Do you ever wish you could still fall asleep as easily as you did when you were a child?

When I interviewed performance expert Greg G. Wells, PhD for the Eat4Earth series, I asked him what he thought was the #1 determinant of health among food, exercise, and sleep.

He said it was sleep.

According to Zach Bush, MD (who I interviewed twice for Eat4Earth), most Americans are carrying around a 20,000 hour sleep debt by age 40.

Sleep debt has become so pervasive that the World Health Organization declared a sleep deprivation epidemic in developed countries.

Obviously, sleep debt can accrue by not sleeping long enough, but it can also add up by not sleeping well, not spending enough time in the various stages of sleep. This is one reason that sleep debt can remain “hidden” from our awareness.

Hidden Sleep Debt

It is possible to have "hidden" sleep debt by being unaware of poor sleep quality and unaware that sleep debt is accumulating. Many people wake up multiple times per night without realizing it and don't spend enough time in deep sleep, even though they spend enough time asleep. And the consequences of poor sleep quality and sleep debt are much greater than most people realize.

One sign of hidden sleep debt is quickly starting to fall asleep as soon as you lie down in the middle of the day. But not falling asleep when you do that does not mean that you do not have sleep debt.

Consequences of Sleep Debt

Sleep debt degrades key regulators of health, such as ...

• Microbiome diversity
• Gut membrane integrity
• Hormone production and balance
• Detoxification
• Immune system competence and balance
• Insulin sensitivity

The long-term consequences of sleep debt include the main health challenges we all want to avoid, such as ...

1. Hormone deficiencies and dysregulation
2. Obesity
3. Diabetes
4. Heart problems, including heart attack
5. Alzheimer’s Disease
6. Cancer

Sleep could be considered the mother of all health influences.

It's absolutely essential to master sleep if you want to be healthy.

By the way, good sleep is also a key to healthy eating and exercise.

Inadequate sleep makes it more difficult to maintain a healthy diet because sleep debt increases cravings for sugary and processed foods.

It also reduces the ability and desire to exercise.

Sleep issues are a big cause of unwanted weight gain via these obvious mechanisms and also via less obvious factors induced by sleep debt, like gut dysbiosis and inflammation.

Often people can start shedding extra fat just by improving their sleep.

49+ Potential Causes of Poor Sleep and Sleep Debt

Here are some potential causes of sleep debt most people have never heard of in connection to  sleep: 

1. Blunted or dysregulated circadian rhythm
2. Vitamin A deficiency and BCMO1 gene polymorphism
3. Vitamin B2 deficiency
4. Vitamin D deficiency
5. Hidden under-hydration
6. Constipation, toxic bowels, toxic bile, and intestinal hyperpermeability
7. Dysbiosis
8. Liver congestion (cholestasis)
9. Mold toxins
10. Parasites
11. Methylation issues
12. High dopamine
13. Low or high serotonin
14. Dysregulated cortisol
15. Inflammation
16. Hypothyroidism
17. Sleep apnea and upper airway restriction syndrome (UARS)
18. Restless Leg Syndrome
19. Copper deficiency
20. Impaired sulfation
21. Impaired sulfur metabolism
22. Sulfite accumulation
23. SUOX gene polymorphism
24. Deficiencies of magnesium or zinc
25. Molybdenum deficiency
26. MOCS1, MOCS2, MOCS3 Gene Polymorphisms
27. Hydrogen sulfide accumulation
28. Oxidative stress
29. Fasting, caloric restriction, and carbohydrate restriction
30. Deficiencies of riboflavin (vitamin B2), coenzyme Q10, iron, glutathione, NADPH, thiamine (vitamin B1), magnesium, copper, niacin (vitamin B3), vitamin B6, and zinc
31. Manganese toxicity and gene polymorphisms for hemochromatosis
32. Gene polymorphisms affecting coenzyme Q10 synthesis, absorption, and transport
33. Statins and possibly bisphosphonate drugs
34. SQOR, TRT, ETHE1 gene polymorphisms
35. CBS and CTH gene polymorphisms
36. ALDH2 gene polymorphism
37. Deficiency of vitamin B3 or low NAD+/NADH ratio
38. Mitochondrial dysfunction
39. High glutamate activity
40. Traumatic brain injury
41. Estrogen dominance
42. Aluminum toxicity
43. Vitamin B6 deficiency
44. Magnesium deficiency
45. Zinc deficiency
46. Low GABA activity
47. Babesia and Bartonella infections
48. Interference fields and blocked meridians
49. Dysautonomia and Dysfunction of the Vagus Nerve and the Polyvagal System

Let's explore each one.

Blunted or Dysregulated Circadian Rhythm

Your circadian rhythm, sometimes referred to as the "rest-activity" circadian rhythm, is the pattern of activity and rest that your body goes through each day. During the day the body focuses on producing energy and seeking nutrients and other resources. At night the body focuses on maintenance tasks like repairing cells and tissues, synthesizing hormones, recycling neurotransmitters, and removing pathogens and toxic substances (both metabolic byproducts and environmental toxins and toxicants taken in through food, water, air, and through the skin).

This daily rhythm is regulated by biological "clocks" in your brain and other organs. These clocks are set by cues that your body receives from its environment and activity, such as exposure of the retina of your eyes to light, when you eat, when you exercise or engage in other physical activities, when you sleep, and more. 

How well you sleep has a great deal to do with how well your circadian rhythm and its clocks are set and working. Your circadian rhythm can be weak, or it can be strong. If your circadian rhythm is weak, this is often referred to as a "blunted" circadian rhythm, which negatively impacts sleep, is associated with an increased rate of biological aging (R), and increases the risk of all-cause mortality, cardiovascular disease mortality, and cancer mortality (R).

In addition to being strong or blunted, your circadian rhythm can also be well-regulated or dysregulated, which simply means that it is not working correctly. Circadian rhythm can become blunted and/or dysregulated if environmental and activity cues are not clear or occur at unnatural times compared to what humans have evolved to respond to. For example, working at night and sleeping during the day causes a specific type of dysregulated circadian rhythm called "shift work sleep disorder". Another example is "jet lag disorder", caused by large, fast changes in patterns of light exposure and activity as a result of air travel across large distances and time zones.

One of the most important environmental cues for your circadian rhythm is light. Your body determines what time of day it is by the intensity and mix of various colors of light, mainly blue and red, that it senses via the retina of the eyes. If you expose your eyes to an insufficient quantity and intensity of both blue and red light during the day, your body will lack a clear and natural signal of when it is daytime. If you expose your eyes to blue light after sunset, your circadian rhythm will be receiving an unnatural cue indicating that it is still daytime rather than nighttime. 

