SLEEPING DISORDERS:

Impact on health & Nutrition interventions

PRESENTED BY:Supta SarkarHHM-2013-10

M.Sc Foods & Nutrition

SEE INSIDE… Introduction Sleep regulation Measuring sleep Types & stages of

sleep Functional changes

during sleep Types of sleeping

disorders Health risk due to SD Nutrition

intervention Conclusion Reference s

Introduction• Sleep can be defined as a reversible behavioural state in which

an individual is perceptually disengaged from and unresponsive to the environment (Carskadon & Dement,2011).

• People generally know little about the importance of this essential activity.

• Sleep actually appears to be required for survival.

• The Guinness World Record for sleep deprivation is 11 days (Gillin, 2002).

• Rats deprived of sleep will die within two to three weeks, a time frame similar to death due to starvation (Rechtschaffen, 1998).

• According to the International Classification of Sleep Disorders (ICSD-2, 2005) there are around 90 distinct sleep disorders.

• The most common are obstructive sleep apnea, insomnia, hypersomnia, parasomnia, narcolepsy, restless legs syndrome and circadian rhythm disorder.

• Large numbers of individuals suffering from these sleep disorders are unaware of—and have not been diagnosed or treated for—their disorder (Strohl et al.,2000).

• Sleep disorders have been associated with fatigue, bad mood, poor performance and also long-term health consequences like hypertension, diabetes, obesity, depression, heart attack, stroke.

• Nutritional status of an individual could play a major role on sleep quality (Partinen et al., 2014).

MISCONCEPTION ABOUT SLEEP:

Misconception 1:

Sleep is time for the body in general and the brain specifically

to shut down for rest.

Misconception 2: Getting just one hour less sleep per night than

needed will not have any effect on daytime functioning.

Misconception 3:

The body adjusts quickly to different sleep schedules.

Misconception 4: People need less sleep as

they grow older.

Misconception 5: A “good night’s sleep” can cure

problems with excessive daytime sleepiness.

SLEEP REGULATIONHow is sleep regulated?

Under the brain’s control Internal factors drive sleep

External factors influence sleep

A. BRAIN’S CONTROL• A small number of brain cells are responsible for

keeping us awake or asleep—some cells promote wakefulness and others promote sleep.

• Neurons that promote wakefulness or arousal: Tuberomammillary Nucleus (TMN).

• Neurons that promote sleep: Ventrolateral Preoptic Nucleus (VLPO).

• TMN release neurotransmitters histamine & orexin (also known as hypocretin).

Wakefulness or arousal: Tuberomammillary nucleus (TMN)

Fig 1: Orexin neurons stimulate the brain’s arousal centers.

Fig 2: Arousal centres send signals that stimulate the cerebral cortex.

SLEEPINESS: VENTROLATERAL PREOPTIC NUCLEUS (VLPO)

Fig: The VLPO promotes sleep by inhibiting activity in the brain’s arousal centers

(Neurotransmitters released from VLPO like GABA, galanin reduce activity in the arousal regions, causing us to pass quickly into the unconscious state of NREM sleep)

B. Internal factors• There are many internal factors: homeostatic

sleep drive and circadian rhythms.

• Homeostatic sleep drive: Drive to sleep that accumulates during prolonged wakefulness & minimize during sleeping.

• Circadian rhythms: Circadian rhythms are endogenously generated, although they can be modulated by external cues such as sunlight and temperature.

CIRCADIAN RHYTHMS The term circadian comes from the Latin ‘circa’, meaning

"around" (or "approximately"), and ‘diem’ or ‘dies’, meaning "day”.

A "master clock" in the brain controls circadian rhythms consists of a group of nerve cells in the brain called the Suprachiasmatic Nucleus, or SCN.

• Retina also contains specialized ganglion cells which are directly photosensitive, and contain the photopigment melanopsin and their signals follow a pathway called the retinohypothalamic tract, leading to the SCN.

• The SCN takes the information on the lengths of the day and night from the retina, interprets it and passes it on to the pineal gland, located on the epithalamus.

• In response, the pineal secretes the hormone melatonin.

• Secretion of melatonin peaks at night and ebbs during the day and its presence provides information about night-length.

• The body's master clock, or SCN, controls the production of melatonin, a hormone that makes one sleepy.

