Increasing BDNF Brain-Derived Neurotropic Factor

Exercise, Nutrition, & Optimized Sleep Supercharges our Brain!

On January 6th, a study predicting dementia prevalence in 204 countries was published in The Lancet: Public Health by the Institute for Health Metrics and Evaluation (IHME). Globally, the study predicts that by 2050, an estimated 153 million people will be living with dementia, up from the current estimate of 57 million in 2019. The authors noted that these findings were consistent with those found in ADI’s 2019 World Alzheimer Report.

Table of Contents

1.1. Resistance Exercise and Enhanced Brain Activity. 4

1.2. Exercise-Induced Brain health and Myokines. 6

1.2.1. Interleukin 6 (IL-6). 7

1.2.2. Irisin/ FNDC5. 8

2. Diet and Brain Health. 9

2.1. Ketogenic Diet improves Brain Activity. 10

2.1.1. Boosting ‘feel good’ neurotransmitters. 11

2.1.2. Bolstering brain power. 11

2.1.3. Exerting potent antioxidant effects. 11

2.2. Omega-3 Supplements to improve Mental Health. 12

2.2.1. How Do Omega-3s Affect the Brain?. 13

3. Mental Health and Sleep. 13

3.1. How Mental Health is related to Sleep?. 14

3.2. Stages of Sleep. 15

3.3. Improving Your Sleep Habits to Enhance Your Mental Health. 16

3.3.1. Create a relaxing environment before bed. 16

3.3.2. Eat dinner no less than two hours before bedtime. 16

3.3.3. Reduce your exposure to light. 16

3.3.4. Watch what you drink. 18

3.3.5. Maintain a cool temperature of your room.. 18

3.4. Sleep-Tracking Devices. 19

3.4.1. What does Sleep Tracking devices monitor?. 19

3.4.2. OURA Ring: Improving self-performance through sleep tracking. 20

4. Tests to monitor brain activity. 21

4.1. CT Scans (Computed Tomography). 21

4.2. Electroencephalography (EEG). 21

4.3. Electromyography (EMG). 22

4.4. Nerve Conduction Studies. 23

5. References. 24

The three pillars of a healthy life are proper nutrition, physical activity, and rest. Several recent studies have suggested that improving all three of these lifestyle factors may be a better way to improve both physical and mental health, even though improvements in just one can help people live longer. The interplay between dietary habits, physical activity, and sleep is intricate and multifaceted. Research has shown that the more of these lifestyle behaviors you improve, the better your well-being is, so it’s important to learn how they all work together.

(Fig.1. Connection between Exercise, Diet, Sleep and Mental Health)

Exercising has been linked to fewer cases of a wide range of health problems, both physiological and psychological. Extensive research has shown that regular exercise can prevent not only cardiovascular disease, colon and breast cancer, and obesity, but also psychological disorders like depression and anxiety.1 Multiple large-scale prospective and cross-sectional observational studies have found that a diet rich in cereals, dark or brightly colored fruits and vegetables, and leafy greens, along with two to five servings of fish per week, is associated with improved cognitive function as people age.2 Therefore, interventions such as diet and exercise have been used to counteract what may be a detrimental effect of ageing on brain function. This paper will explain how physical activity and diet can improve brain function and cognition.

1. Exercise Improves the Brain Activity

Exercising regularly is essential to good health and has numerous positive effects on the body as a whole. Reduced anxiety, lower blood pressure, and improved sleep are just a few of the immediate benefits. Better weight management, stronger bones, and a reduced risk of over 35 diseases are just a few of the long-term benefits of a regular exercise routine.3

The effects of high-intensity exercise on appetite typically last for 30-60 minutes after the workout is over. Exercising after eating can have the additional benefit of making you feel fuller for longer. However, it would appear that the opposite is true for sedentary pursuits. People who spend more time in front of the TV tend to be heavier because of their higher calorie intake and decreased physical activity.4

Several studies have found that regular exercise can help you sleep better. Aerobic exercise (like running or cycling) and resistance exercise (like lifting weights) both contribute to better sleep. Exercise of any kind can help you sleep better, but younger people typically need more of it than older people do. Exercise in the late afternoon or early evening has been shown to improve sleep quality. If you work out right before bed, your stress hormones will rise, making it even harder to fall asleep.5

Physical activity has been linked to a lower incidence of sleep disorders such as insomnia, obstructive sleep apnea (OSA), and restless leg syndrome (RLS). Exercising prior to bedtime has been shown in multiple studies to lower levels of anxiety and increase the quality of sleep for those who suffer from insomnia. In addition to enhancing sleep quality and decreasing daytime fatigue, one study found that a 12-week regimen of aerobic and resistance training led to a 25% reduction in the severity of OSA. In a similar study, participants who participated in a 12-week exercise programme saw a 39% decrease in RLS symptoms.6

(Fig 2. Exercise boosts Cognition)

