Sleep Well
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Sleep Well

Product Highlights

Sleep Well relaxes your mind, enabling you to unwind, become calm, and drift gently into peaceful, restorative sleep. This proprietary formula enables you to relax deeply, minus any negative long-term side effects. 

  • A multy-level relaxing combination of nature’s best sleeping agents
  • Influences and creates a deeply restful sleep
  • Maintains and modulates stress and sleep mechanisms
  • This formula is not sold to any retailer as a private label or store brand. May be supplemented with Tahiro Sleep Forte spray

    Main Properties

    easy_swallow_capsules, freedom_packet_system, vegan, gluten, non_gmo, no_artificial, made_in_usa, sugar_and_cafeine

    Each packet contains


    Piper methysticum, Kava
    Wrriten by Simon Ido | MCS. Forwarded by Prof. Shoseyov Oded

    Written by: Simon Ido | MSc
    Forwarded by; Prof. Shoseyov Oded. Estimated reading time 4 min, 21 seconds
    Last update, Sep, 2021

    Piper methysticum, Kava

    Kava is a plant used traditionally by Pacific Island societies for its relaxing properties[1, 6, 8, 9]. Kava contains kavalactones, which hold anxiolytic and sleep-inducing properties[8, 10]. Kavalactones have GABAergic properties and also affect the endocannabinoid system[7, 8].


    Piper methysticum, otherwise known as Kava, is a tradi- tional plant native to Pacific societies utilized for cen- turies for its soothing effects[6]. Kava has psychoac- tive properties when consumed and is classified as a narcotic[6].
    Kava’s active components consist mainly of kavalactones[6], which are phenolic polyketides with anxiolytic and analgesic properties supported by over 3000 years of traditional use and recent clinical trials[8]. These effects are achieved through modulation of GABA activity via alteration of lipid membrane structure and sodium channel function, monoamine oxidase B in- hibition, and noradrenaline and dopamine re-uptake inhibition[9]. Kava’s components also act on the cannabinoid receptors[8]. More specifically, yangonin is the only kavalactone to bind to the CB1 receptor[7]. Yangonin is also a potent dopamine antagonist, and is thought to aid in limiting the euphoric actions of the kavalactones at higher concentrations[1].
    Current evidence supports the use of kava for mild, generalized anxiety[5, 9, 10] in both animal and early clinical trials. These placebo-controlled trials show im- provements in neurotic, premenopausal, and chronic forms of anxiety with key themes of reductions in stress, calming effects, and improvements in sleep[9].
    Kava was withdrawn from European markets in 2002 due to concerns over hepatotoxicity, however recent re- search has shown that liver damage can be caused usu- ally only in extremely high doses and alongside consump- tion with alcohol or other drugs via modulation of the cytochrome P450 system (CYP)[9]. Water-based con- sumption methods are considered safer than ethanolic extracts, which is supported by traditional methods of use[9].




    Kavalactones are structurally related to liphophilic lac- tones, and have been characterized since the second half of the 19th century[2]. The six major kavalactones, ac- counting for 96% of kava’s lipid extract fraction, are dehydrokavain, dihydrokavain, yangonin, kavain, dihy- dromethysticin and methysticin[2]. Minor constituents include other kavalactones, chalcones, piperidine alka- loids, and essential oils[2].
    The mode of action for which kavalactones affect the body has been fairly well-studied in vitro. One study showed a fast action on voltage-dependent sodium chan- nels, which contributes to the local anaesthetic and an- ticonvulsive properties of kava[3]. However, it is thought that GABAA, dopamine D2, opioid, and histamine re- ceptor interactions are responsible for kava’s anxiolytic, muscle relaxant, and sleep-inducing effects[3].
    These interactions include reduced excitatory neuro- transmitter release due to blockade of calcium ion chan- nels, enhanced ligand binding (no direct binding as is seen with benzodiazepenes) to gamma-aminobutyric acid (GABA) type A receptors, reversible inhibition of monoamine oxidase B, and reduced neuronal reuptake of noradrenaline (norepinephrine) and dopamine[9]. In an- imal models, it was seen that kavalactones did not bind to GABAA receptors - however, the kavalactones were still able to activate GABAergic effects[9].
    Another study examined yangonin, which is a kavalac- tone that was found to be an agonist to the CB1 receptor in vitro[7]. This has implications that kava affects the en- docannabinoid system as one of its modes of action, and also somewhat describes its anxiolytic effects as cannabi- noid antagonists have previously been studied for their anxiolytic properties[7].

    While fears over kava’s hepatotoxic attributes have been found to be related primarily to excessive dosage and use with alcohol, it is considered largely safe to con- sume, especially if consumed via a water-extraction[9]. There are however also potential drug interactions via modulation of the CYP450 system or P-glycoprotein pump[9]. Frequent and heavy use of kava is discour- aged and can have some detrimental side effects such as dermopathy and lower lymphocyte counts[9]. However, infrequent and social use of kava seems to be fairly safe and effective[4, 9].



