Depressive personality and depressive illness are examined from an evolutionary adaptationist standpoint. It is postulated that the depressive state evolved in relation to social competition, as an unconscious, involuntary losing strategy, enabling the individual to accept defeat in ritual agonistic encounters and to accommodate to what would otherwise be unacceptably low social rank.

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Using the frameworks of attachment and social hierarchy theories, strategies seen in depression and in normal life are better understood. A hierarchial encounter elicits the "Involuntary Subordinate Strategy" ("ISS") in the loser, which terminates the "ISS" and brings the encounter to an end. These are psychophysiological mechanisms deeply rooted in our phylogenetic ancestry. Loss of a love object also elicits ineffective anger or rage which may, in turn, trigger the ISS. A prolonged intense ISS manifests in depression. Factors are examined that prevent "acceptance" of losing, thereby contributing to an escalation of the ISS and culminating in depressive illness. Psychotherapeutic implications include cognitive restructuring to enable the patient to explore options that might turn off the ISS such as "acceptance" (without making negative self-evaluations), changing unrealistic ideals and aspirations, leaving the scene, or becoming more self-assertive. Case examples are given to illustrate these interventions.

During pregnancy, elevated levels of PTH-related peptide (PTHrP) persist in the myometrium of the rat uterus. Near term, intrauterine occupancy is correlated with high levels of PTHrP messenger RNA in the gravid horn of the unilaterally pregnant uterus. In nongravid tissue from these same animals the presence of smaller yet significant elevations of PTHrP mRNA suggests that the PTHrP gene also may be regulated by humoral factor(s). To test this hypothesis, we assessed the action of 17 beta-estradiol (E2) on the expression of the PTHrP gene in the uterus of the ovariectomized rat. While low levels of PTHrP mRNA are detected in uteri from ovariectomized rats, a single dose of E2 (4, 40, or 400 micrograms/kg body weight) stimulated a 6- to 8-fold increase in the levels of PTHrP mRNA in the uterus at approximately 2 h after E2 treatment. This increase was transient with levels gradually declining to pretreatment (basal) levels within 24 h. Other steroid hormones tested, including dihydrotestosterone, dexamethasone, and progesterone, failed to stimulate this response. The increase of PTHrP mRNA accumulation required a dose greater than 0.4 micrograms/kg. The magnitude and duration of PTHrP mRNA accumulation were very similar when doses of 40 or 400 micrograms/kg were used. In addition, the stimulation of the PTHrP gene by E2 is neither age dependent nor specific to the rat and is, in part, under transcriptional control. Together, these data indicate that in vivo E2 regulates the levels of PTHrP mRNA in the rat uterus and support a role for E2 in the increased expression of PTHrP mRNA in early gestational tissue, as well as in the nongravid horn of the unilaterally pregnant uterus.

Background: Administration of a single physiological dose of 17beta-estradiol (E2:40 microg/kg) to the ovariectomized immature rat rapidly induces uterine growth and remodeling. The response is characterized by changes in endometrial stromal architecture during an inflammatory-like response that likely involves activated matrix-metalloproteinases (MMPs). While estrogen is known as an inducer of endometrial growth, its role in specific expression of MMP family members in vivo is poorly characterized. E2-induced changes in MMP-2, -3, -7, and -9 mRNA and protein expression were analyzed to survey regulation along an extended time course 0-72 hours post-treatment. Because E2 effects inflammatory-like changes that may alter MMP expression, we assessed changes in tissue levels of TNF-alpha and MCP-1, and we utilized dexamethasone (600 microg/kg) to better understand the role of inflammation on matrix remodeling.

We trace the development of ideas about the relation of mood to social rank and territory. We suggest that elevated mood enabled a person to rise in rank and cope with the increased activities and responsibilities of a leadership role, while depressed mood enabled a person to accept low rank and to forego the rewards associated with high rank. This led to the concept of a trio of agonist/investor strategy sets, each consisting of escalating and de-escalating strategies, one set at each of the three levels of the triune forebrain. Depressed mood can be seen as a de-escalating (appeasement) strategy at the lowest (reptilian) level; this should facilitate de-escalation at the highest (rational) level, but sometimes this rational level de-escalation is blocked (e.g., by stubbornness, courage, pride or ambition) and then clinical depression may ensue. These evolved psychobiological mechanisms survived the partial transition from agonistic to prestige competition. We discuss difficulties which have arisen with our ideas, and their implications for clinical work and research.