Creatine: What It Is, How It Is Used and Why Brain Health Research Is Getting Interesting

Posted on by Stephen Brumwell

Creatine has moved a long way from its old reputation as a gym-only supplement.

For years, most people associated it with bodybuilding, strength training and muscle size. This makes sense, because Creatine monohydrate is one of the most researched supplements in sports nutrition, and its strongest evidence is still in exercise performance.

But recently, the conversation around Creatine has widened.

Research has now started to look more closely on Creatine’s role in brain energy, cognitive performance, and neurological health and support.

In this article, we’ll discuss what Creatine is, what it does, it’s current and future benefits, and what dosing creatine looks like now.

What Is Creatine?

Creatine is a compound made naturally in the body from the amino acids arginine, glycine and methionine. It is also found in animal foods such as meat and fish.

Most creatine is stored in skeletal muscle, but it is also found in other tissues, including the brain. Once stored, creatine helps recycle adenosine triphosphate, or ATP. ATP is the body’s immediate energy currency.

Basically, ATP provides quick energy for cells → ATP is used, phosphate group lost and becomes ADP → Creatine helps donate phosphate group back to ADP → ATP is regenerated!

That creatine-phosphocreatine system is especially useful when energy demand rises quickly. In muscle, that might mean sprinting, lifting or repeated high-intensity efforts. In the brain, it may matter when cognitive demand is high or energy availability is under pressure.

This is why creatine sits in an interesting place. It is not just a performance supplement. It is a bioenergetic compound, meaning it is involved in how cells manage and buffer energy.

Why Creatine Is Still Best Known for Exercise

Creatine’s benefits still lie largely in the realm of supporting physical performance.

The Australian Institute of Sport lists creatine monohydrate as a Group A supplement, meaning it has strong evidence for use in specific sporting situations. Its main role is supporting repeated high-intensity efforts, strength and power-based training, and training blocks where performance and adaptation matter.

Exercise types where Creatine tends to be most relevant include:

  • resistance training
  • sprint work
  • repeated high-intensity intervals
  • power-based sports
  • team sports involving repeated bursts of effort
  • training phases where lean mass and strength are priorities

It is less likely to create obvious benefits for low-intensity activity alone. Someone doing gentle walking or occasional yoga may not notice much from creatine. This is because the energy demand is much less.

When we lift heavy weights, sprint, train hard and do explosive workouts, we will notice it more due to a much higher energy demand.

Creatine Monohydrate vs Other Forms

There are many forms of creatine on the market: creatine hydrochloride, buffered creatine, creatine nitrate, creatine ethyl ester and various blended formulas.

I am honestly not opposed to using the other forms, they have their place. Creatine monohydrate is still probably the direction I would go, purely because it’s the form used in most of the research.

The Australian Institute of Sport notes that creatine monohydrate is well absorbed and that there is no clear scientific reason to choose another form over monohydrate for most uses.

The next step is buying Creatine monohydrate that is most pure. In Australia, most commercially available options are suitable and safe. If you want the purest option though, you can look for products that use either Creapure, Purest or OptiCreatine. Some product examples below.

To avoid overcomplicating it, and just zooming into the benefits of Creatine, start with looking for a product that gives you 3-5g of Creatine per scoop.

Creatine and Brain Energy

The brain is energy hungry. Although it represents only a small percentage of body weight, it uses a large amount of the body’s energy at rest.

This is where creatine research becomes more interesting.

Creatine helps buffer cellular energy. In the brain, that may be relevant during periods of increased demand, such as sleep loss, cognitive stress, ageing, injury or disease states where energy metabolism is altered.

FoundMyFitness (n.d.) highlights this shift well: creatine is no longer being discussed only as a sports supplement. It is also being studied for brain bioenergetics, cognition, sleep deprivation and neurodegenerative conditions.

Pausing here for a second though, The evidence does still show to be more stronger and settled for exercise performance vs brain health. This is not saying it isn’t beneficial, but more that the research is more substantial and available.

Brain-related research is promising, but it’s still developing. Candow et al. (2023) note that dose, duration, age, diet, health status and baseline creatine levels all appear to matter.

What Recent Cognitive Research Suggests

Xu et al. (2024) conducted a systematic review and meta-analysis of 16 randomised controlled trials involving 492 adults. They found that creatine monohydrate supplementation may have benefits for some aspects of cognitive function, particularly memory, attention time and processing speed. The authors also noted that larger, more robust trials are needed.

It does not mean creatine makes everyone smarter. It does not mean every healthy, well-rested adult will feel a dramatic mental boost. It suggests there may be specific cognitive domains and specific contexts where creatine is useful.

From what we can see, Creatine appears have the most measurable impact on a stressed or mentally fatigued brain. This means, we see the highest return on brain-states that are sleep deprived, ageing, have lower dietary creatine intake, or have a higher cognitive workload.

The takeaway is, creatine may be more noticeable when the system is under strain. For someone rested and collected, we’ll see less noticeable improvements.

Creatine and Sleep Deprivation

One of the more interesting newer studies looked at creatine during sleep deprivation.

Gordji-Nejad et al. (2024) gave healthy adults a single high dose of creatine monohydrate, 0.35 grams per kilogram of body weight, during 21 hours of sleep deprivation. The researchers found changes in brain energy markers and improvements in cognitive performance and processing speed compared with placebo.

For an 80 kg adult, 0.35 grams per kilogram is 28 grams of creatine in a single dose. That is much higher than a standard daily maintenance dose. It was used in a controlled research setting, not as a casual daily recommendation.

I would probably not try and consume that bolus of creatine either, it could end up resulting in an immediate trip to the bathroom.

What this really means is, don’t hero dose to get the benefits, spread it out across the day. A simple strategy is often 5g three times daily, or 10g twice daily, it depends on your original tolerance.

Creatine, Ageing and Neurodegenerative Research

FoundMyFitness (n.d.) summarised an early Alzheimer’s disease pilot study where 20 adults with early-stage Alzheimer’s disease took 20 grams of creatine monohydrate per day for 8 weeks, split into two 10 gram doses (see, don’t hero dose it!).

From this study, brain creatine stores increased on average, and several cognitive measures improved, this is amazing.

This study suggests even further than before that higher-dose creatine is capable of increasing brain creatine levels, and the link between creatine and brain-energy research needs more attention.

What was once a supplement just for the gym goer, has almost become a daily wellness or longevity essential. This leads us into the next question.