1.1. Resistance Exercise and Enhanced Brain Activity

When muscles are repeatedly contracted against an external resistance, this is known as resistance exercise. Push-ups and other similar bodyweight exercises, as well as those performed with dumbbells, resistance bands, or exercise machines, all fall into the category of resistance training. Muscle strength increases from this type of training are initially triggered by cellular responses (days to weeks), and then progress to structural changes via synaptogenesis (months to years) in response to continued training (months-years).7

When it comes to MEPs and SICI/CSP during muscle activity, a meta-analysis of 31 studies found that resistance training increases the former and decreases the latter. This data suggests that the corticospinal output to the trained muscle increases after even a short period of resistance training. The global effects of training-induced neuroplasticity are demonstrated by the observation that resistance training increases corticospinal output to both the trained and untrained limb. After 9 sessions of right-leg-only squatting, for instance, the untrained leg showed a greater MEP amplitude and a smaller SICI.8

There is a lack of research on the effects of prolonged resistance training on the corticospinal system, especially for durations longer than three months. Long-term adaptations can only be studied through cross-sectional research designs. Although there were differences in strength between trained and untrained controls, studies of people with years of resistance training experience showed no differences in corticospinal excitability.7 The biceps brachii of the non-dominant arm showed a significant increase in spinal excitability compared to controls, but no differences in corticospinal excitability.9 Longitudinal designs should be implemented in the future to evaluate spinal and supraspinal adaptations after long-term resistance training programs. Although conducting such research may be difficult due to its complexity, it is essential for learning about the neural responses to chronic resistance training and how they differ from acute and transient responses.

After 12 months of twice-weekly resistance training, healthy elderly women showed increased hemodynamic activity in the anterior left middle temporal gyrus, the left anterior insula, and the lateral orbital frontal cortex, as measured by functional magnetic resonance imaging (fMRI). Cognitive enhancements as measured by the Flanker test coincided with these hemodynamic alterations.10 Increased efficiency in activating response inhibition processes contributed to resistance training’s beneficial effects on performance on the Flanker test. Additionally, it has been hypothesized that increased IGF-1 and decreased homocysteine levels play a role in the aforementioned training-induced improvements in cognitive performance and neuroplasticity.11  

 The effects of resistance training on functional connectivity and memory in middle-aged women with mild cognitive impairment were examined using functional magnetic resonance imaging (fMRI). The right lingual gyrus, occipital fusiform gyrus, and right frontal pole showed increased activity during encoding and recall processes after resistance training.12 Improvements in associative memory performance were also positively correlated with increased activity in the right lingual gyrus. Increasing activity in several brain regions implicated in important cognitive functions has been linked to exercise, and these changes have been shown to facilitate improved performance on assessments of these abilities, as shown by fMRI studies.

1.2.  Exercise-Induced Brain health and Myokines.

Brain function can be improved without the use of pharmaceuticals via engaging in physical exercise. Physical activity has been shown to enhance the size and activity of the hippocampus and prefrontal cortex, two brain areas closely associated with memory and reasoning.13 Exercise has been shown to enhance cognitive and physical function in studies of persons with AD, the most prevalent form of dementia. Physically active people also had a 30–40% lower chance of acquiring AD than those who weren’t as active as they could be. 14

(Fig. 3. Myokines and Mental Health)

Exercise stimulates metabolic regulation and changes in gene expression, both of which are adaptive mechanisms that allow skeletal muscle to access energy stores.15 Muscle autocrine regulation of metabolism and the paracrine/endocrine regulation of adjacent/remote organs are both influenced by exercise-induced changes in myokine expression. Exercising has been shown to be good for the brain because it raises myokine levels in the bloodstream. Mood, learning, locomotor activity, and neuronal protection are just some of the brain functions that the myokines regulate in animal or in vitro models.16

The brain’s control of neuronal proliferation and differentiation, plasticity, memory, and learning are all influenced by the increased myokines in the bloodstream brought on by regular exercise.

Muscle and other organs or tissues communicate with one another through the release of myokines, which have provided a new conceptual framework for this study. Skeletal muscle has been found to be an endocrine organ with a robust capacity for the production, expression, and secretion of a number of factors (collectively known as Myokines). The contraction of skeletal muscles causes the release of myokines, which are cytokines and other peptides with autocrine, paracrine, and endocrine effects. Myokine signaling mediates the endocrine loop between muscles and the brain, which facilitates communication between the two.17

1.2.1. Interleukin 6 (IL-6)

Interleukin 6 (IL-6) was the first myokine discovered to be secreted into circulation independently of tumor necrosis factor (TNF), with plasma levels increasing by as much as 100-fold in response to exercise. Circulating IL-6 levels increased during exercise without accompanying muscle damage.18 Brain IL-6 mRNA and protein levels both increased after exercise. Mice that ran on a wheel for two weeks were found to have higher levels of IL-6 in their hippocampi, which may serve to protect the brain by dampening harmful inflammatory responses.19

