Page 1, 2, 3, 4

Conclusion
The metabolic syndrome has no defined etiology that can be targeted by specific treatment, and its use in predicting risks for cardiovascular disease has proven disappointing as well (Kohli et al. 2006). Kahn et al. stated that the new definitions of MSX have major flaws (Kahn R et al. 2005). The definition of MSX is assumed to predict diabetes and cardiovascular disease (CVD), but in fact includes diabetes and CVD. The American Heart Association (AHA) and American Diabetes Association (ADA) have been at odds over the clinical relevance of the metabolic syndrome. The ADA feels that MSX is poorly defined and misleading, and there is no consensus of agreement as to the utility of the grouping of risk factors associated with MSX (Mitka 2006).

It is obvious from the above discussion that the development of MSX is complex and multi-causal. The condition involves not only genetic, lifestyle, environmental, and emotional factors; development and progression is greatly influenced by neuroendocrine and nutritional imbalances.

HTMA may serve as a useful screening tool for assessing individuals with a predisposition toward MSX. Further research will undoubtedly show that HTMA patterns will provide not only an indication of MSX but also reveal factors contributing to the underlying progression of the associated syndromes. HTMA will substantially aid in assessment of the collective factors, which is necessary for determining a specific, targeted nutritional approach in treatment and prevention.

In reviewing this paper, one should be cautious about drawing conclusions and making applications. There are not only biological differences contributing to diabetes and CVD, but also biological variability among each metabolic type. One should not assume that there exists a single mineral pattern and, therefore, a single nutritional approach for all individuals who have MSX. There are several subtype mineral patterns associated with each metabolic type. Consequently, each person should be assessed and treated as an individual rather than grouped under a broad category of disease or syndrome. With the recognition of biological individuality that can be assessed through HTMA and other methods, the concept of one diet or nutritional approach for diabetes, heart disease, and other health conditions is obsolete and can no longer be justified. Quoting Ann Coulston, "Changes in philosophy, scientific recommendations, and terminology shift the nutrition management of diabetes from a mathematical to a cognitive process…" (Coulston 1994). This statement is true for the treatment of most health conditions and provides the opportunity for increasing the effectiveness of nutritional therapy.

Dr. David L. Watts, Director of Research
Trace Elements, Incorporated
4501 Sunbelt Drive, Addison, Texas 75001 USA
(800) 824-2314
(972) 250-6410
Fax: (972) 248-4896

Reprinted with permission from Trace Elements, Inc. Newsletter. January-April 2007; 17 (1,2).

References
Alrefai H, et al. The endocrine system in diabetes mellitus. Endocrin. 2002;18

Batzevich, et al. Hair trace element analysis in human ecologicalstudies. Sci.Total Environ. 1995; 164; 89,98.

Bergman RN, et al. Free fatty acids and pathogenesis of type 2 diabetes mellitus trends. Endocrinol. Metab. 2000;11,9.

Bjorntorp,P, et al. Hypothalamic origin of the metabolic syndrome x. Ann.N.Y.Acad.Sci. 18, 1999.

Bogden, JD, et al. Clinical Nutrition of the Essential Trace Elements and Minerals. New Jersey: Humana Press; 2000.

Bondy PK, et.al. Metabolic Control and Disease. New York: W.B.Saunders;1980.

Bowman B, Russell R., Eds. Present Knowledge in Nutrition, 8th Ed. Washington, DC: ILSI Press; 2001.

Bujaiska I, et al. Does Central Obesity Reflect "Cushing's Disease of the Omentum"? Lancet. 1997;349.

Bureau I, et. al. Effect of hepatic iron on hypercholesterolemia and hypertryglycerolemia in copper-deficient fructose-fed rats. Nutr. 1998;14.

Cebrian A, et.al. Overexpression of parathyroid hormone-related protein inhibits pancreatic beta-cell death in vivo and in vitro. Diabetes. 2002; 51,10.

Chandra RK. Influences of nutritional status and susceptibility to infection. Advances In Nutritional Research.Vol. 2. Draper, HH. Ed. New York: Plenum Pub: 1979.

Coulston A. Nutrition recommendations for people with diabetes mellitus: A break with tradition. Nutr.Today. 1994; 29,3.

Executive Summary. Conference Highlights. Am.J.Clin.Nutr. 1987.

Feldstein, AE, et al. Free fatty acids promote hepatic lipotoxicity by stimulating TNF-alpha expression via a lysosomal pathway. Hepatol. 2004; 40,1.

Fields, M, et al. The interaction of type of dietary carbohydrates with copper deficiency. Am.J.Clin.Nutr. 39,1984.

George K, et al. The metabolic syndrome-a new worldwide definition. Lancet. 2005;366.

Heaney RP. Long-latency deficiency disease: Insights from calcium and vitamin D. Am.J.Clin.Nutr. 2003;78.

Gerl H, et.al. Improvement of diabetes mellitus after excision of a parathyroid adenoma. Wien. Klin. Woch. 1998;110,23.

Graham TE, et al. Retinol-binding protein 4 and insulin resistance in lean, obese, and diabetic subjects. NEJM. 2006; 354,24.