C. External factors1. Sleeping environment: Light, sound, temperature.

2. Jet leg

3. Shift worker

4. Pain, Anxiety, and Other Medical Conditions

5. Alcohol

HOW TO MEASURE SLEEP?The commonly used methods to assess sleep.

1. Polysomnography: study body functions: brain activity (electroencephalogram-EEG), eye movements (electrooculogram-EOG), muscle activity (electromyogram-EMG) are measured.

2. Actigraphy

3. Sleep diary.

TYPES & STAGES: 2 types: NREM & REM

5 stages: NREM(4 stages) & REM

NREM sleep is divided into four stages, which are associated with a progressive increase in the depth of sleep (Carskadon & Dement,2011).

REM sleep is characterized by muscle atonia, bursts of REM and dreaming.

Figure: First, the periods ofNREM and REM sleep alternate

during the night.

Stage-1-4 (NREM)Stage-5 (REM)

Pattern of sleep in different stages

Brain waves formed in different stages

Indication of different Brain Waves:

• Sleep in particular slow-wave sleep (SWS) or deep sleep, is important for recovery (Halson, 2004).

• The synchrony of growth hormone release with SWS occurs in humans (Halson, 2004).

• The duration of SWS is proportional to preceding wakefulness (Shapiro et al., 1981).

• When SWS is decreased by deprivation, an increase in daytime sleepiness and a reduction in performance have been observed (Dijk, 2010).

Changes in the functions of many organ systems during sleep:

Endocrine system:

• Many hormones are secreted into the blood during sleep.

• Growth hormone, follicle stimulating hormone and luteinizing hormone are released during sleep.

• Thyroid-stimulating hormone, are released prior to sleep.

Renal system:• Kidney filtration, plasma flow, and the excretion

of sodium, chloride, potassium, and calcium all are reduced during both NREM and REM sleep.

• These changes cause urine to be more concentrated during sleep.

Alimentary activity:• In a person with normal digestive function, gastric

acid secretion is reduced during sleep.• In those with an active ulcer, gastric acid

secretion is actually increased.

TYPES OF SLEEPING DISORDERs• According to the International Classification of Sleep

Disorders (ICSD-2, 2005) there are around 90 distinct sleep disorders.

• The most common are:-Obstructive Sleep Apnea(OSA), -Narcolepsy, -Restless Legs Syndrome(RLS),-Insomnia, -Parasomnias(Sleep walking & REM Behavior Disorder),-Circadian rhythm disorders: (Jet leg & shift work),-Hypersomnia

IS IT A SLEEPING DISORDER?

Q. Do you…….

• feel irritable or sleepy during the day?• have difficulty staying awake when sitting still, watching

television or reading?• fall asleep or feel very tired while driving?• have difficulty concentrating?• often get told by others that you look tired?• react slowly?• have trouble controlling your emotions?• feel like you have to take a nap almost every day?• require caffeinated beverages to keep yourself going?

If you answered “yes” to any of the previous questions, you

may have a sleep disorder.

Health risks associated with sleeping disorders:

• The cumulative effects of sleep loss and sleep disorders have been associated with a wide range of deleterious health consequences including an increased risk of diabetes, obesity, depression, hypertension,heart attack, stroke and nutritional status of an individual could play a major role on sleep quality (Partinen et al.,2014).

• The exact mechanism by which decreased sleep influences glucose metabolism is thought to be multifactorial and includes decreased brain glucose utilization, alterations in sympathovagal balance, increased evening cortisol, extended night-time growth hormone secretion, and proinflammatory processes (Van Cauter et al., 2008).

HORMONAL IMBALANCE Sleep deprivation results in decreases in leptin

and increases in ghrelin (Van Cauter et al., 2008).

Leptin and ghrelin are hormonal regulators of food intake, with leptin exerting inhibitory effects on food intake and ghrelin being an appetite-stimulating hormone (Van Cauter et al., 2008).

Sleep restriction has also been shown to increase hunger and appetite, especially relating to carbohydrate-rich foods (Spiegel et al., 2004).

FIG: Actions of and relationships between leptin and ghrelin

CORTISOL (the stress hormone):• In studies on individuals who were sleep deprived (four

hours of sleep per night), evening cortisol levels were elevated and the levels decreased six times slower when compared to control subjects.

