Sleep disorder

Zolpidem increased cancer risk in patients with sleep disorder: A 3-year follow-up study

Posted by

0


  Abstract

Background: Zolpidem has been increasingly used in patients with sleep disorder due to its minimal respiratory depressor effects and short half-life. Materials and Methods: Recent case reports indicate that zolpidem usage may be associated with increased cancer mortality. This study aimed to determine the impact of zolpidem usage on the risk of incident cancer events in sleep disorder patients over a 3-year follow-up. Of the 6924 subjects diagnosed with sleep disorder in 2004, 1728 had used zolpidem. A Cox proportional hazard model was performed to estimate 3-year cancer event-free survival rates for patients using zolpidem and those not using it, after adjusting for confounding and risk factors. Results: At the end of follow-up, 56 patients had incident cancers, 26 (1.5%) who used zolpidem, and 30 (0.6%) who did not. After adjustments for gender, age, comorbidities, and other medications, patients using zolpidem had a 1.75 times (95% confidence interval [CI], 1.02–3) greater risk of cancer events than those not using zolpidem during the 3-year follow-up. Greater mean daily dose and longer use were associated with increased risk. Among patients with sleep disorder, mean daily dose >10 mg and length of drug use >2 months was associated with 3.74 times greater risk (95% CI, 1.42–9.83; P = 0.008) of incident cancer events. Conclusions: In this study, zolpidem use increased cancer events risk in sleep disorder patients. Risks and benefits of chronic zolpidem usage should be explained to sleep disorder patients, and long-term use should be monitored.

Keywords: Cancer, hazard ratios, mean daily dose, sleep disorder, zolpidem

 

How to cite this article:
Lin SC, Su YC, Huang YS, Lee CC. Zolpidem increased cancer risk in patients with sleep disorder: A 3-year follow-up study. J Med Sci 2016;36:68-74

 

How to cite this URL:
Lin SC, Su YC, Huang YS, Lee CC. Zolpidem increased cancer risk in patients with sleep disorder: A 3-year follow-up study. J Med Sci [serial online] 2016 [cited 2018 Dec 15];36:68-74. Available from: http://www.jmedscindmc.com/text.asp?2016/36/2/68/181522

 

  Introduction Top

The clinical use of sedatives or hypnotics has increased gradually so that a 53% growth in prescriptions over 5 years was reported in 2006.[1] Some 6–10% of US adults have used hypnotics, and the percentage is higher in Europe.[2] The most commonly prescribed medications are benzodiazepines, nonbenzodiazepines, gamma-aminobutyric acid (GABA) agonists, melatonin receptor agonists, sedating antidepressants, antihistamines, and wake-promoting drugs.[3] However, the potential side effects of hypnotics, such as cancer risk, may be overlooked.

Zolpidem, an imidazopyridine in use since 1980, has been increasingly used in patients with sleep disorder due to its very few respiratory depressor effects and short half-life of 2.5 h.[4],[5] Of the 8607 patients who reported side effects of zolpidem on the eHealthMe website, which continuously monitor drug adverse effects, 71 (i.e. 0.82%) reported incident cancer.[6] Previous studies reported an association of hypnotics and cancer death.[7],[8],[9] However, in these studies, neither the specific hypnotic drug nor the quantity was provided. Furthermore, zolpidem was not included in these series. Recently, Kripke et al. conducted a matched cohort study and found that taking hypnotics, either zolpidem or temazepam, was associated with increased cancer risk in rural US patients.[10] The main limitation of this study was its stratification of hypnotic drug dosage in three equivalent groups to validate the dose-response relationship; however, such stratification is not practical in terms of clinical use.

The critical dosage and length of use at which zolpidem will affect the development of incident cancer events in patients with sleep disorder have not clearly explored. The goals of the current study are (1) to determine the relative risk of incident cancer events associated with zolpidem use in sleep disorder patients using a population-based dataset and (2) to provide the critical dosage and length of zolpidem usage associated with increased cancer risk.

  Materials and Methods Top

Ethics statement

This study was initiated after approval by the Institutional Review Board of Buddhist Dalin Tzu Chi General Hospital, Taiwan. Since all identifying personal information was stripped from the secondary files before analysis, the review board waived the requirement for written informed consent from the patients involved.

Database

The National Health Insurance Program, which provides compulsory universal health insurance, was implemented in Taiwan in 1995. It enrolls up to 99% of the Taiwanese population and contracts with 97% of all medical providers. The resulting database contains comprehensive information on insured subjects including dates of clinical visits, diagnostic codes, details of prescriptions, and expenditure amounts. This study used the Longitudinal Health Insurance Dataset for 2004–2006 released by the Taiwan Nation Health Research Institute. The patients studied did not differ statistically significantly from the general population in age, gender, or health care costs, as reported by the Taiwan National Health Research Institute (www. nhri.org.tw).

Study population

All patient records in the dataset between January 1, 2002, and December 31, 2002, with sleep disorder diagnostic codes (International Classification of Diseases, 9th revision-Clinical Modification [ICD-9-CM] 780.5x) from an urban area were included in the study.[11],[12] Excluded were those with any type of cancer (ICD-9-CM codes 140-208) diagnosed before or during the index ambulatory visit.

Identification of study cohort

A total of 6924 sleep disorder patients were identified. Each patient was tracked for 3 years from his or her index ambulatory visit in 2002 to identify outcomes, including any type of incident cancer (ICD-9-CM 140-208). To maximize case ascertainment, only patients verified by also being in cancer and catastrophic illness patient database were included in the study. These patients were then linked to the administrative data for the period 2002–2004 to calculate cancer disease-free survival time, with cases censored for patients who withdrew coverage from the National Health Insurance Program or were still robust without defined events at the end of follow-up.

Definition of exposure and covariate adjustment

The main exposure of interest was zolpidem. The dosage, date of prescription, supply days, and a total number of pills dispensed were obtained from the outpatient pharmacy prescription database. The mean daily dose was estimated by dividing the cumulative number of pills prescribed by the follow-up time from the date of initiating zolpidem treatment to the date of incident cancer, date of stopping medicine, or end of this follow-up study. The defined daily dose (DDD) was 10 mg for zolpidem. Other medications included in analysis were antihypertensives (i.e. propranolol, terazosin, doxazosin, prazosin, atenolol, furosemide, nifedipine, verapamil, diltiazem, isosorbide dinitrate, lisinopril, amitriptyline, chlorpromazine, or prochlorperazine), psychotropic agents (i.e. diazepam, alprazolam, or haloperidol), oral hypoglycemic agents, and insulin. Information on patients’ age, gender, comorbidities, and monthly income level as a proxy of socioeconomic status (SES) were collected. The comorbidities for each patient was based on the modified Charlson comorbidity index score, a widely used measure for risk adjustment in administrative claims data sets.[13]

Statistical analysis

The SAS statistical package, version 9.2 (SAS Institute, Inc., Cary, NC), and SPSS version 15 (SPSS Inc., Chicago, IL, USA) were used for data analysis. Pearson’s Chi-square test was used for categorical variables, demographic characteristics (age group and gender), comorbidities, and medications.

