title: Three studies on life expectancy and lifespan inequality

authors: Wijesinghe, Jayani

abstract: While life expectancy is a key indicator in public health and demography, it may obscure unequal experiences of different population groups. By contrast, lifespan inequality captures variations in age at death, offering a broader view of health disparities. Focusing on lifespan inequality enables policymakers and researchers to identify vulnerable populations, design more equitable health and social policies, and evaluate progress toward reducing inequities. 
This thesis is comprised of three interrelated studies that examine life expectancy and lifespan inequality from different perspectives. The first study explores state-level variations in life expectancy and lifespan inequality in the US over a 55-year period, employing Theil’s entropy index to measure lifespan inequality and a Panel-Corrected Standard Errors (PCSE) model to assess associated socioeconomic and demographic factors. The analysis reveals a significant negative correlation between life expectancy and lifespan inequality across states. Educational attainment, health insurance coverage, and physician density show negative associations with lifespan inequality, whereas violent crime rates, smoking prevalence, and income inequality exhibit positive associations.
The second study investigates the impact of homicide on life expectancy and lifespan inequality at the state level in the US from 1968 to 2020, focusing on demographic, socioeconomic, and policy determinants. Utilizing data from the US Mortality Database and cause-eliminated life tables and Panel-Corrected Standard Errors (PCSE) models, the study reveals that Southern states experience the most substantial impacts on both life expectancy and lifespan inequality, while the Northeast exhibits comparatively lower effects. Males consistently face greater impacts than females. Key findings underscore systemic inequities: a higher percentage of Black populations and individuals aged 25–34 correlate with greater homicide-related reductions in life expectancy and increased lifespan inequality. Educational attainment, particularly the high school graduation rate, helps mitigate these effects. Corrections and judicial expenditures affect both life expectancy and lifespan inequality. In contrast, police and health spending are associated with decreases in lifespan inequality but no change in life expectancy, whereas welfare expenditures correlate with increased lifespan inequality but are correlated with life expectancy only for the total population.
The final study conducts a comparative analysis of the demographic impacts of three major pandemics: the 1918 influenza pandemic, the HIV/AIDS epidemic, and the COVID-19 pandemic on global life expectancy and lifespan inequality. The study finds that the 1918 influenza pandemic caused the most pronounced reductions in life expectancy, especially among young adults, thereby leading to substantial lifespan inequality. By contrast, HIV/AIDS had a gradual yet enduring impact, predominantly affecting young and middle-aged adults and exacerbating health disparities in regions with limited healthcare resources. The COVID-19 pandemic primarily affected older populations, producing smaller reductions in life expectancy but uniquely decreasing lifespan inequality due to the concentration of mortality among the elderly. Gender-specific effects varied: while the 1918 influenza and COVID-19 pandemics showed relatively uniform gender impacts, HIV/AIDS disproportionately affected women.
Collectively, the findings across these studies underscore the need to address the interconnected issues of life expectancy, lifespan inequality, and systemic disparities. Targeted gender-specific policies and public expenditures (e.g., increased judicial and healthcare funding) have the potential to reshape mortality patterns and mitigate disparities. Pandemic responses should be tailored to protect vulnerable age and demographic groups by ensuring equitable access to healthcare and vaccines.

