Binge Drinking Among Adults, by Select Characteristics and State — United States, 2018

Bohm, Michele K.; Liu, Yong; Esser, Marissa B.; Mesnick, Jessica B.; Lu, Hua; Pan, Y.; Greenlund, Kurt J.

doi:10.15585/mmwr.mm7041a2

Cited by 50 publications

(34 citation statements)

References 10 publications

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“…The use of alcohol, and binge drinking more specifically, are common behaviours in the USA. A recent report found that during 2018, 16.6% of US adults reported binge drinking in the past 30 days 26. Given the strong relationship between alcohol use, and particularly alcohol use disorder and alcohol intoxication, and TBI,20 this puts millions of adults at increased risk of sustaining a TBI.…”

Section: Discussionmentioning

confidence: 99%

“…We calculated mean level of binge drinking across all waves; data on binge drinking was collected in 1982–1985, 1988–1989, 1992, 1994, 2002 and every 2 years starting in 2006 until 2014. Of note, this definition of binge drinking differs from the Centers for Disease Control and Prevention’s definition (four or more drinks for women and five or more drinks for men on one occasion); the implications of which are discussed in the Limitations section 26…”

Section: Methodsmentioning

confidence: 99%

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Does binge drinking mediate the relationship between four adverse childhood experiences and adult traumatic brain injury? Results from the National Longitudinal Survey of Youth 1979 Cohort

et al. 2022

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ObjectiveAdverse childhood experiences (ACEs) are associated with increased risk of sustaining a traumatic brain injury (TBI). Alcohol use may play an important role in this relationship. This study examines whether binge drinking mediates the relationship between four ACEs and TBIs sustained in adulthood.MethodsUsing the National Longitudinal Survey of Youth, 1979 cohort, we conducted longitudinal mediation analyses (n=6317). Interviews occurred annually from 1979 to 1994 and biennially until 2016. We evaluated the direct and indirect effects of individual ACEs (ie, experiencing physical violence, low parental warmth, familial alcoholism and familial mental illness; reported retrospectively) and a cumulative ACEs score on mean level of binge drinking (calculated across waves) and having a TBI in adulthood. To establish temporality, we included binge drinking that was measured at age 18 or older and before any reported TBI.ResultsCumulative ACEs, familial alcoholism and physical abuse exposure were significantly associated with having a TBI through binge drinking, although this only explained a small part of the association between ACEs and TBI. Other ACEs were not significantly associated with binge drinking or TBI.ConclusionThe results indicate that while ACEs and adult TBI risk were significantly associated, lifetime binge drinking explains only a small part of the association. Future research could examine alternative social, biological and behavioural mechanisms along the pathway between ACEs and TBI. Determining this mechanism will allow public health practitioners to design and implement effective TBI prevention programmes for those at higher risk of injury due to ACE exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Does binge drinking mediate the relationship between four adverse childhood experiences and adult traumatic brain injury? Results from the National Longitudinal Survey of Youth 1979 Cohort

et al. 2022

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“…They are then inevitably ingested by humans because they are present in daily food items such as coffee [ 3 ], baked food [ 4 ], bakery products [ 5 , 6 ], roasted meat [ 7 ], pizza [ 8 ], and especially, beer [ 9 , 10 ], the most consumed alcoholic beverage worldwide. Over the past 50 years, total global beer consumption has risen sharply in emerging economies [ 11 , 12 ]. Long-term, excessive beer consumption has been associated with metabolic disease outcomes (obesity, diabetes and non-alcoholic fatty liver disease) and causes preventable death [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Malting barley carbon dots-mediated oxidative stress promotes insulin resistance in mice via NF-κB pathway and MAPK cascade

Zhang

Zhu

et al. 2022

J Nanobiotechnol

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Background Food-borne carbon dots (CDs) are widely generated during food processing and are inevitably ingested by humans causing toxicity. However, the toxic effects of food-borne CDs on the blood glucose metabolism are unknown. Results In this study, we brewed beer via a representative strategy and extracted the melting-barley CDs (MBCDs) to explore the toxic effects on blood glucose in mice. We found the accumulation of fluorescent labeled MBCDs in various organs and oral administration of MBCDs can cause visceral toxicity, manifested as liver damage. Mice were orally administered MBCDs (5 and 25 mg/kg) for 16 weeks, and increased levels of fasting blood glucose were observed in both MBCDs-treated groups. Transcriptomic analyses revealed that MBCDs activate oxidative stress, inflammatory responses, the MAPK cascade, and PI3K/Akt signaling in mice livers. Mechanistically, MBCDs exposure-induced reactive oxygen species (ROS) overproduction activates the nuclear factor-κB (NF-κB) signaling pathway and MAPK cascade, thereby promoting phosphorylated insulin receptor substrate (IRS)-1 at Ser307 and inducing insulin resistance (IR). Meanwhile, the IR promoted gluconeogenesis, which enhanced MBCDs-induced hyperglycemia of mice. Importantly, inhibition of the ROS significantly attenuated the MBCDs-induced inflammatory response and MAPK cascade, thereby alleviating IR and hyperglycemia in mice. Conclusion In summary, this study revealed that MBCDs promote ROS overproduction and thus induced IR, resulting in imbalance of glucose homeostasis in mice. More importantly, this study was further assessed to reveal an imperative emphasis on the reevaluation of dietary and environmental CDs exposure, and has important implications for T2DM prevention research. Graphical Abstract