Studies in vitro demonstrated that IL-6 protects neural cells from Ca2+ and ROS excitotoxicity while also promoting their survival and differentiation. Neurodegenerative diseases, such as Alzheimer’s disease, are affected by il-6. Experiments conducted in vitro showed that the neurotoxicity induced in cortical neurons was exacerbated by the addition of Il-6 to the culture medium. In contrast, IL-6 increased the activation of astrocytes and microglia cells in vivo, resulting in enhanced clearance of plaque A and demonstrating its neuroprotective properties.20

1.2.2. Irisin/ FNDC5

Irisin/fibronectin type III domain-containing protein 5 (FNDC5) is a glycosylated type I membrane protein. Proteolytic cleavage of FDN5C results in the formation of the 112-amino-acid peptide irisin, which is then secreted into the bloodstream.21

Skeletal muscle is the primary source of the circulating levels of FNDC5/IRISIN, which is why exercise is said to induce this myokine. One of the key regulators of post-exercise skeletal muscle plasticity is peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1), which is induced by exercise and promotes irisin synthesis and secretion.22 FNDC5 mRNA was found to be elevated in skeletal muscle cells after exercise in both mice and humans. Blood levels of irisin were found to be noticeably higher in individuals who had just completed an endurance exercise session.23

When mice are used as a model, physical activity increases Fndc5 expression in the hippocampus (a brain region critical for memory and spatial awareness) in a PGC-1-dependent manner. Mice deficient in Pgc1a, also known as Pgc1 / mice, lacked FNDC5 expression. As a result of the activation of the protein kinase B (PKB) and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway, irisin promotes neuronal proliferation and differentiation and contributes to the exercise neuroprotective effects.24 Recent studies in AD mouse models have suggested that irisin plays a role in controlling synaptic function and memory. In the brain of FNDC5 mice, a mice mole of AD, synaptic plasticity and long-term potentiation are compromised, while the FNDC5/irisin re-expression rescued synaptic plasticity and memory impairment.25 Moreover, irisin increase brain-derived neurotrophic factor (BDNF) expression in the brain, which is involved in the cognitive function.26

(Fig. 4. Physical activity enhances circulating levels of myokines in the bloodstream, affects the brain regulating neuronal proliferation and differentiation, plasticity, memory, and learning)

2. Diet and Brain Health

Diet and nutrition affect virtually all aspects of our health. Eating a healthy, balanced diet has been shown to reduce the risk of a myriad of health conditions, from heart disease and stroke, to diabetes and obesity. Diet can also affect our mental health, with several studies suggesting that certain diets may reduce the risk of developing depression and anxiety.27

Ab individual’s dietary choices clearly effect neuroplastic processes in the brain. Adherence to certain dietary interventions such as the Mediterranean diet, ketogenic diet, caloric restriction, intermittent fasting and diet supplementation appear to increase measures of neuroplasticity in the brain. Therefore, routine consumption of unhealthy diets such as those high in calories, saturated fats and sugars conversely leads to negative consequences to brain functioning. Together, these results suggest that dietary factors should be a major consideration when attempting to maximize neuroplasticity induced by training or learning. An individual’s dietary habits will also be valuable information for researchers trying to understand individual differences in responses to the same intervention attempting to induce neuroplasticity, such as exercise or non-invasive brain stimulation.

Food can either fuel or foil a workout, and research shows that combining a healthy diet with adequate exercise offers more benefits than improving diet alone. The right combination of fluids, carbohydrates and protein, eaten at the right time, can improve athletic performance and decrease fatigue. Poor dietary choices, like eating right before a high-intensity cardio workout, can lead to increased nausea and make exercise more challenging.28

What we eat also impacts sleep quality and duration. Caffeine is notorious for making it more difficult to fall asleep and eating too close to bedtime can lead to sleep disruptions. Most health experts recommend avoiding caffeine prior to sleeping. Having too much calories or fat in your diet may make it harder to get enough sleep, as do diets lacking key nutrients, like calcium, magnesium, and vitamins A, C, D, and E.29

2.1. Ketogenic Diet improves Brain Activity

The keto diet is a high-fat, low-carbohydrate, and adequate-protein diet. Eating this way triggers a metabolic process called ketosis. Simply put, it causes the body to burn fat instead of carbohydrates for energy. Despite currently being used as a mainstream weight loss method, it was initially developed to manage seizures in people with epilepsy.

Ketogenic diets show promise for improving mood and research suggests that the diet may possibly benefit a number of mental health conditions such as:

  • Depression
  • Bipolar disorder
  • Schizophrenia
  • Dementia

Ketogenic diets appear to affect the brain in a number of positive ways, such as:

  • Boosting ‘feel good’ neurotransmitters
  • Bolstering brain power  
  • Having antioxidant effects

2.1.1. Boosting ‘feel good’ neurotransmitters

Being in a state of ketosis has been shown to increase production of a common neurotransmitter in the brain called GABA. There is evidence that various anxiety disorders result from dysfunctional GABA activity. Studies conducted on the use of the ketogenic diet in seizure disorders, for example, tend to show that a good balance of GABA leads to better mental focus, reduced stress and anxiety.30

