This article summarizes my scientific work and describes some personal experiences during this period. After my basal medical training (MD) (1971), I obtained a PhD in pharmacology (1976) and ended up as a professor of Physiology. My initial studies were within the field of gastroenterology. I showed that the gastrointestinal hormone gastrin, which stimulates HCL secretion in the stomach, was released in response to stimulation of the vagal nerve. Later I showed that the entire endocrine system of the gastrointestinal (GI) tract that promotes digestion and anabolic metabolism and growth was under vagal nerve control. I also showed that activation of the vagal nerve inhibits the function of the inhibitory substance somatostatin. 10 years later, after some big changes in my personal life, my research focus changed. I became interested in female physiology, particularly the role of oxytocin. In addition, I became aware of the situation of female scientists and started to work with questions regarding equality between women and men. I gathered a group of interested female medical students and midwives around me. We demonstrated that breastfeeding and touch (e.g., between mother and baby), via stimulation of sensory nerves in the skin, activated the endocrine system of the GI tract and, thereby, anabolic processes and growth. The effects were exerted via a vagal mechanism and involved activation of parvocellular oxytocinergic neurons from the paraventricular nucleus (PVN). We also showed that the gastrointestinal hormone cholecystokinin stimulated the release of oxytocin in a calorie-dependent way via an afferent vagal mechanism. In summary, there is a bidirectional, vagally mediated connection between the endocrine system of the GI tract and the oxytocin producing neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus.1. Oxytocinergic neurons from the PVN enhances the activity of the endocrine system of the GI tract and thereby growth and regeneration. The effect is exerted via efferent vagal fibers which inhibit the release of somatostatin. 2. Food in the duodenum triggers a release of cholecystokinin (CCK), which via a vagal afferent mechanism stimulates the release and function of oxytocin. This mechanism is not activated in the absence of food intake. Administration of oxytocin induces a multitude of actions, i.e., anxiolytic and sedative effects, increased pain threshold, lowering of cortisol and blood pressure and an increased activity of the endocrine system of the GI tract. Repeated administration of oxytocin may induce long-term effects and "secondary" mechanisms such as an increased activity of alpha-2- adrenoceptors are involved. Oxytocin released by suckling during breastfeeding or by touch during social interaction will induce a similar effect spectrum. Activation of the parvocellular neurons will stimulate some aspects of social behavior, induce calm and well-being, and decrease levels of fear, stress, and pain. In addition, vagal functions and the activity of the endocrine system of the GI tract will be stimulated. Together, these effects are consistent with the oxytocin-mediated calm and connection response and, in a long-term perspective, with the promotion of well-being and health. A second period of professional difficulties occurred in the late 1990s. I moved to the Swedish University of Agriculture, where I started to investigate the role of oxytocin in interactions between humans and pets, as this type of interaction had been shown to promote health. I continued to study the role of oxytocin in female reproduction, in particular, the role of oxytocin during labor and birth and in the peripartum period. In addition, I started to write books about different aspects of oxytocin. I also wanted to establish a role for oxytocin in the treatment of vaginal atrophy. Several clinical studies show that local intravaginal application of oxytocin in women with vaginal atrophy increases the regeneration of vaginal mucosal cells and function.

