In this article we present an evolutionary theory of altruism-Selective Investment Theory (SIT). The essence of SIT is that human social bonds evolved as overarching, emotion regulating mechanisms designed to promote reliable, high-cost altruism among individuals who depend on one another for survival and reproduction (e.g., offspring, mates, coalition members). We view the social bond as a dynamic memory complex, with cognitive, affective, and neurohormonal features. When activated, this complex works to minimize self versus other motivational conflicts associated with altruistic decision making. Our proposal that social bonds evolved because they promoted giving away (as opposed to getting) valuable resources represents a departure from traditional wisdom, and has important implications for interpreting and investigating close relationship phenomena.

The acquisition of declarative (i.e., facts) and procedural (i.e., skills) memories may be supported by independent systems. This same organization may exist, after memory acquisition, when memories are processed off-line during consolidation. Alternatively, memory consolidation may be supported by interactive systems. This latter interactive organization predicts interference between declarative and procedural memories. Here, we show that procedural consolidation, expressed as an off-line motor skill improvement, can be blocked by declarative learning over wake, but not over a night of sleep. The extent of the blockade on procedural consolidation was correlated to participants' declarative word recall. Similarly, in another experiment, the reciprocal relationship was found: declarative consolidation was blocked by procedural learning over wake, but not over a night of sleep. The decrease in declarative recall was correlated to participants' procedural learning. These results challenge the concept of fixed independent memory systems; instead, they suggest a dynamic relationship, modulated by when consolidation takes place, allowing at times for a reciprocal interaction between memory systems.

It is well known that certain cognitive abilities decline with age. The ability to form certain new declarative memories, particularly memories for facts and events, has been widely shown to decline with advancing age. In contrast, the effects of aging on the ability to form new procedural memories such as skills are less well known, though it appears that older adults are able to acquire some new procedural skills over practice. The current study examines the effects of normal aging on procedural memory more closely by comparing the effects of aging on the encoding or acquisition stage of procedural learning versus its effects on the consolidation, or between-session stage of procedural learning. Twelve older and 14 young participants completed a sequence-learning task (the Serial Reaction Time Task) over a practice session and at a re-test session 24 hours later. Older participants actually demonstrated more sequence skill during acquisition than the young. However, older participants failed to show skill improvement at re-test as the young participants did. Age thus appears to have a differential effect upon procedural learning stages such that older adults' skill acquisition remains relatively intact, in some cases even superior, compared to that of young adults, while their skill consolidation may be poorer than that of young adults. Although the effect of normal aging on procedural consolidation remains unclear, aging may actually enhance skill acquisition on some procedural tasks.

During sequence learning, individuals show motor-skill acquisition and an ability to verbally describe items within the sequence. We disrupted this latter, declarative component by having participants learn a word list immediately after sequence learning. This induced off-line skill improvements. We conclude that off-line memory processing relies not only on the engagement of neuroplastic mechanisms but also on the disengagement of an interaction between declarative and procedural memory systems.

Although a growing body of evidence suggests that giving to (helping) others is linked reliably to better health and longevity for the helper, little is known about causal mechanisms. In the present paper we use a recently developed model of caregiving motivation to identify possible neurophysiological mechanisms. The model describes a mammalian neurohormonal system that evolved to regulate maternal care, but over time may have been recruited to support a wide variety of helping behaviors in humans and other social animals. According to the model, perception of need or distress in others activates caregiving motivation, which in turn, can facilitate helping behavior. Motivational regulation is governed by the medial preoptic area of the hypothalamus, interacting with certain other brain regions, hormones, and neuromodulators (especially oxytocin and progesterone). Consideration of neurohormonal circuitry and related evidence raises the possibility that it is these hormones, known to have stress-buffering and restorative properties, that are responsible, at least in part, for health and longevity benefits associated with helping others.