text: Three studies on life expectancy and lifespan inequality While life expectancy is a key indicator in public health and demography, it may obscure unequal experiences of different population groups. By contrast, lifespan inequality captures variations in age at death, offering a broader view of health disparities. Focusing on lifespan inequality enables policymakers and researchers to identify vulnerable populations, design more equitable health and social policies, and evaluate progress toward reducing inequities. 
This thesis is comprised of three interrelated studies that examine life expectancy and lifespan inequality from different perspectives. The first study explores state-level variations in life expectancy and lifespan inequality in the US over a 55-year period, employing Theil’s entropy index to measure lifespan inequality and a Panel-Corrected Standard Errors (PCSE) model to assess associated socioeconomic and demographic factors. The analysis reveals a significant negative correlation between life expectancy and lifespan inequality across states. Educational attainment, health insurance coverage, and physician density show negative associations with lifespan inequality, whereas violent crime rates, smoking prevalence, and income inequality exhibit positive associations.
The second study investigates the impact of homicide on life expectancy and lifespan inequality at the state level in the US from 1968 to 2020, focusing on demographic, socioeconomic, and policy determinants. Utilizing data from the US Mortality Database and cause-eliminated life tables and Panel-Corrected Standard Errors (PCSE) models, the study reveals that Southern states experience the most substantial impacts on both life expectancy and lifespan inequality, while the Northeast exhibits comparatively lower effects. Males consistently face greater impacts than females. Key findings underscore systemic inequities: a higher percentage of Black populations and individuals aged 25–34 correlate with greater homicide-related reductions in life expectancy and increased lifespan inequality. Educational attainment, particularly the high school graduation rate, helps mitigate these effects. Corrections and judicial expenditures affect both life expectancy and lifespan inequality. In contrast, police and health spending are associated with decreases in lifespan inequality but no change in life expectancy, whereas welfare expenditures correlate with increased lifespan inequality but are correlated with life expectancy only for the total population.
The final study conducts a comparative analysis of the demographic impacts of three major pandemics: the 1918 influenza pandemic, the HIV/AIDS epidemic, and the COVID-19 pandemic on global life expectancy and lifespan inequality. The study finds that the 1918 influenza pandemic caused the most pronounced reductions in life expectancy, especially among young adults, thereby leading to substantial lifespan inequality. By contrast, HIV/AIDS had a gradual yet enduring impact, predominantly affecting young and middle-aged adults and exacerbating health disparities in regions with limited healthcare resources. The COVID-19 pandemic primarily affected older populations, producing smaller reductions in life expectancy but uniquely decreasing lifespan inequality due to the concentration of mortality among the elderly. Gender-specific effects varied: while the 1918 influenza and COVID-19 pandemics showed relatively uniform gender impacts, HIV/AIDS disproportionately affected women.
Collectively, the findings across these studies underscore the need to address the interconnected issues of life expectancy, lifespan inequality, and systemic disparities. Targeted gender-specific policies and public expenditures (e.g., increased judicial and healthcare funding) have the potential to reshape mortality patterns and mitigate disparities. Pandemic responses should be tailored to protect vulnerable age and demographic groups by ensuring equitable access to healthcare and vaccines.

year: 2025

title: Identification of central circuitry components mediating anorexigenic properties of oxytocin