Who Might Be Most Interested in Creatine?

Creatine is still a very useful tool in your toolkit for people who want support for strength, training capacity or energy-demanding activities.

Creatine may also be super useful for the following

  • people doing regular resistance training
  • athletes or active people doing repeated high-intensity work
  • people rebuilding strength after time away from training
  • older adults wanting to support muscle function alongside exercise
  • vegetarians or people with low dietary creatine intake
  • people with ongoing sleep deprivation or sleep deficits (parenting, anyone?)
  • people with high physical or cognitive demands

Please note though, Creatine still works best beside the basics: adequate food, enough protein, progressive training, sleep, hydration and appropriate health care where needed.

Creatine is not a fix all solution, but in fact still a supplemental tool. Foundational health habits should always be covered as well.

Current Dosing Recommendations

For exercise performance and muscle creatine saturation, the standard dosing guidance has not changed dramatically.

Option 1: Loading phase

While less essential to do this now, the thought behind this is saturating muscle stores. This is especially relevant in the strength training or weight lifting area.

The loading approach is around 0.3 grams of creatine monohydrate per kilogram of body weight per day for about 5 days, usually split into 3 to 4 doses with meals.

After loading, a maintenance dose is usually around 3 to 5 grams per day, or about 0.03 grams per kilogram of body weight per day.

Option 2: No loading phase

Many people skip the loading phase and simply take 3 to 5 grams of creatine monohydrate per day.

This can still increase muscle creatine stores over time, but it usually still sufficient for most users.

For general health, training and simplicity, this is often the easiest option. It is cheaper, easier to remember and usually gentler on digestion.

Option 3: Cognitive demand dosing

There is no true exact number for this, so the optimal dose on increasing brain creatine is not clear.

Fabiano and Candow (2025) argue that brain-focused creatine research often uses higher dosing than standard sports nutrition protocols, but the ideal dose is still not clear. The practical approach here would be to split this up twice or three times daily (so 10g or 5g per dose per day).

Of course, if you have any pre-existing kidney or complex health issues, speaking to a health professional first is important before doing this.

Timing: When Should You Take Creatine?

Creatine works by increasing tissue creatine stores over time. It is not like caffeine, where the timing is tightly linked to an immediate stimulant effect.

The Australian Institute of Sport notes that creatine uptake may be supported when taken with meals containing carbohydrate and protein. Taking it after training with a normal post-exercise meal is also a practical habit for many people.

Some good times to fit creatine into your schedule is with breakfast, with lunch, before training, or simply mixed into a smoothie.

If creatine upsets your stomach, try taking it with food, using a smaller dose, or skipping the loading phase.

Common Creatine Myths

Myth 1: Creatine is a steroid

Creatine is not an anabolic steroid. It has a completely different structure and function. It is made naturally in the body and found in food.

Myth 2: Creatine is only for bodybuilders

Creatine is popular in bodybuilding, but its use is broader than that. It may support strength, power, sprint performance, training volume, older-adult muscle function and emerging areas of brain-energy research.

Myth 3: More creatine is always better

Higher doses may be used in specific research settings (such as sleep deprivation or high cognitive load, but for everyday use, 3 to 5 grams per day is still the most practical baseline for most healthy adults.

Myth 4: Creatine causes fat gain

Creatine can increase body weight in some people, often through increased water stored with muscle creatine. That is not the same as fat gain.

Myth 5: Creatine damages kidneys in healthy people

Antonio et al. (2021) note that creatine is generally well tolerated at recommended doses in healthy people. However, people with kidney disease, abnormal kidney markers or complex medical situations should get professional guidance first.

The Takeaway

Creatine monohydrate remains one of the most evidence-backed supplements for strength, power and repeated high-intensity exercise.

What has changed is the conversation around it.

Creatine is now being studied as a broader energy-support compound, particularly for the brain. The newer research into cognition, sleep deprivation, ageing and neurodegenerative conditions is promising, but it is not as settled as the exercise-performance research.

For most healthy adults, the practical starting point is still simple: creatine monohydrate, 3 to 5 grams per day, taken consistently. Loading can be useful when faster muscle saturation is desired, but it is not essential.

The bigger picture still matters. Creatine works best when it sits beside good food, enough protein, regular training, sleep and sensible health care.

If you are unsure whether creatine fits your goals, Stephen can help you look at the full picture: nutrition, training, lifestyle, energy, sleep and whether supplementation is likely to be useful for your situation.

FAQ

What is creatine used for?

Creatine is best known for supporting strength, power, repeated high-intensity exercise and training adaptation. It is also being researched for brain energy, cognition, sleep deprivation and ageing.

What is the best form of creatine?

Creatine monohydrate is the best-supported form and is usually the most practical choice.

How much creatine should I take?

A common daily dose is 3 to 5 grams of creatine monohydrate. A loading phase of around 20 grams per day for about 5 days can saturate muscle stores faster, followed by 3 to 5 grams per day.

Do I need to load creatine?

No. Loading is optional. Taking 3 to 5 grams per day without loading can still increase muscle creatine stores over time.

Can creatine support brain health?

Creatine may support aspects of brain energy metabolism, and research suggests possible benefits for memory, attention time and processing speed in some adults. The evidence is promising but still developing.

Are higher doses needed for brain benefits?

Possibly, but this is not settled. Some brain-focused studies use higher doses than standard sports nutrition protocols, but these are research settings rather than general public dosing advice.

Is creatine safe?

Creatine monohydrate is generally well tolerated in healthy people when used at recommended doses. People with kidney disease, complex medical conditions, pregnancy, breastfeeding or medication concerns should seek professional guidance first.

Does creatine cause weight gain?

It can increase scale weight for some people, often because creatine increases water stored inside muscle. This is not the same as gaining body fat.