2.1.2. Bolstering brain power

Contrary to common belief that glucose is essential for the brain, ketone bodies produced from fat, such as beta hydroxybutyrate, can provide an alternative ready fuel for the brain. Research suggests that ketones may even be a more efficient fuel for the brain than glucose. It is believed that ketones increase the number of energy factories (mitochondria) in brain cells, which boost the energy levels in those cells. This is important, as many mental disorders share one major problem – deficient energy production.31

2.1.3. Exerting potent antioxidant effects

Studies have suggested that the ketogenic diet may reduce oxidative stress and inflammation in the brain. Researchers believe that lower levels of inflammation combined with enhanced energy with ketones used as fuel may contribute to improved brain function. As it turns out, studies have shown that one way the ketogenic diet could work in treating seizures could be by increasing levels of a major antioxidant, called glutathione that protects us against oxidative stress.32

(Fig 5. The cognitive benefits of going Keto)

2.2.  Omega-3 Supplements to improve Mental Health

Omega-3 fatty acids are polyunsaturated fats responsible for most of the brain and mental health benefits of fish oil. Fish oil primarily contains two types of omega-3 fatty acids:

  • EPA
  • DHA

These two fatty acids are components of cell membranes and have powerful anti-inflammatory functions within the body. They are also well known for their critical roles in human development and heart health. In the human diet, EPA and DHA are almost exclusively found in fatty fish and fish oil. Because most people do not consume the recommended amounts of fish, many people likely fall short of getting enough EPA and DHA in their diets.33

The body can make EPA and DHA out of another omega-3 called alpha-linolenic acid (ALA) (ALA). ALA is found in a number of food sources, such as walnuts, flaxseeds, chia seeds, canola oil, soybeans and soybean oil. However, humans can’t convert ALA to EPA and DHA very efficiently, with estimates reporting that less than 10% of the amount of ALA you consume is converted to EPA or DHA.34 Therefore, taking fish oil may be a good option, especially for those who don’t eat much fish but are still looking to gain some of the health benefits of omega-3 fatty acids.

2.2.1. How Do Omega-3s Affect the Brain?

The omega-3 fatty acids EPA and DHA are critical for normal brain function and development throughout all stages of life. EPA and DHA seem to have important roles in the developing baby’s brain. In fact, several studies have correlated pregnant women’s fish intake or fish oil use with higher scores for their children on tests of intelligence and brain function in early childhood. These fatty acids are also vital for the maintenance of normal brain function throughout life. They are abundant in the cell membranes of brain cells, preserving cell membrane health and facilitating communication between brain cells.35

When animals are fed diets without omega-3 fatty acids, the amount of DHA in their brains decreases, and they tend to experience deficits in learning and memory.36 In older adults, lower levels of DHA in the blood have been associated with smaller brain size, a sign of accelerated brain ageing.37 Clearly, it is important to make sure you get enough omega-3 fatty acids to avoid some of these detrimental effects on brain function and development.

3. Mental Health and Sleep

Most people know firsthand that sleep affects their mental state. After all, there’s a reason it’s said that someone in a bad mood “woke up on the wrong side of the bed.”

As it turns out, there’s quite a bit of truth behind this colloquial saying. Sleep is closely connected to mental and emotional health and has demonstrated links to depression, anxiety, bipolar disorder, and other conditions. While research is ongoing to better understand the connections between mental health and sleep, the evidence to date points to a bidirectional relationship. Mental health disorders tend to make it harder to sleep well. At the same time, poor sleep, including insomnia, can be a contributing factor to the initiation and worsening of mental health problems.

Both sleep and mental health are complex issues affected by a multitude of factors, but, given their close association, there is strong reason to believe that improving sleep can have a beneficial impact on mental health and can be a component of treating many psychiatric disorders.

3.1. How Mental Health is related to Sleep?

Brain activity fluctuates during sleep, increasing and decreasing during different sleep stages that make up the sleep cycle. In NREM (non-rapid eye movement) sleep, overall brain activity slows, but there are quick bursts of energy. In REM sleep, brain activity picks up rapidly, which is why this stage is associated with more intense dreaming. Each stage plays a role in brain health, allowing activity in different parts of the brain to ramp up or down and enabling better thinking, learning, and memory.

Research has also uncovered that brain activity during sleep has profound effects on emotional and mental health. Sufficient sleep, especially REM sleep, facilitates the brain’s processing of emotional information. During sleep, the brain works to evaluate and remember thoughts and memories, and it appears that a lack of sleep is especially harmful to the consolidation of positive emotional content. This can influence mood and emotional reactivity and is tied to mental health disorders and their severity, including the risk of suicidal ideas or behaviours.38

As a result, the traditional view, which held that sleep problems were a symptom of mental health disorders, is increasingly being called into question. Instead, it is becoming clear that there is a bidirectional relationship between sleep and mental health in which sleeping problems may be both a cause and consequence of mental health problems.

