Technology and nutrition – a combined approach
Farm technology is an exciting frontier, and it's changing how we manage herds.
The liver doesn't often get the attention it deserves.
Tucked behind the rumen and largely invisible to farm-level observation, it quietly carries the burden of converting nutrients, detoxifying metabolites, and producing energy in the form of glucose to fuel lactation. But during early lactation, when energy demands are highest and intake is lagging, the liver is often overwhelmed. When this happens, fertility can suffer.
It’s time we looked at ketosis not only as a milk production or animal health issue, but as a reproduction issue too. Without a functioning liver, you won’t get functioning ovaries.
The hidden chain reaction
During early lactation, the cow enters a state of negative energy balance. She can’t eat enough to support her output, so she starts mobilising body fat. This fat is converted into non-esterified fatty acids (NEFAs) and sent to the liver for processing. In a well-functioning cow, the liver turns NEFAs into usable energy or exports them as fat. Reductions in liver performance are a common problem across many herds during early lactation when maximum liver capacity is of utmost importance. In cows where the liver is not fully functional, NEFAs are not efficiently utilised, leading to the production of ketone byproducts such as betahydroxybutyrate (BHB) and acetoacetate. This is ketosis in action.
When this imbalance continues, the cow’s immune system weakens, milk production drops, and ketosis, either clinical or subclinical, can set the cow up for fertility issues later on. Ketosis interferes with calcium metabolism and disrupts insulin signalling, which can lead to suppression of ovarian function, delayed estrus, and an increased risk of early embryonic loss.
Ketosis isn't one thing
Not all ketosis is created equal. Ketosis can be categorised into three nutritional causes:
In all cases, the liver’s ability to oxidise fat and fuel the cow is compromised. But each type requires a different nutritional strategy to resolve it.
Fertility fallout
Why does this matter for mating? Because reproduction is an energy-intensive process. The cow must not only resume cycling but also produce viable follicles, ovulate, support embryo survival, and maintain a pregnancy. All of that depends on glucose and, by extension, on a liver that is in good working order.
Insulin resistance, triggered by elevated NEFA and BHB levels, blocks ovulation and can delay return to oestrus. Progesterone levels are affected, conception rates fall, and early embryonic death becomes more likely, leading to apparent failures to conceive or early pregnancy loss.
What you can do now
So, how do we set cows up for better liver function and reproductive success?
Feed for the liver, not just the rumen
Focus on propionic acid precursors (e.g.maize, molasses, protected starches) and bypass amino acids to support gluconeogenesis in the liver. It’s not just about energy, it’s about the type of energy.
Use DCAD strategically
Consider a controlled negative DCAD (dietary cation-anion difference) approach pre-calving to improve calcium availability and reduce metabolic stress. Stable calcium levels in the blood support uterine recovery and ovarian function.
Target minerals that support the liver
Selenium, cobalt, and zinc play important roles in antioxidant activity and enzyme function. Liver health depends on it.
Test, don't guess
Monitor BHB levels in fresh cows to catch subclinical ketosis before it cascades into something worse. A cow with BHB levels above 1.2 mmol/L might look fine, but her liver is under strain, and her reproductive future is at risk.
Watch your silage
Don’t assume goodlooking silage is harmless. High butyric acid can depress appetite and spike BHB production, which are hallmarks of Type 3 ketosis.
When your cows aren’t getting in-calf, it might not be about bull management, synchrony, or timing. It might be about the liver.
Chris Balemi is founder of Agvance Nutrition
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