References

Australian Institute of Sport. (n.d.). Creatine: How and when do I use it? Australian Sports Commission. https://www.ausport.gov.au/ais/nutrition/supplements/group_a/performance-supplements2/creatine/how-and-when-do-i-use-it

Antonio, J., Candow, D. G., Forbes, S. C., Gualano, B., Jagim, A. R., Kreider, R. B., Rawson, E. S., Smith-Ryan, A. E., VanDusseldorp, T. A., Willoughby, D. S., & Ziegenfuss, T. N. (2021). Common questions and misconceptions about creatine supplementation: What does the scientific evidence really show? Journal of the International Society of Sports Nutrition, 18, Article 13. https://doi.org/10.1186/s12970-021-00412-w

Candow, D. G., Forbes, S. C., Ostojic, S. M., Prokopidis, K., Stock, M. S., Harmon, K. K., & Faulkner, P. (2023). “Heads up” for creatine supplementation and its potential applications for brain health and function. Sports Medicine, 53(Suppl. 1), 49-65. https://doi.org/10.1007/s40279-023-01870-9

Fabiano, N., & Candow, D. (2025). Creatine supplementation: More is likely better for brain bioenergetics, health and function. Journal of Psychiatry and Brain Science, 10(4), Article e250006. https://doi.org/10.20900/jpbs.20250006

FoundMyFitness. (n.d.). Creatine. https://www.foundmyfitness.com/topics/creatine

Gordji-Nejad, A., Matusch, A., Kleedörfer, S., Patel, H. J., Drzezga, A., Elmenhorst, D., & Bauer, A. (2024). Single dose creatine improves cognitive performance and induces changes in cerebral high energy phosphates during sleep deprivation. Scientific Reports, 14, Article 4937. https://doi.org/10.1038/s41598-024-54249-9

Xu, C., Bi, S., Zhang, W., & Luo, L. (2024). The effects of creatine supplementation on cognitive function in adults: A systematic review and meta-analysis. Frontiers in Nutrition, 11, Article 1424972. https://doi.org/10.3389/fnut.2024.1424972

Beyond Iron: Why This Mineral Matters for More Than Energy and Fatigue

Posted on by Stephen Brumwell

Most people think about iron when they feel tired, and it’s more relevant for females, too, in this context.

Iron is essential for making haemoglobin, the protein in red blood cells that helps carry oxygen around the body. When iron is low, fatigue, weakness, breathlessness, dizziness and reduced exercise tolerance can be some of the first things people notice.

But iron is not just an energy/fatigue nutrient. It’s also involved in brain function, neurotransmitter production, dopamine signalling, thyroid hormone metabolism, mitochondrial energy production, immune function, muscle performance, sleep quality and restless legs syndrome. This is why low iron can sometimes show up as brain fog, poor concentration, low mood, feeling wired but exhausted, poor sleep, restless legs or anxiety-like symptoms.

That does not mean every tired, anxious or foggy person has low iron. Symptoms overlap with stress, poor sleep, thyroid issues, low B12, low vitamin D, under-eating, heavy training, chronic inflammation, alcohol history, gut issues, medications, pregnancy, postpartum depletion and many other causes, the list goes on.

In this article, we’ll unpack iron, including it’s simple role as a “fatigue” nutrient, and also beyond so that you can understand it further.

What To Know (Article Snapshot)

  • Iron helps carry oxygen through haemoglobin and supports oxygen use in muscles through myoglobin.
  • Iron is also involved in cellular energy production, thyroid hormone metabolism, neurotransmitter synthesis and brain development.
  • Low iron can exist before anaemia shows up on a standard full blood count.
  • Ferritin is commonly used to assess iron stores, but it needs to be interpreted in context because inflammation can raise ferritin.
  • Low iron may contribute to fatigue, reduced exercise tolerance, poor concentration, low mood, restless legs, poor sleep and anxiety-like symptoms in some people.
  • Restless legs syndrome has one of the stronger links with iron regulation, especially brain iron and dopamine pathways.
  • Iron supplements should not be taken casually without testing and guidance. Too much iron can be harmful.

Why Does Low Iron = Low Energy & Fatigue?

Iron is best known for transporting oxygen through-out the body.

Your body uses iron to make haemoglobin, which carries oxygen from the lungs through the bloodstream. Iron is also part of myoglobin, which helps muscles access and use oxygen. So, without iron, these two functions don’t operate per usual, leading to fatigue (NIH Office of Dietary Supplements).

So, all the talk on iron deficiency and fatigue is warranted, iron matters for energy.

But, that’s only the small part of the story.

Iron is also part of the enzymes and proteins that help generate cellular energy, regulate oxidative stress, and support normal neurological function,

When iron status is low, we present with symptoms related to fatigue. It may look like heavy limbs, brain fog, poor motivation, or reduced stress resilience.

Low Iron Is Not Always The Same As Anaemia

This is one of the most important points.

A person can have low iron stores without being anaemic.

Anaemia usually refers to low haemoglobin or a reduced ability of the blood to carry oxygen. Iron deficiency can eventually lead to iron deficiency anaemia, but iron stores may fall before haemoglobin drops below range.

This is where ferritin becomes useful. Ferritin is a protein that stores iron. Low ferritin often suggests depleted iron stores.

Australian Prescriber notes that non-anaemic iron deficiency is common, can cause non-specific symptoms, and is usually seen as low ferritin and low transferrin saturation with normal haemoglobin (Australian Prescriber).

That does not mean ferritin is the only marker that matters. Ferritin can rise with inflammation, infection, liver disease and other contexts, so a result that looks normal does not always tell the whole story.

This is why we generally want to look at the whole picture, and and also assess other factors including inflammatory markers, menstrual loss, diet, lifestyle, and more. (Auerbach et al., 2025)

When iron is low, we should be asking, why is it low and what else is happening around it?

Iron And The Brain

Iron is present throughout the brain and is involved in several processes that matter for cognition, mood, movement and nervous-system function.

A systematic review on women of childbearing age found evidence linking iron deficiency with poorer cognition, mental health scores and fatigue in several studies (Greig et al., 2013).

Although the authors noted more research is warranted, it does underscore the link on iron and brain function. It suggests that iron status can be relevant when someone presents with persistent fatigue, brain fog, low concentration, reduced motivation or mood changes.

If we look further, we can begin to see irons critical role in neurotransmitter synthesis and long-term nerve function.

Iron, Dopamine and Serotonin

Iron is a vital co-factor for enzymes involved in synthesising two key neurotransmitters, Dopamine and Serotonin.

These two fairly well known neurotransmitters are heavily involved in regulating our mood, motivation, focus, hunger and drive (to note a few).

In plain English, iron is part of the biochemical step to make these. When iron status insufficient, we see alterations in dopamine pathways, and impacts in emotional regulation and mood (Pivina et al., 2019).

Interestingly, we also need adequate iron for long-term nerve health. Iron is required for the production of myelin (the coating around our nerves). Some studies suggest early-life iron deficiency can impact this long-term, leading to deficits in neural development (Gao et al., 2025).