3.2. Stages of Sleep

(Fig 6. Stages of Sleep and Brain Activity)

3.3. Improving Your Sleep Habits to Enhance Your Mental Health

Anxiety and despair are only two of the issues that have been connected to a lack of sleep. Having this condition might also interfere with your metabolism and immune system. If you sleep better, you will wake up feeling refreshed and ready to take on the day.

There is a strong correlation between the quality of your sleep and the amount of effort you put into establishing this routine and nighttime habits:

3.3.1. Create a relaxing environment before bed

Some people find that doing things like taking a warm bath, reading in dim light, listening to calming music, or practicing relaxation techniques like deep breathing just before bedtime helps them wind down and get a good night’s sleep.

3.3.2. Eat dinner no less than two hours before bedtime

In the most fundamental sense, digestion prevents the body from entering a restful state as quickly as it might otherwise. Having problems falling asleep and experiencing poor sleep quality are both consequences of this. When digesting food at night, your body does not go to sleep. Because of the link between your digestive system and your brain, you may find it difficult to fall asleep. Inefficient digestion by your digestive tract and the brain’s subsequent efforts to make sense of the situation prevent you from drifting off to sleep.39

In addition to using energy, digestion may prevent you from reaping the benefits of other restorative facets of sleep that might otherwise aid in your recovery. Also, the circadian rhythm, the body’s 24-hour internal clock that controls the sleep/wake cycle, can be disrupted by eating late at night.

3.3.3. Reduce your exposure to light

It’s best to put away the bright screens at least two hours before night. The circadian rhythm is a portion of the body’s biological clock that plays an important role in regulating sleep, and the strongest trigger for it is light. Making the bedroom as dark as possible before bed helps maintain a regular sleep schedule.

Blackout curtains may be able to assist if your room is flooded with sunlight from the outside, the lights in the room, including any bedroom lamps, should be dimmed. Drowsiness and sleepiness may be more easily induced by lighting with a low color temperature and illuminance.40

Sleep masks prevent you from opening your eyes and looking at your alarm clock, which sleep experts suggest should be out of sight from your sleeping posture, or any other temptations or distractions in the room. When there is no light, our brains respond by increasing production of melatonin, the hormone that regulates our sleep and wake cycles, which leads to us feeling sleepier and more ready for bed. Scientists have shown a correlation between sleeping in the dark and more time spent in rapid eye movement (REM) sleep and less time spent awake, both of which improve the quality of sleep and the likelihood that you will get a full night’s rest. They discovered these advantages not just in completely dark rooms, but even while using sleep masks.41

(Fig 7. Sleep Mask for better Sleep)

The use of electronic devices, such as tablets and mobile phones, should be restricted or banned from the bedroom as a means of reducing exposure to artificial light. Watching TV in the bedroom before going to bed, will negatively affect your sleep quality. Blue light from screens is known to mess with people’s circadian rhythms, and the stimulation of the mind caused by staring at a screen can make it difficult to wind down for sleep. If you need to have a gadget in your bedroom, try to keep it out of arm’s reach and avoid using it for an hour or more before night.

Don’t fight your body’s circadian rhythms; instead, work with them (as much as possible). Maintaining a consistent sleep-wake pattern, especially on days off, will assist set your body’s internal clock and improve the quality of your sleep. You probably aren’t getting enough sleep throughout the week if you need to sleep in for several hours on weekends.

3.3.4. Watch what you drink

Caffeine, nicotine, and alcohol all disrupt sleep cycles and should be avoided in the hours leading up to bedtime. Some people find that drinking alcohol helps them fall asleep, however because alcohol disrupts normal sleep patterns, the resulting sleep is not restful. In addition to these issues, alcohol use can exacerbate preexisting conditions including snoring and asthma.

3.3.5. Maintain a cool temperature of your room

 Create a completely dark, completely cool, completely silent space in your bedroom. The use of blackout drapes and fans might be of assistance. If you’ve ever tried to sleep while overheating or shivering, you know how frustrating it can be. The creation of melatonin, which aids in sleep, is stimulated by your body’s temperature dropping from its high late in the afternoon. The sweet spot for a bedroom is between 60 and 65 degrees Fahrenheit, or 16 to 18 degrees Celsius. Rapid eye movement (REM) sleep is particularly disrupted by environmental factors such as heat, cold, and draftiness. When trying to sleep, a room temperature of above 24 degrees Celsius (71 degrees Fahrenheit) or below 12 degrees Celsius (53 degrees Fahrenheit) is not ideal.42

3.4. Sleep-Tracking Devices

Millions of people today wear activity trackers on their wrists to keep tabs on anything from their heart rate and oxygen intake to the amount of steps they take each day. One of the numerous ways in which activity trackers may be useful is by highlighting the role that sleep plays in the user’s overall lack of physical activity.

There is a plethora of sleep monitors available today, and more are being introduced regularly. You may attach several trackers on your wrist and use them that way. Still others might be attached to your pillow or placed on your nightstand.

