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Relax
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STRESS & SLEEP

STRESS

An individual’s adaptive response to stimuli that places excessive psychological or physical demands on that individual is Stress. When this pressure initiates a drive in us to perform it is called Stress and when this pressure becomes unmanageable with strain on our system it is called Distress.

SLEEP

The innate mechanism of our body wherein every day in a 24 hour cycle our internal system slows down the metabolism to a state wherein complete rest is given to us. In this state our conscious mind goes thru a series of complex processes to achieve a shutdown wherein all involuntary critical processes like heart, lungs etc continue to function. This state is extremely essential for regeneration repair and healing.

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  • FAQ
  • References
  • How Much Sleep Do I Need?

    It depends, but adults generally need 7-8 hours per night. Kids and teens need more.

    The exact amount varies from person to person, based on many things, including your age.

    If you didn�t sleep well last night, you may need more to make up for it. As you get older, your sleep patterns may change, with lighter and shorter periods of shut-eye.

    The best way to know if you get enough rest is to notice how you feel during the day. If you�re drowsy or want to nap � or even fall asleep while the sun�s out � you probably need more Zzz�s at night.

  • What Is a Sleep Disorder?

    Everyone has a rocky night every now and then. That can happen if you�re under stress, for instance.

    But if it happens often, ask your doctor to help you figure out what�s going on.

  • How can we have good healthy sleep ?

    Keep regular sleep habits. Establish a rhythm by going to bed at the same time each night and wake up at the same time each morning, including weekends and days off. Exercise regularly, preferably in the morning. If not possible, finish at least three hours before bedtime. Relax. Take a warm bath, drink a cup of warm milk, or read a book. Eat healthy, and while a light snack before bedtime can help promote sound sleep, avoid large meals - especially late. Caffeine, nicotine, and alcohol prior to retiring are additional factors that can worsen one�s ability to fall asleep and stay asleep. Create an environment conducive to sleep. Make your bedroom cool, dark, and quiet. Leave your worries at the bedroom door. If you�re concerned about something, make a list of the steps you�ll take to solve the problem or leave yourself a voicemail message. Your bed should be for sleep or sickness only. If you are unable to fall asleep or stay asleep, leave your bedroom and engage in a quite activity elsewhere. Do not permit yourself to fall asleep outside the bedroom. Return to bed when - and only when - you are sleepy. Repeat this process as often as necessary throughout the night. Do not read, watch TV, or do work in bed for an extended time. Avoid napping during the daytime. If daytime sleepiness becomes overwhelming, limit nap time to a single nap of 20 minutes of less, and no later than 5 p.m.

  • Does diet utrition affect sleep ?

    Nutrition and sleep share several similarities, and the regulation of both is physiologically linked. Research has demonstrated several mechanisms by which nutrition promotes sleep. Sleep can affect nutrition, and sleep abnormalities may disrupt energy homeostasis. Dietary changes can help treat certain sleep disorders.

    MyHealthWorks recommends below given regimen for reversal of Sleep disorder and stress management

    STRESS & SLEEP

    Reversal                                                 Recovery                        Restoration and Maintenance

    SLEEPWELL NANO CURCUMIN MULTIMAX
    BRAIN-O-BOOST PROTOMAX
    PRIMROSE OMEGA-369 COCONUT MIRACLE-X
    SPIRULINA

References

Triethyleneglycol, an active component of Ashwagandha(Withania somnifera) leaves, is responsible for sleep induction. Kaushik MK1,2, Kaul SC3, Wadhwa R3, Yanagisawa M2, Urade Y1. (Author information) Abstract Insomnia is the most common sleep complaint which occurs due to difficulty in falling asleep or maintaining it. Most of currently available drugs for insomnia develop dependency and/or adverse effects. Hence natural therapies could be an alternative choice of treatment for insomnia. The root or whole plant extract of Ashwagandha (Withania somnifera) has been used to induce sleep in Indian system of traditional home medicine, Ayurveda. However, its active somnogenic components remain unidentified. We investigated the effect of various components of Ashwagandha leaf on sleep regulation by oral administration in mice. We found that the alcoholic extract that contained high amount of active withanolides was ineffective to induce sleep in mice. However, the water extract which contain triethylene glycol as a major component induced significant amount of non-rapid eye movement sleep with slight change in rapid eye movement sleep. Commercially available triethylene glycol also increased non-rapid eye movement sleep in mice in a dose-dependent (10-30 mg/mouse) manner. These results clearly demonstrated that triethylene glycol is an active sleep-inducing component of Ashwagandha leaves and could potentially be useful for insomnia therapy.