Milk production and hormonal responses to milking in Holstein cows that were milked twice daily, and that either also nursed calves twice daily 2 h after milking for 9 wk after calving (n = 10) or that served as nonnursing controls (n = 8) were examined to assess how nursing affected responses to machine milking. Milk yield at milking during the 9 wk of nursing was lower in nursing cows compared with control cows (26.1 +/- 1.0 vs. 35.5 +/- 1.1 kg) that were only machine milked. During nursing, the amount drunk by calves increased from 6.5 +/- 0.7 kg/d on wk 1 to 12.5 +/- 1.4 kg/d on wk 9. When this was added to the amount of milk obtained at milking, nursing cows did not differ from control cows in total milk produced (35.5 +/- 1.0 vs. 35.5 +/- 1.0 kg). Residual milk yield, after i.v. injection of oxytocin after milking, was higher in nursing cows than in control cows (8.7 +/- 0.8 vs. 3.2 +/- 0.8 kg). During the 6 wk after weaning, milk production was the same for the nursing and control cows (34.0 +/- 1.35 vs. 34.7 +/- 1.42 kg). Plasma oxytocin levels during milking were greater for control cows than for nursing cows (31.7 +/- 5.4 vs. 18.0 +/- 2.8 pg/mL), but were equivalent to concentrations in nursing cows during nursing (35.5 +/- 7.5 pg/mL). Plasma concentrations of prolactin and cortisol increased after both milking (control vs. nursing: prolactin: 40.2 +/- 6.8 vs. 32.9 +/- 6.1 ng/mL; cortisol: 6.4 +/- 1.23 vs. 7.4 +/- 1.10 ng/mL) and nursing (control vs. nursing: prolactin: 18.6 +/- 7.3 vs. 38.9 +/- 6.6 ng/mL; cortisol: 2.34 +/- 1.15 vs. 7.37 +/- 1.04 ng/mL). In contrast to previous studies, there was no obvious advantage for milk production by keeping a calf with the cow. This appears to result from the reduced oxytocin secretion during milking for the nursing cows.

The physiology of lactation includes development of the mammary gland from the foetal to the adult stage, further development during pregnancy and onset of lactation, with the accompanying metabolic and behavioural adaptation. At the onset of pregnancy the endocrine system undergoes dramatic changes. The growth of the mammary gland is stimulated by growth hormone and prolactin, adrenocortical steroids, oestrogens and progesterone, and that of the gastrointestinal (GI) tract by gastrin, CCK and secretin. The onset of lactation is accompanied by increases in the blood volume, cardiac output, mammary blood flow and blood flow through the GI-tract and liver, aiming to provide the udder with nutrients and hormones for regulation of milk synthesis. Food intake and distribution of nutrients to the mammary gland are partially regulated by hormones as well as the repartitioning of nutrients away from body stores towards the udder. To improve milk production, administration of growth hormone has been practised, but also much discussed. Besides central mechanisms, local mechanisms within the mammary gland regulate initiation of lactation, maintenance, regulation of blood flow and mammary gland cell apoptosis. Most of the milk in a filled dairy cow udder is stored in the alveolar compartments. The milk ejection reflex must be activated to gain access to the udder milk, i.e. oxytocin contracts the myoepithelial cells. Recent studies show that vasopressin may also elicit milk ejection. More efficient oxytocin release is achieved if the cows are fed during milking. Beyond milk let down, oxytocin influences maternal behaviour and metabolism. Furthermore, it has been indicated that suckling or milking activates a vagal reflex, which may link the milk production to the endocrine system of the GI-tract. The question has been raised whether the mammary gland is a supporting or consuming organ.

The aim of this article is to propose that oxytocin not only stimulates milk let down, but also adapts behaviour and physiology to facilitate lactation in mammals including dairy cattle. Circulating oxytocin as well as neurogenic oxytocin participates in these regulatory processes. In short, oxytocin stimulates maternal interaction and attachment between mother and young. It also participates in the metabolic prerequisites for milk production by e.g. stimulating glucagon release and thereby, mobilisation of glucose. Digestive and anabolic aspects of metabolism are also stimulated, e.g. by increased vagal nerve activity. Adaptations consistent with an antistress like pattern are also induced. Cortisol levels are decreased as well as blood pressure, and behaviours characterised by calm, reduced levels of anxiety and more social activity are promoted. These effects seem to be present in monogastric animals as well as in ruminants. The expression of various aspects of these adaptations vary according to the special needs and living environmental circumstances of different species. The mechanisms behind the effect spectrum of oxytocin are being explored in other experimental models. A second aim of this paper is to suggest that efficiency of lactation can be promoted by facilitating oxytocin release in connection with milking by enhancing the amount of sensory stimulation.