So, if you spend all day indoors and exposed to typical indoor lighting without enough exposure to natural outdoor daylight from the sun, your circadian rhythm will be blunted and your sleep will not be as deep and restful as it could be. If you also expose your eyes to blue light and/or green light at night, this also blunts and dysregulates your circadian rhythm. Unnatural exposure to blue and green light comes from most indoor lighting, computer and TV screens, and mobile devices like smart phones. This is why it is important to wear "blue-blocking" glasses (that also block green light) at night between sunset and bedtime, and when you get up at night to use the bathroom if you will be turning on any lights that are not 100% red.

With a blunted and/or dysregulated circadian rhythm, it is as if your body is not 100% certain about what it is supposed to do and when it is supposed to do it. For example, you might want to go to sleep at 10 p.m. so that you can wake up feeling rested by 6 a.m., but your body may not be fully certain that 10 p.m. is the time to go to sleep and therefore does not fully shift into sleep mode. Your mind might still be alert, and your body might still feel energetic and oriented to performing activities, instead of feeling sleepy and easily drifting off into sleep. In contrast, with a strong circadian rhythm, your body is very certain about when it is time to go to sleep and therefore makes you feel sleepy and fully shifts into deep, restful sleep.

Since one of the main cues for your brain's circadian clock is light striking the retina of your eyes, your retinas have to be working correctly for this cue to be perceived and relayed to the part of the brain that mains the brain's circadian clock, the suprachiasmatic nucleus. One of the influences on how well the retina works in this regard is vitamin A status, so vitamin A deficiency can cause or contribute to a blunted or dysregulated circadian rhythm. 

Vitamin A Deficiency and BCOM1 Gene Polymorphism

Vitamin A deficiency can disrupt circadian rhythm via several mechanisms that could alter the body's perception of the light-dark cycle via the retina of the eye and the suprachiasmatic nucleus (SCN) in the brain (R, R). 

Vitamin A can be consumed from animal foods, or the body can produce it from beta carotene in plant foods. The body uses an enzyme called beta carotene oxygenase (BCMO) to convert beta carotene to retinol. The gene for this enzyme is known as BCMO1. Some people have genetic variants in this gene that reduce their ability to convert beta carotene to retinol.

Vitamin A and vitamin D3 need to be in balance with one another. Scientific research suggests that the ratio of these nutrients can be quite broad, ranging from 2:1 to 8:1 in terms of consumption of vitamin A to vitamin D3. So most people seem to be vastly under-consuming vitamin A, especially when they are supplementing with vitamin D3.

Vitamin B2 Deficiency

Vitamin B2 is the precursor for flavin adenine dinucleotide (FAD), which is required for the function of blue-light sensing photoreceptors called cryptochromes that are involved in the regulation of biological clocks, including the circadian clocks (R, R). Since intense blue light during the daytime is one of the essential cues that contributes to a strong circadian rhythm, vitamin B2 deficiency could blunt the circadian rhythm by reducing the ability of FAD-dependent cryptochrome photoreceptors to detect differences in the intensity of blue light throughout the day.

Vitamin D Deficiency

Vitamin D deficiency appears to promote sleep disorders via multiple mechanisms (R).

Hidden Under-Hydration & Reduced Circulating Blood Volume

In my own experiences with sleep challenges, under-hydration has been one of the main causes. I use the term "under-hydration" because I'm referring to a subtle level of suboptimal hydration, not overt dehydration that causes obvious, classic symptoms like dry mouth, feelings of thirst, headaches, or muscle cramps. I'm talking about a level of suboptimal hydration that most people do not realize is occurring. In that sense, it is "hidden" under-hydration.

A small amount of research has identified associations between hydration status and sleep outcomes like sleep duration, but the mechanisms and direction of causality are not clear. Some observers note that the uncomfortable, classic symptoms of dehydration could interfere with sleep. But with what I am calling hidden under-hydration, it's not obvious that there is a hydration issue, and the mechanism by which sleep is negatively impacted is not via the discomfort of classic symptoms of dehydration.

Hidden under-hydration, and overt dehydration, are very common among people with chronic fatigue, mold illness, Lyme disease, other chronic infections, and other conditions that impair the function of the hypothalamus, pituitary gland, adrenal glands, and kidneys, which together regulate blood volume. In general, under-hydration that accompanies these conditions is probably due to low production of antidiuretic hormone by the pituitary gland, aldosterone by the adrenal glands, and/or reduced kidney function.

Hypothalamus-pituitary axis (HPA) dysregulation, hypoadrenalism, dysautonomia, and reduced kidney function can independently or synergistically contribute to reduced blood volume. And this can be worsened by insufficient intake of water and/or dietary sodium (salt). Fasting and low-carb diets tend to cause loss of sodium, which would contribute to reduced blood volume.

2 a.m. and 4 a.m. is the time window during which the body is maximally sensitive to the reduced blood circulating volume. So an adrenal response to low blood volume involving a spike in cortisol and adrenaline is most likely to occur during this time window and cause the person to wake up.

Based on my experiences and how the body regulates fluid balance, I hypothesize that in people who do not produce enough antidiuretic hormone and/or aldosterone, under-hydration could affect sleep via a mechanism related to reduced blood volume.

With under-hydration, blood volume is slightly below normal, causing a drop in blood pressure and a reduction in circulation of blood to the tissues of the body. In people whose hypothalamus, pituitary gland, adrenal glands, and kidneys are working normally, the body could solve (or entirely avoid) the problem of reduced blood volume by increasing production of antidiuretic hormone (vasopressin) and/or aldosterone to signal the kidneys to retain more fluid and maintain appropriate blood volume.

But in people whose bodies do not effectively regulate fluid retention and blood volume, a drop in blood volume caused by under-hydration would require the heart to pump harder and/or more frequently to sufficiently circulate the reduced blood volume to the tissues. In order for this to occur, the nervous system and adrenal glands may secrete neuro-hormones like adrenaline to boost heart function, which increases alertness and impairs sleep.

The heart also has its own internal regulatory mechanisms for adjusting its activity in response to conditions like shifts in blood pressure. The heart engages in cross talk with adrenal glands, and this is mediated by catecholamine neuro-hormones like adrenaline (epinephrine) and noradrenaline (norepinephrine) (R). Even small amounts of cardiac stress in response to suboptimal blood volume would likely elevate systemic catecholamine signaling, leading to increased alertness and impaired sleep..

Constipation, Toxic Bowels, Toxic Bile, and Intestinal Hyperpermeability

Somewhat related to under-hydration, constipation, especially when the contents of the bowel are toxic, can be a significant cause of sleep disturbances. The lower portion of the colon, especially the sigmoid colin, is very efficient at absorbing the water, electrolytes, and other contents of the feces.