Bacopa monnieri(Brahmi) This herb is just amazing. The amount of benefits this herb gives is unreal. Here are just some of the many benefits this herb provides:
Enhanced sleep quality
Enhanced memory
Enhanced concentration
Enhanced cognitive function
Reduced anxiety
Reduced depression

SUMMARY: Used for nearly 3000 years, bacopa monnieri is a fat soluble herb used in traditional Indian cultures. It has been an effective part of Ayurvedic medicine and has lots of research as a useful mental performance tool.

BRAHMI -- boosts brain function and reduces stress and helps in sleep

Exploring the role of "Brahmi" (Bocopa monnieri and Centella asiatica) in brain function and therapy. ShinomolGK1, Muralidhara, Bharath MM. Author information Abstract It has been envisaged that in this century, disorders of the central nervous system will have a significant bearing on the healthcare concerns of the human population worldwide. Such neurological and psychiatric disorders are generally associated with loss of memory, cognitive deficits, impaired mental function etc. Due to the multi-factorial nature of these diseases, modern medicine based psychoactive drugs have met with limited success. Therefore, there is a growing demand for novel products that could target multiple pathways and improve the mental capabilities either independently or in combination with conventional drugs. In the recent times, herbal products based on traditional knowledge have been increasingly used both in developed and developing countries. According to "Ayurveda", the Indian traditional system of medicine, "medhyarasayanas" represent herbal therapeutics that boost memory, restore cognitive deficits and improve mental function. The current review deals with the components and application of such a traditional herb "Brahmi" that corresponds to two plants, Bacopa monnieri and Centellaasiatica. Research evidences clearly indicate that both plants possess neuroprotective properties, have nootropic activity with therapeutic implications for patients with memory loss. The field has witnessed exciting patent activity with most inventions aiming at either (i) improving the methods of herbal extraction or (ii) enrichment and purification of novel compounds from brahmi or (iii) providing novel synergistic formulations for therapeutics in various human ailments. In this review, clinical trials related to the therapeutic properties of brahmi and current patents relevant to the preparation, composition and application have also been included.

Randomized controlled trial of standardized Bacopa monniera extract in age-associated memory impairment. Raghav S1, Singh H, Dalal PK, Srivastava JS, Asthana OP.(Author information) Abstract BACKGROUND: Brahmi (Bacopa monniera) is a traditional Indian medicinal plant which causes multiple effects on the central nervous system. The standardized extract of this plant has shown enhanced behavioural learning in preclinical studies and enhanced information processing in healthy volunteers. AIM: To study the efficacy of standardized Bacopa monniera extract (SBME) in subjects with age-associated memory impairment (AAMI) without any evidence of dementia or psychiatric disorder. METHODS: A double-blind, placebo-controlled randomized study design was employed. The subjects received either 125 mg of SBME or placebo twice a day for a period of 12 weeks followed by a placebo period of another 4 weeks (total duration of the trial 16 weeks). Each subject was evaluated for cognition on a battery of tests comprising mental control, logical memory, digit forward, digit backward, visual reproduction and paired associate learning. RESULTS: SBME produced significant improvement on mental control, logical memory and paired associated learning during the 12-week drug therapy. CONCLUSION: SBME is efficacious in subjects with age-associated memory impairment.

Bramhi

Effects of a standardized Bacopa monnieri extract on cognitive performance, anxiety, and depression in the elderly: a randomized, double-blind, placebo-controlled trial. Calabrese C1, Gregory WL, Leo M, Kraemer D, Bone K, Oken B. Author information