The 3-year cancer event-free survival rate was estimated using the Kaplan–Meier method. The cumulative risk of incident cancer event was estimated as a function of time from initial treatment. A Cox proportional hazard regression model was used to calculate the risk of cancer event in sleep disorder patients who used zolpidem versus those who did not, after adjustments for age, gender, comorbidities, SES and other medication usage. A P < 0.05 was considered statistically significant in the regression models.

  Results Top

The distribution of demographic characteristics for the two cohorts is shown in [Table 1]. Those taking zolpidem were significantly older and more likely to be female than those who did not take it. They were also more likely to have more comorbidities, low SES, and more frequently used antiglycemic drugs, psychotropic agents, and antihypertensive medications.

Table 1: Baseline characteristics (n=6924)

Click here to view

At the end of follow-up, 56 patients had incident cancers, 26 (1.5%) in those using zolpidem, and 30 (0.6%) in those not using it. Patients using zolpidem had an increased risk of cancer events. [Table 2] shows the types of cancer events for the two cohorts stratified by gender. Increased mean daily dose and longer use were associated with increased cumulative risk of cancer events [Figure 1] and [Figure 2]. After adjustments for gender, age, comorbidities, and other medications, patients using zolpidem had a 1.75-times (95% CI, 1.02–3.02) higher risk of cancer events than those who did not use zolpidem during the 3-year follow-up period. [Figure 3] shows the combined effect of mean daily dose and length of zolpidem use on increased cancer risk. [Table 3] shows the adjusted ratios of cancer incidence with zolpidem usage after adjusting for gender, comorbidities, and other medications. Mean daily dose >1 DDD and usage >2 months was associated with 3.74 times (95% CI, 1.42–9.83; P = 0.008) higher risk of incident cancer events in a Cox regression model.

Table 2: Incident tumors in individuals with zolpidem usage and those without by stratification for gender

Click here to view
Figure 1: Effect of zolpidem dose on cancer risk

Click here to view
Figure 2: Effect of zolpidem duration on cancer risk

Click here to view
Figure 3: Combined effect of zolpidem dose and duration on cancer risk

Click here to view
Table 3: Adjusted hazard ratios for zolpidem in patients with sleep disturbance

Click here to view

 

  Discussion Top

Our data showed that zolpidem usage was associated with increased incident cancer risk in patients with sleep disorder. Zolpidem usage >1 DDD for a period >2 months incurred a 3.7-fold higher risk of cancer events. Although zolpidem, the newer nonbenzodiazepine, has been shown to be safe and effective in patients with insomnia,[14] its chronic usage should be carefully restricted and monitored.

Our results suggest that zolpidem usage for more than 2 months increases cancer risk significantly in patients with sleep disorder. Comparing with previous studies, this series further provided a critical period (>2 months) and mean daily dose (>1 DDD) for elevated risk of incident cancer for clinical physicians and the general population.

Due to its short half-life and selective Type I GABAA receptor agonist, zolpidem is a widely used, standard treatment for patients with sleep disorder or insomnia.[3],[15] Of the 8607 patients who reported side effects with zolpidem use on the eHealthMe website, which continuously monitors drug adverse effects, 71 (i.e., 0.82%) reported an incident cancer.[6] In our study, 1.5% persons with zolpidem usage developed incident cancer within 3 years. Zolpidem use was associated with a 1.8-times higher risk of cancer events after adjusting for other medications and confounding factors. Our findings are consistent with Iqbal et al. that zolpidem usage was associated with a 1.13-times higher risk of cancer (95% CI, 1.09–1.17).[16] Higher doses and longer use were positively associated with cancer risk. This series revealed that a mean daily dose >1 DDD and drug usage >2 months was associated with 3.7 times risk (95% CI, 1.4–10) of incident cancer events in patients with sleep disorder.

The exact relationship between zolpidem and infection events remains unknown although several mechanisms are plausible. Benzodiazepines have been found to affect polymorphonuclear cell chemotaxis and phagocytosis.[17] Benzodiazepines in general suppress the immune response through peripheral and central benzodiazepine receptors.[18] The impairment of macrophage spreading could be attributed to the anti-inflammatory effect of the peripheral benzodiazepine receptor on blood cells through inhibition of the release of pro-inflammatory cytokines such as interleukin-6 and interleukin-13.[19] An uncontrolled small case series described carcinogenicity following the prescription of zopiclone or eszopiclone to HIV Type 1 infected individuals.[20] Eszopiclone and zolpidem use have been reported associated with increased risk of infection, raising the speculation that hypnotics impair immune surveillance.[21] A suppression of immune function may partly explain the increased risk of incident cancers. Sparse data on the new hypnotics (eszopiclone, zaleplon, zolpidem, and ramelteon) suggest an increased risk of cancer, which is supported by studies demonstrating a carcinogenic effect in rodents.[22]

Furthermore, hypnotics such as zolpidem can increase the incidence of sleep apnea and may suppress the respiratory drive. Zolpidem increased the apnea index and provoked greater oxygen desaturation than flurazepam and placebo in a controlled, double–blind, cross-over study. Such that 20 mg zolpidem failed to overcome the existing contraindications to administration of hypnotic drugs in patients with heavy snoring and obstructive sleep apnea syndrome.[23] Sleep apnea induced by medication may in turn induce early apoptosis of large granular lymphocytes which further compromises immunity and reduces immune surveillance.[24]

A greater incidence of depression with zolpidem use has been reported.[25] A decrease in the number of natural killer T-cells has also been reported in patients with major depressive disorder.[26] Depressed immunity to varicella zoster in older adults with major depressive disorder has been observed.[27] Compromised immunity may contribute to tumor formation.

Benzodiazepines can decrease lower esophageal sphincter tone, independently of the awareness or drowsiness of patients.[28] Zolpidem reduced the arousal response to nocturnal acid exposure and increased the duration of each esophageal acid reflux event.[29] Gastroesophageal reflux can lead to chronic sinusitis, recurrent croup, and laryngitis.[30] A recent meta-analysis reported an increased risk of infection with zolpidem use.[21] Infection may result from increased gastroesophageal regurgitation or from zolpidem usage and subsequent increased cancer development.[31] However, the exact relationship between zolpidem and cancer event remains unknown, and further research is needed to explore the possible mechanism.

