Introduction
At this point, most people working in the health and fitness industry know not to sleep on the importance of sleep. It’s been permeating the health and fitness industry and even in the mainstream conversation of those not in health and fitness. Information about sleep quality and quantity are showing up on more and more client intake forms and check-in sheets, and for good reason.
For those not familiar, sleep deprivation can lead to a host of short and long term consequences, including aberrancies in thyroid, adrenal health, gut health, and overall transformation capacity. Sleep loss lowers satiety hormones, raises hunger hormones, tanks testosterone in men, and much more.
A Recap on Sleep Hygiene Basics
If only it was as easy as telling your clients to sleep a good quality 8 hours. Many people suffer from sleep latency issues, insomnia, and much more, and much of this is due to the discrepancy in the modern environment versus the environment we evolved in.
There are certain baseline sleep and circadian hygiene practices that facilitate good sleep, which this section will serve as a reminder of. The basics of sleep hygiene include:
- Getting as much morning sunlight exposure to the eyes as possible within 30-60 minutes of waking (10 min minimum).
- Use of blue light blocking glasses if watching TV/engaging in electronics
- If the above doesnt work, an entire electronics cutoff 1-2 hours before bed is warranted.
- Keeping your bed and bedroom only for sleep and sex – No working there
- Keeping your sleeping environment as dark and cool as possible (optimal temperature for sleep quality in studies is 67 F – It should feel chilly to you if you’re not under the covers)
- Cutting off food intake 2-3 hours before bed. But what happens when you’re doing all of the typical sleep hygiene practices and are still suffering from insomnia or poor sleep and fatigue during the day? These are 6 lesser thought-about issues that may be preventing you from getting the good nights rest you need.
What happens, though, when you or your client is doing all of the above perfectly and is still struggling to either fall asleep, getting night wakeups, or still feeling not rested upon waking? If this is you or you have a client like this, you’ve landed on the right post.
Going Beyond the Basics – 6 Overlooked Factors Affecting Sleep
- Obstructive sleep apnea (OSA)
OSA is a disorder caused by upper airway obstruction during sleep, and its both more common and more problematic than you might think. During these episodes, the arterial oxygen saturation falls, which can lead to autonomic dysregulation.
Regulation of the autonomic nervous system is incredibly important for health; this means being in a fight or flight state at the appropriate time (working out, when facing a threat, etc) and being in a rest-and-digest state at the appropriate time (the other 20 hours of the day). The autonomic dysfunction that can occur during OSA basically puts people in a sympathetic nervous system dominant state 24/7, making it nearly impossible to manage stress correctly from a physiological point of view.
These acute changes result over time in increased risk of many chronic conditions: Insulin resistance, metabolic syndrome and type 2 Diabetes, cardiovascular disease, pulmonary disease, and neurocognitive disease. According to a review by Benjafield et al that looked at OSA in over 16 countries, approximately 1 billion people aged 30-65 years are affected by it, and 425 million of those deemed to have moderate to severe OSA.
Basically, 1/8th of the world’s population (probably more since they just looked at 16 countries) is affected by sleep apnea to some degree.
This is a seriously overlooked factor for a lot of coaches that may be keeping their overweight or obese clients from getting the results they desire in both body transformation and health. If you have an obese or high lean mass/large necked client (such as a bodybuilder), it should be a priority question to ask them if they’ve ever done a sleep study to be evaluated for it, and if not, ask if they snore and/or if their partner or spouse has noticed they stop breathing at night. These are tell-tale signs.
OSA produces a chronic inflammatory state, which leads to increased atherosclerotic changes in the blood vessels of an individual. Similar to obesity, which is also considered a low-grade inflammatory state, OSA has been shown to stimulate the white adipose tissue (WAT) leading to the production of inflammatory mediators. OSA leads to sleep fragmentation, low oxygen and increased carbon dioxide in the blood, which in turn, stimulates increased sympathetic activity, increased RAAS signaling, both of which will result in hypertension, increased systemic inflammation, and increased oxidative stress. The end result of these changes is endothelial dysfunction and metabolic dysfunction which accounts for the increase in cardiovascular disease and T2DM.
Therefore, if you have a client with OSA, they’re going to be in a chronic inflammatory state even if they’re not obese, which is going to affect everything from physical transformation to health outcomes.
