• 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

Limitation of oxidative damage

Ketone bodies cause oxidative damage. For example, cell membranes are damaged by lipid peroxidation and proteins are reduced by the oxidation of functional groups and subsequently limited in their function. In humans, oxidative damage is well known as cause of the comorbidities of diabetes mellitus 69.

Oxidative damage is triggered by

  • Direct prooxidant effects of acetone and acetoacetate 70, 71. The body tries to repel these prooxidative effects by converting them into β-hydroxybutyrate, but succeeds only to a limited extent in cases of severe glucose deficit.
  • Indirect prooxidative effect by activation of NADPH oxidases, MAP kinases and NF-κB 69. At the same time, ketone bodies have a pro-inflammatory effect.
  • These indirect prooxidative and proinflammatory effects are exacerbated by high concentrations of NEFA 72, 73.

Accordingly, oxidative damage from ketone bodies is especially to be expected in cases of

  • extreme glucose deficit
  • high NEFA concentrations
  • concomitant existence of inflammatory processes (mastitis, metritis, etc.)

Therefore, sufficient supplementation with antioxidants (vitamin E, β-carotine and selenium) is an important measure for the prevention and treatment of ketosis 21.

Acetoacetic acid

  • good energy carrier
  • moderately biocompatible
  • oxidative damage


  • Develops via spontaneous decarboxylation of acetoacetic acid
  • oxidative damage

ß-hydroxybutyrate (BHB)

  • good biocompatibility: no redox damage

* see also our references page