Poor Sleep and Weight Gain Relationship

Poor Sleep and Weight Gain Relationship

Poor sleep and an obesity profile – Is there a link? Yes, indeed there is. There is well-documented research on the intimate relationship that sleep plays on our BMI (Body Mass Index). In fact, in just one of the studies conducted, perhaps the largest conducted across 1.1 million participants a survey was conducted on sleep duration and frequency of insomnia across the group[1].

An increase in BMI occurred for habitual amounts of sleep less than the recommended 7-8 hours per night. So, if you’re frequently having low levels of sleep, which is less than the recommended 7-8, you will likely see an association with this lack of sleep and weight gain[1,2,3].

Weight Gain?

Ok, so I get less sleep than recommended sure, but how does this equate to weight gain? What does sleep do for me at 8 hours vs 5 for example and weight? Appetite hormones and sleep are directly related in function and reliability.

Leptin, which is a peptide hormone that is secreted from our white adipocytes (fat cells), aids in the regulation of food intake and energy balance. Leptin acts on our central governing nervous system, within this system we have the hypothalamus in the brain – signaling to the hypothalamus as well as insulin-induced changes in lipid/fat metabolism in the body dictate when we are feeling satisfied. This is our ‘satiety hormone’ better known in this industry as such and sleep has a lot to do with leptin which we will breakdown below.

Ok, so I just need more leptin?

Not exactly. Much like insulin resistance, there is a metabolic disorder associated with what is now titled as ‘Leptin Resistance’ and this is where, even with high levels of leptin available in the body – the tissues are no longer receptive to it, receptors are not recognizing this peptide hormone any longer or at the very least in minimum amounts.

High levels of leptin are not a good thing. Leptin, although a necessary hormone - still falls under the common discussion piece of “more is not always better”. Leptin is pro-inflammatory, and in most cases, those with a profile of obesity have excessive amounts of leptin present that appear invisible to the leptin receptors. This seems to confirm the theory that obesity is actually a low-grade pro-inflammatory state[4]. Three common findings in obesity are excessive levels of pro-inflammatory markers/cytokine expression:

  • High levels of Leptin.
  • Interleukin-6 (Pro-inflammatory cytokine/ anti-inflammatory Myokine).
  • Tumour Necrosis factor-α.

    The sparring of Ghrelin and Leptin

    Our hunger hormones, most of us have heard of these two:

    • Ghrelin makes our stomach growl.
    • Leptin leaves us satisfied.

      The easy way we usually associate remembering their roles in the body. These two hormones function to maintain energy homeostasis in the body when functioning correctly. Ghrelin is a peptide hormone produced by the stomach, kidneys, hypothalamus and pituitary gland. Its purpose is to:

      • Drive appetite.
      • Fat production for energy storage.
      • Growth of our body/growth Hormone production.
      • Stimulation of Prolactin production.
      • Stimulation of Adrenocorticotropic hormone (ACTH) via signaling to the pituitary gland. ACTH makes our adrenals capable of response to stress triggers and secretion of cortisol.
      • Diabetogenic effect on Carbohydrate metabolism, this means that it acts as an antagonist to insulin secretion/aims to suppress it.

        This drives us to consume food for survival and growth and leptin comes in usually soon after once signaling has come through as we mentioned above, to have us say ‘ahh, I’m satisfied’. This is the prediction model for the usually expected function of these two peptide hormones. Insulin-like leptin is a signal for decreased feeding behavior. Both are directionally proportional to levels of white fat/white adipocytes in the body and their ability to regulate weight and energy status[5,6].

        Poor sleep and satisfaction

        In another recent population-based study, conducted on 1024 participants in a Wisconsin sleep cohort study; subjects found to receive less than the adequate recommended sleep value of 8 hours showed a direct increase in BMI[7,8]. This directional correlation was concluded when shorter sleep cycles habitually, showed an increase in Ghrelin levels and a decrease in Leptin. This hormonal profile ratio instigates what is commonly seen in:

        • Decreased energy expenditure/fatigue.
        • Higher appetite.
        • Obesity/weight gain.