authors: Klockars, Oscar Andreas

abstract: Recent years have brought exciting discoveries showing that a neurohormone, oxytocin (OT), acts as an appetite suppressant. Importantly, OT decreases energy needs-driven consumption of high-calorie foods by promoting early satiation, and it terminates intake motivated by palatability related to sweet taste. OT’s anorexigenic effects on both aspects of ingestive behavior are mediated by the OT receptor (OTr) expressed broadly in the brain, however, our understanding of which specific sites relay anorexigenic actions of OT is limited. Thus far, only the nucleus accumbens and ventral tegmental area of the mesolimbic system, and the brainstem’s dorsal vagal complex, have been directly implicated in relaying OT-induced hypophagia. Thus, the overarching goal of this thesis was to examine which discrete components of circuitry expressing the OTr mediate OT’s anorexigenic effects on energy- versus reward-driven feeding. The research approaches included intracranial drug administration, analyses of region-specific expression of genes, neuronal activation mapping, and feeding behavior testing in rats.
The first set of studies explored whether extreme overeating induced by a powerful orexigen, butorphanol tartrate (BT), can be alleviated by pharmacologically stimulating the OT receptor in the forebrain versus the hindbrain (via lateral (LV) and fourth ventricular (4V) OT injections, respectively). I established effective doses of BT and LV / 4V OT. Then, I determined doses of LV and 4V OT that reduce hyperphagia produced by BT in sated and deprived rats. Finally, I assessed whether OT’s effects on BT-induced feeding can be suppressed by an OTr antagonist. 4 mg/kg BT increased intake in fed and in deprived rats, whereas LV and 4V OT at 1μg caused a decrease in deprived rats. BT-induced chow intake in hungry and sated animals was suppressed by a very low, 0.1-μg dose of 4V OT, whereas 1μg OT was effective LV. The effect of OT was attenuated by OTr antagonist. The data strongly suggest that while both the forebrain and hindbrain populations of the OTr promote hypophagia, the hindbrain component of the circuitry is particularly sensitive to appetite reducing properties of OT in animals motivated to eat by a potent orexigen, BT.
In the second set of studies, I examined whether either of the two populations of the hypothalamic OTr, in the medial preoptic area (MPOA) or the ventromedial hypothalamic nucleus (VMH), mediates OT-driven hypophagia in energy- and reward-related ingestive behaviors. I provide insights into mechanisms underlying OT-driven anorexia mediated by the hypothalamus by (a) defining whether OT MPOA or VMH administration affects feeding for energy versus palatability; (b) identifying feeding-related sites activated by VMH OT injection; (c) measuring VMH OTr mRNA changes in response to hunger and palatability; and (d) examining how VMH OT affects sweet solution intake in rats. MPOA had no effect on intake of energy-dense chow in deprived rats nor did it decrease intake of calorie-dilute palatable solutions. VMH OT decreased chow intake and the effect was reversed by the antagonist. OT did not affect intakes of saccharin and sucrose solutions. Fos immunoreactivity, a marker of neuronal activation, was elevated in the VMH and energy balance-related paraventricular and arcuate nuclei, but not reward areas. VMH OT receptor expression was higher in hungry than sated rats; saccharin intake had no effect. In sum, MPOA OTr is not involved in OT-driven hypophagia mediated by hypothalamic networks. VMH OT decreases intake driven by energy not by palatability.
Finally, I assessed whether the OTr present in the basolateral (BLA) and central amygdala (CNA), sites implicated in emotional/pleasure processing of food intake, is involved in appetite control by OT. I injected OT in the BLA or CNA and assessed intake of chow induced by energy deprivation and intake of sweet solutions in nondeprived rats. I examined whether these effects are reversible by OTr blockade. I determined the effect of energy deprivation and exposure to saccharin on BLA and CNA expression of OTr mRNA. BLA OT at 0.3 μg and CNA OT at 1 μg reduced chow intake after deprivation. Only BLA OT was effective at suppressing consumption of sucrose and saccharin. The anorexigenic effects of BLA and CNA OT were attenuated by an OTr antagonist. BLA OTr mRNA expression was affected by exposure to saccharin, whereas that of CNA OTr, by energy deprivation. The relationship between amygdalar OT and energy- vs palatability-driven intake depends on the discrete localization of the OTr in this complex structure.
Overall, these findings shed light on the specific elements of brain circuitry mediating anorexigenic properties of OT. Both the forebrain and hindbrain OTr populations are relevant to feeding control. OT’s inhibitory effects on feeding for energy are mediated by a broader network of sites that includes, aside from the previously reported nucleus accumbens and dorsal vagal complex, the VMH, BLA, and CNA. Only the BLA OT modifies eating for reward. Surprisingly, the OTr in the MPOA is not involved in feeding regulation.

