploration at this time.