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Womens Health Update-11-2010

by , , | Nov 1, 2010

Post Categories: Hormone and Metabolic Health | Sleep Disorders

Women’s Health Update

The cortisol-sleep connection

Tori Hudson, N.D. and Bradley Bush

N.D.

Reprinted and updated with permission from Emerson Ecologics

Adaptation to extrinsic and intrinsic forces is a necessity for survival for all living organisms. The hypothalamic-pituitary-adrenal (HPA) axis is an adaptive system with the purpose of maintaining a dynamic equilibrium or homeostasis in a constantly changing environment. Sleep is regulated by the HPA axis in multiple ways and a growing body of research suggests reciprocal associations between sleep and the activity of the HPA axis.

The HPA axis

Corticotropin releasing hormone (CRH) is secreted by a hypothalamic region called the paraventricular nucleus (PVN), and acts on CRH receptors in the anterior pituitary to cause the release of adrenocorticotropic hormone (ACTH) into the blood. ACTH acts on the adrenal cortex which produces and releases cortisol into the blood and participates in maintaining homeostasis throughout the body. CRH also activates the locus ceruleus (LC) which utilizes norepinephrine (NE) and causes further stimulation of the PVN and subsequent release of CRH as well as stimulates the amygdala which is part of the limbic system.1, 2 Elevated brain NE levels and CRH have been implicated in sleep disturbances, including primary insomnia).3, 4 NE levels have also been shown to directly correlate to CRH levels, whereby elevated NE results in elevated CRH and low NE results in low CRH.5, 6

Along with its numerous actions in the body, cortisol has feedback inhibition on the PVN and anterior pituitary to decrease CRH and ACTH production and release, respectively. Many areas of the brainstem, including the LC, are rich in cortisol receptors indicating additional negative feedback mechanisms mediated by the cortisol- HPA axis. 7, 8. Furthermore, the PVN receives GABAergic innervations which can also inhibit the release of CRH.9 These GABAergic neurons are chiefly opposed by the excitatory neurotransmitter glutamate. 10 Therefore, in addition to negative feedback signaling by cortisol, HPA axis regulation also includes NE, GABA, and glutamate modulation.

Normal sleep physiology

Normal sleep architecture is characterized by cycles of light sleep, deeper slow-wave sleep, and REM sleep. Light sleep includes stages 1 and stages 2 in the sleep cylce. Stage 1 sleep is characterized by mixed frequency theta waves, slow rolling eye movements, and slightly reduced eye movement and chin electromyography (EMG). Stage 2 has mixed frequency waves known as sleep spindles and K-complexes as shown by electroencephalograms (EEGs). Deeper slow-wave sleep includes stages 3 and 4. Stage 3 sleep is characterized by 20-50% delta waves and stage 4 has greater than 50% delta waves. Rapid eye movement (REM) sleep has mixed frequency EEGs with theta waves in combination with rapid eye movements and nearly absent chin EMG. REM sleep occurs approximately every 90-110 minutes with a predominance of slow-wave sleep in the first half of the night and a predominance of REM sleep in the second half. 11

The circadian rhythm of cortisol secretion has a waveform pattern with the nadir for cortisol occurring at about midnight. Cortisol levels start to rise about 2-3 hours after sleep onset and continue to rise into the early morning and early waking hours. The peak in cortisol is about 9 a.m. and as the day continues, there is a gradual decline in levels. With the onset of sleep, there is a continued decline until the nadir. Throughout the cycle, there are pulsatile secretions of cortisol of various amplitudes. Cortisol binds to mineralocorticoid receoptors (MRs) and glucocorticoid receptors (GRs) and causes either excitation or inhibition of the PVN depending on the location and type of receptors. Low levels of cortisol in the evening and night are associated with MR binding. When cortisol levels are higher, GRs are activated. In stressful times, NE and GRs may be activated preferentially and thereby increases CRH. This elevated CRH increases sleep EEG frequency, decreases short-wave sleep and increases light sleep and frequent waking.

Sleep/HPA Axis and Cortisol Rhythm

The initiation of sleep occurs when HPA axis activity is lowest, and sleep deprivation is association with HPA activation. Nighttime awakening is associated with pulsatile cortisol, NE and CRH release and is followed by a temporary inhibition of cortisol secretion. Cortisol begins to have a rapid rise upon the first morning awakening and continues to rise for about 60 minutes. This phenomenon is called the awakening response. Nocturnal wake time and daytime sleepiness have been associated with elevations in plasma cortisol.12

Dysfunctional HPA axis activity may play a role in some sleep disorders but in other cases, the HPA axis dysfunction is actually the result of a sleep disorder, as seen in obstructive sleep apnea. HPA axis hyperactivity can lead to fragmentation of sleep, decreased slow-wave sleep, and shortened sleep time. To complicate matters, sleep disturbances can worsen HPA axis dysfunction, thereby worsening the cycle. Both insomnia and obstructive sleep apnea are specific sleep disorders that are associated with HPA dysfunction.