Guyton A, Hall J. Textbook of Medical Physiology. Saunders Co. 1996.

Harris NS, et al. The chemical pathology of insulin resistance and the metabolic syndrome. Med.Lab.Observ. 2004; 36,10.

Hasebe N. Oxidative stress and magnesium. Clin.Calcium. 2005;15,2.

Hjemdahl P. Stress and the metabolic syndrome. Circul. 2002;106.

Huerta MG, et al. Magnesium deficiency is associated with insulin resistance in obese children. Diab. Care. 2005; 28,5.

Iitaki M, et al. Insulin resistance in pituitary, thyroid, and adrenal disease. Nippom, Rinscho. 2000;58.

Iitaka M, et al. Insulin resistance in pituitary, thyroid and adrenal disease. Nippon Rinsho. 2000;58,2.

Kahn R, et al. The metabolic syndrome. Lancet, 366,9501, 2005.

Kikkoris P, et al. Obesity and endocrine disease. Endocrinol. Metabol. Clin. N. Amer. 2003; 32, 4.

Klevay LM. Coronary heart disease: The zinc/copper hypothesis. Am.J.Clin.Nutr. 1975; 28.

Klevay LM. The role of copper and zinc in cholesterol metabolism. In Advances In Nutritional Research. Drapper, HH, Ed. Plen.Pub; 1975.

Koutsari J. Free fatty acid metabolism in human obesity. J.Lipid Res. May 2006;
14.

Kohli P, Greenland P. Role of the metabolic syndrome in risk assessment for coronary heart disease. JAMA. 2006; 295: 6,7.

Kurup RK, et al. Hypothalamic digoxin, hemispheric chemical dominance and syndrome x with multiple lacunar state. A hypothesis. Neurol. Res. 2003;7.

Lal J, et al. Effect of oral magnesium supplementation on the lipid profile and blood glucose of patients with type 2 diabetes mellitus. J.Assoc. Phys. India. 2003;51.

Lal, et al. Neutron activation of trace elements in human hair: Effect of dietary and environmental factors. Int.J.Rad. Appl. Instrum. 1987; 1:4.

Marx, J. Metabolic defects tied to mitochondrial gene. Science. 2004;306.

Mazur A, et al. Magnesium and the inflammatory response: Potential physiopathological implications. Arch.Biochem.Biophys. 2006.

McCarty MF, et al. PTH excess may promote weight gain by impeding catecholamine-induced lipolysis-implications for theimpact of calcium, vitamin D and alcohol on body weight. Med.Hypoth. 2003;61,5-6.

Medeiros DM, et al. A unified perspective on copper deficiency and cardiomyopathy. Proc. Soc. For Exp. Biol. and Med. 1993; 203.

Mitka M. Researchers examine effects of dietary magnesium on type 2 diabetes risk. JAMA. 2004; 291,9.

Mitka M. Groups call truce over metabolic syndrome. JAMA. 2006; 6: 396.

Mooradian, Morley. Am.J.Clin.Nutr. 1987; 45.

Moshen M. A mediterranean-style diet and metabolic syndrome. Nutr.Rev. 2005; 63,9.

Mozaffarian, D, et al. Dietary fats, carbohydrate and progression of coronary atherosclerosis in postmenopausal women. Am.J.Clin.Nutr. 80,5, 2004.

Nordin BEC, ed. Calcium in Human Biology. New York: Springer-Verlag Publishers;1988.

Norman W, et al. Hormones. 2nd Ed. New York: Academic Press; 1997.

Nowak B, et al. Heavy metals in human hair and teeth. The correlation with metal concentration in the environment. Biol.Trace Elem.Res. 1998;62.

Odegaard AO, et al. Trans fatty acids, insulin resistance, and type 2 diabetes. Nutr. Rev. 2006; 64,8.

O'Dell, BL. Dietary carbohydrate source and copper bioavailability. Nutr.Rev. 48,12,1990.

Ogura M, et al. Unilateral adrenalectomy improves insulin resistance and diabetes mellitus in a patient with ACTH independent macronodular adrenal hyperplasia. Endocrin.J. 2003; 50,6.

Oron-Herman, M, et al. Hyperhomocysteinemia as a component of syndrome x. Metabol. 2003; 52, 11.

Page ME. Degeneration Regeneration. Florida: Nutritional Development Publishers;
1949. Reprinted 1977.

Page, ME. Body Chemistry in Health and Disease. Florida: Nutritional Development Publishers.

Pallholz JE, et al. Arsenic and selenium in human hair: A comparison of five countries with and without aresnicosis. Biol.Trace Elem.Res. 2005; 2:106.

Piolino V, et.al. Thermogenic effect of thyroid hormones: Interactions with epinephrine and insulin. Am.J.Physiol. 1990; 259.

Prohaska JR. Biochemical changes in copper deficiency. J.Nutr.Biochem. 1990;1.

Reaven GM. Banting Lecture. Role of insulin resistance in human disease. Diabetes. 1988; 37:12.