This study has several limitations. First, the diagnosis of sleep disorder, incident cancer, and any other comorbid conditions are completely dependent on accurate recording of ICD-9-CM codes. However, the cancer events were further verified by their appearance in the registry for cancer and catastrophic illness patient database. Furthermore, the National Health Insurance Bureau of Taiwan randomly reviews charts and interviews patients to verify diagnosis accuracy. Hospitals with outlier charges or practice may undergo an audit, with subsequent heavy penalties for malpractice or discrepancies. Second, the database did not include detailed information on body mass index, smoking, or alcohol drinking. Further studies linking administrative data and primary surveys of health behaviors are warranted. Third, we did not control for depression, anxiety, and other emotional factors, which may have influenced these results. Fourth, the number of cases was small, warranting caution in interpreting the data. Finally, associations derived from epidemiological studies do not prove causality. It is hard to discern the correlation between the zolpidem usage and the sleep disorder in time sequence. We cannot exclude the possibility that zolpidem usage is a marker for other risk factors or cancer-related illness and acts a confounder in its association with cancer.

In summary, this study found that zolpidem use was associated with increased risk of cancer events in sleep disorder patients. For patients with sleep disorder who chronically use zolpidem, the likelihood of developing cancer events within 3 years is 1.7 times that of those who do not use zolpidem. Risks and benefits of chronic zolpidem usage should be explained to sleep disorder patients. Cognitive-behavioral therapy for patients with chronic insomnia may be more beneficial than use of hypnotics.[32]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

  References Top

 

1.
Mooallem J. The Sleep-industrial Complex. NY Times Magazine; 2007.  Back to cited text no. 1
2.
International Narcotics Control Board. Psychtropic Substances: Statistics for 2008; Assessement of Annual Medical and Scientific Requirements for Substances in Schedules II, II and IV of the Conventions on Pschotropic Substances of 1971. United Nations: New York; 2011.  Back to cited text no. 2
3.
Kryger MH, Roth T, Dement WC, editors. Principles and Practice of Sleep Medicine. 5th ed. St. Louis, Missouri: Elsevier; 2010. p. 483-91.  Back to cited text no. 3
4.
Rhodes SP, Parry P, Hanning CD. A comparison of the effects of zolpidem and placebo on respiration and oxygen saturation during sleep in the healthy elderly. Br J Clin Pharmacol 1990;30:817-24.  Back to cited text no. 4
5.
Drover DR. Comparative pharmacokinetics and pharmacodynamics of short-acting hypnosedatives: Zaleplon, zolpidem and zopiclone. Clin Pharmacokinet 2004;43:227-38.  Back to cited text no. 5
6.
Available from: http://www.ehealthme.com2012. [Last accessed on 2015 Nov 01].  Back to cited text no. 6
7.
Kripke DF, Klauber MR, Wingard DL, Fell RL, Assmus JD, Garfinkel L. Mortality hazard associated with prescription hypnotics. Biol Psychiatry 1998;43:687-93.  Back to cited text no. 7
8.
Mallon L, Broman JE, Hetta J. Is usage of hypnotics associated with mortality? Sleep Med 2009;10:279-86.  Back to cited text no. 8
9.
Belleville G. Mortality hazard associated with anxiolytic and hypnotic drug use in the national population health survey. Can J Psychiatry 2010;55:558-67.  Back to cited text no. 9
10.
Kripke DF, Langer RD, Kline LE. Hypnotics’ association with mortality or cancer: A matched cohort study. BMJ Open 2012;2:e000850.  Back to cited text no. 10
11.
Liu CY HY, Chung YL, Chen YJ, Weng WS, Liu JS, Liang KY. Incorporating development stratification of Taiwan townships into sampling design of large scale health interview survey (in Chinese). J Health Manag 2006;4:1-22.  Back to cited text no. 11
12.
Engström G, Jerntorp I, Pessah-Rasmussen H, Hedblad B, Berglund G, Janzon L. Geographic distribution of stroke incidence within an urban population: Relations to socioeconomic circumstances and prevalence of cardiovascular risk factors. Stroke 2001;32:1098-103.  Back to cited text no. 12
13.
Deyo RA, Cherkin DC, Ciol MA. Adapting a clinical comorbidity index for use with ICD-9-CM administrative databases. J Clin Epidemiol 1992;45:613-9.  Back to cited text no. 13
14.
National Institutes of Health. National Institutes of Health state of the science conference statement on manifestations and management of chronic insomnia in adults, June 13-15, 2005. Sleep 2005;28:1049-57.  Back to cited text no. 14
[PUBMED]
15.
Pinto LR Jr., Alves RC, Caixeta E, Fontenelle JA, Bacellar A, Poyares D, et al. New guidelines for diagnosis and treatment of insomnia. Arq Neuropsiquiatr 2010;68:666-75.  Back to cited text no. 15
16.
Iqbal U, Nguyen PA, Syed-Abdul S, Yang HC, Huang CW, Jian WS, et al. Is long-term use of benzodiazepine a risk for cancer? Medicine (Baltimore) 2015;94:e483.  Back to cited text no. 16
17.
Galdiero F, Bentivoglio C, Nuzzo I, Ianniello R, Capasso C, Mattera S, et al. Effects of benzodiazepines on immunodeficiency and resistance in mice. Life Sci 1995;57:2413-23.  Back to cited text no. 17
18.
Zavala F. Benzodiazepines, anxiety and immunity. Pharmacol Ther 1997;75:199-216.  Back to cited text no. 18
19.
Torres SR, Fröde TS, Nardi GM, Vita N, Reeb R, Ferrara P, et al. Anti-inflammatory effects of peripheral benzodiazepine receptor ligands in two mouse models of inflammation. Eur J Pharmacol 2000;408:199-211.  Back to cited text no. 19
20.
Stebbing J, Waters L, Davies L, Mandalia S, Nelson M, Gazzard B, et al. Incidence of cancer in individuals receiving chronic zopiclone or eszopiclone requires prospective study. J Clin Oncol 2005;23:8134-6.  Back to cited text no. 20
[PUBMED]
21.
Joya FL, Kripke DF, Loving RT, Dawson A, Kline LE. Meta-analyses of hypnotics and infections: Eszopiclone, ramelteon, zaleplon, and zolpidem. J Clin Sleep Med 2009;5:377-83.  Back to cited text no. 21
22.
Kripke DF. Possibility that certain hypnotics might cause cancer in skin. J Sleep Res 2008;17:245-50.  Back to cited text no. 22
23.
Cirignotta F, Mondini S, Zucconi M, Gerardi R, Farolfi A, Lugaresi E. Zolpidem-polysomnographic study of the effect of a new hypnotic drug in sleep apnea syndrome. Pharmacol Biochem Behav 1988;29:807-9.  Back to cited text no. 23
24.
Steiropoulos P, Lourou N, Nakou E, Bouchliou E, Tzouvelekis A, Nena E, et al. Lymphocyte subsets and early apoptosis in the peripheral blood of patients with obstructive sleep apnoea syndrome (Preliminary Results). Pneumon 2009;22:42-5.  Back to cited text no. 24
25.
Kripke DF. Greater incidence of depression with hypnotic use than with placebo. BMC Psychiatry 2007;7:42.  Back to cited text no. 25
26.
Park EJ, Lee JH, Chae JH, Lee KH, Han SI, Jeon YW. Natural killer T cells in patients with major depressive disorder. Psychiatry Res 2006;144:237-9.  Back to cited text no. 26
27.
Irwin MR, Levin MJ, Carrillo C, Olmstead R, Lucko A, Lang N, et al. Major depressive disorder and immunity to varicella-zoster virus in the elderly. Brain Behav Immun 2011;25:759-66.  Back to cited text no. 27
28.
Tutuian R; Clinical Lead Outpatient Services and Gastrointestinal Function Laboratory. Adverse effects of drugs on the esophagus. Best Pract Res Clin Gastroenterol 2010;24:91-7.  Back to cited text no. 28
29.
Gagliardi GS, Shah AP, Goldstein M, Denua-Rivera S, Doghramji K, Cohen S, et al. Effect of zolpidem on the sleep arousal response to nocturnal esophageal acid exposure. Clin Gastroenterol Hepatol 2009;7:948-52.  Back to cited text no. 29
30.
Yellon RF, Goldberg H. Update on gastroesophageal reflux disease in pediatric airway disorders. Am J Med 2001;111 Suppl 8A: 78S-84S.  Back to cited text no. 30
31.
Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell 2010;140:883-99.  Back to cited text no. 31
32.
Jacobs GD, Pace-Schott EF, Stickgold R, Otto MW. Cognitive behavior therapy and pharmacotherapy for insomnia: A randomized controlled trial and direct comparison. Arch Intern Med 2004;164:1888-96.  Back to cited text no. 32

