by Deborah Jeanne Sergeant
Does leaky gut contribute to heat stress and ketosis in dairy cows? Lance Baumgard of Iowa State University presented a webinar on the topic hosted by Ag Model Systems.
His hypothesis is that “the origin of both heat stress — in all farm animals — and ketosis in dairy cows problems is a compromised intestinal integrity.”
His research has explored if the decrease in feed intake explains the reduced milk yield during heat stress.
“If we have a better understanding of the biological reasons why heat stress reduces production, we’ll have a better idea of how to alleviate it,” Baumgard said.
Heat stress can reduce feed intake by about 30 percent, as well as reducing basal and stimulated adipocyte lipolysis. It also increases basal and stimulated insulin secretion.
Baumgard said cows affected by heat stress secrete 400 grams less lactose per day than animals in the control group.
The big question he presented is, “Does the liver produce less glucose or are extra-mammary tissues using more glucose per day.”
Baumgard considered whole body glucose production and said extra mammary tissues use 400 grams more glucose daily during heat stress, which he believes indicates that “glucose is preferentially being utilized for processes other than milk synthesis, maybe by the immune system during heat stress.”
Baumgard reminded webinar attendees that the gastrointestinal tract is a tube that runs the entire route of the animal’s digestion from the mouth to the anus.
“Everything inside the tube is technically outside of the body,” he said.
The gastrointestinal tract lumen is an inhospitable environment to prevent parasites, pathogens enzymes, acids and toxins from infiltrating the rest of the body. It serves as a barrier.
Heat stress can affect gut health because of the diversion of blood flow to skin and extremities to help cool the animal. This causes coordinated vasoconstriction in intestinal tissues, reduced nutrient and oxygen delivery to enterocytes, and hypoxia increases reactive oxygen species. Since there’s less blood flow to organs during heat stress, heat stress affects digestion. This can result in less nutrient uptake.
Baumgard said heat stressed animals eat less. Reduced nutrient uptake increases rumen and intestinal osmolarity in the intestinal lumen. He said there are multiple reasons for increased osmotic stress.
Baumgard showed images displaying intestinal morphology. In a healthy gastrointestinal tract, the villi are long and slender. Unhealthy GI tracts showed pronounced stubbiness in the villi.
“There are hundreds, if not thousands of things you don’t want in the GI tract,” Baumgard said.
Heat stress affects the lining of the digestive system and can promote inflammation production he called a catabolic condition.
“It’s fine if the barrier is intact, but if the barrier function is compromised, now it has a chance to infiltrate the body,” he said.
He thinks of the liver as an immune system organ.
“If it’s overwhelmed, things can go systemic,” he said. “It happens quickly, starting within two hours.”
Heat stress’ direct and indirect effects include lower milk yield, the liver remains sensitive to catabolic signals and continuing leaky gut issues for even up to 10 days after the animal’s heat stress has been relieved.
Baumgard said it’s dogma that excess andipose tissue mobilization causes fatty liver and ketosis.
“This is exacerbated in high-producing cows,” he added.
The industry goal is to reduce blood non-esterified fatty acids (NEFA).
Baumgard said many studies associate NEFA and beta-hydroxybutyrate (BHBA) — though don’t find a direct causal relationship — with increased risk of ketosis, decreased milk yield, LDA, metritis, retained placenta, laminitis or poor reproduction.
“Plasma NEFA are markedly increased following calving in almost all cows,” Baumgard said. “Fifteen to 20 percent get clinical ketosis.”
So what causes these cows to become more susceptible to ketosis?
“Could it be a predisposition to developing fatty liver, or maybe something predisposes them?” Baumgard asked.
About one-third of the human population has a leaky-gut related disease such as Crone’s disease or celiac.
“Humans with intestinal barrier dysfunction have fatty liver, but do not have increased NEFA,” Baumgard said. “Oftentimes, we assume fatty liver is because of high NEFAs. These people with these disease don’t have high NEFAS but have fatty livers.”
