From Tryptophan to Hydroxytryptophan: Reflections on a Busy Life

Abstract

Given the very difficult odyssey of my early years, who could have imagined the incredible and successful journey that constituted my life path after age 13? I was born into a Jewish family in Breslau, Germany, right before the rise of Nazism and Hitler's election. After Kristallnacht, when my father was taken to Buchenwald Concentration Camp, we had to leave Germany as soon as possible. The first opportunity came in May of 1939, when we boarded the SS St. Louis bound for Havana, Cuba. Almost all passengers were denied entrance into Cuba, and the ship had to go back to Europe, where I ended up in France. In December of 1939, during World War II, I was fortunate to be able to leave France. This time I made it to Cuba, where my father was already in residence. A year later, my entire family was allowed into the United States. I took advantage of all the educational resources in this land of opportunity. I graduated valedictorian of my high school class and earned a four-year scholarship to Rutgers University, where I obtained a Bachelor of Science degree. I went on to earn a Master's degree from the University of Connecticut and finally a PhD from the University of Illinois. Within two months after graduating from Illinois, I was hired as an assistant professor of nutritional biochemistry at Rutgers, where I enjoyed a most productive research and teaching career. My PhD research involved tryptophan and niacin metabolism in the chick, and upon arrival at Rutgers I continued amino acid studies with the goal of assessing the essential amino acid requirements for egg production. This research was crowned with success and was followed with amino acid requirement studies for maintenance and for growth in rabbits, and ultimately with a reevaluation of requirements in adult humans. An outgrowth of the maintenance requirements led to a series of investigations into the metabolism of histidine, histamine, and carnosine (a histidine-containing dipeptide). Histamine, we found, plays an important role in wound healing and stress management. Pyridoxal phosphate is the cofactor for the enzyme histidine decarboxylase required for histamine synthesis and similarly serves as a cofactor for hydroxytryptophan decarboxylase, the enzyme that is part of the pathway to serotonin synthesis. Investigations into these pathways led to interesting findings: brain concentrations of serotonin could be increased by supplementing the diet of rats with tryptophan and pyridoxine; the elevated brain serotonin levels had behavioral consequences. Alcohol craving, addiction, and withdrawal symptoms are affected by serotonin concentrations in the brain, and alleviation of these conditions can be achieved with simultaneous administration of serotonin and dopamine agonists. In the midst of our early amino acid studies, we serendipitously also became involved with lipid metabolism in relation to atherosclerosis and blood cholesterol in a chicken model. This work led to the recognition that soluble fibers, like pectin, had strong cholesterol-lowering properties that were beneficial in lowering the incidence of coronary plaque formation. The research success that I have enjoyed has been coupled with the gift of three accomplished children who are making important contributions as professionals in their fields of endeavor. My wife and I are also blessed with 10 wonderful grandchildren, our pride and joy!

Fat discrimination: A phenotype with potential implications for studying fat intake behaviors and obesity

“…While the mechanism behind the fat discrimination phenotype requires additional study, previous researchers have speculated that poor ability to discriminate a particular dietary component might lead to excess intake due to an impaired ability to detect the nutrient at lower levels (19). Further elucidation of potential gustatory mechanisms of fat transduction, such as CD36 and the GPR family of proteins (38), may also help to clarify the mechanism behind fat discrimination. Both CD36, a fatty acid translocase, and GPR40 and GPR120, G-coupled protein receptors, are expressed in the mouth and in the gastrointestinal tract [ for review see (38).…”

“…Further elucidation of potential gustatory mechanisms of fat transduction, such as CD36 and the GPR family of proteins (38), may also help to clarify the mechanism behind fat discrimination. Both CD36, a fatty acid translocase, and GPR40 and GPR120, G-coupled protein receptors, are expressed in the mouth and in the gastrointestinal tract [ for review see (38). Studies in animals suggest that CD36 is necessary for oral fat detection and preference (39;40), while both GPR40 and GPR120 may be involved with preferences for some fatty acids.…”