Iron And Restless Legs

Restless legs syndrome is one of the strongest reasons to think about iron beyond fatigue.

Restless legs can feel like an uncomfortable urge to move the legs, usually worse at rest or in the evening. It can make sleep difficult and leave someone exhausted during the day.

Iron regulation, brain iron and dopamine pathways are central to current discussions of restless legs syndrome. A 2025 review describes the link between iron deficiency and restless legs syndrome and explains how altered iron metabolism may contribute to the condition (Rizvi et al., 2025). A 2025 article in Sleep notes that iron dysregulation in the brain is now thought to play a fundamental role in the pathophysiology of restless legs syndrome (Sleep).

The American Academy of Sleep Medicine’s clinical practice guideline also recommends iron treatment in specific restless legs contexts where iron indices are appropriate, particularly intravenous ferric carboxymaltose for adults with restless legs syndrome and suitable iron status (AASM guideline summary on PubMed).

This does not mean everyone with restless legs should start iron. It means iron studies are often clinically relevant, especially when symptoms affect sleep.

For the average person, the useful takeaway is this: if you have restless legs, poor sleep and fatigue, it may be worth checking ferritin and full iron studies rather than assuming it is just stress, ageing or poor sleep hygiene.

Iron, Thyroid Function And Metabolism

Iron is also relevant to thyroid physiology.

Thyroid peroxidase, an enzyme involved in thyroid hormone synthesis, is iron-dependent. This is one reason iron deficiency has been studied in relation to thyroid function.

A 2023 systematic review and meta-analysis reported relationships between iron deficiency and thyroid function, including differences in TSH, free T4 and free T3 in some groups, particularly pregnant women and women of reproductive age (Garofalo et al., 2023). A 2021 systematic review and meta-analysis also examined iron deficiency as a risk factor for thyroid disorders in reproductive-age and pregnant women (Luo et al., 2021).

This means iron should be used as part of the bigger picture when someone is presenting with fatigue, cold sensitivity, low mood, hair loss. Thyroid function, iron status, inflammation, menstrual blood loss, protein intake, iodine, selenium, stress and sleep can all overlap.

Low Iron and Anxiety

Low iron can contribute to anxiety in a few overlapping ways.

The first is through oxygen delivery. When iron is low, the body may have a harder time making enough haemoglobin and moving oxygen efficiently. That can lead to symptoms such as racing heart, palpitations, shortness of breath, dizziness, poor exercise tolerance and feeling physically unsettled (Healthdirect Australia).

The second pathway is through the brain. Iron is involved in brain energy metabolism, myelination and monoamine neurotransmitter metabolism, including dopamine and serotonin pathways (Kim & Wessling-Resnick, 2014).

As mentioned previously, These neurotransmitters help regulate mood, motivation, focus, emotional steadiness and stress response. When iron availability is poor, these pathways may not function as smoothly, leading to anxiety.

One study in children with iron deficiency anaemia found changes in plasma dopamine, serotonin and brain-derived neurotrophic factor in response to variation in iron availability (Bani-Ahmad et al., 2022).

There is also emerging genetic evidence supporting a relationship between iron status and anxiety risk. A 2024 Mendelian randomisation study found that genetically predicted iron status biomarkers were linked with anxiety disorder risk (Yin et al., 2024).

Who Is More At Risk Of Low Iron?

Iron deficiency can happen because intake is low, needs are higher, absorption is reduced or losses are increased (if you were to look at it fundamentally).

Some common risk factors include:

  • Heavy menstrual bleedin
  • Pregnancy or postpartum recovery
  • Vegetarian or vegan diets without careful planning
  • Low overall food intake
  • Endurance training or high training loads (Foot-strike hemolysis)
  • Frequent blood donation
  • Gut conditions that affect absorption
  • Coeliac disease or inflammatory bowel disease
  • Long-term use of some medications that affect stomach acid or gut function
  • A history of iron deficiency
  • Diets low in iron-rich foods, protein or vitamin C

If iron is low because of heavy menstrual bleeding, gut bleeding, poor absorption or inflammation, simply taking a supplement without understanding the reason can leave the issue unresolved, and does not address the root cause.

Food Sources Of Iron

There are two main types of dietary iron: haem iron and non-haem iron.

Haem iron is found in animal foods and is generally more readily absorbed. Non-haem iron is found in plant foods and fortified foods. The NIH notes that haem iron has higher bioavailability than non-haem iron, and that vegetarian diets usually have lower iron bioavailability than mixed diets containing meat, seafood and vitamin C-rich foods (NIH Office of Dietary Supplements).

The numbers below are approximate iron amounts per 100g. They can vary depending on the cut, cooking method, brand, fortification level and database used (Healthdirect Australia; Nutrition Australia; USDA FoodData Central).

Haem iron foods

  • Beef: approximately 2.5-3.5mg per 100g
  • Lamb: approximately 2.5mg per 100g
  • Kangaroo: approximately 3.2-4.1mg per 100g
  • Chicken: approximately 0.4-1.3mg per 100g
  • Turkey: approximately 0.7-1.4mg per 100g, depending on white or dark meat
  • Fish: approximately 0.3-1.3mg per 100g, depending on the fish
  • Sardines: approximately 2.5-6.1mg per 100g, depending on whether canned or cooked/fried
  • Tuna: approximately 1.1-1.5mg per 100g
  • Oysters and mussels: approximately 6-9mg per 100g
  • Liver or organ meats, where appropriate: approximately 6-11mg per 100g, depending on the type

Non-haem iron foods

  • Lentils: approximately 3.3mg cooked or 9.1mg dry per 100g
  • Chickpeas: approximately 1.8-2.9mg per 100g
  • Beans: approximately 2-3mg per 100g, depending on the type
  • Tofu: approximately 2.9mg per 100g
  • Tempeh: approximately 2.7mg per 100g
  • Pumpkin seeds: approximately 8-9mg per 100g
  • Sesame seeds and tahini: sesame seeds approximately 14mg per 100g; tahini approximately 2-3mg per 100g
  • Cashews: approximately 5mg per 100g
  • Spinach and leafy greens: raw spinach approximately 3mg per 100g; cooked spinach can be higher per 100g because it is more concentrated
  • Quinoa: approximately 1.5mg cooked or 4.6mg dry per 100g
  • Iron-fortified cereals: varies widely, often approximately 8-16mg per serve depending on the product
  • Whole grains: approximately 1-4mg per 100g, depending on the grain
  • Dried apricots: approximately 3.1-6.3mg per 100g

Plant-based eaters can build iron-rich diets, but they usually need to be more intentional about absorption.