(Fig 8. Sleep Tracking)

3.4.1. What does Sleep Tracking devices monitor?

  • Sleep Duration: The gadgets may keep tabs on when you go to bed and when you wake up by recording the total amount of time you spend sleeping or being inactive.
  • Sleep Quality: Quality of sleep may be monitored by wearing a tracker that alerts you if you start tossing and turning or waking up frequently throughout the night.
  • Sleep Phases: Some monitoring systems detect the stages of your sleep and schedule your alarm to go off during a moment when you’re sleeping less deeply. Assuming that’s true, you should find it less of a struggle to awaken.
  • Environmental Factors: Some gadgets keep track of environmental details like the temperature and lighting levels in your sleeping quarters.
  • Life style Factors: Some trackers ask you to input details about your day, such if you drank coffee, ate recently, and how stressful your day was.43

By monitoring your sleep patterns, the OURA RING can help you become a more productive, efficient version of yourself.

3.4.2. OURA Ring: Improving self-performance through sleep tracking

The Oura Ring is a Smart Ring product made to help you get the restful sleep you need to function at your best. It instructs you on how to control your body in accordance with your own circadian rhythm, a 24-hour cycle that determines the tempo at which our bodies and brains function optimally. Our best performance occurs when we allow our bodies to operate at their natural tempo, or circadian rhythm.

Oura keeps tabs on your nightly routine, recording the duration of each stage of sleep. It monitors a plethora of data points, from core body temperature to respiration rate to pulse amplitude to heart rate to heart rate fluctuation to even the tiniest hand and finger motions. Recommendations for aligning activities like exercise, eating, taking breaks, and sleeping with one’s individual circadian rhythm and nocturnal restorative patterns are provided via the Oura app. 44

(Fig 9. AURA Ring for Sleep Tracking)

4. Tests to monitor brain activity

A diagnosis may be suspected based on the patient’s medical history and neurologic exam, but further diagnostic testing may be required to confirm the diagnosis.

4.1. CT Scans (Computed Tomography)

Using specialized X-ray measurements, computed tomography (CT) of the brain generates horizontal or axial pictures (sometimes called slices) of the brain for diagnostic purposes. Compared to traditional head X-rays, brain CT scans can reveal more subtle details about brain tissue and brain architecture, which can aid in the diagnosis and treatment of brain injuries and disorders. The X-ray beam used in a brain CT rotates around the patient’s head and body to get detailed images from a variety of angles. A computer receives the X-ray data, processes it, and then shows the results in a two-dimensional (2D) format on a screen.

CT scans of the brain can be performed with or without the use of contrast. A contrast agent is a chemical that may be either orally or injected into an intravenous (IV) line in order to improve visibility of the organ or tissue of interest. There may be a window of time before a contrast exam during which you must abstain from eating and drinking. Your doctor will provide you this information before the operation.45

4.2. Electroencephalography (EEG)

Electroencephalography (EEG) is a noninvasive technique that uses electrodes to record electrical brain activity as wave patterns on paper or a computer. EEG can be used to diagnose the following:

  • Seizure disorders
  • Sleep disturbances
  • Disorders of brain metabolism or structure

Liver failure (liver encephalopathy) and some medicines can cause mental disorientation, and EEG can assist pinpoint the exact location of the seizure’s onset by revealing any related changes in electrical activity.

The method entails the application of adhesive sensors (electrodes) to the scalp in the shape of tiny, spherical discs. When the electrodes are wired to a computer, the system can record the minute voltage fluctuations picked up by each sensor. The electroencephalogram is based on these recordings (the EEG). One way to record electrical activity in the brain is with an electroencephalogram (EEG). The process is straightforward and comfortable. About 20 little sticky electrodes are implanted on the scalp, and the brain’s activity is recorded under normal settings. Sometimes the person is subjected to various stimuli, such as bright or flashing lights, to try to cause a seizure.46

(Fig 10. Electroencephalogram (EEG) test to monitor Brain Activity)

4.3. Electromyography (EMG)

Electromyography (EMG) is a diagnostic procedure in which a thin needle is placed into a muscle to record the electrical activity of the muscle both at rest and during contraction. No normal electrical activity is seen in resting muscle. There is some electrical activity with even a mild contraction, and it grows stronger as the contraction does.

An electromyogram is the record kept by an EMG machine. Symptoms of muscle weakness that originate from the spinal cord, the peripheral nervous system, the muscles, or the neuromuscular junction are indicative of something being wrong. Electromyography (EMG) and the patient’s history and symptoms allow for a diagnosis of the underlying cause of the anomalies.

