One of the biggest parts of this book is that your baby will be required to go 4 hours between feedings during the day in order to achieve sleeping through the night and 12 hours without any feedings, the primary goal of the book.
12 Hours Of Sleep By 12 Weeks Pdf Download
Download File: https://7olgusubsda.blogspot.com/?download=2vDopE
Yes, there are instructions in the book for breastfeeding moms, but keep in mind that if you go 12 hours without breastfeeding or expressing/pumping your milk, you may experience a drastic drop in milk supply. Breastfeeding and sleep training can go together but we typically keep at least one night feeding until 6-10 months old, depending on the situation and the baby. You can surely get to 12 hours of sleep even if you still have one night feeding, though, and most of the moms we work with are totally fine with that.
For the first few weeks after birth, baby sleep may be all over the map. They may sleep so much you find yourself wondering why other new mommies seem so tired. Or they may never sleep for more than 45-minute windows leaving you wondering how you can possibly make it through one more night.
Although it is known that alcohol can decrease sleep latency when consumed by healthy persons [124], chronic use leads to increased sleep latency, consistent with individual self-report. Published studies show that SL is prolonged during periods of drinking [9, 33, 85, 199, 221], during acute withdrawal (e.g., weeks 1 and 2 of abstinence) [9, 33, 85, 199, 221], and during post-acute withdrawal (e.g., weeks 2 through 8) [33], (Table 2) with evidence for sleep latency prolongation in inpatient and outpatient settings (e.g., [83, 123, 183]), and when controlled for age and sex, among other variables [26]. After the second month of abstinence, sleep latency may still be increased [213], or normalized [174], with evidence for normalization also present after five [69] and 9 months of abstinence [213].
Congruent with increased sleep latency, total sleep time is reduced in persons with alcohol use disorders during periods of drinking, acute withdrawal, and post-acute withdrawal [33, 85, 86, 199, 221], with very few exceptions [9]. Numerous studies examining total sleep time from 2 to 4 weeks of abstinence document reduced sleep time compared to healthy controls [69, 83, 183] (Table 2). Reduced total sleep time has also been observed in study designs that control for age and sex, among other variables [26].
Considerable evidence points to deficits in slow wave sleep time (i.e. stage 3 and stage 4 sleep, or stage N3 sleep in the newer nomenclature) or slow-wave sleep activity (i.e. EEG spectral power in the slow wave frequency range) in persons with alcohol use disorders [33]. Most of this evidence comes from studies reporting results from the first few weeks of abstinence, including acute withdrawal [196], subacute withdrawal (i.e. days 8 and 12); [106] (Table 2), and beyond [26, 69, 83, 127].
Notwithstanding the above findings, the literature on alcohol and REM sleep has some inconsistencies (Table 2). For example, a meta-analysis examined six studies that did not consider covariates and four studies that controlled for variables such as age and sex (all participants abstinent for at least 3 weeks). Even though the analyses among all subjects showed no differences in REM measured as the percentage of total sleep (REM%), the analyses did find increased REM% in persons with AUD compared to controls when controlling for some variables [26]. Other studies have found no difference in REM% between chronic alcohol users and normal controls in the second [106] and third [83] week of abstinence. Additionally, supporting the finding of no difference in REM between chronic alcohol users and controls, a study examining REM time after 4 weeks of abstinence found no difference between subjects with AUD and normal controls [183]. Another discrepancyappears in the form of a study that found REM% among participants with AUD to be reduced after 12 weeks of abstinence in comparison with REM% after 4 weeks of abstinence, arguing against a lasting REM rebound [171].
Mixed findings implicate objective sleep measurements as predictors of clinical outcomes in AUD. For example, increased sleep latency measured within the first 2 weeks of inpatient admission increased the odds of relapse to alcohol use within the following 5 months [34]. Similarly, increased sleep latency and decreased sleep efficiency after 16 days and 19 weeks of abstinence were associated with lower rates of abstinence at 14 months [69]. However, one study found no difference in sleep latency at 5 days abstinent between persons who subsequently relapsed and those who remained abstinent [82].