Abstract OBJECTIVES: Study aims were to evaluate effects of Bacopa monnieri whole plant standardized dry extract on cognitive function and affect and its safety and tolerability in healthy elderly study participants. DESIGN: The study was a randomized, double-blind, placebo-controlled clinical trial with a placebo run-in of 6 weeks and a treatment period of 12 weeks. SETTING/LOCATION: Volunteers were recruited from the community to a clinic in Portland, Oregon by public notification. SUBJECTS: Fifty-four (54) participants, 65 or older (mean 73.5 years), without clinical signs of dementia, were recruited and randomized to Bacopa or placebo. Forty-eight (48) completed the study with 24 in each group. INTERVENTIONS: Standardized B. monnieriextract 300 mg/day or a similar placebo tablet orally for 12 weeks. OUTCOME MEASURES: The primary outcome variable was the delayed recall score from the Rey Auditory Verbal Learning Test (AVLT). Other cognitive measures were the Stroop Task assessing the ability to ignore irrelevant information, the Divided Attention Task (DAT), and the Wechsler Adult Intelligence Scale (WAIS) letter-digit test of immediate working memory. Affective measures were the State-Trait Anxiety Inventory, Center for Epidemiologic Studies Depression scale (CESD)-10 depression scale, and the Profile of Mood States. Vital signs were also monitored. RESULTS: Controlling for baseline cognitive deficit using the Blessed Orientation-Memory-Concentration test, Bacopa participants had enhanced AVLT delayed word recall memory scores relative to placebo. Stroop results were similarly significant, with the Bacopa group improving and the placebo group unchanged. CESD-10 depression scores, combined state plus trait anxiety scores, and heart rate decreased over time for the Bacopa group but increased for the placebo group. No effects were found on the DAT, WAIS digit task, mood, or blood pressure. The dose was well tolerated with few adverse events (Bacopa n = 9, placebo n = 10), primarily stomach upset. CONCLUSIONS: This study provides further evidence that B. monnierihas potential for safely enhancing cognitive performance in the aging.

Ashwagandha for stress relief

Direct evidence for GABAergic activity of Withaniasomniferaon mammalian ionotropicGABAA and GABA?receptors. CandelarioM1, Cuellar E1, Reyes-Ruiz JM2, DarabedianN3, Feimeng Z3, Miledi R2, Russo-NeustadtA1, Limon A4. Author information Abstract ETHNOPHARMACOLOGICAL RELEVANCE: Withaniasomnifera(WS) has been traditionally used in Ayurvedicmedicine as a remedy for debility, stress, nervous exhaustion, insomnia, loss of memory, and to enhance cognitive function. This study provides an empirical evidence to support the traditional use of WS to aid in mental process engaging GABAergicsignaling. AIM OF THE STUDY: We evaluated the effect of aqueous WS root extract (aqWS), and its two main components, withaferinA and withanolideA, on the main inhibitory receptors in the central nervous system: ionotropicGABAA receptors. MATERIALS AND METHODS: The pharmacological activity of aqWS, withaferinA and withanolideA, was tested on native rat brain GABAA channels microtransplantedinto Xenopusoocytes and GABA?1 receptors heterologouslyexpressed in oocytes. The GABAergicactivity of aqWScompounds was evaluated by the two-electrode voltage-clamp method and the fingerprint of the extract was done by LC-MS. RESULTS: Concentration-dependent inward ion currents were elicited by aqWSin microtransplantedoocytes with an EC50 equivalent to 4.7 mg/mL and a Hill coefficient (nH) of 1.6. The GABAA receptor antagonist bicucullineblocked these currents. Our results show that aqWSactivated inotropic GABAA channels but with lower efficacy compared to the endogenous agonist GABA. We also demonstrate for first time that aqWSis a potent agonist of GABA?1 receptors. GABA?1 receptors were 27 fold more sensitive to aqWSthan GABAA receptors. Furthermore, aqWSactivated GABA?1 receptors eliciting maximum currents that were no significantly different to those produced by GABA (paired t-test; p=0.533). The differential activity on GABAA and GABA ?1 receptors and the reported lack of significant GABA presence in WS root extract indicates that the GABAergicactivity of aqWSis not mediated by GABA. WS main active components, witaferinA and withanolideA, were tested to determine if they were responsible for the activation of the GABA receptors. Neither compound activated GABAA nor GABA?1 receptors, suggesting that other constituent/s in WS are responsible for GABAA receptor mediated responses. CONCLUSIONS: Our results provide evidence indicating that key constituents in WS may have an important role in the development of pharmacological treatments for neurological disorders associated with GABAergicsignalingdysfunction such as general anxiety disorders, sleep disturbances, muscle spasms, and seizures. In addition, the differentialactivation of GABA receptor subtypes elucidates a potential mechanism by which WS accomplishes its reported adaptogenicproperties.