How To Improve Iron Absorption From Food

Iron absorption depends on the type of iron, the meal composition and the person’s current iron status.

Simple food-first strategies include:

  • Pair plant-based iron foods with vitamin C, such as citrus, kiwi, berries, capsicum or tomato.
  • Include haem iron foods if they fit your diet and values.
  • Avoid drinking tea or coffee directly with iron-rich meals if iron status is low.
  • Be mindful that calcium supplements can reduce iron absorption when taken at the same time.
  • Build meals around protein, colourful plants and enough overall food, not just one iron-rich ingredient.

Harvard’s Nutrition Source notes that vitamin C and haem iron can improve non-haem iron absorption, while phytates, tannins and large amounts of calcium can inhibit non-haem iron absorption (Harvard T.H. Chan School of Public Health).

Why You Should Not Self-Prescribe Iron

While supplementing with iron can be the most simple solution, consuming too much iron is equally as harmful as consuming too little.

Having too much iron in the body is toxic and can be fatal, and this is because it’s highly oxidative (think of too much oxidation as cellular rust).

Some people are also at risk of iron overload conditions such as haemochromatosis. This condition involves the inability to metabolise and clear iron from the body as fast as most people These people often need to give blood or reduce iron consumption, so if you have this condition, you definitely do not want to be touching an iron supplement.

Some iron supplements can also cause constipation, nausea, stomach pain and digestive discomfort. Usually, this depends on the type of supplement and iron source you choose, so it’s always good to discuss with a health practitioner first before supplementing with iron.

A sensible approach to take before taking an iron supplement includes:

  1. Test your iron levels first and understand your serum iron, ferritin and transferrin levels.
  2. Discuss with a health professional to understand the broader scope or other causative factors.
  3. Implement food first approaches alongside a good, bioavailable iron supplement.
  4. Recheck levels at a later date to measure against your first test baseline.
  5. Stop, reduce or adjust when appropriate.

When To Seek Professional Guidance

It is worth seeking guidance if you have ongoing symptoms such as:

  • Fatigue that does not improve with rest
  • Breathlessness on exertion
  • Dizziness or light-headedness
  • Poor concentration or memory issues
  • Restless legs or sleep disruption
  • Heavy menstrual bleeding
  • Hair shedding with fatigue or low mood
  • Reduced exercise tolerance
  • Pale skin or unusual weakness
  • A history of low ferritin or iron deficiency
  • Gut symptoms, blood in stool or unexplained weight changes

It is especially important to seek medical care if symptoms are severe, new, worsening or linked with possible blood loss or fainting.

Seeking out a Naturopath or Nutritionist can help interpret your blood results in context with other factors that could be causative factors to your low iron and overall fatigue picture.

The Takeaway

Iron is bigger than energy and fatigue.

It helps carry oxygen, but it also supports cellular energy production, brain function, dopamine-related pathways, sleep, restless legs, thyroid physiology and nervous-system resilience.

That is why low iron can sometimes feel like more than tiredness. It may show up as fogginess, poor concentration, low motivation, poor sleep, restless legs, reduced exercise tolerance or feeling wired but depleted.

But symptoms alone are not enough to diagnose low iron.

The smart approach is to test, interpret the results properly and understand why iron may be low in the first place. Food can help. Absorption strategies can help. Supplements may be useful when there is a confirmed need. But iron should not be taken casually without testing and guidance.

If you are dealing with fatigue, brain fog, restless legs, poor sleep, low mood, heavy periods or reduced exercise tolerance, Stephen can help you look at the bigger picture: diet, iron intake, ferritin and iron studies, nervous-system load, sleep, stress, training, thyroid context and other nutrients that may be part of the pattern.

FAQ

Why is iron more than an energy nutrient?

Iron helps carry oxygen, but it is also involved in cellular energy production, brain function, neurotransmitter synthesis, dopamine pathways, thyroid hormone metabolism, immune function and nervous-system health. That is why low iron can affect more than fatigue.

Can low iron cause anxiety-like symptoms?

Low iron can sometimes contribute to symptoms that overlap with anxiety, such as shortness of breath, racing heart, restlessness, poor sleep, dizziness, fatigue and reduced stress tolerance. It is not the only possible cause, so testing and proper assessment matter.

What is ferritin?

Ferritin is a protein that stores iron. Low ferritin can suggest low iron stores, even when haemoglobin is still normal. Ferritin can also rise with inflammation or illness, so it should be interpreted alongside symptoms, full blood count, iron studies and health context.

Can you have low iron without being anaemic?

Yes. Iron stores can become low before haemoglobin drops low enough to be classified as anaemia. This is often called non-anaemic iron deficiency. It may still be associated with symptoms such as fatigue, poor concentration, reduced exercise tolerance or restless legs.

Can low iron affect sleep?

Low iron can be linked with restless legs syndrome, which can disrupt sleep. Low iron may also contribute indirectly to fatigue, restlessness or poor recovery. Sleep problems can have many causes, so iron is one possible factor to investigate.

What foods contain iron?

Animal sources include beef, lamb, poultry, fish, seafood and organ meats. Plant sources include lentils, beans, chickpeas, tofu, tempeh, pumpkin seeds, tahini, leafy greens, quinoa and iron-fortified cereals. Pairing plant iron with vitamin C-rich foods can improve absorption.

Should I take iron supplements without testing?

No. Iron supplements should not be taken casually without testing or professional guidance. Too much iron can be harmful, and symptoms of low iron can overlap with many other issues. It is better to confirm whether iron is low, understand the cause and use the right approach.

Is plant-based iron enough?

It can be, but plant-based eaters usually need to be more intentional. Plant foods contain non-haem iron, which is less readily absorbed than haem iron and more affected by meal composition. Vitamin C-rich foods, adequate protein and smart meal timing can help.

How long does it take to improve low iron?

It depends on the severity, cause, treatment approach, absorption, diet and whether ongoing blood loss is present. Some people feel better within weeks, while iron stores may take longer to rebuild. Follow-up testing helps confirm whether the plan is working.

