Impact of Sleep and Meal Timing on Food Intake Regulation
| Status: | Recruiting |
|---|---|
| Conditions: | Obesity Weight Loss, Peripheral Vascular Disease, Diabetes, Diabetes |
| Therapuetic Areas: | Cardiology / Vascular Diseases, Endocrinology |
| Healthy: | No |
| Age Range: | 20 - 49 |
| Updated: | 4/21/2016 |
| Start Date: | October 2014 |
| End Date: | March 2016 |
| Contact: | Marie-Pierre St-Onge, PhD |
| Email: | ms2554@columbia.edu |
This study will test the hypothesis that a late sleep (Ls) and/or late meal (Lm) behavioral
pattern, with equal sleep duration, will promote positive energy balance and insulin
resistance (IR).
pattern, with equal sleep duration, will promote positive energy balance and insulin
resistance (IR).
Sleeping patterns affect aspects of metabolism that may impact obesity risk; our lab is
interested in studying whether sleep patterns play a role in the development of obesity.
Individuals with late bedtimes and late rise times tend to have greater food intake which
includes more fast food and sugar-sweetened beverages, less fruits and vegetables [1],
larger portions, and later eating times [2] than those with earlier bedtimes. This sleeping
pattern is highly prevalent: ~15 million Americans work on shifts other than regular day
hours [3] and others subject themselves to 'social jetlag' (time difference between the
middle of the sleep episode [midpoint of sleep] on work days and non-work days, similar to
travel across time zones) [4]. The shift in sleep and meal times associated with these
lifestyles results in misalignment of sleep and eating behaviors with the circadian clocks.
These clocks, located in the brain and organs throughout the body, regulate metabolism and
behavior and are affected by sleep and feeding. Disruption of clock genes in individual
organs may be in part responsible for metabolic dysregulation [5]. Altering the coordination
of sleep and meal timing may affect food reward valuation (brain) and metabolism (peripheral
organs) to promote obesity and IR, observed more frequently in shift workers. This is the
focus of this randomized, crossover, controlled study of 4 phases:
- Normal sleep (Ns; 0000-0800 h), Normal meals (Nm=meals at 1, 5, 11, and 12.5 h after
awakening)=Ns/Nm
- Normal sleep (Ns; 0000-0800 h), Late meals (Lm=meals at 4.5, 8.5, 14.5, and 16 h after
awakening)=Ns/Lm
- Late sleep (Ls; 0330-1130 h), Normal meals (Nm=meals at 1, 5, 11, and 12.5 h after
awakening)=Ls/Nm
- Late sleep (Ls; 0330-1130 h), Late meals (Lm=meals at 4.5, 8.5, 14.5, and 16 h after
awakening)=Ls/Lm Aim 1: To determine whether Ls and/or Lm, in individuals with habitual
normal sleep duration and timing, alters one or both sides of energy balance, i.e. food
intake and energy expenditure (EE), relative to Ns and Nm.
- Hypothesis 1: (a) Ls and Lm will have independent and interactive effects on food
intake and EE. Intake at an ad libitum test meal and during a 24 h period, measured
after 3 d of each intervention, will be greater during Ls and Lm, and this will be
enhanced when Ls and Lm are combined, compared to Ns and Nm. (b) Resting metabolic rate
(RMR) will be lower during the Ls and Lm phases, and this will be further reduced when
Ls and Lm are combined compared to the Ns and Nm phases (Ns/Nm
Aim 2: To determine whether neuronal responses to food stimuli in brain regions related to
reward value explain differences in food intake.
• Hypothesis 2: (a) Increased brain activity in response to visual presentation of food
stimuli, using functional magnetic resonance imaging (fMRI), will be seen in Ls and Lm
compared to Ns and Nm in the insula and the orbitofrontal cortex. Enhanced neuronal activity
in response to foods will be most pronounced in the Ls/Lm phase (Ns/Nm
hypocretin-1, and subsequent food intake.
Exploratory Aim 3: To determine whether meal or sleep timing affect glucose homeostasis and
appetite-regulating hormones.
• Hypothesis 3: Ls and Lm will result in lower insulin sensitivity (frequently sampled i.v.
glucose tolerance test [FSIVGTT] and meal tolerance test [MTT]) than Ns and Nm
(Ns/Nm>Ls/Nm≥Ns/Lm>Ls/Lm). Sleep and meal timing will have independent and interactive
effects on the 24-h pattern of hormones regulating food intake (lower leptin and
glucagon-like peptide-1 [GLP-1]; higher ghrelin, NPY and hypocretin-1).
interested in studying whether sleep patterns play a role in the development of obesity.