How to Stop Snoring

Posted by

1


The very often problem that happened to a lot of people is snoring, it affects nearly 90 million men and women in the United States only. You know that this irritating sound can disrupt your sleep as well as your partner’s.

It happens when relaxed structures in the throat vibrate and start making noise. It is very often considered as a sleep disorder about heavy snoring can have serious medical and social consequences.

How to Stop Snoring

So you have this habit of snoring, right away you need to take the necessary steps and fight with the problem. Be thoughtful and realize that everyone need their rest and with the snoring problem your nights simply can not be restful and peaceful.
We know that there are variety of products available to prevent snoring, but jet most of them have not been proven as effective. There is no miracle cure for snoring, but certain lifestyle changes and easy home remedies can be a big help in controlling it.
Here are the 10 home remedies for snoring.

how-to-stop-snoring-opt

1. Peppermint

The calming property in peppermint helps reduce swelling of the membranes in the coating of the throat and nostrils, in this way advancing simple and smooth breathing. Peppermint cures function well for temporary snoring due to allergies, a cold or dry air.
Add one or two drops of peppermint oil to a glass of water. Gargle with it before going to bed. Make sure not to swallow this solution. Do this daily until you get the desired result.
If dry air and congestion are causing your snoring, add a few drops of peppermint oil (you can also use eucalyptus oil) to a humidifier about 30 minutes before you go to bed and turn it on. Run the humidifier overnight. This will help open up your airways so you don’t snore.
You can also rub a little peppermint oil into the lower portions of each side of your nose before going to bed.

2. Olive oil

Being a strong anti- inflammatory agent, olive oil facilitates the tissues up and down the respiratory entries, lessening the swelling to give a clear passage for air. It can likewise diminish soreness. Utilize this cure frequently to additionally diminish the vibrations in the throat and quit snoring.

Take two or three sips of olive oil before going to bed daily
Combine one – half teaspoon each of olive oil and honey. Take it every night before going to bed.

3. Steam
The one of the main reason behind snoring is nasal congestion. But there is one simple and on of the best solution for reducing congestion and that is to inhale steam.
-In one large bowl pour hot boiling water.
-Add three or four drops of eucalyptus natural essential oil or tea tree natural essential oil.
-Put and hold a towel over your head and inhale the steam deeply through your nose for ten minutes.
-Make this remedy daily before going to bed until your congestion clears.

4. Clarified Butter
Clarified butter is also known as ghee, it has certain medicinal properties that can help you open up blocked nasal passages. This will help you to reduce your snoring and to improve your sleeping.
-Slightly warm a small amount of clarified butter in a microwave.
Use a dropper to put two or three drops of lukewarm clarified butter in each nostril.
-Do this daily before going to bed and again after waking up the next morning.

5. Cardamom
Cardamom is an expectorant and decongestant, making it successful for opening up blocked nasal sections. Free air entry will bring about less snoring.

6. Turmeric
Known by its purpose as powerful antiseptic and antibiotic agent, turmeric can treat inflammation and also help reduce heavy snoring. In the event of treating snoring turmeric should be taken together with milk. This following drink will help you to breathe freely while you sleep and also boost your immune system.
-In a glass with warm milk add two teaspoons of turmeric powder.
-30 minutes before going to bed and sleep drink it
-Do this every night

7. Nettle

nettle-opt

There is something like seasonal allergy that causing the nasal passages to get inflamed and you snore only at a particular time of the year. The nettle has the anti- inflammatory as well as antihistamine properties and the temporary snoring can be treated with this.
-Put one tablespoon of dried leaves of nettle in one cup of boiling water.
-Allow it to steep for five minutes, and then strain it.
-Just before bedtime drink the hot tea.
Drinking two to three cups of nettle leaf tea daily during the allergy season can prevent snoring.

8. Garlic

garlic-fresh-opt

Garlic helps reduce mucus build-up in the nasal passages as well as inflammation in the respiratory system. So, if you snore due to sinus blockage, garlic can give you relief.
Chew on one to two raw garlic cloves and then drink a glass of water. Do this daily, preferably before bedtime to enjoy sound sleep and reduce snoring.
Also use garlic while cooking your dinner and eat your food while it is hot.

9. Honey

honey-opt

The honey can be one of the option for snorers. Due to its anti-inflammatory properties, honey can reduce the swelling around the throat area that can obstruct airways. Plus, honey lubricates the throat, which prevents the snoring vibrations from occurring.
-In a glass of hot water mix one tablespoon of honey and drink it before going to bed. Do this every night.
-Also you can use honey to sweeten herbal tea that you prefer to drink after your dinner.