If the feces contain a lot of toxic substances, such as those that the body is trying to get rid of via the bile, some of the toxic substances can be absorbed into the portal vein and travel directly back to the liver. This causes the liver to have to work harder, and when this occurs at night, the stress that the liver experiences often wakes people up between 1 a.m. and 3 a.m. at night, the time when the liver is most active, according to Traditional Chinese Medicine. 

The feces can also be toxic due to bacteria and/or parasites that produce endotoxins and waste products like ammonia. Overgrowth of bacteria in the small intestine can also produce more hydrogen sulfide than the body can process, potentially resulting in mitochondrial dysfunction and high levels of neurotoxic sulfite, S-sulfocysteine (a glutamate analog that triggers the NMDA receptor), and glutamate, factors that promote sleep challenges and are discussed further below.

Toxic bowels become especially problematic if the bowels have developed hyperpermeability ("leaky gut syndrome"). One of the most common causes of hyperpermeability is dysbiosis.

Dysbiosis

Dysbiosis is a term used to describe an imbalanced gut microbiome in which there are too many pathogenic bacteria and/or too few beneficial bacteria. Some types of dysbiotic bacteria such as Klebsiella pneumoniae produce an enzyme called beta glucuronidase that "deconjugates" toxins and toxicants from the glucuronic acid that was used in "phase 2" detoxification processes to conjugate (bind with) toxins or toxicants to make them easier to eliminate from the body (typically via the bile).

Other types of bacteria that sometimes overgrow in the small intestine produce high amounts of phenols that can be problematic for people that cannot readily clear these phenols via sulfation, a "phase 2" detoxification process, leading to an accumulation of dopamine, which can cause symptoms like anxiety and insomnia, as described later in this article.

Many pathogenic bacteria have components of their outer membrane generally referred to as endotoxin, one of which is lipopolysaccharide (LPS). LPS is a strongly inflammatory, and in the liver this inflammation causes a reduction in bile excretion, leading to "cholestasis" (congestion and stagnation of the liver due to reduced bile flow) (R), which contributes to problems with sleep. LPS appears to also affect sleep in a dose-dependent manner, most likely via its effects on the immune system's response to the LPS (R, R, R).

Here are some of the most well-known causes of dysbiosis:

1. Past use of antibiotics, especially if broad-spectrum antibiotics were used and/or if multiple courses were used back-to-back, not allowing time for the microbiome to recover between courses of antibiotics.
2. Chronic stress alters the microbiome in unfavorable ways.
3. A diet with lots of non-organic foods, which carry residues of the herbicide glyphosate, which is a potent antibiotic. Glyphosate contributes to low bile production and excretion, another factor that contributes to dysbiosis.
4. A diet high in processed foods and low in plant polyphenols and fibers.
5. Low stomach acid production (which can be caused by a variety of factors like chronic stress, H. pylori infection, hypothyroidism, and deficiencies in various nutrients, such as iodine and zinc), which impairs the body’s ability to kill pathogenic or opportunistic bacteria that enter the body in food and drinking water.
6. Low bile production, which impairs the body to keep the small intestine clear of bacteria that should not be there. 
7. Sleep deprivation or low-quality sleep alters the microbiome in unfavorable ways.

Here are some less-known causes of dysbiosis:

1. Dysautonomia and/or vagus nerve dysfunction
2. Vitamin B1 deficiency
3. Heavy metal toxicity
4. Parasites
5. Lyme disease
6. Mitochondrial dysfunction in the cells of the small and/or large intestine

Liver Congestion (Cholestasis)

Liver congestion, more technically referred to as "cholestasis", is reduced flow of bile (and the toxins it should carry) out of the liver. When the liver is congested, it does not process toxins effectively, so toxins back up into the blood stream and can inflame the brain. According to Traditional Chinese Medicine, when the liver is congested, the body can feel unsettled at night, especially during the part of the night when the liver is most active, between 1 a.m. and 3 a.m.. Sleep disturbances have been found to be a common feature of people with chronic liver disease (R).

Mold Toxins

Mycotoxins like ochratoxin-A promote liver inflammation (R). And mycotoxins are well-known in the livestock industry to cause liver dysfunction (R) and humans. Mycotoxins are a significant cause of cholestasis.

Parasites

Parasites are often more active at night, potentially irritating the liver with their metabolic waste or movement. On the other hand, parasite infection might increase sleep duration, perhaps as a response of the body to improve its immune response to the parasites since sleep deprivation appears to reduce immunity to parasites (R).

Methylation Issues

Methylation is a process the body uses to add a single carbon atom (and three hydrogen atoms) to other atoms or molecules. Methylation is used in the process of producing melatonin from serotonin, so impaired methylation could impair the synthesis of melatonin, a key factor for sleep. 

Methylation is also used to inactivate the stimulatory catecholamine neurotransmitters dopamine, norepinephrine, and epinephrine. In this process, the enzyme catechol-O-methyltransferase (COMT) transfers a methyl group from S-adenosylmethionine (SAM) to one of these catecholamine neurotransmitters, rendering it inactive. Impairments in the methylation cycle that lower the availability of SAM can result in a reduced ability to clear these neurotransmitters, potentially impairing sleep. And certain genetic variants in COMT genes result in reduced activity the COMT enzyme and reduced clearance of catecholamine neurotransmitters by COMT.

Methylation is also necessary for the final step in the synthesis of melatonin, which plays a key role in managing the sleep/wake cycle. Melatonin is formed when the enzyme acetylserotonin O-methyltransferase (ASMT) transfers a methyl group from SAM to N-acetylserotonin, creating melatonin. So problems in the methylation cycle resulting in low levels of SAM could interfere with the ability to synthesize melatonin.

High Dopamine

Elevated dopamine can promote anxiety, restlessness, and insomnia. As described above, dopamine can be elevated by problems with methylation. Other causes of dopamine elevation are discussed further below.

Low or High Serotonin

Serotonin has a complex relationship with sleep. Serotonin has been found to be necessary for sleep (R), and low blood levels of serotonin are associated with disordered breathing during sleep (R). Yet serotonin levels are lowest during sleep. Serotonin is generally a waking state neurotransmitter, and in obstructive sleep apnea (and probably other types of sleep apnea), the brain increases serotonin signaling in order to rouse the brain from sleep (R). So it seems that low or high levels of serotonin, or dysregulation of serotonin, can promote problems with sleep.

Dysregulated Cortisol

Cortisol can become elevated by many things, including elevated serotonin. A common cause of elevated nighttime cortisol is an "inverted" cortisol rhythm. Normally, cortisol peaks shortly after waking in the morning and declines over the course of the day, reaching it's lowest point at night. But chronic stress (including from chronic illness) can cause the adrenal glands to produce more cortisol than normal at night, causing problems with sleep. 

