Health promotion programs for middle-aged adults that promote physical activity or healthy eating and involve local governments and health services: A rapid review.

BACKGROUND: Noncommunicable diseases can be prevented or delayed through health promotion programs. Little is known about programs delivered by partnership organisations that address lifestyle behaviours. The study's purpose was to review the literature on physical activity or healthy eating health promotion programs, delivered in partnership by the local government and local health services, to describe characteristics of programs and their impact on physical activity, healthy eating or related health outcomes among middle-aged adults. METHODS: This rapid review was conducted from November 2021 to June 2022, informed by the Cochrane Rapid Reviews Methods guidance for conducting rapid reviews. Articles published in English since 2000 were identified in Medline, Embase, CINAHL, AgeLine and Scopus databases. A narrative synthesis was performed. RESULTS: Ten articles involving 19 802 participants were identified from a total of 4847 articles identified from the search. The primary role of the partnership was providing funds. Other roles were facilitating stakeholder involvement, program development, delivery and recruitment. Positive outcomes were likely if programs were developed by collaborative stakeholder partnerships, informed by previous research or a behaviour change framework. The heterogeneity of study designs and reported outcomes did not permit meta-analysis. CONCLUSION: This review highlights the lack of evidence of local government-health service partnerships delivering physical activity or healthy eating health promotion programs for middle-aged adults. Programs designed collaboratively with an evidence base or a theory base are recommended and can guide future work investigating strategies for partnership development. SO WHAT?: Physical activity or healthy eating health promotion programs need early stakeholder collaborative input designed with a theory/evidence base. This can guide future work for investigating strategies for partnership development.

Stress rapidly suppresses in vivo LH pulses and increases activation of RFRP-3 neurons in male mice

Restraint stress is a psychosocial stressor that suppresses reproductive status, including LH pulsatile secretion, but the neuroendocrine mechanisms underlying this inhibition remains unclear. Reproductive neural populations upstream of gonadotropin-releasing hormone (GnRH) neurons, such as kisspeptin, neurokinin B and RFRP-3 (GnIH) neurons, are possible targets for psychosocial stress to inhibit LH pulses, but this has not been well examined, especially in mice in which prior technical limitations prevented assessment of in vivo LH pulse secretion dynamics. Here, we examined whether one-time acute restraint stress alters in vivo LH pulsatility and reproductive neural populations in male mice, and what the time-course is for such alterations. We found that endogenous LH pulses in castrated male mice are robustly and rapidly suppressed by one-time, acute restraint stress, with suppression observed as quickly as 12­18 min. This rapid LH suppression parallels with increased in vivo corticosterone levels within 15 min of restraint stress. Although Kiss1, Tac2 and Rfrp gene expression in the hypothalamus did not significantly change after 90 or 180 min restraint stress, arcuate Kiss1 neural activation was significantly decreased after 180 min. Interestingly, hypothalamic Rfrp neuronal activation was strongly increased at early times after restraint stress initiation, but was attenuated to levels lower than controls by 180 min of restraint stress. Thus, the male neuroendocrine reproductive axis is quite sensitive to short-term stress exposure, with significantly decreased pulsatile LH secretion and increased hypothalamic Rfrp neuronal activation occurring rapidly, within minutes, and decreased Kiss1 neuronal activation also occurring after longer stress durations.

Acute Psychosocial Stress Inhibits LH Pulsatility and Kiss1 Neuronal Activation in Female Mice.

Psychosocial stress, such as isolation and restraint, disrupts reproductive neuroendocrine activity. Here we investigate the impact of psychosocial stress on luteinizing hormone (LH) pulses and gene expression and neuronal activation within Rfrp and Kiss1 cells in female mice. Mice were ovariectomized (OVX) and handled daily to habituate to the tail-tip blood collection procedure. Blood was collected every 5 minutes for 180 minutes for measurement of LH. After 90 minutes, stress animals were placed into restraint devices and isolated to new cages. No-stress control animals remained in their home cages. LH pulses occurred at regular intervals during the entire 180-minute sampling period in controls. In contrast, stress induced a rapid and robust suppression of pulsatile LH secretion. Stress reduced the frequency of pulses by 60% and diminished basal LH levels by 40%; pulse amplitude was unaffected. In a separate cohort of OVX females, brains were collected after 45, 90, or 180 minutes of stress or in no-stress controls. At all time points, stress induced a potent decrease in arcuate Kiss1 neuronal activation, using cfos induction as a marker, with a 50% to 60% suppression vs control levels, whereas Rfrp and cfos coexpression in the dorsal-medial nucleus was elevated after 45 minutes of stress. Although arcuate Kiss1 gene expression remained stable, Rfrp expression was elevated 20% after 180 minutes of stress. These findings demonstrate rapid suppression of LH pulsatile secretion by psychosocial stress, associated with reduced cfos induction in Kiss1 neurons and time-dependent increases in Rfrp neuronal activation and messenger RNA.