That is why a progressive, inquisitive nutritional team at CMC matters: continually questioning assumptions, following the evidence and turning better understanding into better outcomes for our customers.

Below I have used three examples from transition-cow nutrition that illustrate the point.

Ketosis: not just an empty fuel tank

We traditionally described ketosis as a simple energy problem. After calving, the cow cannot eat enough to meet the demands of milk production. She mobilises body fat, the liver becomes overwhelmed and ketones accumulate. The obvious answer was more energy. This information is still useful but no longer enough.

We now recognise inflammation and cortisol as important drivers of metabolic dysfunction. Over-conditioned cows can enter transition with chronic, low-grade inflammation; intermittent dry matter intake creates stress and raises cortisol; lameness adds both inflammation and stress. These pressures impair insulin signalling, increase insulin resistance and accelerate body-fat mobilisation. Fatty acids flood the liver, fat accumulates and liver function deteriorates, compromising glucose production and fat export. A self-reinforcing cycle develops that simply adding dietary energy may not resolve.

The challenge is not just how much energy enters the cow, but how effectively she can use and partition it.

Calcium: more than milk fever maths

Our traditional approach to milk fever was reassuringly mechanical. The cow suddenly requires large amounts of calcium for colostrum and milk. If absorption from the gut and mobilisation from bone cannot respond quickly enough, blood calcium falls. Again, correct but incomplete.

Calcium regulation and inflammation are closely connected. Inflammation can interfere with the cow’s normal metabolic response around calving, while low calcium can reduce feed intake, impair muscle and rumen function and weaken immune-cell activity. Each can therefore make the other worse.

Managing calcium remains essential, but successful transition management must also reduce the wider pressures driving inflammation and metabolic stress.

Methionine and choline: not just another brick in the wall

Methionine was once discussed mainly as an amino acid - a building block for milk protein. Choline was viewed separately, principally as a nutrient supporting liver function.

We now understand they are also connected through methylation. Methylation is a vital cellular control system, passing tiny chemical “tags” between molecules. These help regulate genes and metabolic pathways, process fats in the liver, build important compounds and respond to oxidative and inflammatory stress.

Methionine provides methylation capacity. Choline can also contribute methyl groups and may therefore spare methionine for some of its other essential roles. But they are partners, not substitutes: methionine is still required for protein production, while choline has distinct roles in exporting fat from the liver.

The objective is no longer simply to add more protein or an isolated amino acid. It is to support the connected metabolic system.

So, were we wrong?

Occasionally. More often, we were describing the part of the picture we could see at the time. The important thing is to keep making that picture bigger, clearer, more detailed, and to change our advice when the evidence tells us we should.

At Crediton Milling, we have a team ready to meet these challenges, whether that’s our nutritionists optimising the diet, our focus team providing mobility and condition scoring, or our forage team helping you get the most out of your farm’s resources. We are always investing in knowledge and information to help you see the picture more clearly and prepare for the challenges of an ever-changing world.