Prof. Lance BAUMGARD


Lance Baumgard is a Distinguished Professor and the Normal Jacobson Professor of Nutritional Physiology in the Department of Animal Science at Iowa State University. Lance’s researches milk fat synthesis, metabolism, energetics of the transition and heat-stressed cow, and immunometabolism. He teaches Principals of Nutrition for undergraduates, and Bioenergetics and Advanced Ruminant Nutrition at the graduate level. Lance and his colleagues have recently focused their research efforts on the energetic and mineral requirement of an activated immune system. In particular, he and his group are describing how immune activation alter nutrient trafficking and ultimately reduce farm animal productivity in multiple on farm scenarios. Professor Baumgard and his students have published more than 200 peer reviewed publications, 120 conference proceedings and more than 300 abstracts.

Lance is a native of southwest Minnesota who grew up on a swine and row-crop farm. He has a B.S. and M.S. degree from the University of Minnesota and a PhD from Cornell University. He joined the University of Arizona faculty as an Assistant Professor in the Fall of 2001 and joined Iowa State University in 2009. Dr. Baumgard also teaches in the graduate School of Global Food Resources at Hokkaido University in Japan. Lance and his wife, Dr. Aileen Keating and children, Cian and Med Baumgard live in Ames.

Company and / or University
Professor of Nutritional Physiology in the Department of Animal Science at Iowa State University

United States 🇺🇸


Gut derived inflammation and its role in transition cow success.

Correlation analysis, retrospective classification, and epidemiology fueled the theory that adipose tissue released NEFA, the resulting hepatic derived ketones, and subclinical hypocalcemia (SCH) lead to inappetence, immune suppression, and ultimately morbidity and infertility.

The tenet has evolved into a dogma that therapeutically treating subclinical hyperketonemia (SHK) and SCH improves cow health and productivity. But according to recent NAHMS reports, cow health is not improving, so it is appropriate to question whether we are medicating the causes or simply treating the symptoms. Adipose mobilization and ketogenesis are in fact necessary for high production in the transition and experimentally blunting them directly reduces milk yield. Furthermore, acute and transient SCH is normal in high producing cows. These observations suggest there are alternative explanations to periparturient failures other than SHK and SCH. Recently, it has become firmly established that immune activation and the ensuing inflammatory response are a normal component of transition cow biology. We believe that a significant portion of the systemic inflammation stems from the gastrointestinal tract. Regardless of origin, if inflammation is persistent it both reduces feed intake and causes SCH. During established lactation, immune activation causes an immediate decrease in both milk yield and feed intake but in early transition the evolutionary drive to synthesize milk continues in spite of inadequate feed intake. The simultaneous requirements of immune activation and milk synthesis create an energetic and mineral imbalance characterized by SHK and SCH, a metabolic profile that is similar to a healthy high producing transition cow. Our hypothesis is that immune activation and its induction of hypophagia are responsible for some cows with SHK and SCH and this explains why they are occasionally correlated with poor health, production, and infertility. We argue that changes in circulating NEFA, ketones, and calcium are simply reflective of either: 1) normal homeorhetic adjustments healthy high producing cows use to prioritize milk synthesis or 2) the consequence of immune activation. Research to understand and ameliorate causes of excessive inflammation should be prioritized over efforts to reduce SHK and SCH which are non-specific symptoms of the underlying problem.