• These elevations in cortisol further increase the likelihood of developing diabetes and obesity.

• Saliva cortisol has shown to decrease immediately after a nap (Faraut et al., 2011).

INSULIN:• Poor sleep is also associated with increases in the

secretion of insulin following a meal. • Higher levels of insulin are associated with weight gain,

a risk factor for diabetes.

OBESITYStudies have shown that people who habitually sleep less than 7

hours per night are much more likely to have a higher average BMI and more likely to be obese (Gangwisch et al, 2005).

SLEEP DEPRIVATION

Increased Hunger

Increased opportunity to Eat

Altered thermoregulation

Increased fatigue

Increased caloric intake

Reduced Energy

Expenditure

OBESITY

↑Ghrelin

↓Leptin

DIABETES• Both laboratory and epidemiological studies support the notion that chronic partial sleep loss can increase the risk of obesity and diabetes (Knutson et al.,2007).

• Potential mechanisms include changes in glucose regulation by insulin resistance, dysregulation of neuroendocrine control of appetite and/or increased energy intake (Knutson et al., 2007 & Spiegel, 2005).

• In addition, researchers have correlated obstructive sleep apnea—a disorder in which breathing difficulties during sleep lead to frequent arousals—with the development of impaired glucose control similar to that which occurs in diabetes.

Fig: Schematic diagram of the potential pathways leading from sleep loss to diabetes risk.(Reproduced from Siegel et al.)

Acute sleep deprivation

Glucose level

Decreased glucose

tolerance

Appetite dysregulation

& risk of weight gain

Normal glucose levelInsulin levels

Chronic sleep

deprivation

Insulin resistance

Increased risk of type II diabetes

Even minor periods of inadequate sleep can cause an elevation in blood pressure.

Studies have found that a single night of inadequate sleep in people who have existing hypertension can cause elevated blood pressure throughout the following day.

This effect may begin to explain the correlation between poor sleep and cardiovascular disease and stroke.

Sleeping too little (less than six hours) or too much (more than nine hours) increased the risk of coronary heart disease (Ryu et al., 2008).

HYPERTENSION & CVD

MOOD DISORDERS

Given that a single sleepless night can cause people to be irritable and moody the following day, it is conceivable that chronic insufficient sleep may lead to long-term mood disorders.

Sleeping four hours per night showed declining levels of optimism and sociability as a function of days of inadequate sleep (Haack and Mullington, 2005).

IMMUNE FUNCTION• Increasing amounts of evidence suggest that sleep deprivation can

have detrimental effects on immune function, and that immune responses feed back on sleep architecture (Bollinger et al., 2010).

• In a recent review examining the link between sleep and immunity, it was concluded that sleep improves immune responses and that most immune cells have their peak pro-inflammatory activity at night (Bollinger et al., 2010).

• Short sleep duration(<7hr) was found to be associated with 30 % lower NK cell activity when compared with normal sleep (Fondell et al., 2011).

• Increasing sleep duration (from 8 to 10 h) or napping (30 min) following 1 night of sleep deprivation (only 2 h of sleep) both resulted in a return of leukocyte values to normal ranges (Faraut et al., 2011).

• Markers of the acute inflammatory system, such as interleukin (IL)-1b, tumour necrosis factor-a, IL-6, and C-reactive protein are all influenced following the manipulation of sleep (Mullington et al., 2010).

• In addition, patients with insomnia and sleep apnea have elevated inflammatory markers (Mullington et al., 2010).

***

RECOMMENDED AVERAGE SLEEP TIME:AGE TOTAL SLEEP/DAY

(hour)1-15 days 163-5 months 146-23 months 13.52-3 years 123-5 years 11.55-9 years 1110-13 years 1014 – 18 years 8.519-30 years 833-45 years 7.550-70 years 770-80 years 6.5

Data source: Roffwang, H.P., Muzic, J.N and Dement,W.C. 1966. Ontogenic development of human sleep-dream cycle. Science.

152: 604-619.

NUTRITION INTERVENTIONS IN

SLEEPING DISORDERS

Many different neurotransmitters, neuromodulators and hormones have an important role in regulation of sleep and wakefulness, and in eating behaviour.