10. Chamomile

chamomile-tea-opt

A herbal with very well – known anti- inflammatory effects that can help you stop snoring is the chamomile. But also it is a nerve and muscle relaxant that can ease tense muscles and nerves around the throat and help you sleep and rest better.
Add one tablespoon of chamomile flowers (or one chamomile tea bag) to one cup of water.
Boil it for about 15 minutes.
Strain it and add one teaspoon of honey.
Drink the warm tea before going to bed.
Some additional tips that can help stop snoring include:
In case you’re overweight, get more fit and lose weight. Individuals who are overweight have additional tissues in the throat that add to the process of snoring.
Sleep over your side as opposed to your back. When you think about your back, your tongue and delicate sense of taste rest against the back of your throat, hindering the aviation route and bringing about snoring.
Raise the head of your bed by around four inches or utilize additional pillow to keep the tissues in your throat from falling into your air entries.
Use nasal strips to help you inhale effectively as you rest.
Abstain from drinking alcohol drinks no less than two hours prior to sleep time. Liquor can discourage your central nervous system, causing snoring.
Try singing before going to bed. Singing helps enhance muscle control of the delicate sense of taste and upper throat.

Stopped or eliminate smoking as it can irritate the coating of the nasal cavity and throat, bringing about swelling and eventually snoring.
By incorporating these preventive measures along with any of the remedies above, you’ll be able to reduce or eliminate snoring and get a good night’s sleep.

Late afternoon and early evening caffeine can disrupt sleep at night.

Posted by

0


A new study shows that caffeine consumption even six hours before bedtime can have significant, disruptive effects on sleep.

“Sleep specialists have always suspected that caffeine can disrupt sleep long after it is consumed,” said American Academy of Sleep Medicine President M. Safwan Badr, MD.  “This study provides objective evidence supporting the general recommendation that avoiding caffeine in the late afternoon and at night is beneficial for sleep.”

Results show that 400 mg of caffeine (about 2-3 cups of coffee) taken at bedtime, three and even six hours prior to bedtime significantly disrupts sleep. Even when caffeine was consumed six hours before going to bed, objectively measured total sleep time was dramatically reduced (more than one hour).  However, subjective reports suggest that participants were unaware of this sleep disturbance.

The study is in the Nov. 15 issue of the Journal of Clinical Sleep Medicine, which is published by the American Academy of Sleep Medicine.

“Drinking a big cup of coffee on the way home from work can lead to negative effects on sleep just as if someone were to consume caffeine closer to bedtime,” said lead author Christopher Drake, PhD, investigator at the Henry Ford Sleep Disorders and Research Center and associate professor of psychiatry and behavioral neurosciences at Wayne State University in Detroit, Mich. “People tend to be less likely to detect the disruptive effects of caffeine on sleep when taken in the afternoon,” noted Drake, who also is on the board of directors of the Sleep Research Society.

Drake and his research team studied 12 healthy normal sleepers, as determined by a physical examination and clinical interview. Participants were instructed to maintain their normal sleep schedules.  They were given three pills a day for four days, taking one pill at six, three and zero hours prior to scheduled bedtime.  One of the pills contained 400 mg of caffeine, and the other two were a placebo.  On one of the four days, all three pills were a placebo.  Sleep disturbance was measured subjectively with a standard sleep diary and objectively using an in-home sleep monitor.

According to the authors, this is the first study to investigate the effects of a given dose of caffeine taken at different times before sleep.  The results suggest that caffeine generally should be avoided after 5 p.m. in order to allow healthy sleep.

Opioids Prove Effective for Restless Legs Syndrome.

Posted by

0


In a new, placebo-controlled study, prolonged-release opioid treatment with an oxycodone-naloxone combination product produced impressive relief of symptoms in patients with severe restless legs syndrome for whom other therapies had failed.

The study, published online October 18 in Lancet Neurology, was led by Claudia Trenkwalder, MD, Paracelsus-Elena Hospital, Kassel, Germany.

“We found an 8-point reduction in the mean International RLS Study Group rating scale sum score vs placebo,” Dr. Trenkwalder commented to Medscape Medical News. “This is the most effective treatment response ever seen in restless legs syndrome. A reduction of more than 3 points is thought to be clinically significant. While between-study comparisons are always difficult, dopaminergic drugs ― the main agents used ― are associated with reductions of about 4 to 6 points vs placebo. A reduction of 8 points has never been seen before.”

Professor Trenkwalder explained that there has been much interest in using opioids in restless legs syndrome for many years, after a small study conducted in 1993 showed a positive effect in 8 patients. This has been followed by other small case series and anecdotal reports, but there has never been a controlled clinical trial before.

“This trial is long overdue. It has taken us 20 years to get it done, largely because no one wanted to pay for it. But we eventually managed to get funding from MundiPharma and have now definitely proven that this opioid-based combination works and works very well in reducing all symptoms of restless legs syndrome ― sensory, restlessness, pain, and sleep,” she said.

She added that doctors have been using different opioids at different dosages over the years, but this study provides solid evidence in support of one combination product used at a low dosage and given twice a day.

Professor Trenkwalder noted that the inclusion of the opioid antagonist naloxone counters peripheral side effects of the oxycodone in the gastrointestinal system and so minimizes constipation, the major side effect of long-term opioid therapy. She also highlighted the importance of taking the drug combination twice a day ― morning and evening. “Some people just take medication for restless legs syndrome at night, but you then get high levels at night and a trough during the day. It is important to have stable levels of opiates in the brain to get good symptom improvement.”

In an accompanying commentary, Arthur S. Walters, MD, Vanderbilt University School of Medicine, Nashville, Tennessee, says that the data are “especially convincing because the study included patients who were refractory to other treatments. Such patients would normally be much more likely to fail an alternative treatment than patients who have not had previous treatment failure.”

Although he notes that no direct comparisons can be made between drugs, “the treatment difference between groups of 8.15 points is much greater than that for most approved drugs for restless legs syndrome.”

For the study, Professor Trenkwalder and colleagues randomly assigned 306 patients who had had symptoms for at least 6 months and whose International RLS Study Group severity rating scale sum score was at least 15 to study drug or placebo. Study drug was oxycodone 5 mg, naloxone 2.5 mg twice daily, up-titrated according to investigator’s opinion to a maximum of oxycodone 40 mg, naloxone 20 mg twice daily.

The primary outcome was mean change in severity of symptoms according to the International RLS Study Group severity rating scale sum score at the end of the 12-week double-blind phase.

Mean score at baseline was 31.6. This was reduced by 16.5 points in the oxycodone-naloxone group vs 9.4 points in the placebo group ― a difference of 8.15 points.