On the other extreme, if cortisol dips lower than normal at night, this can reduce blood volume and pressure enough to cause a compensatory spike in production of cortisol, adrenaline, and norepinephrine by the adrenal glands in order to raise blood pressure and perfusion of tissues, especially the brain. This was discussed in the section about under-hydration and reduced blood volume.

Inflammation

Another common cause of elevated cortisol is inflammation since cortisol is one of the body's main anti-inflammatory substances. Elevation of cortisol by inflammation can happen at night if the liver is exposed to bacterial endotoxins from the gut (due to dysbiosis and/or intestinal hyperpermeability) or if the liver is exposed to toxins and toxicants that were excreted by the liver when bile is reabsorbed rom the gut. 

Inflammation also elevates serotonin, which needs to be at its lowest level at night to promote sleep since serotonin promotes wakefulness. Chronic inflammation might be a contributor to the type of sleep apnea caused by elevations in serotonin during sleep in response to interruptions in breathing.

Inflammation also interferes with energy production in the mitochondria of the cells. When energy production is compromised by inflammation, many processes related to sleep do not work as well, such as methylation, which depends on the availability of ATP from mitochondrial energy production. 

And when mitochondrial energy production is compromised, it can trigger a stress response that elevates the production of cortisol and adrenaline in an attempt to raise energy production.

Inflammation from pathogens, traumatic brain injury, cancer, cardiovascular disease, and stroke are often associated with disturbed sleep (R).

Hypothyroidism

Hypothyroidism and subclinical hypothyroidism are connected with sleep abnormalities (R, R) and can be caused or contributed to by dysregulated cortisol, liver congestion / cholestasis, inflammatory in the gut, and other factors.

Low thyroid function often causes ...

1. Sluggish liver function and cholestasis, a cause of sleep disturbances discussed previously.
2. Dysregulated cortisol, a cause of sleep disturbances discussed previously. 
3. Estrogen dominance, a cause of sleep disturbances that is discussed later in this document.
4. Mitochondrial dysfunction, a cause of sleep disturbances that is discussed later in this document.
5. Restless leg syndrome, a cause of sleep disturbances that is discussed later in this document.
6. Sleep apnea, a cause of sleep disturbances that is discussed below.

Hypothyroidism is often not detected because the standard approach to diagnosing it is inadequate. Typically, endocrinologists measure only TSH, T4, and T3. If TSH does not exceed 4.5, and if T4 and T3 are within the broad laboratory ranges that define 95% of the population as "normal" or "healthy", then typically hypothyroidism is not diagnosed.

However, this approach misses a far more important signal of hypothyroidism: the ratio of free T3 to reverse T3.  Since reverse T3 competes with T3, the ratio of the two affects how well the thyroid receptor can be activate by T3.  So measuring reverse T3 and calculating the ratio of T3 to reverse T3 is more important than measuring TSH and only looking at whether T3 and T4 are within "normal" laboratory ranges.

Endocrinologists often also fail to test thyroid antibodies, which if elevated are a sign of autoimmune thyroid disease, often referred to as Hashimoto's thyroiditis. This condition can create symptoms of hypothyroidism with normal levels of thyroid hormones (R).

The bottom line is that if a person has low body temperature and/or other signs of hypothyroidism and has a low ratio of free T3 to reverse T3, or elevated thyroid antibodies, they almost certainly have hypothyroidism, regardless of their levels of TSH and thyroid hormones.

Sleep Apnea and Upper Airway Restriction Syndrome (UARS)

Most people are familiar with the phenomenon of sleep apnea, but few have heard of upper airway restriction syndrome (UARS). In both sleep apnea and UARS, the brain wakes up at least partially many times each night due to breathing difficulties. In sleep apnea, the airway typically closes partially or completely, causing partial or complete cessation of breathing. In UARS, the airway does not close, but restriction of the airway diameter forces increased breathing effort. In both cases, the brain responds by waking up at least partially to increase airflow, which leads to less restful sleep. 

Sleep apnea can be caused by obesity and/or hypothyroidism, and UARS seems to be related to underdeveloped jaws, skulls, and airways, a growing issue in industrialized societies where the food supply is increasingly nutrient-deficient and composed of soft foods that require less chewing effort, which is a signal that is necessary for full development of the jaws, skull, and airways.

Restless Leg Syndrome

If you have restless leg syndrome, you already know how it can interfere with sleep. The question then becomes, what causes restless leg syndrome? Restless leg syndrome appears to be caused by malfunctioning dopamine receptors and low levels of iron in the brain connected to chronic inflammation. But the solution is not to increase dopamine or iron because it is not a deficiency of dopamine or iron that is the problem. The solution involves correcting the cause of inflammation and restoring normal function of dopamine receptors and normal iron regulation, which can involve other factors like vitamin A status and copper metabolism.

Copper Deficiency

As described in connection with restless leg syndrome, copper could be involved with iron dysregulation involved with restless leg syndrome.  Copper is also involved with dopamine metabolism. The enzyme that converts dopamine to norepinephrine, dopamine beta hydroxylase (DBH), requires copper as a cofactor. So a deficiency of copper can result in reduced DBH activity and accumulation of dopamine.

Impaired Sulfation

The activity of dopamine beta hydroxylase (DBH) is impaired by phenols (including polyphenols in foods), so an accumulation of phenols can slow down the conversion of dopamine to norepinephrine, leading to higher dopamine. The body uses sulfation to process phenols and various other substances (e.g. some mycotoxins). So if sulfation is impaired, phenols can accumulate, potentially impairing the DBH enzyme and causing dopamine to accumulate, potentially impairing sleep. Sulfation can be impaired by a deficiency of sulfate and/or certain genetic variants in genes that code for sulfation enzymes.

Impaired Sulfur Metabolism

The sulfate needed for sulfation of phenols so that they do not accumulate and potentially cause dopamine to accumulate (as described in the previous section) is generally created in the body by the conversion of sulfite to sulfate by the enzyme oxidase (SUOX). If the conversion of sulfite to sulfate is impaired, sulfite accumulates and promotes sleep-disrupting neurotoxicity and excitotoxicity in the brain via sulfite directly and indirectly by increasing S-sulfocysteine and glutamate, which trigger the NMDA receptor. Another aspect of impaired sulfur metabolism that can affect sleep is the accumulation of hydrogen sulfide, which can also promote the accumulation of sulfite. How sulfite and hydrogen sulfide accumulate and potentially contribute to sleep disturbances is described further in other sections below.

Sulfite Accumulation

Sulfite is directly neurotoxic (R) and promotes excitatory neurotransmitter activity in a variety of ways. For example, promotes the degranulation of mast cells and their release of histamine, which can act as an excitatory neurotransmitter. Thus, sulfite could be a factor in developing allergies or Mast Cell Activation Syndrome. 

