• Ketone bodies are “the killers” being responsible for all subsequent negative effects (oxidative stress/ oxygen radicals)

  • Early detection and interference are key to prevent clinical effects and economical losses caused by ketone bodies! Go and check your dry cows’ feed intake and BCS on regular scale

  • Undetected subclinical ketosis can also lead to cellular damages, immunosuppression and in consequence increased incidence of secondary diseases e.g. mastitis, metritis and ketosis Go and check regularly blood BHBA levels of your fresh cows!

  • Did you ever wonder about your poor first service conception rates? SCK could be one of the causes you can fix to improve reproductive outcome.

  • Did you already know? Latest investigations reveal a strong correlation between excessive loss of BCS and increased risk of lameness. Go for our updated BCS Cowdition App to get in control of your herd.

  • Negative impact of (subclinical) ketosis on milk yields and subsequent diseases still seems to be underestimated Take your time to make a cost-benefit calculation

Ketone bodies

Ketone bodies, in the strict sense, are acetoacetate and acetone resulting from spontaneous decarboxylation. These are particularly harmful due to their high oxidative potential and associated induction of oxidative damage 12. They are not measured in the blood diagnostically, however, due to extensive efforts with regards to sample storage and analysis.

β-hydroxybutyrate (BHBA) arises from acetoacetate when  there is sufficient availability of NADH + H+ and is more biocompatible. Because of its storage stability, it is more convenient for the diagnosis of (sub) clinical ketosis compared to acetoacetate and acetone 15.

However, BHBA is also formed in the rumen epithelium from butyrate if there is an adequate energy supply. Measurement  of BHBA also includes  decreased hepatic extraction of BHBA formed in the rumen in addition to the formation of ketone bodies in the liver. Thus, BHBA is strictly speaking an "indirect" ketosis marker.

Therefore, it is difficult to set well-founded limits for the diagnosis of ketosis.

  • Low limits (< 0.9 mmol/l) have good sensitivity but poor specificity and are therefore only suitable as a herd standard to derive possible health impairments.
  • Higher limits (1.2 – 1.4 mmol/l) feature increased specificity for the individual animal with decreasing sensitivity 18.

Cases of clinical ketosis are frequently associated with BHBA concentrations of > 3 mmol/l. In spite of this, in individual cases, cows may have serum BHBA concentrations of > 3 mmol/l without showing any clinical symptoms (own unpublished data).

Ketone bodies can also non-invasively be determined in urine and milk – but with lower precision.


  • good energy carrier
  • poorly biocompatible
  • oxidative damage
  • spontaneous decarboxylation to acetone


  • Develops due to spontaneous decarboxylation of acetoacetate
  • Poorly biocompatible
  • oxidative damage

ß-hydroxybutyrate (BHBA)

  • main ketone body
  • good energy carrier
  • highly biocompatible: no oxidative damage
  • NADH + H+ necessary for formation (deficiency in hypoglycemia!)

Ketone bodies measurable on farm 42

Early detection of endangered cows in the dry phase 44

Cows with subclinical ketosis ate less in the week before and 2 wk after calving.

* see also our references page