Research has identified a number of neurotransmitters associated with the sleep–wake cycle. These include 5-HT, gamma-aminobutyric acid (GABA), orexin, melanin-concentrating hormone, cholinergic, galanin, noradrenaline, and histamine (Saper et al., 2005).

Dietary precursors can influence the rate of synthesis and function of a small number of neurotransmitters, including 5-HT (Silber & Schmitt, 2010).

• Ingestion of other forms of protein generally decrease the uptake of Trp into the brain, as Trp is the least abundant amino acid and therefore other LNAA are preferentially transported into the brain (Silber & Schmitt, 2010).

• Carbohydrate, however, increases brain Trp by insulin stimulation of LNAA into skeletal muscle, which results in an increase in free Trp (Fernstrom & Wurtman,1971).

ROLE OF DIFFERENT NUTIENTS IN INFLUENCING SLEEP

CARBOHYDRATEYear Scientis

t Title STUDY & RESULT

1981 Porter & Horne

Bed-time food supplements and sleep: effects of different

carbohydrate levels

• Six male subjects with a high-carbohydrate meal (130 g), a low-carb meal (47 g), or a meal containing no carb was provided 45 min before bedtime.

• The high-carbohydrate meal (130g) resulted in increased REM sleep, decreased light sleep, and wakefulness (Porter and Horne,1981).

2007 Afaghi et al.

High-glycemic-

index carbohydrate

meals shorten sleep

onset

• High or low glycemic index (GI) meals were given 4 h or 1 h before sleep

• The high GI meal significantly improved sleep-onset latency above the low GI meal, and providing the meal 4 h before sleep was better than providing the meal 1 h before sleep.

Sleepy patients with hypersomnias should avoid rapidly absorbing carbohydrates at daytime to minimize afternoon sleepiness. Adenosine is accumulating in the brain, notably in the basal forebrain, during wake, increasing the sleep pressure (Porkka-Heiskanen & Kalinchuk, 2011).

PROTEINYear Scientis

t Title RESULT

1978 Lacey et al.

Effects of dietary protein on sleep EEG in normal

subjects

• Studied women for 7 days with either high protein (>100 g), low protein (<15 g), or normal daily protein intakes.

• Low-protein intakes resulted in lower amounts of SWS.

2013 Lindseth et al.

Nutritional effects on sleep

• The diet of 44 adults were manipulated for 4 days.

• Diets were either high protein (56 % protein, 22 % carbohydrate,22 % fat), high carbohydrate (22 % protein, 56 % carbohydrate, 22 % fat), or high fat (22 % protein, 22 % carbohydrate, 56 % fat).

• Diets higher in carbohydrate resulted in shorter sleep-onset latencies, and diets higher in protein resulted in fewer wake episodes (Lindseth et al. ,2013).

Grandner et al., 2013 examined the dietary intake (by means of questionnaires) of 459 postmenopausal women over 7 days.

The only significant finding was that fat intake was negatively associated with total sleep time.

From the above study it appears that diets high in fat may negatively influence total sleep time.

FAT

TRYPTOPHAN Synthesis of 5-HT is dependent on the availability of

its brain precursor, Trp.

Furthermore, 5-HT is a precursor to melatonin in the pineal gland.

There have been numerous investigations of the effects of tryptophan supplementation on sleep (Silber and Schmitt, 2010)

Trp doses as low as 1 g can improve sleep latency and subjective sleep quality (Silber and Schmitt, 2010).

MELATONIN The ingestion of tart cherries may

increase exogenous melatonin, and when consumed over a 2-week period was shown to improve subjective insomnia symptoms when compared with placebo (Pigeon, 2010).

Tart cherries also contain antioxidant and anti-inflammatory phytochemicals that may influence sleep by means of cytokines associated with the sleep–wake cycle (Howatson, 2011).

CAFFEINE• The stimulant and wake-producing properties of

caffeine depend on its ability to reduce adenosine transmission in the brain.

• Caffeine acts as an antagonist to adenosine A1 and especially to adenosine A2 receptors. (Fisone et al., 2004; Burdakov et al., 2005).

FATTY ACIDS• Fagioli et al.,1989 conducted a small

study with eight children.

• They were fed by total parenteral nutrition without essential lipids and seven other children who received a daily supplement of essential lipids in their parenteral nutrition.