When sulfite accumulates, it combines with the amino acid cystine to form S-sulfocysteine, an excitatory neurotransmitter that is an analog of glutamate and activates NMDA receptors. Sulfite also inhibits the enzyme glutamate dehydrogenase, promoting an accumulation of glutamate, an excitatory NMDA receptor stimulating neurotransmitter that becomes excitotoxic in excess. 

Based on what is known about the NMDA receptor, elevated S-sulfocysteine could increase the risk of insomnia, anxiety, depression, eating disorders, obsessive-compulsive tendencies, addiction, and PTSD. It could also have less predictable effects on bipolar disorder, schizophrenia, and ADHD.

Sulfite also inhibits malate dehydrogenase, an enzyme important to energy production in the Krebs/ Citric Acid Cycle. The Krebs / Citric Acid Cycle is the main source of citrate, the primary building block of myelin, the insulating sheath that enables nerves to conduct electrical impulses. So impairment of the Kreb's / Citric Acid Cycle in the brain could lead to demyelination that contributes to neurological issues that could disturb sleep.

Excess sulfite can further disrupt mitochondrial function by opening the mitochondrial permeability transition pore, allowing substances into the mitochondria that should not be there. Impairment of energy production in the brain limits the brain's ability to manage the highly energy-intensive process of regulating neurotransmitters. Lower energy production also reduces the synthesis of myelin. 

Sulfite depletes the electron donor NADPH by activating the enzyme NADPH oxidase that uses NADPH to produce superoxide to fight pathogens. NADPH is required to recycle tetrahydrobiopterin (BH4), a cofactor in the enzymes that convert amino acids into neurotransmitters.

When BH4 gets depleted (for example due to NADPH depletion), this leads to altered neurotransmitter metabolism because the synthesis of many key neurotransmitters depends on BH4. And this can cause problems for sleep.

For example, one of the enzymes that requires BH4 as a cofactor is phenylalanine hydroxylase, the enzyme that converts the amino acid phenylalanine to tyrosine, which is necessary for the production of dopamine, norepinephrine, and epinephrine. Accumulation of phenylalanine competes with the amino acid tryptophan for entry into the brain and also inhibits the enzyme that converts tryptophan into serotonin, the precursor for melatonin. 

Another enzyme that requires BH4 as a cofactor is tryptophan hydroxylase, the enzyme that initiates the process of converting tryptophan into serotonin, which is required to produce melatonin. As you probably know, melatonin is often thought of as the "sleep hormone" because it is an important instigator of sleep, though it has many more functions than promoting sleep.

Usually, the net effect of sulfite-induced neurotransmitter dysregulation tends toward excitatory states like anxiety, mania, OCD, insomnia, chronic pain, hypersensation, and muscle spasticity or tension. The effects of elevated sulfite on sleep are likely due to increases in the excitatory neurotransmitter S-sulfocysteine, accumulation of glutamate via inhibition of glutamate dehydrogenase, and reduced synthesis of serotonin and melatonin via inhibition of hydroxylase enzymes. 

The effects of impaired sulfite clearance on neurotransmitters also increase the risk of seizures, tremors, tics, jerks, Parkinsonian movement disorders, gait disorders, and other neurological disorders.

SUOX Gene Polymorphism

Genetic single nucleotide polymorphisms (SNPs) in the SUOX gene reduce the activity of this enzyme, thereby reducing conversion of sulfite to sulfate. This can lead to a deficiency of sulfate, reduced sulfation, reduced clearance of phenols, and an accumulation of dopamine that can interfere with sleep. Slow function of sulfite oxidase also allows sulfite to accumulate, interfering with sleep via its direct neurotoxic and indirect neuroexcitatory effects in the brain that are mediated by the NMDA receptor.

Deficiencies of Magnesium or Zinc

The NMDA receptor is stabilized and even considered "blocked" by magnesium and zinc, so deficiencies in these minerals can make you vulnerable to excitability of the NMDA receptor by glutamate and S-sulfocysteine.

Molybdenum Deficiency

The SUOX enzyme (that converts sulfite to sulfate) requires molybdenum as its cofactor, so a molybdenum deficiency impairs the function of the SUOX enzyme, contributing to sulfate deficiency and consequently impaired sulfation of phenols, phenol accumulation, and elevated dopamine. 

Molybdenum is also a cofactor in the enzyme aldehyde oxidase (R) that breaks down aldehydes. Toxic aldehyde metabolites of dopamine, norepinephrine and serotonin cause neuroinflammation, neurodegeneration, and sleep dysregulation (R). Molybdenum deficiency would reduce the ability of aldehyde oxidase to protect the brain from toxic aldehydes.

However, another type of aldehyde-degrading enzyme, aldehyde dehydrogenase (ALDH) (10), could be more important in processing these neurotoxic aldehydes, and ALDH enzymes do not depend on molybdenum. ALDH enzymes are discussed in another section further below.

MOCS1, MOCS2, MOCS3 Gene Polymorphisms

Another factor that can impair the function of enzymes that require molybdenum as a cofactor, such as sulfite oxidase and aldehyde oxidase, is a deficiency in "molybdenum cofactor" (Moco), which enables molybdenum to perform as a cofactor for these enzymes. In other words, having enough molybdenum is not enough for these molybdenum-dependent enzymes to function. Molybdenum cofactor (Moco) is needed for molybdenum to function as a cofactor for these enzymes.

Molybdenum cofactor (Moco) is synthesized in a multi-step process by enzymes that are coded for by the genes MOCS1, MOCS2, and MOCS3. Genetic variants in one or more of these genes can result in limited production of molybdenum cofactor, thereby limiting the ability of molybdenum to function as a cofactor and limiting the function of molybdenum-dependent enzymes like sulfite oxidase to convert sulfite to sulfate and aldehyde oxidase to clear toxic metabolites of catecholamine neurotransmitters.

Molybdenum cofactor deficiency (MoCD) is a well-studied genetic disorder, and it can be "early onset" in childhood or "late onset" in adulthood.  Late onset MoCD is considered rare because it is rarely diagnosed, but I suspect that mild versions of it escape diagnosis because they are mild and are therefore not considered. Some of the people I have worked with have had the genetic variants in the MOCS genes that cause MoCD, along with symptoms suggesting sulfite toxicity, which is the main consequence of MoCD.

The synthesis of molybdenum cofactor (Moco) via the MOCS1, MOCS2, and MOCS3 enzymes depends on the availability of guanosine triphosphate (GTP), a compound similar to ATP. GTP synthesis is dependent on a variety of nutrients, including B1 and B3 (as NAD+), both of which are often depleted in people with chronic stress or illness. So perhaps deficiency of these nutrients plays a role in late onset MoCD. GTP synthesis is also dependent upon lipoic acid and coenzyme A, which is derived from vitamin B5.