Individuals with late bedtimes and late rise times tend to have greater food intake which
includes more fast food and sugar-sweetened beverages, less fruits and vegetables [1],
larger portions, and later eating times [2] than those with earlier bedtimes. This sleeping
pattern is highly prevalent: ~15 million Americans work on shifts other than regular day
hours [3] and others subject themselves to 'social jetlag' (time difference between the
middle of the sleep episode [midpoint of sleep] on work days and non-work days, similar to
travel across time zones) [4]. The shift in sleep and meal times associated with these
lifestyles results in misalignment of sleep and eating behaviors with the circadian clocks.
These clocks, located in the brain and organs throughout the body, regulate metabolism and
behavior and are affected by sleep and feeding. Disruption of clock genes in individual
organs may be in part responsible for metabolic dysregulation [5]. Altering the coordination
of sleep and meal timing may affect food reward valuation (brain) and metabolism (peripheral
organs) to promote obesity and IR, observed more frequently in shift workers. This is the
focus of this randomized, crossover, controlled study of 4 phases:
- Normal sleep (Ns; 0000-0800 h), Normal meals (Nm=meals at 1, 5, 11, and 12.5 h after
awakening)=Ns/Nm
- Normal sleep (Ns; 0000-0800 h), Late meals (Lm=meals at 4.5, 8.5, 14.5, and 16 h after
awakening)=Ns/Lm
- Late sleep (Ls; 0330-1130 h), Normal meals (Nm=meals at 1, 5, 11, and 12.5 h after
awakening)=Ls/Nm
- Late sleep (Ls; 0330-1130 h), Late meals (Lm=meals at 4.5, 8.5, 14.5, and 16 h after
awakening)=Ls/Lm Aim 1: To determine whether Ls and/or Lm, in individuals with habitual
normal sleep duration and timing, alters one or both sides of energy balance, i.e. food
intake and energy expenditure (EE), relative to Ns and Nm.
- Hypothesis 1: (a) Ls and Lm will have independent and interactive effects on food
intake and EE. Intake at an ad libitum test meal and during a 24 h period, measured
after 3 d of each intervention, will be greater during Ls and Lm, and this will be
enhanced when Ls and Lm are combined, compared to Ns and Nm. (b) Resting metabolic rate
(RMR) will be lower during the Ls and Lm phases, and this will be further reduced when
Ls and Lm are combined compared to the Ns and Nm phases (Ns/Nm
Aim 2: To determine whether neuronal responses to food stimuli in brain regions related to
reward value explain differences in food intake.
• Hypothesis 2: (a) Increased brain activity in response to visual presentation of food
stimuli, using functional magnetic resonance imaging (fMRI), will be seen in Ls and Lm
compared to Ns and Nm in the insula and the orbitofrontal cortex. Enhanced neuronal activity
in response to foods will be most pronounced in the Ls/Lm phase (Ns/Nm
hypocretin-1, and subsequent food intake.
Exploratory Aim 3: To determine whether meal or sleep timing affect glucose homeostasis and
appetite-regulating hormones.
• Hypothesis 3: Ls and Lm will result in lower insulin sensitivity (frequently sampled i.v.
glucose tolerance test [FSIVGTT] and meal tolerance test [MTT]) than Ns and Nm
(Ns/Nm>Ls/Nm≥Ns/Lm>Ls/Lm). Sleep and meal timing will have independent and interactive
effects on the 24-h pattern of hormones regulating food intake (lower leptin and
glucagon-like peptide-1 [GLP-1]; higher ghrelin, NPY and hypocretin-1).
Inclusion Criteria:
- Participants free of any current and past sleep and psychiatric disorders, including
eating disorders (ex.anorexia, bulimia, night eating syndrome)
- Participants will not have diabetes and will normally consume a meal within 1 h after
awakening at least 5 times/wk
- Participants with normal scores on the Pittsburgh Quality of Sleep Questionnaire [78]
(global score <5) and Epworth Sleepiness Scale [79] (score <10), no indication of
sleep apnea (Berlin Questionnaire) [80], sleep disorders (Sleep Disorders Inventory
Questionnaire) [81], depression (Beck Depression Inventory II) [82], significant
delayed or advanced sleep phase (Composite Scale of Morningness/Eveningness) [83],
and involuntary sleep movement, by self-report.
Exclusion Criteria:
- Smokers (smoking any cigarettes or ex-smokers <3 y)
- Non-day and rotating shift workers
- Persons who plan to travel across time zones within 4 wk of the study
- Persons with a history of drug and alcohol abuse, drowsy driving, or excessive
caffeine intake (>300 mg/d)
- Persons with recent weight change or who actively participated in a diet or weight
loss program in the previous 3 mo.
- Individuals with a neurologic condition that may disrupt the procedures will be
excluded
- Persons with low hematocrit (<30%) due to the high blood sampling protocol *Women who
are pregnant or <1 y post-partum
- Individuals with contraindications for fMRI
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