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“…Furthermore, a recent study has found that heavy drinking during early adulthood to midlife years was associated with increased risk for AD ( Langballe et al, 2015 ). The majority of individuals that binge-drink are in late adolescent to mid-life years (18–44 yo) and “age-out” of heavy drinking, with low rates in aged populations ( Bohm et al, 2021 ). This suggests that these epidemiological findings in humans could be due to persistent effects of binge ethanol during young adulthood to midlife years that increase risk for AD.…”

Section: Introductionmentioning

confidence: 99%

Chronic Ethanol Causes Persistent Increases in Alzheimer’s Tau Pathology in Female 3xTg-AD Mice: A Potential Role for Lysosomal Impairment

Tucker

Pauneto

Barnett

et al. 2022

Front. Behav. Neurosci.

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Epidemiological studies have found that heavy alcohol use is associated with increased risk for Alzheimer’s disease (AD), with frequent drinking earlier in adulthood increasing risk. The increases in neuroinflammation featured in both heavy alcohol use and AD may be partially responsible for this link. However, it is unknown if abstinence mitigates this risk. We hypothesized that binge ethanol during mid adult life would persistently increase AD pathology even after prolonged abstinence. Male and female 3xTg-AD mice (APPSwe, tauP301, Psen1tm1Mpm) which feature progressive amyloid (Aβ) and tau pathology, received chronic binge ethanol (5g/kg/day, 5-days-on/2-days-off, i.g.) or water during adulthood (from 5.5 to 9 months of age), followed by abstinence and assessment at 14 months of age. The effects of ethanol on protective AD genes (e.g., APOE and TREM2) as well as proinflammatory genes were measured by PCR. Levels of pathologic tau and Aβ were measured by immunohistochemistry and western blot. Ethanol caused persistent reductions in protective AD genes: APOE (25% reduction, *p < 0.05), TREM2 (28%, *p < 0.05), LPL (40%, **p < 0.01), and CTSD (24%, *p < 0.05) and promoted a proinflammatory gene signature in female, but not male cortex. Concurrently, ethanol increased total and hyperphosphorylated tau (AT8) in piriform cortex and hippocampus of females, but not males. Levels of AT8 were negatively correlated with APOE (R = –0.67, *p < 0.05) and TREM2 (R = –0.78, **p < 0.005) suggesting protective roles in pathogenesis. No differences were found in levels of main regulators of tau phosphorylation state (GSK3β, PKA, PP2A), suggesting ethanol disrupted clearance of tau. Therefore, we measured the effect of ethanol on lysosomes, which degrade tau, and lysosomal localization of tau using co-immunofluorescence. In females, ethanol caused a persistent reduction in mature LAMP1 lysosomes in CA1 of hippocampus (35%, *p < 0.05), along with a 60% increase in total tau (*p < 0.05). Thus, chronic binge ethanol during mid adult life causes a persistent enhancement of tau pathology in cortical and hippocampal brain regions of females. Persistent AD pathology was associated with an increased proinflammatory signature and a reduction of mature lysosomes. This implicates binge ethanol exposure with increased risk of AD pathologic progression in females.

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Binge Drinking Among Adults, by Select Characteristics and State — United States, 2018

Cited by 50 publications

References 10 publications

Does binge drinking mediate the relationship between four adverse childhood experiences and adult traumatic brain injury? Results from the National Longitudinal Survey of Youth 1979 Cohort

Does binge drinking mediate the relationship between four adverse childhood experiences and adult traumatic brain injury? Results from the National Longitudinal Survey of Youth 1979 Cohort

Malting barley carbon dots-mediated oxidative stress promotes insulin resistance in mice via NF-κB pathway and MAPK cascade

Chronic Ethanol Causes Persistent Increases in Alzheimer’s Tau Pathology in Female 3xTg-AD Mice: A Potential Role for Lysosomal Impairment

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