Hydrogen Sulfide Accumulation

Aside from a reduced ability of sulfite oxidase to convert sulfite to sulfate due to molybdenum deficiency, Moco deficiency, and/or SUOX genetic polymorphisms, sulfite can also accumulate due to excess hydrogen sulfide. Elevated hydrogen sulfide can lead to elevated sulfite in a variety of ways.

One route from hydrogen sulfide to sulfite is in the breakdown of hydrogen sulfide, which begins when the enzyme sulfide-quinone reductase (SQR, SQOR gene) converts hydrogen sulfide to thiosulfate, and then the enzymes sulfotransferase (TRT gene) and ethylmalonic encephalopathy protein 1 (ETHE1 gene), a.k.a. persulfide dioxygenase convert thiosulfate to sulfite (R).

The accumulation of hydrogen sulfide also promotes sulfite elevation via it's impact on mitochondrial function and oxidative stress. Hydrogen sulfide releases free iron and impairs Complex IV in the mitochondria's electron transport chain (ETC), which lead to lower glutathione levels.

When glutathione is low, and when there are other signals of oxidative stress, the body upregulates its production of cysteine from homocysteine for use in glutathione synthesis. This occurs by increased activity of the Transsulfuration Pathway that consists primarily of the enzymes cystathionine beta synthase (CBS) and cystathionine gamma-lyase (CTH).

Increased production of cysteine increases sulfite because sulfite is a byproduct when excess cysteine gets oxidized (broken down) for energy, which also occurs during fasting or carbohydrate restriction. In other words.

Hydrogen sulfide can be produced by certain gut bacteria that can be involved with dysbiosis, especially small intestine bacterial overgrowth (SIBO). In the gut, excess hydrogen sulfide promotes diarrhea, loose stools, or excessive intestinal motility. This can promote nutrient deficiencies with broad effects throughout the body, including on the body's ability to process hydrogen sulfide and sulfite.

Oxidative Stress

It bears emphasizing that other sources of oxidative stress, not just excess hydrogen sulfide, also tend to lower glutathione and increase the production (and subsequent breakdown / catabolism) of cysteine, thereby raising sulfite and the excitatory, NMDA-stimulating neurotransmitter, S-sulfocysteine.

There also seems to be a reciprocal relationship between oxidative stress and glutamate activity (R), which means that oxidative stress in the brain elevates glutamate activity, and elevated glutamate activity increases oxidative stress. 

GABA neurons are particularly susceptible to damage from oxidative stress (R). So oxidative stress can lower GABA activity in the brain.

Fasting, Caloric Restriction, and Carbohydrate Restriction

It also bears repeating that when the body needs more glucose, one of the ways it can generate it is by breaking down cysteine, which releases sulfite. So, fasting, caloric restriction, or carbohydrate restriction could trigger elevated levels of sulfite, especially if there are bottlenecks in the conversion of sulfite to sulfate, such as molybdenum deficiency or polymorphisms in genes like SUOX, MOCS2, MOCS2, or MOCS3, as discussed previously.

Even if fasting, caloric restriction, or carbohydrate restriction aren't triggering issues with sulfur metabolism, they can still cause upregulated production of cortisol and adrenaline by the adrenal glands to release glucose from glycogen stores and/or promote glucose production from other sources like amino acids. Fasting, caloric restriction, and carbohydrate restriction also tend to cause sodium depletion, which can reduce blood volume sufficiently to cause spikes in the production of cortisol, adrenaline, and norepinephrine to restore adequate blood volume and pressure, as described in previous sections about cortisol dysregulation and reduced blood volume.

Deficiencies of Riboflavin (Vitamin B2), Coenzyme Q10, Iron, Glutathione, NADPH, Thiamine (Vitamin B1), Magnesium, Copper, Niacin (Vitamin B3), Vitamin B6, and Zinc

Whereas molybdenum is essential for the function of sulfite oxidase for converting sulfite to sulfate, a variety of nutrients are needed for the function of the enzymes that convert hydrogen sulfide to sulfite. 

The first enzyme in the process of breaking down hydrogen sulfide, sulfide-quinone reductase (SQR) requires riboflavin (vitamin B2) as the precursor of its cofactor, flavin adenine dinucleotide (FAD). In SQR's process of converting hydrogen sulfide to thiosulfate, Coenzyme Q10 is needed to receive an electron from hydrogen sulfide.

In the step of converting thiosulfate to sulfite, sulfotransferase requires vitamin B6 in its pyridoxal-5-phosphate form, and persulfide dioxygenase / ethylmalonic encephalopathy protein 1 requires iron and possibly glutathione as cofactor(s). Plus glutathione acts as a receiver of a sulfane group when TRT and ETHE1 convert thiosulfate to sulfite.

Glutathione's role in the breakdown of hydrogen sulfide is particularly vulnerable because it gets depleted by the combination of the prooxidative effects of hydrogen sulfide and sulfite and its use in the process of converting thiosulfate to sulfite.

As described previously, glutathione is depleted by the hydrogen sulfide's effects on mitochondrial energy production that promote oxidative stress (releasing iron from iron-sulfur clusters and displaces oxygen at Complex IV in the Electron Transport Chain). 

As if that weren't enough, sulfite stimulates NADPH oxidase (NOX) enzyme to use NADPH to produce superoxide, depleting NADPH, which is required for recycling glutathione. So factors affecting the ability to recycle NADPH affect the ability to recycle glutathione. Much of NADPH recycling occurs via the action of the pentose phosphate pathway, which depends heavily on thiamine (vitamin B1) and magnesium. So deficiencies in these two nutrients would potentially impair the recycling of NADPH and glutathione, which in turn slows the breakdown of hydrogen sulfide and increases the production of cysteine and sulfite via the Transsulfuration Pathway as it gets upregulated in response to glutathione depletion and other signals of oxidative stress.

Since hydrogen sulfide generated by bacteria in the gut is typically metabolized in the gut by the SQR, TRT, and ETHE1 enzymes, other factors affecting the production of these enzymes could play a significant role in hydrogen sulfide metabolism. One such factor is thiamine (vitamin B1) depletion in the gut, which can impair mitochondrial function in the gut and the production of many types of enzymes. So vitamin B1 deficiency could impair metabolism of hydrogen sulfide and lead to its accumulation. 

All of the enzymatic steps described above would also be affected by polymorphisms in any of these genes, as described further below. 

The synthesis of coenzyme (needed in the first step of metabolizing hydrogen sulfide) can be reduced by deficiencies in total calories, protein (especially phenylalanine and tyrosine), carbohydrates, chloride, copper, iron, magnesium, niacin, potassium, thiamine, riboflavin, B6, and zinc. Anything affecting methylation (which is affected by deficiencies of 26+ nutrients).