Similar to clinical studies examining sleep latency and SWS, REM sleep measurements appear to be important in clinical outcomes, but with conflicting results. The differences observed here might be consistent with the differences in the measurement of REM sleep in persons with AUD described above. For instance, while one study indicated a positive correlation between low REM% with response rate in a button-press task to obtain an alcoholic drink [8], Gillin et al. showed increased REM% and shorter REM latency upon admission and upon discharge from a four-week admission among relapsers in comparison with abstainers [82]. Another study showed that increased REM latency decreased the odds of relapsing [34], and one study found no connection between REM latency measured at 19 weeks of abstinence and subsequent relapse [69]. The variation in results regarding REM sleep may be due to the different effect that acute and chronic use, have on REM sleep, and be due to changes in REM sleep as the number of days abstinent increases. Another important consideration is that achieving long periods of abstinence (e.g., like 19 weeks) is in general a good predictor of abstinence and does so to a much greater degree than the predictive qualities of other physiological measurements obtained early in abstinence.
Withdrawal from cocaine is characterized by numerous subjective complaints, including sleep and sleep-related complaints. The first several days to 1 week after cocaine cessation are characterized by sleep disturbances, hypersomnia, bad dreams, depressed mood, psychomotor agitation and retardation, fatigue, and increased appetite [38, 59, 80]. With continued abstinence, however, there is subjective improvement of sleep as well as improvements in other cocaine withdrawal measures [209], with apparent normalization of subjective sleep over the course of several weeks [80].
Chronic cocaine users appear to have dramatically diminished slow-wave sleep time relative to age-matched healthy sleepers [13, 147] (Table 2). More limited evidence suggests that slow-wave activity is increased by cocaine self-administration earlier in the day, with a subsequent loss of slow-wave activity in the first several days of abstinence followed by a rebound over the next 2 weeks of abstinence [148]. More substantial evidence indicates that slow-wave sleep time increases modestly from the first to the third week of abstinence [138], but at 3 weeks of abstinence is still 50 % less than age-matched healthy sleepers [13]. This deficit in slow-wave sleep generation is associated with impaired slow-wave sleep specific, sleep-dependent learning [149], and is consistent with or more profound than similar findings in chronic users of alcohol, cannabis, other stimulants, and heroin [25, 27, 175, 192] suggesting an abnormality in sleep homeostasis [145] that may be common to chronic, regular use of addictive substances.
Cocaine administration acutely suppresses REM sleep [104, 162, 207], with a subsequent rebound evident as an increase in REM sleep time and/or percent of total sleep time spent in REM (REM%), and a decrease in REM latency [81, 104, 121, 149, 153, 192, 207]. However, in chronic cocaine users, REM sleep decreases following the rebound, with low REM times observed during the second and third weeks of abstinence [13, 104, 138, 147, 149, 153, 192] (Table 2). This diminished REM sleep time is associated with cognitive consequences like poor procedural learning [149], suggesting an abnormality of REM homeostasis during abstinence from chronic use. Consistent with this idea is the observation that REM latency is higher in the third week of abstinence relative to the first [149] and at 3 weeks abstinence does not differ substantially from healthy sleepers [147] (Table 2), despite low REM sleep time.
There is a limited number of reports studying the effects of withdrawal and abstinence from chronic opiate use. Asaad et al. reported insomnia, hypersomnolence, increased sleep latency, and reduced sleep duration in individuals with opioid use disorder after 3 weeks of abstinence [17].
Methadone maintenance is widely used and a standard pharmacotherapy for treating patients with opioid use disorders [18, 68, 71, 197, 220]. Chronic methadone use is more commonly associated with tolerance to the sleep problems compared to other opioids [113, 134, 159, 204]. However, more than three-quarters of persons receiving methadone maintenance therapy (MMT) still report sleep complaints [151, 156, 186]. This is complicated by the fact that about 50 % of MMT patients report use of both illicit drugs and legal medications to help with sleep [156, 186]. Methadone and electrostimulation (ES) have been used to treat insomnia in the first 30 days of opioid withdrawal [84]. In the first 2 weeks of withdrawal patients treated with electrostimulation had shorter sleep time and more awakenings than patients receiving methadone. They also found that subjects in the ES group who remained in treatment experienced more sleep disturbance than those who dropped out prematurely. Overall methadone and ES were not efficient in treating insomnia associated with withdrawal. Stein et al. tested whether trazodone (50 mg/night), one of the most commonly prescribed medications for treatment of insomnia, improved sleep among methadone-maintained persons with PSQI score of six or higher [187]. They found that trazodone did not improve subjective or objective sleep problems in this group of patients. 2ff7e9595c
Comments