Depression and other stress-related disorders are also associated with sleep disturbances, elevated cortisol 13 , altered NE levels, 14 and HPA axis dysfunction. 15 Interestingly, chronic insomnia without depression occurs with elevated cortisol levels, particularly in the evening and the first part of the night time sleep period.16, 17,18,19. This elevation in cortisol may be a primary cause of the sleep disturbance. In addition, the elevated cortisol may be a marker for increased CRH activity as well as a marker for increased CNS norepinephrine. 20, 21,22

In children, significant associations between reported sleep-wake behavior problems and cortisol reactivity have been found, with greater sleep-wake behavior problems associated with decreased cortisol responses.23 Elderly individuals tend to have higher cortisol concentrations, which may account for the increased incidence of sleeplessness in that population.24 In one study, healthy older women and men with higher levels of free cortisol (24 hour urine level) under a mild stress condition had impaired sleep (lower sleep efficiency; fewer minutes of stages 2, 3, and 4 sleep; more EEG beta activity during non-rapid eye movement sleep). Cortisol levels and sleep in this study correlated most strongly in men.25 Chronic “burnout”, characterized by symptoms of emotional exhaustion, physical fatigue, and cognitive weariness, has been associated with heightened salivary cortisol levels.26

In summary, HPA axis hyperactivity can have a negative impact on sleep, leading to sleep fragmentation, decreased deep slow-wave sleep, and shortened sleep time. In turn, sleep problems including insomnia and obstructive sleep apnea can further propagate HPA axis dysfunction.

Interventions to normalize HPA axis abnormalities, decrease nocturnal CRH hyperactivity, and decrease cortisol may be beneficial in treating insomnia and other sleep disorders.

Alternative Approach to the hypercortisol induced sleep problems

An effective way to manage chronically elevated cortisol levels is to ensure that the adrenal glands are supported by proper nutrition. Vitamin B6, pantothenic acid, and vitamin C, often become depleted with prolonged hyperactivity of adrenal gland activity and increased production of cortisol. 27 These nutrients play a critical role in the optimal functioning of the adrenal gland and in the optimal manufacturing of adrenal hormones. Levels of these nutrients can be diminished during times of stress. For instance, urinary excretion of vitamin C is increased during stress which is evidence of vitamin C “dumping”. Consequently, additional symptoms may develop with these nutritional deficiencies. Evidence supporting this claim has shown that deficiencies in pantothenic acid results in fatigue, headaches, and insomnia.

L-tyrosine and L-theanine support the adrenal glands by supporting NE production and is beneficial in combating fatigue and anxiety symptoms related to stress. 28, 29 L-theanine supplementation has been shown to stimulate relaxation-inducing alpha brain waves in the occipital and parietal regions of the brains of human subjects, with a more pronounced effect in those experiencing anxiety.30 31 In addition, the cortisol feedback mechanisms are dependent on adequate amounts of calcium, magnesium, potassium, manganese and zinc.32 Therefore, supplementation of these nutrients along with other supporting agents, such as L-tyrosine and L-theanine, may help ameliorate some symptoms as well as assist in proper HPA axis functioning.

Ashwagandha (Withania somnifera), also known as Indian ginseng, has been shown to reduce corticosterone, a glucocorticoid hormone present in amphibians, reptiles, rodents and birds and is structurally similar to cortisol.33, 34 An array of clinical trials and laboratory research also support the use of ashwagandha in enhancing mood, reducing anxiety and increasing energy. 35, 36,37, 38

Magnolia (Magnolia officinalis), was studied in a randomized, parallel, placebo controlled study in overweight premenopausal women and resulted in a decrease in transitory anxiety, although salivary cortisol levels were not significantly reduced. 39 Magnolia has been demonstrated to improve mood, increase relaxation, induce a restful sleep and enhance stress reduction. 40

In an unpublished study conducted at the Living Longer clinic, in Cincinnati, Ohio, a proprietary blend of Magnolia officinalis and Phellodendron amurense was shown clinically to normalize the hormone levels associated with stress-induced obesity. It was demonstrated that this combination lowered cortisol levels by 37 percent and increased DHEA by 227 percent.

Phosphatidylserine (PS), also known as lecithin phosphatidylserine, is known to blunt the rise in cortisol and ACTH following strenuous training, and significantly reduce both ACTH and cortisol levels after exposure to physical stress.41, 42 Phosphatidylserine also has been shown to improve mood.43, 44

Another modality to improve sleep is targeting GABA activity. Increasing GABA activity will decrease LC, PVN, and resultant HPA axis activity. One method to support GABA functioning is to decrease glutamate signaling. Glutamate and GABA activity oppose each other therefore decreasing glutamate activity will support healthy HPA axis activity. L-theanine is a glutamate receptor antagonist and has been shown to decrease brain NE levels secondarily to increasing GABA levels. 45, 46 Interestingly, N-acetylcysteine (NAC) is a known precursor for cysteine, necessary for the synthesis of glutathione, 47, 48 but also has been shown to decrease glutamate levels. NAC decreases glutamate by enhancing the activity of a cystine/glutamate antiporter. Glutamate is regulated by a cystine/glutamate antiporter that exchanges extraceullular cystine for intracellular glutamate. 49 Ultimately, the actions of this antiporter serve to lessen synaptic glutamate levels. Furthermore, glutamate is involved in immune cell signaling to increase dendritic cell maturation following the exposure to antigens. To address elevated glutamate at its source, evaluation of intestinal permeabilities, food sensitivities/allergies, bacterial and/or viral infections need to be considered due their relationship to dendritic cell maturation via increase antigen presence. 50