A neurologist is needed for EMG because only they can choose the nerves and muscles to test and interpret the data, unlike technicians who can do CT and EEG frequently.47

(Fig 11. Electromyography (EMG) Test)

4.4. Nerve Conduction Studies

Motor and sensory nerve impulse conduction times can be determined by nerve conduction investigations. Testing is done by sending a tiny electrical current along the nerve. Multiple needles implanted along the nerve’s course or electrodes put on the skin’s surface can be used to supply the current. Once the impulse reaches the muscle, it triggers a contraction. Doctors can determine nerve conduction speed by timing how long it takes an impulse to travel from a stimulating electrode or needle to the targeted muscle. It is possible to stimulate the nerve once or several times (to determine how well the neuromuscular junction is functioning).48

5. References

  1. Gómez-Pinilla, F. (2011). The combined effects of exercise and foods in preventing neurological and cognitive disorders. Prevent. Med. 52:S75–S80.
  2. Parrott, M., and C. Greenwood (2007). Dietary influences on cognitive function with aging from high-fat diets to healthful eating Ann. N.Y. Acad. Sci. 1114:389–397.
  3. Booth, F. W., Roberts, C. K., & Laye, M. J. (2012). Lack of exercise is a major cause of chronic diseases. Comprehensive Physiology, 2(2), 1143–1211.
  4. Bowman S. A. (2006). Television-viewing characteristics of adults: correlations to eating practices and overweight and health status. Preventing chronic disease, 3(2), A38.
  5. Dolezal, B., Neufeld, E., Boland, D., Martin, J., & Cooper, C. (2017). Interrelationship between Sleep and Exercise: A Systematic Review. Advances in Preventive Medicine.
  6. Kline, C. (2014). The bidirectional relationship between exercise and sleep: Implications for exercise adherence and sleep improvement. American Journal of Lifestyle Medicine, 8(6), 375–379.
  7. Tallent J., Woodhead A., Frazer A. K., Hill J., Kidgell D. J., Howatson G. (2021). Corticospinal and spinal adaptations to motor skill and resistance training: potential mechanisms and implications for motor rehabilitation and athletic development. Eur. J. Appl. Physiol. 121 707–719. 10.1007/s00421-020-04584-2.
  8. Goodwill A. M., Pearce A. J., Kidgell D. J. (2012). Corticomotor plasticity following unilateral strength training. Musc. Nerve 46 384–393. 10.1002/mus.23316.
  9. Philpott D. T., Pearcey G. E., Forman D., Power K. E., Button D. C. (2015). Chronic resistance training enhances the spinal excitability of the biceps brachii in the non-dominant arm at moderate contraction intensities. Neurosci. Lett. 585 12–16. 10.1016/j.neulet.2014.11.009.
  10. Liu-Ambrose T., Nagamatsu L. S., Voss M. W., Khan K. M., Handy T. C. (2011). Resistance training and functional plasticity of the aging brain: a 12-month randomized controlled trial. Neurobiol. Aging 33 1690–1698. 10.1016/j.neurobiolaging.2011.05.010.
  11. Vincent K. R., Braith R. W., Bottiglieri T., Vincent H. K., Lowenthal D. T. (2003). Homocysteine, and lipoprotein levels following resistance training in older adults. Prev. Cardiol. 6 197–203. 10.1111/j.1520-037X.2003.01723.
  12. Nagamatsu L. S., Handy T. C., Hsu C. L., Voss M., Liu-Ambrose T. (2012). Resistance training promotes cognitive and functional brain plasticity in seniors with probable mild cognitive impairment. Arch. Intern. Med. 172 666–668. 10.1001/archinternmed.2012.379.
  13. Beck E. C., Dustman R. E. (1975). “Changes in evoked responses during maturation and aging in man and macaque,” in Behavior and Brain Electrical Activity, eds Burch N., Altshuler H. L. (Boston, MA: Springer), 431–472. 10.1007/978-1-4613-4434-6_19.
  14. Özkaya G. Y., Aydin H., Toraman F. N., Kizilay F., Özdemir Ö, Cetinkaya V. (2005). Effect of strength and endurance training on cognition in older people. J. Sport. Sci. Med. 4:300. 
  15. Widmann M., Nieß A.M., Munz B. Physical Exercise and Epigenetic Modifications in Skeletal Muscle. Sports Med. 2019;49:509–523. doi: 10.1007/s40279-019-01070-4.
  16. Pedersen B.K. Physical activity and muscle-brain cross-talk. Nat. Rev. Endocrinol. 2019;15:383–392. doi: 10.1038/s41574-019-0174-x.
  17. Pedersen B.K., Febbraio M.A. Muscles, exercise and obesity: Skeletal muscle as a secretory organ. Nat. Rev. Endocrinol. 2012;8:457–465. doi: 10.1038/nrendo.2012.49.
  18. Fischer C.P. Interleukin-6 in acute exercise and training: What is the biological relevance? Exerc. Immunol. Rev. 2006;12:6–33.
