Tag Archives: long-term effects

Benzodiazepine use and risk of Alzheimer’s disease

Benzodiazepine use is associated with an increased risk of Alzheimer’s disease. The stronger association observed for long term exposures reinforces the suspicion of a possible direct association, even if benzodiazepine use might also be an early marker of a condition associated with an increased risk of dementia. Unwarranted long term use of these drugs should be considered as a public health concern. Continue reading

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Benzodiazepine use associated with increased risk of dementia.

Conclusions In this prospective population based study, new use of benzodiazepines was associated with increased risk of dementia. The result was robust in pooled analyses across cohorts of new users of benzodiazepines throughout the study and in a complementary case-control study. Considering the extent to which benzodiazepines are prescribed and the number of potential adverse effects of this drug class in the general population, indiscriminate widespread use should be cautioned against. Continue reading

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Risk factors for progression of brain atrophy in aging: six-year follow-up of normal subjects.

Neurology. 2005 May 24;64(10):1704-11. Risk factors for progression of brain atrophy in aging: six-year follow-up of normal subjects. Enzinger C1, Fazekas F, Matthews PM, Ropele S, Schmidt H, Smith S, Schmidt R. Author information Abstract OBJECTIVES: To determine the rate of brain atrophy in neurologically asymptomatic elderly and to investigate the impact of baseline variables including conventional cerebrovascular risk factors, APOE epsilon4, and white matter hyperintensity (WMH) on its progression. METHODS: We assessed the brain parenchymal fraction at baseline and subsequent annual brain volume changes over 6 years for 201 participants (F/M … Continue reading

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Hyperglycemia is associated with subtle brain injury and impaired attention and memory even in young adults

Neurology. 2015 Jun 9;84(23):2329-37. doi: 10.1212/WNL.0000000000001655. Epub 2015 May 6. Glucose indices are associated with cognitive and structural brain measures in young adults. Weinstein G1, Maillard P2, Himali JJ2, Beiser AS2, Au R2, Wolf PA2, Seshadri S2, DeCarli C2. Author information Abstract OBJECTIVE: To evaluate the possible early consequences of impaired glucose metabolism on the brain by assessing the relationship of diabetes, fasting blood glucose (FBG) levels, and insulin resistance with cognitive performance and brain integrity in healthy young and middle-aged adults. METHODS: The sample included dementia-free participants (mean age 40 ± 9 … Continue reading

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Association between benzodiazepine use and occurrence of benign brain tumors.

J Neurol Sci. 2014 Jan 15;336(1-2):8-12. doi: 10.1016/j.jns.2013.11.009. Epub 2013 Nov 16. An association between benzodiazepine use and occurrence of benign brain tumors. Harnod T1, Lin CL2, Sung FC2, Kao CH3. Author information Abstract OBJECTIVE: This study was designed to evaluate the impact of long-term benzodiazepine use on the subsequent risk of benign brain tumor (BBT) or malignant brain tumor (MBT) development. METHOD: We used data from the National Health Insurance System of Taiwan. For the study cohort, we identified 62,186 patients who had been prescribed benzodiazepine for at least 2 … Continue reading

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Alzheimer dementia and diabetes

Alzheimer’s disease [AD] is the most common cause of dementia in North America. Despite 30+ years of intense investigation, the field lacks consensus regarding the etiology and pathogenesis of sporadic AD, and therefore we still do not know the best strategies for treating and preventing this debilitating and costly disease. However, growing evidence supports the concept that AD is fundamentally a metabolic disease with substantial and progressive derangements in brain glucose utilization and responsiveness to insulin and insulin-like growth factor [IGF] stimulation. Moreover, AD is now recognized to be heterogeneous in nature, and not solely the end-product of aberrantly processed, misfolded, and aggregated oligomeric amyloid-beta peptides and hyperphosphorylated tau. Other factors, including impairments in energy metabolism, increased oxidative stress, inflammation, insulin and IGF resistance, and insulin/IGF deficiency in the brain should be incorporated into all equations used to develop diagnostic and therapeutic approaches to AD. Herein, the contributions of impaired insulin and IGF signaling to AD-associated neuronal loss, synaptic disconnection, tau hyperphosphorylation, amyloid-beta accumulation, and impaired energy metabolism are reviewed. In addition, we discuss current therapeutic strategies and suggest additional approaches based on the hypothesis that AD is principally a metabolic disease similar to diabetes mellitus. Ultimately, our ability to effectively detect, monitor, treat, and prevent AD will require more efficient, accurate and integrative diagnostic tools that utilize clinical, neuroimaging, biochemical, and molecular biomarker data. Finally, it is imperative that future therapeutic strategies for AD abandon the concept of uni-modal therapy in favor of multi-modal treatments that target distinct impairments at different levels within the brain insulin/IGF signaling cascades.
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Mobile phone and cordless phone use and brain tumor risk