text: Identification of central circuitry components mediating anorexigenic properties of oxytocin Recent years have brought exciting discoveries showing that a neurohormone, oxytocin (OT), acts as an appetite suppressant. Importantly, OT decreases energy needs-driven consumption of high-calorie foods by promoting early satiation, and it terminates intake motivated by palatability related to sweet taste. OT’s anorexigenic effects on both aspects of ingestive behavior are mediated by the OT receptor (OTr) expressed broadly in the brain, however, our understanding of which specific sites relay anorexigenic actions of OT is limited. Thus far, only the nucleus accumbens and ventral tegmental area of the mesolimbic system, and the brainstem’s dorsal vagal complex, have been directly implicated in relaying OT-induced hypophagia. Thus, the overarching goal of this thesis was to examine which discrete components of circuitry expressing the OTr mediate OT’s anorexigenic effects on energy- versus reward-driven feeding. The research approaches included intracranial drug administration, analyses of region-specific expression of genes, neuronal activation mapping, and feeding behavior testing in rats.
The first set of studies explored whether extreme overeating induced by a powerful orexigen, butorphanol tartrate (BT), can be alleviated by pharmacologically stimulating the OT receptor in the forebrain versus the hindbrain (via lateral (LV) and fourth ventricular (4V) OT injections, respectively). I established effective doses of BT and LV / 4V OT. Then, I determined doses of LV and 4V OT that reduce hyperphagia produced by BT in sated and deprived rats. Finally, I assessed whether OT’s effects on BT-induced feeding can be suppressed by an OTr antagonist. 4 mg/kg BT increased intake in fed and in deprived rats, whereas LV and 4V OT at 1μg caused a decrease in deprived rats. BT-induced chow intake in hungry and sated animals was suppressed by a very low, 0.1-μg dose of 4V OT, whereas 1μg OT was effective LV. The effect of OT was attenuated by OTr antagonist. The data strongly suggest that while both the forebrain and hindbrain populations of the OTr promote hypophagia, the hindbrain component of the circuitry is particularly sensitive to appetite reducing properties of OT in animals motivated to eat by a potent orexigen, BT.
In the second set of studies, I examined whether either of the two populations of the hypothalamic OTr, in the medial preoptic area (MPOA) or the ventromedial hypothalamic nucleus (VMH), mediates OT-driven hypophagia in energy- and reward-related ingestive behaviors. I provide insights into mechanisms underlying OT-driven anorexia mediated by the hypothalamus by (a) defining whether OT MPOA or VMH administration affects feeding for energy versus palatability; (b) identifying feeding-related sites activated by VMH OT injection; (c) measuring VMH OTr mRNA changes in response to hunger and palatability; and (d) examining how VMH OT affects sweet solution intake in rats. MPOA had no effect on intake of energy-dense chow in deprived rats nor did it decrease intake of calorie-dilute palatable solutions. VMH OT decreased chow intake and the effect was reversed by the antagonist. OT did not affect intakes of saccharin and sucrose solutions. Fos immunoreactivity, a marker of neuronal activation, was elevated in the VMH and energy balance-related paraventricular and arcuate nuclei, but not reward areas. VMH OT receptor expression was higher in hungry than sated rats; saccharin intake had no effect. In sum, MPOA OTr is not involved in OT-driven hypophagia mediated by hypothalamic networks. VMH OT decreases intake driven by energy not by palatability.
Finally, I assessed whether the OTr present in the basolateral (BLA) and central amygdala (CNA), sites implicated in emotional/pleasure processing of food intake, is involved in appetite control by OT. I injected OT in the BLA or CNA and assessed intake of chow induced by energy deprivation and intake of sweet solutions in nondeprived rats. I examined whether these effects are reversible by OTr blockade. I determined the effect of energy deprivation and exposure to saccharin on BLA and CNA expression of OTr mRNA. BLA OT at 0.3 μg and CNA OT at 1 μg reduced chow intake after deprivation. Only BLA OT was effective at suppressing consumption of sucrose and saccharin. The anorexigenic effects of BLA and CNA OT were attenuated by an OTr antagonist. BLA OTr mRNA expression was affected by exposure to saccharin, whereas that of CNA OTr, by energy deprivation. The relationship between amygdalar OT and energy- vs palatability-driven intake depends on the discrete localization of the OTr in this complex structure.
Overall, these findings shed light on the specific elements of brain circuitry mediating anorexigenic properties of OT. Both the forebrain and hindbrain OTr populations are relevant to feeding control. OT’s inhibitory effects on feeding for energy are mediated by a broader network of sites that includes, aside from the previously reported nucleus accumbens and dorsal vagal complex, the VMH, BLA, and CNA. Only the BLA OT modifies eating for reward. Surprisingly, the OTr in the MPOA is not involved in feeding regulation.

