Sleep and its link with depression & anxiety

sleep

This is the tenth and final post in a series on some of the physiological (non-psychological) causes of depression and/or anxiety.

The amount and quality of sleep we get has a significant impact on every system of our body. Sleep is not a state of inactivity but a necessary phase for deep regeneration. Prolonged sleep deprivation can have serious consequences including depression. Both chronic and acute sleep deprivation are associated with alterations in brain function and increased inflammation markers.

Sleep deprivation is physiologically stressful on the body. This means that your body activates the stress response via the release of stress hormones like cortisol. Chronically elevated cortisol levels have an impact on our brain chemistry and function. Increased cortisol causes a reduction in the expression of a brain chemical known as brain derived neurotrophic factor (BDNF). Evidence suggests that among its many roles, BDNF promotes the survival and differentiation of serotonin receptors in the brain and is also involved in the regulation of GABA transporters. Among other factors, low BDNF levels have been implicated in the pathogenesis of depression.

Aside from affecting neurotransmitters involved in mood regulation, sleep deprivation also affects the way our bodies regulate blood sugar. Research as shown that sleep restriction reduces insulin sensitivity. Furthermore, and after only one night of poor sleep, individuals tend to have increased cravings for refined foods high in sugar. As noted in a previous post in this series, poor blood sugar regulation can play havoc with mood regulation and affect feelings of wellbeing.

On an interesting note, the ratio of fatty acids/prostaglandins appears to play an important role in the regulation of sleep. Two prostaglandins have been identified as of particular importance: prostaglandin D2 series (PGD2) functions to promote sleep, whilst PGE2 appears to suppress sleep. Thus, alterations in the production of PGD2 can contribute to a shift in sleep patterns. Research also demonstrates the role of omega-3 EFAs in the pineal gland in relation to melatonin. It was found from animal studies that there appears to be some evidence of omega-3’s influence on melatonin synthesis and secretion from pineal gland, and that supplementation with DHA returns melatonin secretion to normal. Melatonin is a potent antioxidant hormone that signals and facilitates sleep.

A note of caffeine:

Caffeine stimulates the stress response and decreases melatonin synthesis by acting as an adenosine receptor antagonist. Adenosine is one of the main sleep molecules in the brain and it increases the production of the enzyme involved in melatonin synthesis.  Whenever possible, limit your intake of caffeine for a good night’s sleep.

What to do about poor sleep?

In addition to following sleep hygiene guidelines, a qualified naturopath can assist you via the prescription of herbs and nutrients shown to be effective in improving the onset and quality of sleep.

If you struggle with poor sleep, anxiety and/or depression and would like an individual naturopathic consultation, please contact me to schedule your appointment.

Yours in Health,
Micaela

 

References

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Basta, M, Chrousos, G, Vela-Bueno, A & Vgontzas, A 2007, ‘Chronic Insomnia and Stress System’, Sleep Medicine Clinics, vol. 2, no. 2, pp. 279-291.

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Brogan, K 2016, A Mind of Your Own, Harper Collins Publishers, NY, USA.

Buckley, T & Schatzberg, A 2005, ‘On the Interactions of the Hypothalamic-Pituitary-Adrenal (HPA) Axis and Sleep: Normal HPA axis Activity and Circadian Rhythm, Exemplary Sleep Disorders’, Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 5, pp. 3106-3114.

Buxton, O, Pavlova, M, Reid, E, Wang, W, Simonson, D & Adler, G 2010, ‘Sleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men’, Diabetes, vol. 59, pp. 2126-2133.

Castren, E & Rantamaki, T 2010, ‘The Role of BDNF and Its Receptors in Depression and Antidepressant Drug Action: Reactivation of Developmental Plasticity’, Developmental Neurobiology, vol.70, no. 5, pp. 289-297.

Hayaishi, O 1991, ‘Molecular mechanisms of sleep-wake regulation: roles of prostaglandins D2 and E2’, The Journal of the Federation of American Societies for Experimental Biology, vol. 5, no. 11, pp. 2575-2581.

Irmisch, G, Schlafke, D, Gierow, W, Herpertz, S & Richter, J 2007, ‘Fatty acids and sleep in depressed inpatients’, Prostaglandins, Leukotrienes and Essential Fatty Acids, vol. 76, no. 1, pp. 1-7.

Irwin, M, Wang, M, Ribeiro, D, Cho, H, Olmstead, R, Breen, E, Martinez-Maza, O, Cole, S 2008, ‘Sleep Loss Activates Cellular Inflammatory Signalling’, Biological Psychiatry, vol. 64, no. 6, pp. 538-540.

Knutson, K, Spiegel, K, Penev, P & Cauter, E 2007, ‘The Metabolic Consequences of Sleep Deprivation’, Sleep Medicine Reviews, vol. 11, no. 3, pp. 163-178.

Lane, J, Pieper, C, Phillips-Bute, B, Bryant, J & Kuhn, C 2002, ‘Caffeine Affects Cardiovascular and Neuroendocrine Activation of Work and Home’, Psychosomatic Medicine, vol. 64, pp. 595-603.

Martinowich, K & Lu, B 2008, ‘Interaction between BDNF and Serotonin: Role in Mood Disorders’, Neuropsychopharmacology, vol. 33, pp. 73-83.

Nedeltcheva, A.V., Kilkus, J.M., Imperial, J., Kasza, K., Schoeller, D.A. and Penev, P.D., 2009. Sleep curtailment is accompanied by increased intake of calories from snacks. The American Journal of Clinical Nutrition, 89(1), pp. 126-133.

Peuhkuri, K, Sihvola, N & Korpela, R 2012b, ‘Dietary factors and fluctuating levels of melatonin’, Food & Nutrition Research, vol. 56.