Reaven GM. The insulin resistance syndrome: Definition and dietary approaches to treatment. Ann. Rev. Nutr. 2005; 35.

Reaven GM. Banting Lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988; 37.

Reaven GM. Do high carbohydrate diets prevent the development or attenuate the manifestations (or both) of syndrome x. A viewpoint strongly against. Curr. Opin. Lipidol. 1997; 1.

Richards ML, et.al. Diabetes mellitus with hyperparathyroidism: Another indication for parathyroidectomy. Surg. 1999;126,6.

Rodriguez-Moran M, et al. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: A randomized double-blind control trial. Diab.Care. 2003;26,4.

Saari, et al. Early and advanced glycation end-products areincreased in copper deficiency. J.Nutr.Biochem. 1999;10,4 1999.

Sawada Y, et al. PTHrP increases pancreatic beta-cell-specific functions in well differentiated cells. Mol. Cell Endocrinol. 2001;182,2.

Schuschke DA. Dietary copper in the physiology of microcirculation. J. Nutr. 1997; 127.

Seelig MS. Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications. J.Am.Col.Nutr. 1994;13,5.

Seelig MS. Metabolic syndrome X. Min. Res. Int. 2002.

Shulman AI, Mangelsdorf DJ. Retinoid X receptor heterodimers in the metabolic syndrome. NEJM. 2005;353 (6).

Simopoulos A. Genetic variation and nutrition: Population differences due to single gene defects and population differences in multifactorial disease due to polygenic effects.
Nutr. Today. 1995;30 (4).

Srikumar, et al. Trace elements status in healthy subjects switching from a mixed to a lactovegetarian diet for 13 months. Am.J.Clin.Nutr. 1992; 55.

Sternberg S. Metabolic syndrome guidelines expand. Available at: www.usatoday.com/news/health /2005-09-12-metabolic-guide_x.htm.

Taneja SK, et al. Detection of potential myocardial infarction susceptible individuals in Indian population: A mathematical model based on copper and zinc status. Biol.Trace Elem.Res. 2000;75.

Tataranni P, et al. Body fat distribution and energy metabolism in obese men and women. J. Am.Col.of Nutr. 1994; 13,6.

Toxic trace elements in mammalian hair and nails. EPA-600 4.70049. August 1979.

Uno K, et.al. Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity. Science. 2006;312.

Vague J. The degree of masculine differentiation of obesities: A factor determining predisposition to diabetes, atherosclerosis, gout, and uric acid calculus disease. Am.J.Clin.Nutr. 1956; 4.

Watson G. Nutrition and Your Mind. New York: Harper and Row; 1972.

Watts DL. HTMA – Useful as a metabolic indicator. TEI Newslet. 2005; 16 (1).

Watts DL. Mineral imbalance, endocrines and hair tissue mineral analysis. TEI Newslet. 1993; 6 (2).

Watts DL. Indications of parathyroid activity in hair tissue mineral patterns. TLDP. October 1989.

Watts DL. Metabolic manifestation of disease, sympathetic-parasympathetic. TEI Newslet. 1989; 3 (3).

Watts DL. The immune system and hair tissue mineral patterns. Nutritonal, neuro-endocrine immunology. TEI Newslet. 1994; 7 (1).

Watts DL. Questions on hormones, heavy metals and other tests. TEI Newslet. 1999; 11 (3).

Watts DL. Trace elements and neuropsychological problems as reflected in tissue mineral analysis patterns. J. Orthomol. Med. 1990; 5 (3).

Watts DL. Neurological effects upon nutritional status. Digest of Chiro. Econ. May/Jun 1991.

Watts DL. Trace elements and other essential nutrients. clinical application of tissue mineral analysis. TEI. 1995.

Watts DL. Disease clusters. Clinical observations. TEI Newsletter. 1990; 5, 4.

Watts DL. Answers to criticism of hair mineral analysis. TEI News Let. 1999;11, 1.

Watts, DL. Hair mercury testing. An accepted and valuable test. TEI News Let. 2000;12,2.

Watts DL, et al. A response to the article; assessment of commercial laboratories performing hair mineral analysis. JAMA. 2001; 1: 285,1.

Watts DL. Variations in hair trace element concentrations: Importance of proper specimen collection. TLDP. November 2000.

Watts DL. Identifying disease clusters. Health Cons. November/December 1991

Watts DL. Nutrient interrelationships minerals-vitamins-endocrines. J Orthomol.Med. 1990;5,1.

Watts DL. HTMA – useful as a metabolic indicator. TEI Newslet. 1989; 3: 3.

Watts DL. The nutritional relationships of iron. J.Orthomol.Med. 1988; 3 (3).

Watts DL. The nutritional relationships of copper. J. Orthomol.Med. 1989; 4 (2).

Watts DL. The nutritional relationships of vitamin A. J.Orthomol.Med. 1991;6,1.

Watts DL. The nutritional relationships of calcium. J.Orthomol.Med. 1990;5,2.

Williams B. Insulin resistance: The shape of things to come. Lancet. 1994; 344.

Page 1, 2, 3, 4