Manganese Toxicity and Gene Polymorphisms for Hemochromatosis

A study in yeast and fruit flies demonstrated that the mechanism of manganese toxicity is inhibition of coenzyme Q10 synthesis and that this is a mechanism that is conserved across species from yeast to animals. (R)

Manganese inhibits the synthesis of coenzyme Q10 by displacing iron in an enzyme involved in coenzyme Q10 synthesis that requires iron as a cofactor. People with low iron could be more vulnerable to the iron-displacing effect of manganese.

Furthermore, gene polymorphisms for hemochromatosis (iron overload) appear to also cause manganese overload. 9% of people globally have heterozygous or homozygous polymorphisms in the HFE gene, usually either the more impactful C282Y variant or the H63D variant. Other genes involved in hemochromatosis besides HFE include HFE2, HAMP, TFR2, and SLC40A1.

Gene Polymorphisms Affecting Coenzyme Q10 Synthesis, Absorption, and Transport

Genes affecting the synthesis, absorption, and transport of coenzyme Q10 would affect the metabolism of hydrogen sulfide (and mitochondrial function, another factor in sleep discussed further below) and could therefore negatively affect sleep. These genes are too numerous to cover here.

Statins and Possibly Bisphosphonate Drugs

Statins, whether from drugs or food sources like red rice yeast, inhibit coenzyme Q10 synthesis and would thereby impair the metabolism of hydrogen sulfide and mitochondrial function in general, thereby potentially impairing sleep. Bisphosphonate drugs probably also inhibit coenzyme Q10 synthesis.

SQOR, TRT, ETHE1 Gene Polymorphisms

Since the SQOR, TRT, and ETHE1 genes code for the enzymes involved in metabolizing hydrogen sulfide to sulfite, genetic variants in these genes could slow the metabolism of hydrogen sulfide, promoting its accumulation and its negative effects on mitochondrial function and its promotion of oxidative stress and sulfite-elevating cysteine production and catabolism.

ALDH2 Gene Polymorphism

As mentioned previously, aldehyde dehydrogenase enzymes breaks down toxic aldehyde metabolites of dopamine, norepinephrine and serotonin that cause neuroinflammation, neurodegeneration, and sleep dysregulation.

A single nucleotide polymorphism (SNP) in the ALDH2 gene, a gene that codes for one of the ALDH enzymes appears to promote sleep dysregulation (R) .

Deficiency of Vitamin B3 or Low NAD+/NADH Ratio

The aldehyde dehydrogenase (ALDH) enzymes are required to break down toxic aldehyde metabolites of dopamine, norepinephrine, and serotonin that contribute to sleep dysregulation, depend on NAD+ or NADP+ as their cofactor. Magnesium may increase the function of ALDH enzymes but is not a required cofactor.

So, a deficiency of vitamin B3 (niacin) or a low ratio of NAD+/NADH could contribute to sleep dysregulation via accumulation of the aldehyde metabolites of neurotransmitters. And a deficiency of magnesium might further contribute to suboptimal function of ALDH enzymes.

An elevated NAD+/NADH ratio can be caused by eating too much too close to bedtime. This is one of the reasons that it is best to finish eating 3 hours before you go to sleep. An elevated NAD+/NADH ratio can also be caused by mitochondrial dysfunction.

Mitochondrial Dysfunction

Mitochondrial dysfunction can occur at various steps in the process of generating ATP in the mitochondria of our cells. Dysfunction in the Electron Transport Chain (ETC) results in the accumulation of electrons in the ETC instead of being transferred to oxygen (along with hydrogen protons) to form water. 

When electrons accumulate in the ETC, additional electrons (and hydrogen protons) cannot be transferred to the ETC by NADH and FADH2, the molecules that transfer electrons and protons from the Krebs Cycle / Citric Acid Cycle. This leads to an accumulation of NADH and a low rate of recycling of NADH to NAD+, a low NAD+/NADH ratio, and reduced availability of NAD+ for various reactions that require it, such as the aldehyde dehydrogenase enzymes needed for breaking down toxic, sleep-dysregulating metabolites of neurotransmitters.

Mitochondrial dysfunction in the electron transport chain that can lead to a low NAD+/NADH ratio can be caused by various factors, such as the following:

• Nutrient deficiencies (e.g. copper, iron, and coenzyme Q10)
• Insulin resistance
• Toxicants that impair mitochondrial function (typically by impairing complexes in the ETC)
• Chronic infections (can promote the Cell Danger Response that shifts mitochondrial function away from energy production)
• Excess hydrogen sulfide (impairs the function of Complex IV in the ETC)
• Excess sulfite (impairs conversion of glutamate to alpha-ketoglutarate, an important compound in mitochondrial energy production, and opens the mitochondrial permeability transition pore, allowing substances to enter and exit the mitochondria that shouldn't)

This is a very short list of mitochondria-dysregulating factors.  There are many others.

High Glutamate Activity

Glutamate is an excitatory neurotransmitter, and elevated glutamate is a common cause of insomnia. Many factors can elevate glutamate, including inflammation and other factors listed below.

Traumatic Brain Injury

Traumatic brain injury can elevate glutamate activity in the brain (R, R).

Estrogen Dominance

Estrogen increases glutamate activity and pregnenolone reduces glutamate activity (R), so estrogen dominance would likely overly elevate glutamate activity.

Estrogen also increases the production of hydrogen sulfide in the body, which could increase the potential for interference with sleep in anybody with impaired sulfur metabolism, whereby the accumulation of hydrogen sulfide and/or sulfite could damage mitochondrial function and also promote excess excitatory signaling at the NMDA receptor in the brain via S-sulfocysteine, as discussed earlier in this article. 

Aluminum Toxicity

Aluminum appears to reduce the activity of glutamic acid decarboxylase (GAD), the enzyme that converts the excitatory neurotransmitter glutamate to the calming neurotransmitter gamma amino butyric acid (GABA) (R, R).

Vitamin B6 Deficiency

Vitamin B6 is a cofactor for glutamic acid decarboxylase (GAD), the enzyme that converts the excitatory neurotransmitter glutamate to the calming neurotransmitter gamma amino butyric acid (GABA). It requires the activated pyridoxal-5-phosphate  (P5P) form, and some people are genetically impaired in making the conversion from the form of B6 in plants and some supplements to the P5P form of B6.

Magnesium Deficiency

In addition to vitamin B6, magnesium is a cofactor for glutamic acid decarboxylase (GAD), the enzyme that converts the excitatory neurotransmitter glutamate to the calming neurotransmitter gamma amino butyric acid (GABA). 