  19. Funk J.A., Gohlke J., Kraft A.D., McPherson C.A., Collins J.B., Harry G.J. Voluntary exercise protects hippocampal neurons from trimethyltin injury: Possible role of interleukin-6 to modulate tumor necrosis factor receptor-mediated neurotoxicity. Brain Behav. Immun. 2011;25:1063–1077. doi: 10.1016/j.bbi.2011.03.012.
  20. Erta M., Quintana A., Hidalgo J. Interleukin-6, a Major Cytokine in the Central Nervous System. Int. J. Biol. Sci. 2012;8:1254–1266. doi: 10.7150/ijbs.4679.
  21. Schumacher M.A., Chinnam N., Ohashi T., Shah R.S., Erickson H.P. The structure of irisin reveals a novel intersubunit beta-sheet fibronectin type III (FNIII) dimer: Implications for receptor activation. J. Biol. Chem. 2013;288:33738–33744. doi: 10.1074/jbc.M113.516641.
  22. Bostroem P., Wu J., Jedrychowski M.P., Korde A., Ye L., Lo J.C., Rasbach K.A., Bostroem E.A., Choi J.H., Long J.Z., et al. A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nat. Cell Biol. 2012;481:463–468. doi: 10.1038/nature10777. 
  23. Nygaard H., Slettaløkken G., Vegge G., Hollan I., Whist J.E., Strand T., Rønnestad B.R., Ellefsen S. Irisin in Blood Increases Transiently after Single Sessions of Intense Endurance Exercise and Heavy Strength Training. PLoS ONE. 2015;10:e0121367. doi: 10.1371/journal.pone.0121367. 
  24. Li D.J., Li Y.H., Yuan H.B., Qu L.F., Wang P. The novel exercise-induced hormone irisin protects against neuronal injury via activation of the Akt and ERK1/2 signaling pathways and contributes to the neuroprotection of physical exercise in cerebral ischemia. Metabolism. 2017;68:31–42. doi: 10.1016/j.metabol.2016.12.003.
  25. Lourenco M.V., Frozza R.L., De Freitas G.B., Zhang H., Kincheski G.C., Ribeiro F.C., Gonçalves R.A., Clarke J.R., Beckman D., Staniszewski A., et al. Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models. Nat. Med. 2019;25:165–175. doi: 10.1038/s41591-018-0275-4.
  26. Pedersen B.K. Physical activity and muscle-brain cross-talk. Nat. Rev. Endocrinol. 2019;15:383–392. doi: 10.1038/s41574-019-0174-x.
  27. Bremner, J. D., Moazzami, K., Wittbrodt, M. T., Nye, J. A., Lima, B. B., Gillespie, C. F., Rapaport, M. H., Pearce, B. D., Shah, A. J., & Vaccarino, V. (2020). Diet, Stress and Mental Health. Nutrients, 12(8), 2428.
  28. Clark J. E. (2015). Diet, exercise or diet with exercise: comparing the effectiveness of treatment options for weight-loss and changes in fitness for adults (18-65 years old) who are overfat, or obese; systematic review and meta-analysis. Journal of diabetes and metabolic disorders, 14, 31.
  29. Grandner, M. A., Kripke, D. F., Naidoo, N., & Langer, R. D. (2010). Relationships among dietary nutrients and subjective sleep, objective sleep, and napping in women. Sleep medicine, 11(2), 180–184.
  30. Erecińska, M., Nelson, D., Daikhin, Y., & Yudkoff, M. (1996). Regulation of GABA level in rat brain synaptosomes: fluxes through enzymes of the GABA shunt and effects of glutamate, calcium, and ketone bodies. Journal of neurochemistry67(6), 2325-2334.
  31.  Owen, O. E. (2005). Ketone bodies as a fuel for the brain during starvation. Biochemistry and molecular biology education33(4), 246-251.
  32. Jarrett, S. G., Milder, J. B., Liang, L. P., & Patel, M. (2008). The ketogenic diet increases mitochondrial glutathione levels. Journal of neurochemistry106(3), 1044-1051.
  33. Papanikolaou, Y., Brooks, J., Reider, C., & Fulgoni, V. L. (2014). US adults are not meeting recommended levels for fish and omega-3 fatty acid intake: results of an analysis using observational data from NHANES 2003–2008. Nutrition journal13, 1-6.
  34. Gerster, H. (1998). Can adults adequately convert a-linolenic acid (18: 3n-3) to eicosapentaenoic acid (20: 5n-3) and docosahexaenoic acid (22: 6n-3)?. International journal for vitamin and nutrition research68(3), 159-173.
  35. Helland, I. B., Smith, L., Saarem, K., Saugstad, O. D., & Drevon, C. A. (2003). Maternal supplementation with very-long-chain n-3 fatty acids during pregnancy and lactation augments children’s IQ at 4 years of age. Pediatrics111(1), e39-e44.
  36. Sinclair, A., Begg, D., Mathai, M., & Weisinger, R. (2007). Omega 3 fatty acids and the brain: review of studies in depression.
  37. Tan, Z. S., Harris, W. S., Beiser, A. S., Au, R., Himali, J. J., Debette, S., … & Seshadri, S. (2012). Red blood cell omega-3 fatty acid levels and markers of accelerated brain aging. Neurology78(9), 658-664.
  38. Bernert, R. A., Kim, J. S., Iwata, N. G., & Perlis, M. L. (2015). Sleep disturbances as an evidence-based suicide risk factor. Current psychiatry reports, 17(3), 554.
  40. Noguchi, H., & Sakaguchi, T. (1999). Effect of illuminance and color temperature on lowering of physiological activity. Applied human science : journal of physiological anthropology, 18(4), 117–123