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Heroin Deaths In Connecticut Increase 87 Percent



More-educated adults in the United States tend to live longer than less-educated individuals. The differences increase in a stair-step pattern by education level, with the widest difference between college graduates and those without high school degrees. This gap has widened over the past two decades, resulting in part from steep increases in drug overdose deaths among those without college degrees, reports Ho in an article published in the journal Demography.3




Heroin Deaths in Connecticut Increase 87 Percent



Her analysis shows that between 1992 and 2011 drug overdose deaths represented a sizable share of the widening difference in life expectancy among college graduates and those with less education. For example, among non-Hispanic whites, opioid deaths account for 99 percent of the growth in the life expectancy gap between men with college degrees and those without high school diplomas; among women, opioid deaths could be blamed for 42 percent of the growth in the life expectancy gap between the two education groups.


For 2015, they calculate that the opioid-related overdose mortality rate for whites was 12.2 per 100,000, nearly twice the rate for blacks (about 6.6 per 100,000). However, between 2000 and 2015, the opioid death rate increased 51 percent among whites but 87 percent among blacks.


A possible consequence of prescription opioid misuse is fatal overdose, which can occur because opioids suppress breathing. In 2016, 7,109 women and 9,978 men died from prescription opioid overdose (a total of 17,087)* which is about 19 women per day compared to about 27 men dying from overdosing on prescription opioids. However, from 1999 to 2016, deaths from prescription opioid overdoses increased more rapidly for women (596 percent or sevenfold) than for men (312 percent or fourfold). Women between the ages of 45 and 54 are more likely than women of other age groups to die from a prescription opioid overdose.72


Drinking over the long term is more likely to damage a woman's health than a man's, even if the woman has been drinking less alcohol or for a shorter length of time.77,78 Comparing people with alcohol use disorders, women have death rates 50 to 100 percent higher than do men, including deaths from suicides, alcohol-related accidents, heart disease, stroke, and liver disease.79 In addition, there are some health risks that are unique to female drinkers. For example, heavy drinking is associated with increased risk of having unprotected sex, resulting in pregnancy or disease,80 and an increased risk of becoming a victim of violence and sexual assault. In addition, drinking as little as one drink per day is associated with a higher risk of breast cancer in some women, especially those who are postmenopausal or have a family history of breast cancer.79


Of the 70,200 overdose deaths in the US in 2017, opioids were involved in 47,600.[6] This is an increase from 2016 where over 64,000 died from drug overdose, and opioids were involved in over 42,000.[7] In 2017, the five states with the highest rates of death due to drug overdose were West Virginia (57.8 per 100,000), Ohio (46.3 per 100,000), Pennsylvania (44.3 per 100,000), Kentucky (37.2 per 100,000), and New Hampshire (37.0 per 100,000).[3]


Similar to human clinical studies, rodents exposed to heroin or morphine have a lower birthweight (Eriksson and Ronnback, 1989; Lu et al, 2012; Zagon and McLaughlin, 1977b, 1977c) and impaired learning and memory (Steingart et al, 2000a; Wang and Han, 2009). Numerous structural and functional alterations have been found that could underlie the effects of prenatal opiates on cognition, including perturbations in dendritic length, synaptic plasticity, neuronal proliferation, and cholinergic function. Prenatal heroin or morphine exposure decreases dendritic branch length in layer II/III pyramidal neurons in somatosensory cortex, which is thought to be specific to opiate receptor activation, as it can be blocked by co-administration of an opiate receptor antagonist (Lu et al, 2012; Ricalde and Hammer, 1990). Long-term potentiation, long-term depression, and proteins associated with synaptic transmission are all attenuated with perinatal morphine exposure (Villarreal et al, 2008; Yang et al, 2006). Decreased proliferation in the developing striatum (Harlan and Song, 1994) and increased apoptosis in dopaminergic cell cultures and the hippocampus have been observed with perinatal heroin or morphine exposure (Oliveira et al, 2003; Oliveira et al, 2002; Svensson et al, 2008; Wang and Han, 2009).


Perinatal heroin and morphine exposure also disrupt maturation of the opiate receptor system. Postnatal morphine exposure decreases mu opioid receptor binding in the striatum, NAc, amygdala, hypothalamus, and spinal cord (Hammer et al, 1991; Kirby, 1983; Tempel, 1991). Perinatal morphine exposure also induces morphine tolerance (Chiang et al, 2010; Eriksson and Ronnback, 1989; Hovious and Peters, 1984), although an increased sensitivity to morphine analgesia has been reported in female offspring (Arjune and Bodnar, 1989). Aroyewun and Barr (1982) proposed that postnatal morphine also accelerates the maturation of some aspects of opiate-dependent behaviors, such as opiate antagonist-induced anorexia, that normally only occurs after P14. Postnatal morphine exposure accelerated the appearance of this behavior to P10 and 12 (Aroyewun and Barr, 1983), but the observed hypophagia could also have been induced by the precipitation of opiate withdrawal. In addition, perinatal morphine or heroin has also been shown to alter sexual behavior (Vathy and Katay, 1992), NE turnover and release (De Vries et al, 1991), neuroendocrine function (Litto et al, 1983), and several other important structures and processes that this review cannot cover (for a comprehensive review of the developmental effects of illicit opiates see Slamberova (2012)).


Fewer animal studies have been published for perinatal buprenorphine than methadone and heroin/morphine, but perinatal buprenorphine appears to produce alterations common to opiate exposure. Like other opiates, perinatal buprenorphine produces morphine tolerance (Chiang et al, 2010; Robinson and Wallace, 2001), delayed acquisition of developmentally timed behaviors (Robinson and Wallace, 2001), and increased sensitization to METH (Chiang et al, 2013). Chiang et al (2013) also found decreased D1 receptor mRNA, basal cyclic AMP, and D1 receptor induced adenylyl cyclase activity in the NAc of buprenorphine-exposed offspring, suggesting disrupted signal transduction may underlie the increased METH sensitization. Although mu opioid receptor binding is decreased at birth, it corrects by postnatal day 7 (Belcheva et al, 1998; Belcheva et al, 1994; Hou et al, 2004). Perinatal buprenorphine does not appear to cause hyperactivity in animal models to date, although this has been reported in some clinical studies (Hutchings et al, 1996; Sundelin Wahlsten and Sarman, 2013). Effects on striatal acetylcholine levels are dose dependent with high doses causing a decrease at P4 and 21 but low doses producing an increase at P21 (Guo et al, 1990; Robinson, 2002). Altered myelination, which has been observed in clinical studies of opiate-exposed neonates (Walhovd et al, 2012), also occurs, producing increased myelinated axon caliber with disproportionately thin myelin sheaths potentially due to changes in myelin basic proteins and myelin-associated glycosylation (Sanchez et al, 2008). Additional observations in animal models of perinatal buprenorphine exposure have been reviewed comprehensively by others (Farid et al, 2008).


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