Primary Outcome: International RLS Study Group Severity Rating Scale Sum Score at 12 Weeks

Oxycodone-Naloxone Placebo Treatment Difference (95% CI) PValue
Mean sum score at 12 weeks 15.1 22.1 8.15 (5.46 – 10.85) <.0001

Snoring mothers-to-be linked to low birth weight babies.

Posted by

0


Experts say snoring may be a sign of breathing problems that could deprive an unborn baby of oxygen

A newborn baby. Scientists found that women who snored both before and during pregnancy were more likely to have smaller babies and elective C-sections. Photograph: Christopher Furlong/Getty Images

Mothers-to-be who snore are more likely to give birth to smaller babies, a study has found. Snoring during pregnancy was also linked to higher rates of Caesarean delivery.

Experts said snoring may be a sign of breathing problems that could deprive an unborn baby of oxygen.

Previous research has shown women who start to snore during pregnancy are at risk from high blood pressure and the potentially dangerous pregnancy condition pre-eclampsia.

More than a third of the 1,673 pregnant women recruited for the US study reported habitual snoring.

Scientists found women who snored in their sleep three or more nights a week had a higher risk of poor delivery outcomes, including smaller babies and Caesarean births.

Chronic snorers, who snored both before and during pregnancy, were two-thirds more likely to have a baby whose weight was in the bottom 10%.

They were also more than twice as likely to need an elective Caesarean delivery, or C-section, compared with non-snorers.

Dr Louise O’Brien, from the University of Michigan’s Sleep Disorders Centre, said: “There has been great interest in the implications of snoring during pregnancy and how it affects maternal health but there is little data on how it may impact the health of the baby.

“We’ve found that chronic snoring is associated with both smaller babies and C-sections, even after we accounted for other risk factors. This suggests that we have a window of opportunity to screen pregnant women for breathing problems during sleep that may put them at risk of poor delivery outcomes.”

Women who snored both before and during pregnancy were more likely to have smaller babies and elective C-sections, the researches found. Those who started snoring only during pregnancy had a higher risk of both elective and emergency Caesareans, but not of smaller babies.

Snoring is a key sign of obstructive sleep apnoea, which results in the airway becoming partially blocked, said the researchers, whose findings appear in the journal Sleep.

This can reduce blood oxygen levels during the night and is associated with serious health problems, including high blood pressure and heart attacks.

Sleep apnoea can be treated with CPAP (continuous positive airway pressure), which involves wearing a machine during sleep to keep the airways open.

Dr O’Brien added: “If we can identify risks during pregnancy that can be treated, such as obstructive sleep apnoea, we can reduce the incidence of small babies, C-sections and possibly NICU (neo-natal intensive care unit) admission that not only improve long-term health benefits for newborns but also help keep costs down.”

Morbidity and mortality in children with obstructive sleep apnoea: a controlled national study.

Posted by

1


Abstract

Background Little is known about the diagnostic patterns of obstructive sleep apnoea (OSA) in children. A study was undertaken to evaluate morbidity and mortality in childhood OSA.

Methods 2998 patients aged 0–19 years with a diagnosis of OSA were identified from the Danish National Patient Registry. For each patient we randomly selected four citizens matched for age, sex and socioeconomic status, thus providing 11 974 controls.

Results Patients with OSA had greater morbidity at least 3 years before their diagnosis. The most common contacts with the health system arose from infections (OR 1.19, 95% CI 1.01 to 1.40); endocrine, nutritional and metabolic diseases (OR 1.30, 95% CI 0.94 to 1.80); nervous conditions (OR 2.12, 95% CI 1.65 to 2.73); eye conditions (OR 1.43, 95% CI 1.07 to 1.90); ear, nose and throat (ENT) diseases (OR 1.61, 95% CI 1.33 to 1.94); respiratory system diseases (OR 1.78, 95% CI 1.60 to 1.98); gastrointestinal diseases (OR 1.34, 95% CI 1.09 to 1.66); skin conditions (OR 1.32, 95% CI 1.02 to 1.71); congenital malformations (OR 1.56, 95% CI 1.31 to 1.85); abnormal clinical or laboratory findings (OR 1.21, 95% CI 1.06 to 1.39); and other factors influencing health status (OR 1.29, 95% CI 1.16 to 1.43). After diagnosis, OSA was associated with incidences of endocrine, nutritional and metabolic diseases (OR 1.78, 95% CI 1.29 to 2.45), nervous conditions (OR 3.16, 95% CI 2.58 to 3.89), ENT diseases (OR 1.45, 95% CI 1.14 to 1.84), respiratory system diseases (OR 1.94, 95% CI 1.70 to 2.22), skin conditions (OR 1.42, 95% CI 1.06 to 1.89), musculoskeletal diseases (OR 1.29, 95% CI 1.01 to 1.64), congenital malformations (OR 1.83, 95% CI 1.51 to 2.22), abnormal clinical or laboratory findings (OR 1.16, 95% CI 1.06 to 1.27) and other factors influencing health status (OR 1.35, 95% CI 1.20 to 1.51). The 5-year death rate was 70 per 10 000 for patients and 11 per 10 000 for controls. The HR for cases compared with controls was 6.58 (95% CI 3.39 to 12.79; p<0.001).

Conclusions Children with OSA have significant morbidities several years before and after their diagnosis.

Source: Thorax

Deficits caused by workweek sleep loss not totally recouped by sleeping in on the weekends

Posted by

0


In many modern societies, adults often sacrifice sleep during the workweek to make time for other demands, then snooze longer on the weekends to recoup that lost sleep. Research has shown that even a few days of lost sleep can have adverse effects, including increased daytime sleepiness, worsened daytime performance, an increase in molecules that are a sign of inflammation in the body, and impaired blood sugar regulation. These last two could be partially responsible for why sleeping less negatively affects health in other ways and shortens the lifespan. Though many people believe they can make up sleep lost during the workweek by sleeping more on the weekend, it’s unknown whether this “recovery” sleep can adequately reverse these adverse effects.

To help answer this question, researchers led by Alexandros N. Vgontzas of the Penn State University College of Medicine, placed 30 volunteers on a sleep schedule that mimicked a sleep-restricted workweek followed by a weekend with extra recovery sleep. At various points along this schedule, the researchers assessed the volunteers’ health and performance using a variety of different tests.

The researchers found that the volunteers’ sleepiness increased significantly after sleep restriction, but returned to baseline after recovery sleep. Levels of a molecule in blood that’s a marker for the amount of inflammation present in the body increased significantly during sleep restriction, but returned to normal after recovery. Levels of a hormone that’s a marker of stress didn’t change during sleep restriction, but were significantly lower after recovery. However, the volunteers’ measures on a performance test that assessed their ability to pay attention deteriorated significantly after sleep restriction and did not improve after recovery. This last result suggests that recovery sleep over just a single weekend may not reverse all the effects of sleep lost during the workweek.