Magnesium inhibits the excitatory NMDA/glutamate receptor, and a deficiency of magnesium leads to greater NMDA receptor activity (R).

As mentioned previously, magnesium appears to improve the function of aldehyde dehydrogenase (ALDH) enzymes that break down toxic, sleep-dysregulating metabolites of neurotransmitters. So a magnesium deficiency could reduce the potential efficiency of ALDH enzymes.

Zinc Deficiency

Like magnesium, zinc inhibits the NMDA receptor (R).

Low GABA Activity

The calming neurotransmitter gamma amino butyric acid (GABA) is important for sleep, and some sleep medications are based on improving GABA receptor activity (R). Impairments in glutamic acid decarboxylase (GAD), the enzyme that converts glutamate to GABA, such as aluminum toxicity or deficiencies of vitamin B6 or magnesium (as described previously) could lead to low GABA and impaired sleep. 

Babesia and Bartonella Infections

Babesia, a protozoan parasite similar to the one that causes malaria, and Bartonella, a bacterium, that are common Lyme disease coinfections are known to cause sleep disturbances. 

Interference Fields and Blocked Meridians

The acupuncture meridians of the body are electrical circuits composed of the fascia connective tissue sheath that surrounds muscle groups that store electrical charge (voltage) and serve as "battery packs" that supply voltage to the meridians / circuits. 

Meridians / circuits deliver voltage to organs, tissues, and cells served by the circuit in question. For example, the Stomach/Spleen meridian/circuit is the battery pack for the endocrine system, and the Heart/Small Intestine meridian/circuit is the battery pack for the autonomic nervous system. 

Sleep is regulated in part by the functions of the endocrine system and the autonomic nervous system, so dysfunction in these meridians/circuits can substantially impair sleep. 

Meridians/circuits/battery packs lose their voltage when something blocks or otherwise interferes with production of energy to supply voltage and/or the flow of voltage through the circuit. 

Things that interfere with the flow of voltage through circuits are referred to as "interference fields" and essentially "short-circuit" the meridian/circuit. This causes loss of voltage in the circuit. When the voltage is low in the circuit, it cannot deliver voltage to the organs and other tissues on that circuit, and dysfunction and disease then develop in those organs and tissues.

According to Jerry Tennant, MD, author of the Healing is Voltage book series, a symptom of a loss of voltage in the Stomach/Spleen meridian/circuit is an inability to go to sleep before 11:00 p.m. and waking up tired despite sleeping an adequate number of hours. This circuit is very commonly affected by interference fields on the midline of the body, which are often associated with scars such as C-section, hysterectomy, and episiotomy scars. The Stomach/Spleen meridian/circuit is also vulnerable to being blocked by chronic worry, which tends to lodge in that meridian/circuit.

If you are not yet familiar with the "healing is voltage" concept, you can learn more in a 3-part article series that begins here. 

Dysautonomia and Dysfunction of the Vagus Nerve and the Polyvagal System

Dysautonomia is dysfunction of the autonomic nervous system, the part of the nervous system that regulates internal organs, smooth muscles, and glands. Sleep and dysautonomia have a bidirectional relationship in that sleep disorders can contribute to dysautonomia, and dysautonomia can cause sleep abnormalities, which are more common in people with dysautonomia than in the general population (R). 

The vagus nerve, also known as the 10th cranial nerve, is considered part of the autonomic nervous system, which regulates a variety of processes that influence sleep. According to Stephen Porges' concept of the "polyvagal system", activation of the ventral branch of the vagus nerve promotes a sense of safety, which promotes restful sleep.

Though not part of the vagus nerve, the sympathetic nervous system, which is another part of the autonomic nervous system, works in concert with the branches of the vagus nerve and is responsible for the "fight or flight" response, increasing alertness and interfering with sleep.

Activity of the ventral branch of the vagus nerve serves as a "brake" on sympathetic activity, maintaining a calm state under safe conditions. On the other hand, reduced activity of the ventral branch of the vagus nerve and/or increased activation of the sympathetic nervous system allows elevated states of neuroendocrine arousal and alertness.

Activity of the dorsal branch of the vagus nerve is associated with a response to the perception of extreme danger and a "freeze" response, and this can interfere with sleep in a variety of ways. For example, a state of low energy and lethargy resulting from activation of the dorsal branch of the vagus nerve can disrupt normal sleep-wake cycles by interfering with sleep initiation or the body's ability to enter deep restorative sleep stages.

Slowing of gut motility due to the physiological "shutdown" aspect of dorsal vagus nerve activation can cause discomfort (e.g. bloating or indigestion) that can disturb sleep. Dorsal vagus nerve activation can also result in impaired regulation of breathing during sleep, which can exacerbate conditions like sleep apnea, leading to frequent awakenings.

Dorsal vagal activation is often linked to emotional shutdown, dissociation, or feelings of helplessness or depression, which can lead to sleeplessness. Prolonged dorsal vagal activation may also disrupt the smooth cycling between REM and non-REM sleep necessary for recovery.

Dysfunction of the vagus nerve and polyvagal system can have a variety of causes, including but not limited to the ones listed below:

1. Psychological trauma in the past
2. Chronic psychological stress in the present
3. Head or neck injuries
4. Forward head posture and other misalignments in the neck
5. Cranio-cervical instability (CCI)
6. Low production of acetylcholine, the neurotransmitter used by the vagus nerve
7. Deficiencies of choline and/or vitamin B1, which are necessary to produce acetylcholine
8. Direct infection of the vagus nerve, sometimes occurring due to dysbiosis in the gut

And it is possible that the polyvagal system is involved as a mediator of the effects of many more of the other causes and contributors to sleep challenges described in this article. For example, when polyvagal dysfunction causes the type of dysautonomia that impairs HPA function, this can reduce sodium retention and blood volume, potentially causing awakening at night (usually between 2 a.m. and 4 a.m.), as described in the previous section about under-hydration and reduced blood volume.

As a side note, although transcutaneous vagus nerve stimulation has been shown to be effective with primary insomnia (insomnia with no known cause) (R), vagus nerve stimulation was shown in another study to increase complications related to sleep apnea among suffers of sleep apnea (R). Other approaches to improving vagus nerve function may be more appropriate, at least in some situations.

What Can You Do With This Information?

One of the things that you can do is start testing to find out if any of the factors described in this article might be the cause of sleep challenges you might be experiencing. But realize that the list in this article is just the tip of the ice berg when it comes to potential causes of problems with sleep.

If you would like help with resolving causes of poor sleep and restoring effortless, restful sleep, check out the Bio-Individual Blueprint Roadmap to learn how I work with clients and schedule a time to talk. Or if you have already seen that, you can proceed to schedule a free 15-minute or 45-minute consultation.