References

American Academy of Sleep Medicine. (2025). Treatment of restless legs syndrome and periodic limb movement disorder: An American Academy of Sleep Medicine clinical practice guideline. https://pubmed.ncbi.nlm.nih.gov/39324694/

Auerbach, M., DeLoughery, T. G., & Tirnauer, J. S. (2025). Iron deficiency in adults: A review. JAMA, 333(20), 1813-1823. https://doi.org/10.1001/jama.2025.0452

Australian Prescriber. (2021). Non-anaemic iron deficiency. https://australianprescriber.tg.org.au/articles/non-anaemic-iron-deficiency.html

Bani-Ahmad, M., Ahmad, M., Obeidat, M., & Barqawi, M. (2022). The modulation of plasma levels of dopamine, serotonin, and brain-derived neurotrophic factor in response to variation in iron availability. Acta Biomedica, 93(6), e2022293. https://doi.org/10.23750/abm.v93i6.13276

Gao, Q., Zhou, Y., Chen, Y., Hu, W., Jin, W., Zhou, C., Yuan, H., Li, J., Lin, Z., & Lin, W. (2025). Role of iron in brain development, aging, and neurodegenerative diseases. Annals of Medicine, 57(1), 2472871. https://doi.org/10.1080/07853890.2025.2472871

Garofalo, V., Condorelli, R. A., Cannarella, R., Aversa, A., Calogero, A. E., & La Vignera, S. (2023). Relationship between iron deficiency and thyroid function: A systematic review and meta-analysis. https://pubmed.ncbi.nlm.nih.gov/38004184/

Greig, A. J., Patterson, A. J., Collins, C. E., & Chalmers, K. A. (2013). Iron deficiency, cognition, mental health and fatigue in women of childbearing age: A systematic review. https://pubmed.ncbi.nlm.nih.gov/25191562/

Harvard T.H. Chan School of Public Health. Iron. https://nutritionsource.hsph.harvard.edu/iron/

Healthdirect Australia. How to meet your iron needs. https://www.healthdirect.gov.au/how-to-meet-your-iron-needs-infographic

Healthdirect Australia. Iron deficiency. https://www.healthdirect.gov.au/iron-deficiency

Kim, J., & Wessling-Resnick, M. (2014). Iron and mechanisms of emotional behavior. Journal of Nutritional Biochemistry, 25(11), 1101-1107. https://doi.org/10.1016/j.jnutbio.2014.07.003

Luo, J., Wang, X., Yuan, L., & Guo, L. (2021). Iron deficiency, a risk factor of thyroid disorders in reproductive-age and pregnant women: A systematic review and meta-analysis. https://pmc.ncbi.nlm.nih.gov/articles/PMC7947868/

National Institutes of Health, Office of Dietary Supplements. Iron: Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/Iron-HealthProfessional/

Nutrition Australia. (2021). Iron. https://nutritionaustralia.org/resources/iron/

Pivina, L., Semenova, Y., Doşa, M. D., Dauletyarova, M., & Bjørklund, G. (2019). Iron deficiency, cognitive functions, and neurobehavioral disorders in children. Journal of Molecular Neuroscience, 68(1), 1-10. https://doi.org/10.1007/s12031-019-01276-1

Rizvi, S., et al. (2025). Restless legs and iron deficiency: Unravelling the hidden link and current evidence. https://pmc.ncbi.nlm.nih.gov/articles/PMC12084866/

Sleep. (2025). Bringing iron to the brain for restless legs. https://academic.oup.com/sleep/article/48/7/zsaf128/8129076

U.S. Department of Agriculture. FoodData Central. https://fdc.nal.usda.gov/

Yin, R., Gao, Q., Fu, G., & Zhao, Q. (2024). The causal effect of iron status on risk of anxiety disorders: A two-sample Mendelian randomization study. PLOS ONE, 19(3), e0300143. https://doi.org/10.1371/journal.pone.0300143

Circadian Rhythm: Why Light Timing Matters for Sleep, Energy and Mood

Posted on by Stephen Brumwell

Morning sunlight can sound like one of those simple wellness habits that gets overhyped online. Wake up, get outside, fix your sleep, improve your mood, change your life.

The reality is, it’s so important, and it supports your circadian rhythm, your body clock.

Morning light is one of the strongest signals your body uses to understand what time of day it is. Your sleep, energy, alertness, body temperature, hormone rhythms, appetite patterns and mood are all influenced by internal timing systems. Those timing systems do not run in isolation. They respond to light, darkness, meals, movement, stress, work routines and social cues.

This is why morning sun can be helpful. Not because sunlight is magic, and not because it replaces proper sleep, nutrition, mental health support or medical care. It helps because the body is designed to read light as a timing signal.

If your sleep is drifting later, your mornings feel flat, your energy is scattered or your nights are full of screen light and late meals, morning light is one of the simplest places to start.

What To Know (Article Snapshot)

  • Circadian rhythms are roughly 24-hour biological patterns that help regulate sleep, alertness, body temperature, hormones, metabolism and stress responses.
  • Light is the strongest daily timing cue because the brain’s master clock is highly responsive to light and darkness.
  • Morning light tends to shift the body clock earlier, which can help support earlier sleepiness at night and easier waking in the morning.
  • Evening light can push the clock later, so bright light and screens at night may delay sleep timing.
  • UV safety still matters in Australia. Morning light can be useful, but sunburn is never the goal.

What Is Circadian Rhythm?

Circadian rhythm refers to the body’s roughly 24-hour timing system. It helps coordinate when you feel alert, when you feel sleepy, when body temperature rises and falls, when certain hormones change and how your body lines up with the day-night cycle.

The Sleep Health Foundation explains that circadian rhythms are closely connected to the 24-hour cycle of night and day, and that the brain’s internal clock is located in the suprachiasmatic nucleus, or SCN. The SCN is sensitive to light, which is why light plays such a central role in sleeping patterns (Sleep Health Foundation).

You can think of circadian rhythm as part of the body’s timing infrastructure. It does not control everything by itself, but when it is well aligned, sleep, energy and routine tend to make more sense.

When it is poorly aligned, people may notice patterns such as:

  • Feeling tired in the morning but wired at night
  • Struggling to fall asleep despite being exhausted
  • Needing alarms but still waking unrefreshed
  • Getting a second wind late in the evening
  • Feeling more alert after dark than during the day
  • Having irregular appetite, energy or motivation patterns

These patterns can have many causes, so they should not all be blamed on light exposure. But light timing is often worth reviewing because it is one of the easiest variables to change.

Why Morning Light Matters

Light and darkness are powerful time cues. In sleep science, these cues are sometimes called zeitgebers, which simply means time-givers.