• Slow wave sleep was significantly decreased in the group of children who did not receive fatty acids as compared to those who did.

• Observational studies have shown a link between sleep (Partinen ,2009) and vitamins and minerals, whether taken in combination or individually.

• Unlike other dietary supplement ingredients, vitamins and certain minerals are considered essential nutrients for which standards of adequacy are needed.

VITAMINS AND MINERALS

VITAMIN A Barcelo et al.,2006 reported that patients with obstructive sleep

apnea syndrome have a decreased antioxidant capacity of vitamin A and E levels.

It has been suggested that retinoid signalling pathways are important for adult neural function in health and disease (Sei, 2008).

A definitive role for vitamin A signalling however is evident in the regulation of delta oscillations which contribute to slow wave sleep (SWS). (Maret et al.,2005)

Study of sleep in mouse models of ageing shows involvement of vitamin A in the regulation of delta oscillations (Ransom et al., 2013).

Vitamin A deficiency is known to significantly reduce the power of the delta oscillation in mice (Kitaoka et al., 2007).

VITAMIN B B vitamins have been advanced as a preventive

for insomnia based on research that suggests deficiencies in vitamin B6 promote psychological distress and ensuing sleep disturbances (Baldewicz et al., 1998).

Vitamin B12 has been shown to modulate human melatonin secretion (Yamazaki et al., 1991).

The potential role of diet including vitamin C that was associated independently with non-restorative sleep has been reported which shows associations between sleep symptoms and diet/metabolism, potentially explaining associations between sleep and CVD. (Grandneret al.,2013; Grandner et al., 2014).

In restless leg syndrome (RLS), vitamins C and E and their combination are used as safe and effective treatments for reducing the severity of RLS in hemodialysis patients (Sagheb et al.,2012).

VITAMIN C

VITAMIN DVitamin D enhance the synthesis and transmission of

serotonin, leading to improvement in mood & sleep. (Privette et al, 1991)

Persistent inadequacy of vitamin D may also increase the risk for obstructive sleep apnea by promotion of adenotonsillar hypertrophy, airway muscle myopathy, and/or chronic rhinitis (McCarty et al.,2013).

VITAMIN E Vitamin E normalize chronic sleep deprivation

(Alzoubi, et al, 2012).

Decreased levels of antioxidants and lower performance on the neuropsychological tasks were observed in patients with obstructive sleep apnea (Sales et al.,2013).

Limited research indicates that supplemental vitamin E may reduce symptom occurrence in restless leg syndrome (Sagheb et al.,2012).

Zinc is an important cofactor for metabolism relevant to neurotransmitters, prostaglandins, and melatonin, and indirectly affects dopamine metabolism (Prasad,1985).

Magnesium has beneficial effects on mood and is crucial, together with zinc, in the endogenous synthesis of melatonin (Nordlander,1953).

The administration of nightly melatonin, magnesium, and zinc appears to improve the quality of sleep and the quality of life in long-term care facility residents with primary insomnia (Nowak et al., 2002).

ZINC & MAGNESIUM

IRON

In restless legs syndrome S-ferritin is often low, in which case, giving iron per os, or intravenously in more severe cases, should be part of the treatment.

In patients with RLS 45 μg/L is usually used as a limit when one should consider giving iron supplement even if hemoglobin is normal (Partinen et al., 2009).

SELENIUM• Selenium may have some role in regulation of

sleep and in development of insomnia as lack of selenium was statistically significantly associated with difficulty falling asleep in a recent large survey (Chiu et al., 2003).

• Infusion of tetravalent selenium compounds, reversibly, time- and dose-dependently inhibited both nonrapid eye movement (NREM) and rapid eye movement (REM) sleep during the daytime (Gumustekin et al., 2004).

DIETARY GUIDELINES:Several practical recommendations may be suggested (Halson,2004):

• High GI foods may promote sleep.

• Diets high in carbohydrate may result in shorter sleep latencies.

• Diets high in protein may result in improved sleep quality.

• Diets high in fat may negatively influence total sleep time.

• When total caloric intake is decreased, sleep quality may be disturbed.

• Small doses of tryptophan (1 g) may improve both sleep latency and sleep quality.

• The hormone melatonin and foods that have a high melatonin concentration may decrease sleep onset time.

CONCLUSION

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