The study is entitled “The Effects of Recovery Sleep After One Workweek of Mild Sleep Restriction on Interleukin-6 and Cortisol Secretion and Daytime Sleepiness and Performance.” * It appears in the American Journal of Physiology-Endocrinology and Metabolism, published by the American Physiological Society.

Methodology

The researchers recruited 30 healthy adults who were normal sleepers and put them on a 13-day schedule that involved spending nights in a sleep lab. For the first four nights, the subjects were allowed to sleep for 8 hours, setting a baseline for a healthy, normal amount of sleep. For the next six nights, the researchers woke the subjects up 2 hours earlier. For the following three nights, the subjects were allowed to sleep for 10 hours. The researchers monitored the volunteers’ brain waves during these sleep sessions. At three points during the 13-day schedule, the volunteers spent whole days at the lab taking part in various tests: after the 4 days of baseline sleep, after 5 days of restricted sleep, and after 2 days of recovery sleep. On these days, the subjects had catheters inserted into their arms, and the researchers sampled blood every hour, testing it for levels of interleukin-6 (a marker of inflammation) and cortisol (a hormone secreted during stress). They also participated in a test of how quickly they fell asleep when allowed to nap several times during those days (an objective measure of sleepiness) and filled out questionnaires to assess how sleepy they felt (a subjective measure of sleepiness). To assess their performance, they participated in a test in which they were asked to press a button whenever a dot appeared on a screen, which measured how well they were able to pay attention.

Results

Not surprisingly, the researchers found that after 5 days of restricted sleep, the subjects were significantly sleepier on both objective and subjective tests compared to baseline levels. Their interleukin-6 levels increased sharply during restricted sleep, though their cortisol levels remained the same. Their performance on the attention test deteriorated. After 2 days of recovery sleep, both objective and subjective tests showed that the volunteers were less sleepy. Their interleukin-6 levels reduced, and their cortisol levels decreased significantly compared to baseline, possibly suggesting that the volunteers were sleep deprived before the study started. Notably, their performance on the attention test didn’t improve after recovery sleep.

Importance of the Findings

Though many indicators of health and well being improved after recovery sleep, these findings suggest that extra sleep may not fix all the deficits caused by lost sleep during the workweek.

“Two nights of extended recovery sleep may not be sufficient to overcome behavioral alertness deficits resulting from mild sleep restriction,” the authors write. “This may have important implications for people with safety-critical professions, such as health-care workers, as well as transportation system employees (drivers, pilots, etc.).”

The authors also suggest that even though these results provide some insight on the health effects of a single week of sleep loss and recovery, reliving the cycle over and over again may have more significant health effects that this study wouldn’t show.

“The long-term effects of a repeated sleep restriction/sleep recovery weekly cycle in human remains unknown,” they write.

Drug Helps Relieve Disrupted Night time Sleep in Narcolepsy.

Posted by

0


Patients with narcolepsy who have disordered nighttime sleep benefited more from sodium oxybate (SXB) than from modafinil or placebo, according to a randomized trial that documented fewer shifts from sleep stage 2 to 4 or rapid eye movement (REM) to stage 1 or full wakefulness in patients receiving SXB.

“In this retrospective analysis, sodium oxybate appeared to improve polysomnograms and patient-reported measures of disrupted nighttime sleep in narcolepsy,” said Yves Dauvilliers, MD, PhD, from the Reference National Center for Narcolepsy at Gui de Chauliac Hospital in Montpellier, France.

“Disrupted nighttime sleep (DNS) is a clinically common complaint, occurring in almost all patients with narcolepsy,” he said. The important features of DNS are frequent shifts to lighter sleep, awakenings after sleep onset, and poor sleep quality. Researchers retrospectively analyzed data from a randomized trial to evaluate the effects of 3 common narcolepsy treatments.

SXB is approved for the treatment of cataplexy and excessive daytime sleepiness in narcolepsy. Polysomnography has suggested that SXB can also increase slow-wave sleep and reduce sleep fragmentation.

“There have been no data, however, related to sleep continuity or patient sleep quality ratings,” Dr. Dauvilliers noted.

The current study, therefore, evaluated the effects of narcolepsy treatment modalities on REM and non-REM sleep-shift changes and sleep quality by retrospective analysis of data from a phase 3 randomized trial.

The findings were presented here at the American Neurological Association (ANA) 2013 Annual Meeting.

Study Details

The study included 278 patients with narcolepsy who were randomly assigned to 1 of 4 treatment groups: SXB, 9 g/day; modafinil, 200 to 600 mg/day; the combination of the 2 agents; or placebo. Patients take 1 dose of SXB before going to sleep and must wake up during the night to take a second dose.

Polysomnograms and sleep quality, as assessed by the Pittsburgh Sleep Quality Index (PSQI)— specifically, question 6 (“During the past month, how would you rate your sleep quality overall?”)—were obtained at baseline and at 8 weeks. The analysis was performed on the 222 patients with evaluable sleep stage and sleep-quality PSQI data.

SXB alone and in combination with modafinil was associated with significant reductions at week 8 in the number of shifts relative to baseline. The reductions with SXB and the combination were greater than those observed with placebo. Modafinil was not associated with any shift stage reductions at week 8, Dr. Dauvilliers reported.

In shifting from stage 2/3/4 REM to stage 1/wake sleep, the median change from baseline was –13.0 (from 40.9 at baseline) in patients receiving SXB alone (P < .001) and –11.5 with the combination (P < .001). No significant reductions in these shifts were observed with modafinil alone or placebo.

In shifting from sleep-stage REM to stage 1/wake, the median change from baseline was –7.0 with SXB alone (P < .001) and –5.0 with the combination (P = .001).

“With SXB, we saw a huge decrease in the number of shift stages and from REM to stage1/wake,” he noted.

Patient-reported sleep quality also significantly improved from baseline with SXB and SXB plus modafinil. The change from baseline was –0.46 with SXB (P < .001) and –0.48 with the combination (P < .001), while modafinil and placebo demonstrated little to no change.

Nausea, vomiting, and dizziness were significantly more common with SXB than with modafinil or placebo, and more treatment discontinuations occurred among patients taking SXB alone or in combination with modafinil.

“SXB improved sleep continuity and sleep quality, and we believe this makes for an improvement in daytime functioning,” Dr. Dauvilliers concluded.

