drinking alcohol on airplanes is harmful

 

A recent article assessed the impact of moderate alcohol consumption in people on long-haul airplane flights (see alcohol dec ox sat in plane thorax2024 in dropbox, or doi:10.1136/thorax-2023-220998).

 

Details:

-- two groups of healthy individuals spent two nights with a 4-hour sleep opportunity in a sleep laboratory

    -- control group: 23 individuals, under conditions of normobaric normoxia at 53 m altitude corresponding to air pressure of 1010 hPa

    -- In-Flight Group: 17 individuals, in simulated crew-rest compartment in the altitude chamber corresponding to air pressure decreased to 753 hPa, simulating the minimal pressure inside an airplane cabin at cruising altitude; there was also realistic noise that had been recorded in a prior flight (70 db(A))

-- these two groups were assessed one night without any alcohol consumption and one night with recent alcohol consumption

    -- the amount of alcohol was determined by the anticipated need to achieve a target value of 0.06% blood-alcohol concentration by drinking 114.5 mL of pure vodka, typically equivalent to drinking two cans of beer (5% alcohol) or two glasses of wine (175 mL, 12% alcohol) at 11:15 PM

-- demographics:

 

 

-- exclusion criteria for this study included those with physical, psychological, or intrinsic sleep or circadian disorders

-- blood oxygen saturation and polysomnography were conducted with evaluation of sleep stages and EEG documented arousals

 -- sleep stages: 

    -- Stage N1: also known as the transition stage; N1 occurs when one first falls asleep and during brief arousals within sleep. It is the lightest stage of sleep and usually lasts 1–7 minutes. During N1, the brain starts producing theta waves, which can lead to hypnagogic hallucinations (about 70% of people experience these hallucinations, which occur as one is falling asleep). N1 typically accounts for 2–5% of total sleep time.

    -- Stage N2: also known as a more subdued state; N2 occurs throughout the sleep period and typically lasts 30–60 minutes. During N2, one's body temperature drops, muscles relax, and breathing and heart rate slow down. N2 typically accounts for 45–55% of total sleep time.

    -- Stage N3: also known as deep sleep; N3 occurs mostly in the first third of the night and typically lasts 20–40 minutes. During N3, it's harder to wake someone up (increased muscle tone), pulse and breathing rates decrease, and brain activity produces a pattern of delta waves. N3 typically accounts for 10–20% of total sleep time.  However, the total amount of deep sleep in N3 decreases with age. 

    – REM sleep: about 20-25% of total sleep. REM sleep also decreases with age (about 0.6% per decade from age 19 to 75)

 

-- Outcomes measured: total sleep time (TST), sleep efficiency (ie total sleep time/time in bed times 100), sleep onset latency (SOL, defined as the first occurrence of any sleep stage deeper than N1), duration of sleep in stages N1-3 and REM, wake after sleep onset (WASO, duration of wake between sleep onset and end of time in bed), number of sleep stages per hour of total sleep time and number of arousals per hour of sleep time, mean heart rates for total sleep time, N1-3, and REM sleep

 

Results:

-- blood-alcohol level measured at 11:45 PM (30 minutes after drinking the alcohol): 0.043% in both groups

-- blood-alcohol level at 6 AM was 0% in both groups

 

-- given the complexity of these multiple analyses, I will display their summary effects of no alcohol and  moderate alcohol consumption in normobaric and hypobaric conditions from the article:

 

 

Commentary:

-- as we know, air travel is remarkably common and increasingly so: in 2002 there were were about 1 billion air travelers per year taking long-haul flights, in 2018 that number had quadrupled

-- the minimal cabin pressure on commercial flights is equivalent to 2483 m (753 hPa), as was re-created in the above sleep laboratory (as mentioned above, the air pressure at 53m is 1010 hPa)

 

-- Other studies have found:

     -- the duration of N3 and REM sleep was shortened by higher altitude simulation

    -- in athletes, altitude was associated with decreased oxygen saturation (89.6% versus 95.4%) and increased heart rate (55.6 beats per minutes versus 51.3 bpm) compared with normobaric normoxia

    -- moderate altitude itself (1630m and 2590m) during 4 consecutive days was associated with increased periodic breathing (increased apnea-hypopnea index) and sleep disturbance

    -- Several prior studies have found that alcohol reduces sleep onset latency (i.e. one falls asleep faster), and increases N2 sleep duration

 

-- this study found that a single exposure to moderate alcohol intake just before bedtime led to:

    -- reduced N1 and REM sleep by 3.5 min and 4.5 min, respectively

    -- decreased sleep onset latency and a longer N2, but these were not statistically significantly differet. Neither was total sleep time

    -- oxygen saturation by hypobaric conditions alone decreased by 1% to a median of 95% (where the normal oxygen saturation values are 96%-98%) and heart rate increased by 13 bpm to median of 77

    -- alcohol on top of hypobaric conditions reduced REM further by 7.5 minutes and showed a trend to shortening SOL, prolonging N2 and decreasing N3; it also further decreased oxygen saturation by 3% and led to an increase in heart rate of 15 beats per minute

    -- adding hypobaric conditions to alcohol reduced REM by 18 minutes and decreased N3 duration by 38 minutes, increased N2 duration and WASO as compared to alcohol exposure alone, and decreased oxygen saturation by 10% and increased pulse by 11 beats per minute

        -- this all suggests that there is a synergistic effect between alcohol and hypobaric conditions, though hypobaric conditions were the primary driver of these changes in sleep architecture

 

-- potential mechanisms are:

    --  alcohol induces peripheral systemic vasodilation which triggers the baroreceptor reflects resulting in increased heart rate

    -- alcohol facilitates sleep by a rapid increase in cerebral adenosine receptor availability

    -- alcohol initially acts as a sedative that interacts with several neurotransmitter systems involved in sleep regulation, leading to more sleep disruptions in the second half of the night and daytime fatigue: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5821259/

        -- these sleep disruptions can take weeks of no alcohol to normalize:

 

Limitations:

-- though in this experiment they did try to mimic the conditions of an actual airplane flight, there do remain questions as to whether it is only the altitude assessed in a laboratory that plays a role in the effect of alcohol on oxygenation. Are there other aspects of an actual flight that might alter the effects of alcohol? Foods eaten? Stress related to an actual flight? Psychologic state of the individual (especially since those with psychological problems were excluded from this study)? Engaging in conversations with one’s neighbor, perhaps inducing anxiety? do different types of alcoholic drinks lead to different effects on sleep? do underlying medical conditions/comorbidities that also led to exclusion in the study? Or medications taken on an actual flight (e.g. sedatives, sleeping medications, scopolamine patches)?

-- In this study participants slept in the supine position, reflecting those on airplanes in the first and business class sections and not the much larger economy class. Do these results apply to what the majority in economy class experience (given their typically less good sleep overall)?

-- it is difficult to have a double-blind study with alcohol consumption, since the participants are quite likely to know if they are drinking alcohol.

 

So, the issue here is that alcohol consumption does interfere with blood oxygenation and sleep architecture when taken before sleep, though it does decrease the time to get to sleep. This all brings up a few concerns:

    -- though the changes in the above airplane study were pretty small, changes in sleep architecture (amount of sleep in different stages) might have important clinical effects despite these small numbers: for example, a pretty recent study found that a 5% decrease in REM sleep was associated with a 13% higher all-cause mortality: https://pubmed.ncbi.nlm.nih.gov/32628261/ )

    -- and, the effects of changing sleep architecture may be more evident clinically if the individual has significant underlying heart or lung disease (and perhaps other comorbidities as well). For example, a study of 23 healthy males who had obstructive sleep apnea, mean age 46, drinking moderate amounts of alcohol (0.5-1.0g alcohol per kg body weight/day) within 30 minutes before retiring to bed had a significantly higher apnea-hypopnea index (mean 7.2 events/hour vs 2.9 events/hour on a non-alcohol drinking day), and lower arterial oxygen saturation of 94.5% vs 95.7%; there was also a substantial decrease in oxygen saturation to 95.4% when drinking alcohol more remotely at dinner (see alcohol before bed dec ox sat EnvHealthPrevMed2005 in dropbox, or Izumi I et al, Environmental Health and Prev Med 10, 16-20, January 2005). This study also found that the percentage of time where patients had oxygen saturation <92% during the early half of sleep (4.9%) was significantly higher than in an alcohol-free day (1.2%)  and when having alcohol with more remotely at dinner (1.4%)

    -- one concern about drinking alcohol before bed in order to fall asleep faster is that it might well be misconstrued as an overall sleep benefit. Patients should understand that regular pre-bed alcohol is actually harmful to sleep architecture and can promote day-time somnolence.

    -- this all adds to the increasing concern about alcohol consumption, reinforcing the pretty clear message that zero alcohol is best for health: https://gmodestmedblogs.blogspot.com/2023/11/alcohol-use-disorder-meds.html

 

geoff

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