Morning light helps tell the brain that the day has started. This can reduce melatonin signalling, support alertness and help anchor the body’s internal rhythm to the external day. As the day moves toward evening and light drops, melatonin can rise more appropriately and support sleepiness.

The CDC’s NIOSH training material on shift work explains the timing effect clearly: bright morning light tends to advance the circadian rhythm, meaning people feel sleepy earlier in the evening and wake earlier in the morning. Bright evening light tends to delay the rhythm, pushing sleepiness and waking later (CDC NIOSH).

A recent study on sunlight exposure and sleep found that morning sunlight was associated with sleep timing and overall sleep quality. In that study, every additional 30 minutes of morning sun exposure before 10 a.m. was associated with an earlier midpoint of sleep, and more morning sun exposure was linked with lower Pittsburgh Sleep Quality Index scores, suggesting better sleep quality (PubMed).

For people who feel stuck in late nights and slow mornings, this matters. Instead of only trying harder at bedtime, it can help to influence the clock earlier in the day.

Morning Light, Mood and Energy

Circadian rhythm is not only about sleep. It intersects with hormones, body temperature, nervous-system tone, alertness, cognitive function, appetite and stress regulation. Sleep Foundation notes that circadian rhythms help regulate sleeping and waking, core body temperature, hormones, metabolism, cognitive function and the body’s reaction to stress (Sleep Foundation).

Practically, this is why a dark indoor morning can feel different from a morning where you step outside, walk for 10 minutes and let your eyes register natural light.

If this is happeningMorning light may help by
You feel slow and foggy in the morningGiving the brain a clearer start-of-day signal.
You feel more alert late at nightHelping shift the rhythm earlier when used consistently.
Your routine has become irregularRebuilding a daily anchor point.
You spend most of the day indoorsIncreasing natural light exposure compared with dim indoor lighting.
Your mood dips during darker monthsSupporting rhythm, alertness and daily structure as part of a broader plan.

A practical starting point is 5 to 15 minutes outside in the morning, ideally within the first hour or two of waking. If the day is cloudy, you may still get useful outdoor light because outside light is usually much brighter than typical indoor light.

Some people may benefit from longer exposure, such as 20 to 30 minutes, especially if they are trying to shift a late sleep pattern earlier. But more is not automatically better, and Australian UV safety matters.

Helpful options include:

  • Drinking your morning coffee or tea outside
  • Taking a short walk before work
  • Sitting near outdoor light while eating breakfast
  • Walking the dog soon after waking
  • Doing gentle mobility outside
  • Opening curtains early, then getting outdoors when practical

Do not stare at the sun. The aim is outdoor light exposure, not direct sun-gazing.

Cancer Council Australia explains that UV radiation is both the major cause of skin cancer and the best natural source of vitamin D, and that Australians need to balance skin cancer risk with maintaining adequate vitamin D levels. They recommend sun protection when the UV Index is 3 or above, or when spending extended periods outdoors (Cancer Council Australia).

While the sun is beneficial for Vitamin D, excessive sun exposure can cause skin damage, which ultimately can have negative effects on our health (and longevity).

The Takeaway

Morning sunlight is a simple habit with a strong biological reason behind it, It is often core to supporting good sleep hygiene.

Your body uses light to help set its internal timing system. Morning light tends to support an earlier, clearer sleep-wake rhythm, while evening light can push the rhythm later. That is why morning sun can be useful for sleep, energy, alertness and daily routine.

The goal is not to turn sunlight into a cure-all. The goal is to use light intelligently.

Get outside early where possible. Keep it safe. Respect the Australian UV context. Pair morning light with consistent sleep timing, food, movement and lower evening stimulation. If sleep or mood symptoms are ongoing, get proper support rather than trying to solve everything with one habit.

If you are trying to rebuild your sleep, energy and nervous-system foundations, Stephen can help you look at the bigger picture: sleep timing, morning light, alcohol, caffeine, nutrition, stress, training, pathology and sustainable routine changes.

FAQ

Does morning sunlight help circadian rhythm?

Morning light is one of the strongest signals for the body’s internal clock. It can help tell the brain that the day has started and may support an earlier sleep-wake rhythm.

How soon after waking should I get sunlight?

A practical target is within the first hour or two of waking. It does not need to be perfect. The main goal is to give your body a regular morning light signal.

Can I get morning light on a cloudy day?

Yes. Outdoor light on a cloudy day is usually still much brighter than typical indoor lighting. It may not feel as intense, but it can still provide a useful timing cue.

Should I look directly at the sun?

No. Do not stare at the sun. The aim is outdoor light exposure through normal daylight, not direct sun-gazing.

Do I need sunscreen for morning sunlight?

It depends on the UV Index, your location, skin type, time outside and personal risk factors. Cancer Council Australia recommends sun protection when the UV Index is 3 or above, or when spending extended periods outdoors. if you decide to use sun protection, use an all-natural, zinc-based sunscreen!

What if I work night shift?

Shift work changes the timing equation. Bright light can help or hinder, depending on when it is used. If you work nights or rotating shifts, it is worth getting personalised advice (from someone like me!)

References

Cancer Council Australia. (2026). Vitamin D. https://www.cancer.org.au/cancer-information/causes-and-prevention/sun-safety/vitamin-d

CDC NIOSH. (2020). Effects of Light on Circadian Rhythms. https://www.cdc.gov/niosh/work-hour-training-for-nurses/longhours/mod2/19.html

Sleep Foundation. (2025). Circadian Rhythm. https://www.sleepfoundation.org/circadian-rhythm

Sleep Health Foundation. (n.d.). Circadian Rhythm Disorders. https://www.sleephealthfoundation.org.au/sleep-categories/circadian-rhythm-disorders

Teixeira, G. P., et al. (2025). The role of sunlight in sleep regulation: analysis of morning, evening and late exposure. PubMed. https://pubmed.ncbi.nlm.nih.gov/41053799/

Neurotransmitters: Understanding the Neurochemistry Behind Addiction and Sobriety

Posted on by Stephen Brumwell

I think since the day I started my nutrition degree, I had always been fascinated by the brain, but I never really knew why.

This all changed when I was introduced to the world of antidepressants, something that came into regular use as I tried to cope with alcohol addiction.

See, I never knew much about antidepressants at that point, and the extent of my knowledge of neurotransmitters was pretty basic.

