Biography
Dr. Nielsen grew up on a small dairy farm in central Wisconsin, and received his Bachelor's degree in 1963, Master's degree in 1966, and Doctor of Philosophy degree in 1967, all in Biochemistry, from the University of Wisconsin, Madison. After completing two years of military service with the U.S. Army's Medical Research and Nutrition Laboratory in Denver, CO, Dr. Nielsen, as a Research Chemist, was the first staff member hired for the present day Grand Forks Human Nutrition Research Center, and arrived in Grand Forks shortly before the building officially opened in 1970. He served as Center Director from June, 1985, to March, 2001. In his current position as a Research Nutritionist, he is determining whether sub-clinical magnesium deficiency through exacerbating chronic inflammation is a significant factor in the occurrence of chronic disease, particularly bone loss leading to osteoporosis, associated with obesity.
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Research Interests
Past research of Dr. Nielsen focused on determining the needs for essential nutrients for and beneficial action of bioactive trace minerals on bone health, cardiovascular function, and neuropsychological function. Dr. Nielsen’s current research program is focused on determining whether bone health adversely affected by obesity-induced chronic inflammation is exacerbated by pro-inflammatory factors (e.g., magnesium deficiency).
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Research Accomplishments
Senior member of the team that produced evidence that boron is a beneficial, perhaps essential nutrient for higher animals. Found that boron deprivation is detrimental to trabecular bone micro-architecture and cortical bone strength, and adversely affects behavior in experimental animals.
Produced evidence that boron has diverse beneficial effects through influencing the formation and/or utilization of S-adenosylmethionine, which participates in a variety of biochemical processes. Found that boron deprivation increased circulating homocysteine (a product of S-adenosylmethionine utilization), which has been associated with osteoporosis and mental disorders.
Produced evidence that boron has diverse beneficial effects through influencing the formation and/or utilization of S-adenosylmethionine, which participates in a variety of biochemical processes. Found that boron deprivation increased circulating homocysteine (a product of S-adenosylmethionine utilization), which has been associated with osteoporosis and mental disorders.
Senior member of a team that showed boron is a bioactive element that has beneficial, possibly essential, actions in humans. Found that supplementation of a low boron diet with an amount of boron commonly found in diets high in fruits and vegetables improved cognitive and psychomotor functions, modified calcium and magnesium metabolism, and enhanced and mimicked some of the effects of estrogen therapy.
Senior member of a team that showed for the first time that sub-clinical magnesium deficiency, induced by low dietary intake alone, has adverse effects in humans. Magnesium deprivation caused heart rhythm abnormalities, energy inefficiency during controlled exercise, and altered calcium metabolism.
Led the research effort showing that low magnesium intakes similar to that of 10% of adults older than 51 years are associated with increased chronic inflammatory stress and changes in bone composition associated with increased bone loss and decreased bone strength.
Led the research effort that found a sub-clinical zinc deficiency with copper intakes just above the estimated average requirement resulted in heart rhythm abnormalities and increased oxidative stress in postmenopausal women.
Led the research effort that showed silicon enhances wound healing and immune function. Found that silicon affects mainly trabecular bone turnover and structure, apparently through affecting collagen metabolism and cytokine action.
Produced evidence that nickel is a beneficial bioactive element in higher animals. Found that nickel deprivation in experimental animals affects the response to deficient intakes of vitamin B-12 (can affect central nervous system function), can increase blood pressure, and exacerbates the response to a high salt intake.
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