SXB Should Not Be Misused

Session moderator Beth Ann Malow, MD, professor of neurology at Vanderbilt University and director of the Vanderbilt Sleep Disorders Center, Nashville, Tennessee, emphasized that the study was conducted in patients with narcolepsy, and the findings should not be extrapolated to the general population with sleep latency.

“This is an innovative study, looking at this drug in sleep latency, since its traditional use is for improving daytime sleepiness. But it’s important to realize that this is in narcolepsy, not the general population, and this drug has abuse potential,” Dr. Malow said.

“My concern would be that the results are extrapolated to a population where the drug is not FDA [Food and Drug Administration]-approved. We must make this distinction,” she added. “I’m not saying it doesn’t have a role, but we should be careful.”

Comorbidities Common in Narcolepsy.

Posted by

0


Individuals diagnosed with narcolepsy have substantially higher rates of psychiatric and medical conditions than the general population, a new study shows.

“We found that 27% of persons with narcolepsy had a mood disorder, 37% were taking an antidepressant — 3 times higher than the general population — and anxiety disorders were also prevalent,” said Maurice M. Ohayon, MD, DSc, PhD, professor of psychiatry and behavioral sciences at Stanford University School of Medicine, and director of the Stanford University Sleep Epidemiology Research Center in California.

In addition, chronic medical conditions were also greatly increased, said Dr. Ohayon, who noted, “Individuals affected with narcolepsy represent a vulnerable segment of the population. However, we only have a partial understanding of this vulnerability.”

The high prevalence of both medical conditions and psychiatric disorders seen in association with narcolepsy needs to be addressed when developing a treatment plan, Dr. Ohayon concluded.

He presented the findings at the American Neurological Association (ANA) 2013 Annual Meeting here. They were also recently publishedin Sleep Medicine.

High Frequency of Psychiatric Conditions

The study examined psychiatric disorders and medical conditions associated with narcolepsy in 320 narcoleptic patients, who were compared with a sample of 1464 persons matched for age, sex, and body mass index.

Study participants were interviewed regarding sleep habits, health, medication, medical conditions, sleep disorders, and mental disorders using the Sleep-EVAL. Mental disorders were classified according to theDiagnostic and Statistical Manual, 4th edition.

A high proportion of narcoleptic patients reported psychiatric disorders, especially major depressive disorder and social anxiety disorder, which affected nearly 20% of these individuals, Dr. Ohayon reported.

Table. Proportion of Mental Disorders in Narcoleptics vs Matched Controls

Disorder Narcolepsy (%) Controls (%) Adjusted Odds Ratio P Value
Major depressive disorder 17.1 6.4 2.7 <.001
Bipolar disorder 8.5 1.9 4.6 <.001
Post-traumatic stress disorder 11.3 5.3 2.1 <.001
Social anxiety 21.1 8.7 2.4 <.001
Panic disorder 12.5 3.9 3.2 <.001
Agoraphobia 8.5 1.3 6.5 <.001
Simple phobia 5.2 1.3 4.1 <.001
Obsessive-compulsive disorder 3.7 1.0 3.8 <.001
Generalized anxiety disorder 5.5 1.7 3.3 <.001

Five medical diseases were also more frequently observed among narcoleptic participants: hypercholesterolemia, digestive diseases, heart disease, upper respiratory tract disease, and hypertension. The highest odds ratios were for diseases of the digestive system, which were noted in 16.3% of the narcoleptic population vs 5.0% of the controls, a 3-times-increased risk (P < 0.001), and for upper respiratory tract diseases, which were noted for 27.5% and 10.9%, respectively, for an odds ratio of 2.5 (P < 0.001).

“In addition, 34% of narcoleptics were obese, and this was with matching for body mass index in the study, and they are more likely to have hypercholesterolemia and hypertension than the general population,” Dr. Ohayon added.

He said that major depressive disorder mostly developed after the onset of narcolepsy (88%), while social anxiety was present before the onset of narcolepsy in about half the cases. He further noted that several comorbid conditions were autoimmune disorders, such as inflammatory bowel disease, asthma, and allergies.

Dr. Ohayon concluded, “We don’t know how to interpret these data. These are just facts, but we don’t know what they mean.”

Session moderator Louis Ptacek, MD, Howard Hughes Investigator in the Department of Neurology at the University of California, San Francisco School of Medicine, commented on the study for Medscape Medical News.

“The study is quite fascinating, given the statistical significance of the findings,” Dr. Ptacek said. “It’s not surprising that people who might be predisposed to psychiatric disorders could have these precipitated by a stressful event such as narcolepsy, though in some patients the psychiatric diagnosis preceded the narcolepsy. While it’s important to identify these comorbidities, we don’t yet understand the connection or causality yet, as the author pointed out.”

Source: Medscape.com

Shorter Sleep Duration and Poorer Sleep Quality Linked to Alzheimer’s Disease Biomarker.

Posted by

0


Poor sleep quality may impact Alzheimer’s disease onset and progression. This is according to a new study led by researchers at the Johns Hopkins Bloomberg School of Public Health who examined the association between sleep variables and a biomarker for Alzheimer’s disease in older adults. The researchers found that reports of shorter sleep duration and poorer sleep quality were associated with a greater β-Amyloid burden, a hallmark of the disease. The results are featured online in the October issue of JAMA Neurology.

“Our study found that among older adults, reports of shorter sleep duration and poorer sleep quality were associated with higher levels of β-Amyloid measured by PET scans of the brain,” said Adam Spira, PhD, lead author of the study and an assistant professor with the Bloomberg School’s Department of Mental Health. “These results could have significant public health implications as Alzheimer’s disease is the most common cause of dementia, and approximately half of older adults have insomnia symptoms.”

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. According to the National Institutes of Health, as many as 5.1 million Americans may have the disease, with first symptoms appearing after age 60. Previous studies have linked disturbed sleep to cognitive impairment in older people.

In a cross-sectional study of adults from the neuro-imagining sub-study of the Baltimore Longitudinal Study of Aging with an average age of 76, the researchers examined the association between self-reported sleep variables and β-Amyloid deposition. Study participants reported sleep that ranged from more than seven hours to no more than five hours. β-Amyloid deposition was measured by the Pittsburgh compound B tracer and PET (positron emission tomography) scans of the brain. Reports of shorter sleep duration and lower sleep quality were both associated with greater Αβ buildup.

“These findings are important in part because sleep disturbances can be treated in older people. To the degree that poor sleep promotes the development of Alzheimer’s disease, treatments for poor sleep or efforts to maintain healthy sleep patterns may help prevent or slow the progression of Alzheimer disease,” said Spira.  He added that the findings cannot demonstrate a causal link between poor sleep and Alzheimer’s disease, and that longitudinal studies with objective sleep measures are needed to further examine whether poor sleep contributes to or accelerates Alzheimer’s disease.