Who Let The Dogma Out Of Transition Cow Management? Dr. Lance Baumgard, Iowa State University

Nutritionists are often blamed for transition cow problems like high NEFAs, clinical and subclinical ketosis, and subclinical hypocalcemia. Dr. Baumgard suggests these symptoms are a result of one of two situations: 1. These are highly productive, healthy, and profitable cows; or 2. The symptoms are the metabolic reflection of immune activation, likely stemming from metritis, mastitis, pneumonia, or GI tract inflammation. In the first scenario, the nutritionist deserves a raise; in the second, these are mostly management issues not caused by nutrition. (1:26) 

If listeners are interested in more detail on this topic, Dr. Baumgard suggests reading this 2021 review in the Journal of Dairy Science: “ Invited review: The influence of immune activation on transition cow health and performance—A critical evaluation of traditional dogmas.” 

Link: https://www.sciencedirect.com/science/article/pii/S0022030221006329

Dr. Baumgard highlights key concepts that underpin his thinking regarding transition cows: The best indicators of health are feed intake and milk yield, it’s too easy to overthink the immune system, Mother Nature is rarely wrong, and inconsistent or non-reproducible data should create doubt. He goes on to review the incidence of metabolic disorders in early lactation and the energy balance dynamics of the transition period. (4:29)

For decades, we’ve had the assumption that NEFAs and ketones are causing many of the health issues in transition cows. NEFAs, BHBs, and calcium have been correlated and associated with negative outcomes. However many other studies do not find these negative correlations or associations. Plasma NEFA is markedly increased following calving in almost all cows, yet only 15-20% get clinical ketosis. Dr. Baumgard suggests that it’s presumptuous and reductionist of us to assume we can use one metabolite to diagnose the disease. Little mechanistic evidence exists to explain how these symptoms cause metabolic disease issues.  (10:29)

If hyperketonemia, high NEFA, and subclinical hypocalcemia are causing disease, then therapeutically treating these disorders would improve overall cow health. NAHMS data does not back that up. Dr. Baumgard dissects the dogma of ketosis. In short, mobilization of adipose tissues and partial conversion of NEFA to ketones is essential for maximum milk yield. (18:35)

High-producing cows are more hypoinsulinemic compared to low-producing cows, and transition period insulin concentrations are inversely related to whole lactation performance. Low insulin concentrations coupled with insulin resistance allow for fat mobilization. (29:02)

Post-calving inflammation occurs in all cows. Sources include the mammary gland, the uterus,  and the gut. Severe inflammation precedes the clinical presentation of the disease. In one experiment, all cows exhibited some inflammation in very early lactation. However, cows that were culled or died before 100 days in milk were already severely inflamed during the first few days of lactation. Dr. Baumgard thinks inflammation is the simplest and most logical explanation for why some cows don't eat well before and after calving.  (31:13)

While clinical hypocalcemia (milk fever) is pathological and requires immediate intervention, is subclinical hypocalcemia detrimental to health, productivity, and profitability? (36:33)

Dr. Baumgard’s paradigm-shifting concept suggests that increased NEFA and hyperketonemia are caused by immune activation-induced hypophagia, and hypocalcemia is a consequence of immune activation. He goes on to use a high-producing, a low-producing, and a sick cow to illustrate this concept. (43:26)

In summary, the metabolic adjustments in minerals and energy during the transition period are not dysfunctional and don’t need to be “fixed.” The real fix