Risk factors for OSA:
- Obesity and high BMI are the biggest independent risk factors
- Neck circumference greater than 17 inches (43cm) in men and 15 inches (38cm) in women irrespective of BMI status
- This is one of the reasons bodybuilders suffer from OSA at similar rates as obese individuals – neck circumference plays a large role independent of obesity
- Being male or a postmenopausal woman (estrogen/progesterone have roles in maintaining good upper airway tone, and progesterone is a natural bronchodilator (opens airways))
- >50 years of age
- Being on testosterone replacement therapy
- One study tracked men as they began TRT, doing a sleep study before and a sleep study after. Prior to TRT, none of the men had sleep apnea. After beginning TRT, 52% of the men developed sleep apnea.
- Alcohol consumption can exacerbate OSA in those who already have it by causing increased relaxation of the upper airway, contributing to upper airway collapse.
- Eating large meals closer to bedtime also causes increased relaxation of the upper airway.
Treatment Options
The biggest effect is going to be reducing body fat levels into a healthy range. For many people this will get rid of their apnea, however, folks with apnea may need treatment in order to help reach their weight loss goals given that OSA will reduce overall daytime energy levels as well as produce an inflammatory state.
For that, the gold standard is a CPAP machine; CPAP stands for continuous positive airway pressure. The machine delivers a stream of oxygenated air into the lungs during sleep. Treatment with a CPAP has been shown to alleviate a lot of the negative side effects associated with sleep apnea. It may take a week or two for you or your client to get used to sleeping with a CPAP, as it’s a bit unwieldy.
Mandibular advancement devices (MADS) are another option. These are little devices you place in your mouth that work by forcing the jaw and tongue forward during sleep. In studies, it doesn’t show as much efficacy as a CPAP in reducing hypertension and other risk factors associated with sleep apnea, but it does improve them over no treatment, and in all studies compliance with MADs was better than CPAPs. CPAPs can be unwieldy and are not exactly comfortable.
For non-obese individuals that just have large necks (bodybuilders etc); if the individual does not want to lose lean mass to help with neck size reduction, then a CPAP or MAD is advised.
2. Dietary Sensitivities and Gut Dysbiosis
The gut influences most of our physiology, and in this case it influences sleep as well through the gut-brain axis. It’s rather obvious that actual symptoms such as bloating, gas, diarrhea, etc can interrupt sleep just from physical discomfort, but even if gut-related symptoms aren’t present, a dysbiosis can still potentially lead to issues with insomnia. In addition to dysbioses, dietary intolerances can potentially elevate histamine, and histamine is a wake-promoting chemical amongst other things.
You may be thinking, “Is it the chicken or the egg?”. Does sleep deprivation alter the microbiome or does the dysbiosis of the microbiome alter sleep? Well the answer is that it might be both. Surprisingly, not many studies have been done looking at the effects of sleep restriction on the microbiome, but the ones that have been done have conflicting results.
In two studies looking at sleep deprivation’s effects on the microbiome, one study looked at 9 healthy men and sleep restricted them over the course of two nights, and looked at fecal microbiome samples before and after. The men had slightly higher firmicutes:bacteroidetes ratio after sleep restriction, which is considered to be more towards an “obesogenic” microbiome profile.
However, another study of 11 men that were restricted to 4 hours of sleep for 20 days showed no significant changes in microbiome status as measured by fecal microbiome sample before and after sleep restriction, so we have some conflicting data. Both of the studies used the same testing methods as well.
We do however, have a solid piece of literature looking at the converse of how dysbiosis affects sleep and sleep architecture. This particular human RCT used actigraphy to quantify sleep measures coupled with gut microbiome sampling to determine how the gut microbiome correlates with various measures of sleep physiology.
The study found positive correlations between total microbiome diversity and better sleep architecture, lower incidences of night waking, and lower sleep latency. Analysis of microbiome composition revealed that within phyla richness of Bacteroidetes and Firmicutes were positively correlated with sleep efficiency as well as lateral thinking and abstract thinking. They also found that several taxa (Lachnospiraceae, Corynebacterium, and Blautia) were negatively correlated with all sleep measures.
Regardless of the chicken or the egg question, we can see that dysbiosis can induce insomnia and lower quality sleep. This is further cemented by looking at studies that tested the effects of probiotics on insomnia. Now, if someone has bad dysbiosis, then a whole gut protocol may be needed, but an easy way to look at changes in the microbiome and its effects on sleep in studies would just be probiotic supplementation since we know that it’s going to alter microbial composition of the gut in some form.