4-amino-3-phenylbutyric acid is a synthetic amino acid sold as a nutritional supplement that crosses the blood brain barrier and is a GABA agonist. 51 Like many other GABA agonist, 4-amino-3-phenylbutyric acid can promote sleep by stimulating sleep promoting centers in the brain and supports healthy cortisol levels by inhibiting the LC release of NE into the PVN.

Rhodiola rosea is an adaptogenic herb that modulates cortisol. 52 It reduces catecholamine release and prevents catecholamine depletion from the adrenal glands. In addition, research that was conducted in Russia indicates that it may stimulate opioid receptors 53 which in turn can reduce NE excitability in the PVN and HPA axis activity. 54

Many traditional botanicals: American ginseng, ashwagandha, Asian ginseng, astragalus, cordyceps, reishi, eleutherococcus, holy basil, rhodiola, schisandra, maca, licorice and common nutritional supplements: phosphatidylserine, L-theanine, 4-amino-3-phenylbutyric acid and N-acetylcysteine have been utilized for their stabilizing effect on the HPA axis. Combination/multi-ingredient formulations are common in a whole system approach to restoring HPA axis dysfunction, whether to increase or decrease cortisol levels.

Reducing cortisol levels and stabilizing HPA axis dysfunction can be a very effective approach to addressing sleep disturbances, while also reducing the long term risks associated with elevated cortisol levels.

**Sections of this article are reprinted with permission from Emerson Ecologics.

Disclosures:

Tori Hudson, N.D. Director of Education/Research, Vitanica; Scientific Advisory boards: ITI, Nordic Naturals, NHI, Gaia Herbs, Biogenesis

Bradley Bush, N.D. Director of Clinical Affairs, Neuroscience.

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Authors

  • Ann D. Sawyer

    At age 77, Ann is still working part-time as a psychotherapist, a career she loves. Educated at the University of Michigan, BA Psychology, and the University of Chicago (MA Social Work), she then earned her LCSW license. At the same time her personal life was also progressing with marriage and the birth of three children, followed by the fun of raising them. Multiple Sclerosis interrupted her life, taking her to full disability, then her years of recovery. Ann then dedicated some years to spreading the good word about recovery which culminated in the book, “The MS Recovery Diet,” Avery/Penguin, 2007 with Judith E. Bachrach. A bout with cancer followed before she returned to her profession. With many interests, among them traveling, writing, family now with 6 grandchildren, friends, church and organizations, Ann enjoys life.

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  • Bradley J Bush, ND
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  • Tori Hudson, ND

    Dr. Tori Hudson, Naturopathic Physician, graduated from the National University of Natural Medicine (NUNM) in 1984 and has served the college in several capacities, including: Medical Director, Associate Academic Dean, and Academic Dean. She is currently a clinical adjunct professor at NUNM), Southwest College of Naturopathic Medicine, Bastyr University and the Canadian College of Naturopathic Medicine. Dr Hudson has been in practice for 40 years, is the medical director of her clinic, “A Woman’s Time” in Portland, Oregon, co-owner and director of product research and education for VITANICA and the program director for the Institute of Women’s Health and Integrative Medicine. She is also the founder and co-director of NERC (Naturopathic Education and Research Consortium), a non-profit organization for accredited naturopathic residencies.

    Dr. Hudson has been appointed as a faculty member of the Fellowship in Integrative Health and Medicine, Academy of Integrative Health & Medicine.

    Dr. Hudson was awarded the 1990 President’s award from the American Association of Naturopathic Physicians for her research in women’s health, the 1999 prestigious Naturopathic Physician of the Year award, the 2003 NUNM Alumni Pioneer Award., the 2009 Natural Products Association Pioneer Award and in 2012 was inducted into the NUNM Hall of Fame. In 2016, she was the recipient of the annual Oregon Association of Naturopathic Physician’s “Living Legends” award.

    In 2021 she received the 2020 American Botanical Council’s prestigious Fredi Kronenberg Excellence in Research and Education in Botanicals in Women’s Health Award for 2020.

    She is a nationally recognized author (book: Women’s Encyclopedia of Natural Medicine second edition, McGraw Hill 2008) and the Menopause Companion (2023), speaker, educator, researcher, and clinician. Dr. Hudson serves on several editorial boards, advisory panels and as a consultant to the natural products industry. She also writes monthly columns and freelance articles for several publications.

    www.drtorihudson.com
    www.instituteofwomenshealth.com
    www.awomanstime.com
    www.vitanica.com

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Ann D. Sawyer

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