    The pharmacological effects of kava has been shown in multiple studies to be statistically significant in reducing anxiety[5, 9, 10].
    These studies and literature searches are early clinical trials, where the patients take about 1-2 months to see an improved anxiolytic effect over the placebo[9]. These placebo-controlled trials also show improvements in neu- rotic, premenopausal, and chronic forms of anxiety with key themes of reductions in stress, calming effects, and improvements in sleep[9].
    Kava also has sleep inducing effects[10] which is thought to be caused by changes of the activity of 5- HT neurons, while its relaxing effects are attributed to activation of the mesolimbic dopaminergic neurons[1].
    In clinical considerations, studies highlight the impor- tance of high-quality herbal material and high standards of manufacturing[9].
    There have been some reported side effects from Kava, mostly in the form of nausea and gastrointenstinal discomfort[1, 9, 10].



    Kava has been traditionally an essential component of many Pacific Island societies, traditionally used during religious and and cultural ceremonies as a psychoactive and used in social settings as an inebriate beverage that elicits relaxation[6, 9].
    As described above, kava can be used in a social set- ting as a water-based extraction (tea) for its relaxing properties[6].
    It can also be recommended by clinicians for use in general anxiety disorder[1, 9, 10].




    [1] S. S. Baum, R. Hill, and H. Rommelspacher. Ef- fect of kava extract and individual kavapyrones on neurotransmitter levels in the nucleus accumbens of rats. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 22(7):1105–1120, 1998.

    [2] A. R. Bilia, L. Scalise, M. C. Bergonzi, and
    F. F. Vincieri. Analysis of kavalactones from piper methysticum (kava-kava). Journal of Chromatog- raphy B, 812(1):203–214, 2004. Biomedically Rele- vant Plant Components: Active Principles and Tox- icants.
    [3] D. Dinh, U. Simmen, K. Berger Beuter, B. Beuter,
    K. Lundstrom, and W. Schaffner. Interaction of var- ious piper methysticum cultivars with cns receptors in vitro.
    [4] E. Ernst. A re-evaluation of kava (piper methys- ticum). British Journal of Clinical Pharmacology, 64(4):415–417, 2007.
    [5] M. Feltenstein, C. Lambdin, M. Ganzera, H. Ran- jith, W. Dharmaratne, N. P. D. Nanayakkara, I. A. Khan, and K. J. Sufka. Anxiolytic properties of piper methysticum extract samples and fractions in the chick social–separation–stress procedure. Phy- totherapy Research, 17(3):210–216, 2003.
    [6] V. Lebot and J. Lèvesque. The origin and distri- bution of kava (piper methysticum forst. f., piper- aceae): A phytochemical approach. Allertonia, 5(2):223–281, 1989.
    [7] A. Ligresti, R. Villano, M. Allarà, I. Ujváry, and
    V. Di Marzo. Kavalactones and the endocannabi- noid system: The plant-derived yangonin is a novel cb1 receptor ligand. Pharmacological Research, 66(2):163–169, 2012.
    [8] T. Pluskal, M. Torrens-Spence, T. Fallon,
    A. De Abreu, C. Shi, and J. Weng. The biosynthetic origin of psychoactive kavalactones in kava. Nature Plants, 5(8):867, 878.
    [9] J. Sarris, E. LaPorte, and I. Schweitzer. Kava: A comprehensive review of efficacy, safety, and psychopharmacology. Australian & New Zealand Journal of Psychiatry, 45(1):27–35, 2011. PMID: 21073405.
    [10] Y. Singh and N. Singh. Therapeutic potential of kava in the treatment of anxiety disorders.


    Read More
    Neuroanatomy of Sleep
    Wrriten by Maya Gosztyla | Neuroscience and Molecular Genetics. Double B.S. degree

    WRITTEN BY MAYA GOSZTYLA. Estimated reading time 4 min, 21 seconds
    Last update, Dec, 2021

    Neuroanatomy of Sleep

    We spend a third of our entire lives asleep. For us and most other animals to spend so much time in such a vulnerable state, it must serve some important evolutionary purpose. Yet, surprisingly, scientists still do not fully understand what sleep is and why we do it. Sleep remains an enigmatic but crucial component of our daily lives. This article will give a brief overview of what we do know about sleep and the brain regions controlling it.


    Sleep can be broken into two major categories: rapid eye movement (REM) sleep and non-REM sleep. Dreaming occurs during REM sleep, which is why the eyes are often moving beneath the eyelids. Your brain waves during REM sleep appear similar to when you are awake. Non-REM sleep is the deeper form of sleep when it is the most difficult to be awakened, characterized by long and slow brain waves. Throughout the night, you cycle between REM and non-REM sleep several times, which each cycle lasting between 1.5 and 2 hours. Most people will undergo between 4 and 6 sleep cycles per night before beginning to approach wakefulness.


    Your brain uses distinct mechanisms to regulate the states of wakefulness, REM sleep, and non-REM sleep. Let’s discuss each of them to understand how they work.