A double-blind, placebo-controlled study of 38 healthy volunteers assigned to an experimental or control group assumed a daily dose of a probiotic mixture (containing Lactobacillus fermentum LF16, L. rhamnosus LR06, L. plantarum LP01, and Bifidobacterium longum BL04) or placebo, respectively, for 6 weeks. Mood, personality dimensions, and sleep quality were assessed four times (before the beginning of the study, at 3 and 6 weeks, and at 3 weeks of washout). A significant improvement in mood was observed in the experimental group, with a reduction in depressive mood state, anger, and fatigue, and an improvement in sleep quality only after 6 weeks. Meaning they didn’t see the benefit in sleep until they’d been supplementing for 6 weeks.
As stated earlier, histamine issues can also result in insomnia. If you’re histamine intolerant, this would be a big contributor. But in general, dietary sensitivities have the ability to increase histamine secretion in the body, which promotes wakefulness.
Once again, if someone has bad gut issues, you probably don’t just want to throw probiotics at it and call it a day; it’ll probably take more than that. That study above was just to illustrate that changing the composition of the gut microbiome can indeed improve sleep.
A better order of operations as a coach would be first cleaning up someone’s diet by eating mostly whole, micronutrient and fiber dense foods. If that doesn’t fix the issue, then you’ll be looking at a 4R/5R elimination diet protocol with use of probiotics, enzymes, and antimicrobials IF needed. Also be on the lookout for histamine intolerance: reactions to leftover foods, fermented foods, cured meats, etc
3. Micronutrient Deficiencies or Excesses
Most people may be familiar with the fact that taking magnesium before bed can help induce sleep regardless of deficiency status, but low levels or deficiencies of certain micronutrients can also potentially lead to insomnia, so let’s go beyond magnesium here.
A large 2017 review study looked at micronutrient deficiencies associated with poor sleep architecture and insomnia. In the articles reviewed, researchers generally supported the role of repletion of iron, magnesium, and vitamin A in improving sleep architecture in the young and reversing age-related decline of sleep architecture.
Micronutrient status has also been linked to sleep duration, with sleep duration positively associated with adequate iron, zinc, and magnesium levels, and negatively associated with elevated copper as found in hair samples.
Potassium and vitamin B12 supplements prior to bed also increased sleep latency and night wake-ups. The mechanisms underlying these relationships include the impact of micronutrients on excitatory/inhibitory neurotransmitters and the expression of circadian genes.
For example, retinoic acid, a metabolite of vitamin A, regulates the expression of two core circadian genes, CLOCK and BMAL1. Magnesium, iron, and zinc play roles in suppressing excitatory neurotransmission. Ensuring appropriate levels of micronutrients is important here, and you may want to avoid taking any large supplemental doses of B12 or potassium prior to bed. Foods containing them are fine, this is more for large supplemental doses.
4. Nocturnal Hypoglycemia or Blood Sugar Instability Throughout the Night
Nocturnal hypoglycemia, and even a drop back to baseline from a blood sugar high can cause increased night wakeups and decreased sleep quality. When blood sugar drops, this causes a release in glucagon and catecholamines in order to increase blood sugar. All of these hormones are wake-promoting and may cause night wakeups.
The obvious individuals who might suffer from these things are individuals with insulin resistance, metabolic syndrome, or T2DM. The post-meal curves of insulin and blood sugar in an individual with metabolic syndrome may result in reactive hypoglycemia regardless of the time of day. The loss or dampening of first-phase insulin response in metabolic syndrome and T2DM results in an exaggerated second-phase insulin response which can drop blood sugar below baseline.
If this particular avatar has any sized meal with carbohydrates prior to bed, they may suffer from a blood sugar low, causing those hormones we talked about earlier to suddenly elevate in order to get them up. This may be one reason that time restricted feeding with an earlier eating window (stopping eating at 6PM) instead of a later eating window (2PM – 10PM for example) may be more efficacious from a health standpoint for those with metabolic syndrome or T2DM as opposed to the average healthy individual. Since the last meal is many hours before bed, this gives the chance for blood sugar to drop and stabilize prior to actually going to bed.
Your body senses relative changes and not necessarily absolute, so a blood sugar drop from a high level, even if it doesn’t necessarily drop below baseline, can also lead to night wake-ups from the same mechanism: increased glucagon + catecholamines. However, for a healthy person with no insulin resistance, this would probably necessitate eating a larger meal prior to bed. Which we know disrupts sleep architecture anyway apart from any sort of blood sugar effects.
For the individual with advanced insulin resistance or Type 2 Diabetes, it would be best to either stop eating 3-4 hours prior to bed, or if they’re very hungry, have a high protein, low-moderate carb with low GI carb snack before bed would be okay.