He also observed that incidences of clinical ketosis in Southwestern versus Midwestern and Northeast animals — .5 percent vs. 10 to 15 percent — seems to indicate heat stress cows have increased incidence of fatty liver.
“Ketosis isn’t a problem in the Southwest,” Baumgard said. “Why do we have these huge regional differences?”
Diet plays a role. Animals fed ground grain experience systemic inflammation and those fed alfalfa pellets experience no inflammation. Since haylage is fed in the Southwest, Baumgard thinks that lowers their risk of ketosis.
In further research, Baumgard wanted to confirm that the biomarkers of leaky gut increase during the transition period for clinically ketotic cows.
“A compromised gastrointestinal barrier and subsequent ednotoxin infiltration may play a causative key role in ketosis development,” he said.
For a month, he and his research team sampled every cow going through the transition period at a 3,500-cow dairy. The herd’s veterinarian helped them focus on cows treated for ketosis except for obvious reasons. They looked at cows between days five and 14 of milk.
Though they did not end up with causative data — after all, their research sample was rather small — Baumgard feels confident that there’s the same associative problem that NEFA and ketones have with ketosis.
Baumgard also researched if intentionally induced gastrointestinal permeability reduces productivity and alter energetic and inflammatory indices in otherwise healthy dairy cows.
“We anticipated leaky gut would have a negative impact on feed intake,” Baumgard said. “When they get leaky gut, they essentially stop eating. You don’t need PhD in gastrointestinal physiology to know that the leaky gut is causing intestinal damage.
He believes that GSI morphologically alter villi architecture and biomarkers of the acute phase protein response: characteristics consistent with leaky gut.
“Introduced leaky guy markedly affected production and metabolism responses similar to ketosis,” Baumgard said. “Feed restriction by itself negatively affected intestinal barrier function. Feed restriction may be a useful tool to test molecules targeting leaky gut mitigation.”
Baumgard also researched to identify the magnitude of feed restriction that would reliably cause increased leaky gut and inflammation.
He found that “all markers of inflammation increase with advancing feed restriction on leaky gut.”
That was based upon 50 percent feed restriction for 12 hours.
“How often are cows without feed for more than six hours on your farm?” Baumgard asked. “I think it happens a lot more than we like to admit.”
The feed restriction doesn’t appear to cause hypoglycemia in dairy cows; it only does in pigs.
Baumgard also found that lipopolysaccharide (LPS) “stimulates or at least augments glucose stimulated insulin secretion,” he said. “LPS activates the immune system.”
Insulin promotes andipose tissue accretion. It also partitions nutrients away from muscle and lactation.
“From a milk production standpoint, insulin is not our friend,” Baumgard said.
He encourages producers to always make sure feed is available for animals so they can eat on demand.
“Anything that prevents the animal from eating when it wants to eat can cause leaky gut,” Baumgard said.
He also believes that decreasing environmental stress, especially while cows are transitioning, can help mitigate the effects of inflammation.
“We need to stop calling the transitioning cow metabolically stressed,” Baumgard said.
Baumgard wants farmers to intervene in ketosis cases when they observe evidence of high ketones and cows not coming into milk, not aggressively eating, looking lethargic/melancholic, or have a mild fever. But farmers don’t need to treat high ketones cows that are eating well, milking well, looking good and lacking a fever.
“Heat stress, ketotic and feed restricted cows have a similar metabolic and edocrine fingerprint,” Baumgard said. “Leaky gut is a common denominator. The activated immune system utilizes an enormous amount of glucose.”
“Leaky gut and endotoxin infiltration may play important roles — if not the origin — in suboptimal productivity commonly observed in animal agriculture.”
Though more research needs to be done to develop strategies to improve intestinal integrity, Baumgard believes that if leaky gut is “the fundamental cause of many typical on-farm problems, then it is financial problem that dwarfs all others combined.”