          There is one caveat to this and that is both the stage of sleep and the type of hormone present at the time. A variable that has been newly established in the current literature. Administration of leptin and ghrelin can alter sleep itself, pulling somewhat of a reverse UNO on everything we just lead to up until now. How? Well, in the recent example ghrelin administration appeared to increase non-rem sleep in both humans and mice in the studies conducted[9]. This is possibly due to its role in the growth hormone-releasing hormone (GHRH). More research is being conducted in this area at current on patients with a correlation of high ghrelin levels and sleep apnoea compared with matching BMI control subjects.

          REM (Rapid Eye Movement) Sleep dictates Leptin levels upon waking

          We established above that higher levels of ghrelin induce larger amounts of non-REM sleep in total, in comparison to that of leptin where there is little impact on leptin levels from non-REM. Changes in waking levels of leptin occur when we are getting rem sleep, and below we will explain this in more detail.

          Higher levels of REM sleep lead to a reduction of waking leptin – this is important to note because you don’t want constantly high levels of leptin, you want functioning leptin receptors that are sensitive to leptin. Remember we discussed earlier what leptin resistance was. So, in the instance of REM sleep which is the Rapid Eye Movement phase of sleep, most adults get a few good hours of REM[10,11]. This allows a reduction of serum leptin while we sleep so that when we wake our receptors are sensitive and ready for this hormone once excreted. Which makes sense, we aren’t eating while we are asleep.

          Poor levels of REM sleep – leads to poor leptin sensitivity as there is no real alterations or necessary reduction in serum levels upon waking. This goes hand in hand with other studies that suggest that little amounts of REM achieved lead to lower levels of leptin, but more so in fact lower secretion as serum levels are attempted to be accounted for[12].

          The vicious cycle of poor sleep

          We have now covered off that higher amounts of leptin present also expose us to a pro-inflammatory state of being, when we are less receptive to leptin at the receptor sites the body is signaled to produce more in an attempt to at least get some coming through to facilitate the function of leptin in its normal state. These higher levels of leptin facilitate the increased secretion of pro-inflammatory cytokines such as:

          • Tumour Necrosis Factor.
          • Interleukin-1.
          • Interleukin-6.

            Conversely, from here these inflammatory cytokines actually loop back to increase the production of leptin in adipose tissue creating an inflammatory cytokine storm[13].

            We all know what comes in to mediate inflammation… cortisol. So you have this big loop happening, poor sleep from high cortisol from poor sleep, higher Ghrelin levels as a result, lower sensitivity to high serum levels of leptin, higher inflammation, higher demand on cortisol to mediate the inflammation, which places more demand on Ghrelin’s function in the production of ACTH and Cortisol from the adrenals and high levels of cortisol indicate a stress response and survival response. Cortisol acts as an antagonist to insulin shuttling glucose to muscle stores and rather instead, creating an insulin resistance profile.

            Higher ghrelin means we eat more, in a high inflammatory state, more is stored as fat tissue due to the cortisol switching off glycogen storage and long-term survival in the form of fat as energy and we have ourselves the perfect recipe for an Obesity profile.

            The bottom line?

            Find ways to improve your sleep, if you are intentionally giving no regard to the importance of your sleep, then let this be an eye-opener to nurture the need for sleep especially if you are a health-conscious person or working towards a physique goal and wondering why you are having to push so much harder to hit these goals.

            Getting insatiable cravings for sweet things after a meal (insulin resistance sign 101) and binging on sweets, staying up late, and having things that interrupt your capacity to reach REM, etc. Control what you can and start placing more importance on the quality of your sleep and your health with thank you for it.


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            9. Rhythms of ghrelin, leptin, and sleep in rats: effects of the normal diurnal cycle, restricted feeding, and sleep deprivation. Bodosi B, Gardi J, Hajdu I, Szentirmai E, Obal F Jr, Krueger JM Am J Physiol Regul Integr Comp Physiol. 2004 Nov; 287(5):R1071
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            11. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. Spiegel K, Leproult R, L'hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E J Clin Endocrinol Metab. 2004 Nov; 89(11):5762-71.
            12. Olson, C. A., Hamilton, N. A., & Somers, V. K. (2016). Percentage of REM sleep is associated with overnight change in leptin. Journal of sleep research, 25(4), 419–425. https://doi.org/10.1111/jsr.12394
            13. Endotoxin stimulates leptin in the human and nonhuman primate.Landman RE, Puder JJ, Xiao E, Freda PU, Ferin M, Wardlaw SL J Clin Endocrinol Metab. 2003 Mar; 88(3):1285-91.