5. Imbalanced Estradiol and Progesterone
Both estradiol and progesterone play important roles in the regulation of sleep. In animal studies, it has been verified that progesterone is capable of altering the sleep pattern as an agonist of the GABA-A receptors. This effect was reversed when the animals received an antagonist of the GABA-A receptor (meaning the receptor was blocked from progesterone), confirming the relationship between the progesterone and gabaergic receptors. It is very likely that progesterone does not act directly on GABA-A receptors though, but rather involves the activity of a metabolite named allopregnanolone.
In terms of estrogen, evidence coming from estrogen replacement therapy suggests a hypnotic effect, since it ameliorates most of the sleep-related complaints of perimenopausal women. Additionally, data on rodents suggest that estrogen seems to have an important effect on the consolidation of the sleep-wake cycle, as ovariectomized female rats treated with estrogen display a better balance of sleep when compared with the controls.
In this case, estrogen promoted both REM and non-REM sleep during their natural sleep phase and reduced it during the time they were awake. The mechanisms underlying hypnotic effects of estrogen probably involve signaling via E2 receptors on areas such as the ventrolateral preoptic area, involved in sleep onset and maintenance, and the lateral hypothalamus.
It has also been postulated that estrogen may exert its effects through progesterone, as adequate/increased estradiol levels have been shown to increase levels of progesterone receptors.
However, excess estrogen, or when estrogen is out of balance with progesterone, has also been shown to increase glutamate neurotransmitter signaling. Glutamate is one of the brain’s principal excitatory neurotransmitters, so this can also result in anxiety, irritability, and you guessed it – insomnia.
We can kind of see this across the normal menstrual cycle, as well. Evidence suggests that sleep is mostly disturbed during the mid-late luteal phase, when steroidal hormone levels start to decline. During this phase, women tend to experience an increased number of awakenings and arousals during sleep if you look at it compared with the follicular phase.
Taken together, these findings correlate the impact of hormonal oscillations with the onset of sleep complaints. The same impact might be seen across the lifespan, as shifts on hormonal patterns observed during puberty, during pregnancy, and the menopausal transition are associated with increased prevalence of insomnia.
All that being said, if a woman is in a state of health where progesterone is quite low and estradiol is too high, or if both sex hormones are quite low, this is going to affect sleep. Parsing out the cause could be a greater challenge; but I would gauge an individuals whole body stress load in terms of overtraining, under-eating (RED-S), gut dysbiosis, obesity and/or insulin resistance, PCOS, systemic inflammation from another source, etc.
Postmenopausal women can consider hormone replacement therapy here as there are numerous studies showing increased sleep quality and quantity from hormone replacement therapy. When done correctly, there is little risk to estradiol and progesterone replacement post-menopause as long as the route of administration (transdermal for estradiol and oral for progesterone), forms of the hormones (bioidentical estradiol and bioidentical, micronized progesterone), and time course when starting (within 5 years of beginning menopause or in perimenopause) are correct.
6. Past Trauma
PTSD and past trauma can potentially result in alterations of neurobiology and neuroendocrinology that affects sleep. In fact, long-lasting insomnia is a core factor of PTSD that’s well-known amongst the medical community and in scientific literature.
Lesser traumas that don’t necessarily result in a PTSD diagnosis may also have the same effect. Brain changes in those with trauma include volumetric reductions in the hippocampus and anterior cingulate cortex as well as functional dysregulation in the amygdala and medial prefrontal cortex.
The combination of the dysregulation of amygdala and medial prefrontal cortex, as well as reduced volume in the hippocampus result in increased excitatory transmission as well as a lower threshold for excitatory transmission, resulting in it being significantly harder to “come down” as they say.
Prolonged hyperactivity of the amygdala (as in PTSD) might increase the generation of nightmares and alter neural activity in the brainstem and forebrain sleep-regulating centers. The amygdala (together with the hippocampus and ACC) plays a key role in the processing of fear consolidation, fear extinction, and emotional distress, processes that underlie nightmare generation and are capable of affecting activity in the brain stem and hypothalamic autonomic centers.
Again, studies show these structural amygdalar alterations are associated with sleep disturbances not only in PTSD patients, but also in traumatized controls who do not develop the other criteria for PTSD.
The remedy here is to deal with the trauma; easier said than done I know, and can be a long process. Various forms of therapy from CBT to others can assist in non-PTSD trauma and also aid in trauma-induced PTSD, although the latter can be tough to treat.
More promising treatments are on the horizon, however, namely MDMA-assisted psychotherapy, which is showing serious promise in phase III clinical trials right now with efficacy miles above any other drug or therapy currently available.
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