year: 2019

title: An exploration of different outlooks on science: towards an understanding of the under-representation of girls, and of Maori and Pacific Island students, in science

authors: Stead, Keith Eric

abstract: The research reported here was undertaken as a supplementary study to the Learning in Science Project conducted at Waikato University (1979-1981) and sought to understand why girls, Maori and Pacific Island students, are under-represented in the sciences. Two distinctive, but complementary, perspectives were developed; one qualitative, the other quantitative, to provide data from which an understanding of the problem was sought.
The qualitative perspective was provided by using a Kelly Repertory Grid methodology and intensive individual interviews with 26 students (and many of their parents) carefully chosen to provide a reasonably heterogeneous sample of students from a variety of different schools, of both sexes, of the three major ethnic groups (European, Maori, and Pacific Island), and from each of the four middle-school form levels (Fl to F4, inclusively).
The quantitative perspective was provided by a series of empirical measures chosen, not only to identify the students for the qualitative sample but also, to investigate particular variables suggested by the literature search to have possible implications for the teaching and learning of science. 
The resultant analyses suggested the sex differences in the students’ outlooks on science could be accounted for by the existence of a broad based ‘gender-related inequality’ in the way science is presented to them by the communication media, home, and school.
Similarly, the ethnic differences in students’ outlooks on science could be accounted for by the ‘cultural inequality’ present in New Zealand society which was identified in the way many of the Polynesian students and their parents, perceived the products, processes, and practitioners of science. 
The simplification presented here masks the complexity of the issues involved but, series of educational within these two broad postulates, a series of educational recommendations was suggested for affecting current educational practices identified as maintaining (or even creating) the existing under-representation of girls, Maori and Pacific Island students in the sciences. 
These included:
(i) Student beliefs about science need to be explored, challenged, modified, and/or extended
(ii) Students’ perceptions of other people’s views need to be identified, explored, challenged and/or extended 
(iii) Teachers’ styles of teaching science need to be examined
(iv) Parents’ own outlooks on science need to be developed.
This research has emphasised the need to have all students, but particularly girls, Maori, and Pacific Island students, develop positive outlooks on science in order that the current imbalance of girls and Polynesians in the sciences be redressed.

text: An exploration of different outlooks on science: towards an understanding of the under-representation of girls, and of Maori and Pacific Island students, in science The research reported here was undertaken as a supplementary study to the Learning in Science Project conducted at Waikato University (1979-1981) and sought to understand why girls, Maori and Pacific Island students, are under-represented in the sciences. Two distinctive, but complementary, perspectives were developed; one qualitative, the other quantitative, to provide data from which an understanding of the problem was sought.
The qualitative perspective was provided by using a Kelly Repertory Grid methodology and intensive individual interviews with 26 students (and many of their parents) carefully chosen to provide a reasonably heterogeneous sample of students from a variety of different schools, of both sexes, of the three major ethnic groups (European, Maori, and Pacific Island), and from each of the four middle-school form levels (Fl to F4, inclusively).
The quantitative perspective was provided by a series of empirical measures chosen, not only to identify the students for the qualitative sample but also, to investigate particular variables suggested by the literature search to have possible implications for the teaching and learning of science. 
The resultant analyses suggested the sex differences in the students’ outlooks on science could be accounted for by the existence of a broad based ‘gender-related inequality’ in the way science is presented to them by the communication media, home, and school.
Similarly, the ethnic differences in students’ outlooks on science could be accounted for by the ‘cultural inequality’ present in New Zealand society which was identified in the way many of the Polynesian students and their parents, perceived the products, processes, and practitioners of science. 
The simplification presented here masks the complexity of the issues involved but, series of educational within these two broad postulates, a series of educational recommendations was suggested for affecting current educational practices identified as maintaining (or even creating) the existing under-representation of girls, Maori and Pacific Island students in the sciences. 
These included:
(i) Student beliefs about science need to be explored, challenged, modified, and/or extended
(ii) Students’ perceptions of other people’s views need to be identified, explored, challenged and/or extended 
(iii) Teachers’ styles of teaching science need to be examined
(iv) Parents’ own outlooks on science need to be developed.
This research has emphasised the need to have all students, but particularly girls, Maori, and Pacific Island students, develop positive outlooks on science in order that the current imbalance of girls and Polynesians in the sciences be redressed.

year: 1984