    Wakefulness is largely controlled by neurons in the brainstem, which send signals to the brain via two different circuits. The upper circuit goes to a brain region called the thalamus, which controls movement and sensation. People with damage to this circuit are awake but in an unresponsive vegetative state. The lower circuit connects to several brain regions, including the hypothalamus, basal forebrain, and cortex. This circuit is believed to control the conscious experience of being awake, as damage can result in narcolepsy, a disease of excessive sleepiness.



    How does this neuronal signaling actually work? Neurons communicate via chemicals called neurotransmitters. There are several neurotransmitters with particular importance for maintaining wakefulness. One example is norepinephrine, which is largely produced in a small brainstem region called the locus coeruleus (Latin for “blue dot”, named for the blue norepinephrine that’s highly concentrated there). These signals are important for inducing hyper-wakefulness during a stressful event, such as a life-threatening emergency. Other examples include orexins, which are required for maintaining long periods of wakefulness, and serotonin, which promotes general wakefulness.


    Non-REM sleep is regulated by molecules called somnogens, which gradually accumulate in your body the longer you’re awake and decrease as you sleep. The higher your somnogen levels, the more sleepy you will feel, and as a result, longer periods of wakefulness are followed by longer periods of non-REM sleep. The most well-understood somnogen is adenosine. During wakefulness, adenosine builds up in your brain, causing you to feel more and more tired as the day

    goes on. This system is actually how caffeine works: caffeine prevents adenosine from binding to its receptors, thus blocking adenosine signaling and allowing you to feel less sleepy.


    Non-REM sleep is largely controlled by the preoptic area, a subregion of the hypothalamus. Preoptic neurons inhibit the wakefulness-promoting signals in the brainstem and hypothalamus, increasing the feeling of tiredness. These neurons fire more quickly the longer you stay awake.


    A region of the brainstem called the pons is crucial for REM sleep. Neurons in the pons signal to other neurons in the brainstem medulla and spinal cord in order to produce muscle paralysis. This is why being awakened during REM sleep can sometimes cause “sleep paralysis,” where you are awake but temporarily unable to move. It is also why sleepwalking typically occurs during non-REM sleep, since your muscles are not paralyzed during those stages of sleep.


    The neurotransmitters controlling REM sleep remain poorly understood by science. A molecule called acetylcholine appears to be important for entering REM sleep from a non-REM stage. However, the maintenance of REM sleep does not seem to involve acetylcholine. More research is being done to understand this mysterious dreaming stage of sleep.


    Behind all of the neural circuitry controlling wakefulness, REM sleep, and non-REM sleep, there’s a single master regulator that’s crucial for it all: the suprachiasmatic nucleus (SCN). A subregion of the hypothalamus, the SCN is your body’s pacemaker for circadian rhythms, which are any biological signaling patterns that follow the day-night cycle.


    For our ancient hunter-gatherer ancestors, it would have been crucial to be awake during the day and asleep at night, as the darkness offered protection from predators. To ensure our sleep-wake cycles stay in sync with the day-night cycles, the SCN uses external cues (called zeitgebers, a German word for “time giver”) to predict the time of day and sends signals to the rest of the brain based on this information.


    The most important zeitgeber is light, since a decrease in light indicates the end of the day. This is why exposure to bright device screens at night can interfere with sleep, as it tricks your SCN into thinking that it’s still daytime. Another zeitgeber is melatonin, a hormone released by the pineal gland during periods of darkness. Melatonin supplements are poor at promoting sleep, but they can be useful for training your body to adopt a new sleeping pattern, such as getting used to an earlier wake-up time for school or work.


    • Brainstem

      • Rostral brainstem: The rostral brainstem promotes wakefulness by signaling to the cortex via an upper and lower circuit.
        • [Note: “rostral” means “front,” ie the side where the face is.]
      • Pons: REM sleep
        • Locus coeruleus: The locus coeruleus promotes hyper-wakefulness during highly stress events.
      • Forebrain
        • Hypothalamus
          • Caudal hypothalamus: The caudal hypothalamus promotes the conscious experience of being awake.
            • [Note: “caudal” means “back,” ie the side where the back of the head is.]
          • Preoptic area: The preoptic area promotes non-REM sleep by inhibiting wakefulness-promoting signals from other brain regions.
          • Suprachiasmatic nucleus: The suprachiasmatic nucleus keeps your circadian rhythms in sync with the day-night cycle.
        • Basal forebrain: The basal forebrain promotes the conscious experience of being awake.
        • Thalamus: The thalamus promotes sensation and movement during wakefulness.


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    How long does it take before you start feeling results? Most customers report improved sleep within 3-5 days. For best results, take Sleep Well as part of a sleep practice which may include, consistent bed time, no electronics one hour before going to sleep, no coffee past 3pm, exercise and or nightly body scan meditation.
    Do I have to take both capsules at the same time? Yes. recommended use is to take both capsule at the same time 30 minutes before the desired bed time.
    What is your 30-day money-back guarantee? We formulated the products with your brain on our mind . If for some reason the product didn't work for you, let us know and we'll process your refund.

    a word from our team

    Nir Avraham, MSc. Biochemistry

    Master Formulator

    “The most exiting part in creating our proprietary formulas was witnessing first hand how today’s science proves anciant knowlage”

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