Induction of lactation

The successful induction of lactation in non-maiden mares was first reported in 2002. The original treatment protocol consisted of the administration of estradiol, progesterone (or altrenogest) and a dopamine-D2 antagonist (sulpiride or prolactin) to stimulate prolactin secretion. Since the original report, hundreds, perhaps thousands, of mares have been successfully induced to produce milk, adopt an orphan foal and raise it to weaning age.

The most important conclusions of the research and clinical reports are summarised below:
• The milk that is produced by hormonal induction has the same composition as milk from naturally lactating mares; foals raised by mares with induced lactation appear healthy and have a similar growth curve as naturally raised foals.
• The induced lactation does not start with colostrum production, as occurs in foaling mares, but rather starts with the production of normal milk, similar to a mare at a week or more post-partum. Attempts to induce colostrum production have not been successful to date.
• Once lactation has been set in motion (after 7–10 days of hormonal treatment), milk production continues without sustained hormonal treatment on condition that mares are milked frequently (probably more than 7–8 milkings/ day) or are nursed frequently by an adopted foal.
• When a foal is grafted to a mare with induced lactation, the regular suckling of the foal stimulates sufficient milk production (with no requirement for hormonal treatment) until the foal reaches weaning age. The amount of milk produced appears to result in the same growth as in naturally raised foals.
• Estradiol is an essential ingredient in the induction of lactation. It is not possible to induce lactation using only dopamine antagonists (sulpiride or domperidone) in mares without an endogenous source of oestrogen (ovariectomised and anestrous mares). It has been demonstrated that estradiol has a synergistic or priming effect on prolactin secretion if given prior to, or during, the dopamine-D2 antagonist treatment. However, estradiol administration to mares is not possible in most European countries. Experimental and clinical evidence demonstrates that lactation can only be achieved in mares with sufficient endogenous estradiol production provided by growing follicles. Without access to estradiol, it is advised that only normal cyclic mares with follicular activity are used for induction of lactation.
• Clinical experience tells us that lactation can be successfully induced in about 90% of cyclic mares.
• The induction protocol can be stopped at any stage without an increased risk of mastitis if a lactating mare is no longer required.

Previous treatment protocols consisted of the administration of a luteolytic dose of PGF2α on day 1 of the treatment followed by daily administration of estradiol, progesterone/ altrenogest and a dopamine-D2 antagonist (sulpiride or domperidone). The logic behind this treatment was to simulate the prepartum endocrine environment. The main reason for progesterone administration was to suppress (exaggerated) oestrous behaviour that occurs subsequent to PGF2α and estradiol administration; it very likely does not play a role in the stimulation of lactation. Later, the protocol was modified to accommodate the fact that we could no longer administer estradiol to mares in Europe. The new protocol is limited to mares that have cyclic ovarian activity (anoestrus mares are not good candidates). The PGF2α is still administered on day 1, to lyse any active corpus luteum that might be present and thus induce oestrus, follicular growth and increased estradiol secretion by the growing follicle(s). Progesterone/altrenogest is no longer part of the protocol as there did not seem to be any advantage to its inclusion. The dopamine-D2 antagonist is administered twice daily for 7–10 days to stimulate prolactin secretion. It is recommended to start milking around day 5 of treatment. Clinical observations indicated that this treatment protocol is as efficient as the original protocol and it has been used in several adoption centres for over a decade.

Treatment protocol

• Day 1: Make sure the mare has foaled in the past and has regular cyclic ovarian activity. The presence of a corpus luteum and the interval since the last ovulation are irrelevant (including if the mare has recently ovulated and is unlikely to respond to the PGF2α treatment). Administer a normal luteolytic dose of PGF2α and start dopamine-D2 antagonist treatment (sulpiride 300–400 mg i.m. every 12 h or domperidone 1.1 mg/kg bwt orally every 12 h). Sulpiride is available as a human drug in most European countries under the trade name Dogmatil®. In most countries it is available as an injectable formulation in 100 mg/2 mL ampoules. When oral medication is used, one should use this at three times the i.m. dose every 12 h. Domperidone, commonly known under the brand name Motilium® in human medicine, is also available as an oral paste for horses under the brand name Equidone® and is only of limited availability in Europe.
• Continue dopamine antagonist treatment for 7–10 days.
• Around day 4–7, one should notice swelling of the mammary gland and normal milk present in the teats. Since mares have a very limited storage capacity (foals nurse very frequently), it is advised to start milking the mares 5–8 times per day starting around day 5. If no milk secretion is observed by day 7–10 of treatment, it is advised to stop the treatment as it is unlikely that the mare will start lactation. In practice, we observe about 10% of mares that fail to make milk.
• In most mares, sufficient milk is produced to adopt a foal by day 5–10.
• After 10–14 days the treatment should be stopped as it has been reported that with prolonged treatment the effect on prolactin secretion decreases. In the majority of cases, the frequent nursing of the foal and interaction between mare and foal will quickly result in a further increase in milk production. When in doubt, we recommend to stop treatment for 1 week and then resume treatment for 1 week. This has proven to further increase milk production in mares with induced lactation that were machine-milked.