We made a pooled analysis of two case-control studies on malignant brain tumours with patients diagnosed during 1997–2003 and 2007–2009. They were aged 20–80 years and 18–75 years, respectively, at the time of diagnosis. Only cases with histopathological verification of the tumour were included. Population-based controls, matched on age and gender, were used. Exposures were assessed by questionnaire. The whole reference group was used in the unconditional regression analysis adjusted for gender, age, year of diagnosis, and socio-economic index. In total, 1498 (89%) cases and 3530 (87%) controls participated. Mobile phone use increased the risk of glioma, OR = 1.3, 95% CI = 1.1–1.6 overall, increasing to OR = 3.0, 95% CI = 1.7–5.2 in the >25 year latency group. Use of cordless phones increased the risk to OR = 1.4, 95% CI = 1.1–1.7, with highest risk in the >15–20 years latency group yielding OR = 1.7, 95% CI = 1.1–2.5. The OR increased statistically significant both per 100 h of cumulative use, and per year of latency for mobile and cordless phone use. Highest ORs overall were found for ipsilateral mobile or cordless phone use, OR = 1.8, 95% CI = 1.4–2.2 and OR = 1.7, 95% CI = 1.3–2.1, respectively. The highest risk was found for glioma in the temporal lobe. First use of mobile or cordless phone before the age of 20 gave higher OR for glioma than in later age groups.
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Special issue on panic disorder: Actual separations and losses during childhood, such parental death, parental separation or divorce (CPL), effect lifelong alterations in the physiological reactivity of the endogenous opioid system of healthy adults.

This is the final, published version of our paper, published in the special issue of Neuroscience & Biobehavioral Reviews Volume 46, Part 3, October 2014, Pages 345–351 Translational approaches to panic disorder http://www.sciencedirect.com/science/article/pii/S0149763414000827 PDF: Preter Klein 2014 final journal version Nov 20 2014  FULLTEXT:  Article outline Highlights Abstract Keywords 1. Panic and comorbid conditions 2. Testing the panic-suffocation-false alarm-endogenous opioid connection References Neuroscience & Biobehavioral Reviews Volume 46, Part 3, October 2014, Pages 345–351 Translational approaches to panic disorder Review Lifelong opioidergic vulnerability through early life … Continue reading

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Autoimmune disease, inflammation and the brain

Went to a fabulous lecture by  Dr. Souhel Najjar on autoimmune encephalitis this morning. As a reminder, bad relationships (including with one’s self-image etc.) can also cause/contribute to inflammatory burden. Below is a well-informed and written piece on Anti-NMDA-receptor encephalitis (one of many), courtesy of Wikipedia. Last edited 11 days ago by an anonymous user Anti-NMDA receptor encephalitis Watch this page Anti-NMDA (N-methyl D-aspartate) receptor antibody encephalitis, also termed NMDA receptor antibody encephalitis, is an acute form of encephalitis which is potentially lethal but has high probability for … Continue reading

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Association of Childhood Adversities and Early-Onset Mental Disorders With Adult-Onset Chronic Physical Conditions

Important paper on childhood adversities an adult-age chronic medical conditions, published just before our study on endogenous opioid dysregulation after early childhood adversity in psychiatrically and physically “healthy” adults.   Archives of General Psychiatry August 2011, Vol 68, No. 8 > < Previous ArticleNext Article > Original Article | Aug 2011 Association of Childhood Adversities and Early-Onset Mental Disorders With Adult-Onset Chronic Physical Conditions Kate M. Scott, PhD; Michael Von Korff, ScD; Matthias C. Angermeyer, MD, PhD; Corina Benjet, PhD; Ronny Bruffaerts, PhD; Giovanni de Girolamo, MD; Josep Maria Haro, MD, MPH, … Continue reading

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BMJ.org: Research News Benzodiazepines may be linked to Alzheimer’s disease, study finds

Research News Benzodiazepines may be linked to Alzheimer’s disease, study finds BMJ 2014; 349 doi: http://dx.doi.org/10.1136/bmj.g5555 (Published 10 September 2014)Cite this as: BMJ 2014;349:g5555 Article Related content Metrics Responses Get access to this article and to all of thebmj.com for 14 days. Sign up today for a 14 day free trial. Access to the full version of this article requires a subscription payment. Please login or subscribe below. Zosia Kmietowicz Author affiliations Taking benzodiazepines is associated with an increased risk of developing Alzheimer’s disease, particularly in long term users, a study has … Continue reading

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Maurice Preter MD and Donald F. Klein, MD, DSc: Lifelong opioidergic vulnerability through early life separation: A recent extension of the false suffocation alarm theory of panic disorder.

“[…W]e objectively, experimentally showed a physiological link between endogenous opioid system deficiency and panic-like suffocation sensitivity in healthy adults. This is consonant with the expanded Suffocation-False Alarm Theory of panic suggesting an episodic functional endogenous opioid deficit (Preter and Klein, 1998). The specificity of the naloxone + lactate model of clinical panic should be tested using specific anti-panic components, possibly including opioidergic mixed agonist-antagonists such as buprenorphine. If specific, the naloxone + lactate effect in normal humans affords a screening method for testing putative anti-panic drugs which is currently not available. This could obviate the experimental treatment of panic disorder patients in drug development.
Our data also show for the first time that actual separations and losses during childhood, such parental death, parental separation or divorce (CPL), effect lifelong alterations in the physiological reactivity of the endogenous opioid system of healthy adults.
This result encourages epigenetic inquiry into the effects of CPL on endogenous opioid systems, and their role in resilience under extreme stress. In addition, a redefinition of what constitutes a (truly) healthy control in clinical research protocols may be called for.” Continue reading

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