A double-blind, placebo-controlled evaluation of the anxiolytic efficacy ff an ethanolic extract of withania somnifera. Andrade C1, Aswath A, Chaturvedi SK, Srinivasa M, Raguram R. Author information Abstract A double-blind, placebo-controlled study was conducted to evaluate the efficacy an ethanolicextract of Aswagandha (Withania somnifera), in patients with ICD10 anxiety disorders. The sample comprised 39 subjects, of whom 20 received the drug and 19 received placebo. The two groups were sociodemographically and clinically similar at baseline. At 2 and 6 weeks follow-up, data from approximately 85% of patients in each group were available for analysis. Statistical trends favouring the drug were observed at both time points. At 6 weeks, significantly more patients met a priori response criteria in the drug group (88.2%) as compared with the placebo group (50%). The drug was well-tolerated and did not occasion more adverse effects than did placebo. It is concluded that this ethanolicextract of Withania somnifera has useful anxiolytic potential and merits further investigation.

Ashwagandha for stress relief

Naturopathic care for anxiety: a randomized controlled trial ISRCTN78958974. Cooley K1, SzczurkoO, PerriD, Mills EJ, Bernhardt B, Zhou Q, Seely D. Author information Abstract BACKGROUND: Anxiety is a serious personal health condition and represents a substantial burden to overall quality of life. Additionally anxiety disorders represent a significant cost to the health care system as well as employers through benefits coverage and days missed due to incapacity. This study sought to explore the effectiveness of naturopathic care on anxiety symptoms using a randomized trial. METHODS: Employees with moderate to severe anxiety of longer than 6 weeks duration were randomized based on age and gender to receive naturopathic care (NC) (n = 41) or standardized psychotherapy intervention (PT) (n = 40) over a period of 12 weeks. Blinding of investigators and participants during randomization and allocation was maintained. Participants in the NC group received dietary counseling, deep breathing relaxation techniques, a standard multi-vitamin, and the herbal medicine, ashwagandha(Withaniasomnifera) (300 mg b.i.d. standardized to 1.5% with anolides, prepared from root). The PT intervention received psychotherapy, and matched deep breathing relaxation techniques, and placebo. The primary outcome measure was the Beck Anxiety Inventory (BAI) and secondary outcome measures included the Short Form 36 (SF-36), Fatigue Symptom Inventory (FSI), and Measure Yourself Medical Outcomes Profile (MY-MOP) to measure anxiety, mental health, and quality of life respectively. Participants were blinded to the placebo-controlled intervention. RESULTS: Seventy-five participants (93%) were followed for 8 or more weeks on the trial. Final BAI scores decreased by 56.5% (p0.0001) in the NC group and 30.5% (p 0.0001) in the PT group. BAI group scores were significantly decreased in the NC group compared to PT group (p = 0.003). Significant differences between groups were also observed in mental health, concentration, fatigue, social functioning, vitality, and overall quality of life with the NC group exhibiting greater clinical benefit. No serious adverse reactions were observed in either group.

Ashwagandha (Withania somnifera) reverses B-amyloid1-42 induced toxicity in human neuronal cells: implications in HIV-associated neurocognitive disorders (HAND). Kurapati KR1, Atluri VS, SamikkannuT, Nair MP.Authorinformation Abstract Alzheimer's disease (AD) is characterized by progressive dysfunction of memory and higher cognitive functions with abnormal accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles throughout cortical and limbic brain regions. At present no curative treatment is available, and research focuses on drugs for slowing disease progression or providing prophylaxis. Withaniasomnifera(WS) also known as 'ashwagandha' is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer. However, there is a paucity of data on the potential neuroprotective effects of W.somniferaagainst B-Amyloid (1-42)-induced neuropathogenesis. In the present study, we have tested the neuroprotective effects of methanol:Chloroform(3:1) extract of ashwagandhaagainst B-amyloid induced toxicity and HIV-1Ba-L (clade B) infection using a human neuronal SK-N-MC cell line. Our results showed that B-amyloid induced cytotoxic effects in SK-N-MC cells as shown by decreased cell growth when tested individually. Also, confocal microscopic analysis showed decreased spine density, loss of spines and decreased dendrite diameter, total dendrite and spine area in clade B infected SK-N-MC cells compared to uninfected cells. However, when ashwagandhawas added to B-amyloid treated and HIV-1 infected samples, the toxic effects were neutralized. Further, the MTT cell viability assays and the peroxisome proliferator-activated receptor-? (PPAR?) levels supported these observations indicating the neuroprotective effect of WS root extract against B-amyloid and HIV-1Ba-L (clade B) induced neuropathogenesis.