Fast forward to late 2017, I came across a fantastic little book called Brain in Balance: Understanding the Genetics and Neurochemistry Behind Addiction and Sobriety. That book was a gold mine for simplifying the science of neurochemistry and how it relates to addiction. It got me deep in the weeds of how substance abuse can impact our neurochemical state.

Neurotransmitters can sound like a very technical subject, but they are really just chemical messengers that help your brain and nervous system communicate. They influence mood, motivation, sleep, appetite, stress response, focus, pain, cravings, pleasure, memory and the way you respond to everyday life.

That is why they matter so much in addiction recovery, alcohol recovery, substance abuse and sobriety.

When someone has been drinking heavily, using substances, sleeping poorly, under-eating, living under long-term stress or running on inconsistent routines, brain chemistry can feel out of balance. This does not mean every low mood, craving or poor sleep pattern can be neatly blamed on one neurotransmitter. The brain is far more complex than that.

But it does mean neurotransmitters are worth understanding.

Alcohol and other substances can affect several major neurotransmitter systems, including dopamine, GABA, glutamate, serotonin, opioid peptides, noradrenaline, acetylcholine and the endocannabinoid system. These systems help explain why early recovery can involve low motivation, anxiety-like symptoms, irritability, poor sleep, emotional sensitivity, cravings and that flat feeling where normal life does not feel rewarding yet (NIAAA, 2024; Yang et al., 2022).

The goal of this article is not to diagnose neurotransmitter deficiencies. It is to give you a clearer, practical understanding of how these systems work, why recovery can feel the way it does, and what kinds of foundations can support healthy brain chemistry over time.

What To Know (Article Snapshot)

  • Neurotransmitters are chemical messengers used by the brain and nervous system.
  • Serotonin has multiple receptor types throughout the body, often referred to as 5-HT receptors, and I like to describe these receptors as switches on a switchboard.
  • Alcohol and substance abuse affect multiple neurotransmitter systems, not just dopamine.
  • Dopamine is involved in reward, motivation, learning and habit formation.
  • GABA and glutamate help regulate the balance between calm and excitement in the nervous system.
  • Serotonin is involved in mood, appetite, sleep, pain sensitivity and emotional regulation.
  • Opioid peptides and endorphins are involved in pleasure, pain relief and reward reinforcement.
  • Noradrenaline is tied to alertness, stress response, arousal, focus and fight-or-flight physiology.
  • The endocannabinoid system helps regulate appetite, mood, pain, stress and neurotransmitter release.
  • Acetylcholine supports attention, memory, learning, REM sleep and parasympathetic nervous system activity.
  • In recovery, neurotransmitter systems can improve over time, but timelines vary. Some brain and cognitive changes may improve over months of abstinence, especially with consistent support (NIAAA, 2024; Powell et al., 2024).
  • Symptoms alone are not enough to diagnose a neurotransmitter problem. Diet, sleep, stress, alcohol history, medications, mental health, pathology and professional assessment all matter.

What Are Neurotransmitters?

Neurotransmitters are chemical signals used by our nervous system to transmit messages between neurons, or nerve cells.

We have billions of these neurons. The body could almost be considered a big battery, using neurons to send electrochemical signals across the brain and body.

These neurotransmitters are often grouped into different systems that you may have heard of before, including serotonin, dopamine, GABA and glutamate.

Some neurotransmitters are more excitatory. They help switch the system on, increase alertness, support learning and drive action. Others are more inhibitory. They help slow the system down, support calm, regulate sleep and stop the brain from running too hot.

Most of them are not simply good or bad. Dopamine is not just pleasure. Serotonin is not just happiness. GABA is not just calm. Glutamate is not just stress. Each one has multiple roles depending on the receptor, brain region, timing, context and the rest of the body.

In alcohol recovery, the useful way to think about neurotransmitters is this: repeated alcohol exposure can train the brain toward reward, relief and habit loops. When alcohol is removed, the brain has to recalibrate. That recalibration can affect mood, motivation, sleep, cravings, stress tolerance and emotional regulation.

Serotonin

Serotonin is one of the most well-known neurotransmitters, usually discussed in relation to mood.

But serotonin does much more than mood. It is involved in appetite, pain perception, sleep, arousal, gut function, sensory processing, impulse control and emotional regulation. Genetic variability in serotonin-related systems has also been studied in relation to behaviour and psychiatric disorders (Nordquist & Oreland, 2010).

Serotonin acts through many receptor types, often referred to as 5-HT receptors. I like to think of these receptors like switches on a switchboard. Some switches may increase activity in one pathway, while others may reduce activity somewhere else. That is one reason serotonin is not as simple as “more serotonin equals better mood.”

Alcohol can interact with serotonin systems and the wider reward circuitry of the brain. Serotonin also interacts with dopamine and GABA, which means it can influence reward, inhibition, mood and alcohol-related behaviour in complex ways (Lovinger, 1997; Marcinkiewcz, 2015).

Serotonin primary functions

  • Mood regulation
  • Appetite and satiety
  • Sleep and arousal rhythm
  • Pain sensitivity
  • Gut motility
  • Impulse control
  • Sensory processing
  • Emotional flexibility

Serotonin deficiency

Possible serotonin-related patterns may include low mood that feels worse during winter, anxiety or social anxiety patterns, aggression, OCD-type tendencies, carbohydrate cravings, constipation, low pain tolerance, poor dream recall, insomnia, impulsive tendencies or low self-esteem.

These patterns do not prove low serotonin. Similar symptoms can come from poor sleep, low protein intake, low iron, thyroid issues, trauma, medication changes, chronic stress, blood sugar instability or mental health conditions.

Serotonin excess

Possible serotonin excess can be more serious and may involve confusion, agitation, sweating, diarrhoea, nausea, muscle twitching or tremor. This is especially important if medications or supplements that affect serotonin are involved. Seek medical advice if symptoms are sudden, severe or medication-related.

If you have low serotonin production

A sensible serotonin-supportive foundation starts with the basics: regular meals, enough protein, daylight exposure, movement, sleep consistency and stress support.

Vitamin D status may also be worth considering, especially if mood feels worse in winter or sunlight exposure is low.

Tryptophan, an amino acid found in protein-containing foods, is a precursor for serotonin. But the answer is not to chase one amino acid in isolation. It is usually more useful to build consistent meals that contain quality protein, colourful plants, fibre and enough overall energy.

Dopamine

Dopamine is often described as the pleasure chemical, but that is only part of the story.

Dopamine is deeply involved in motivation, reward learning, drive, anticipation, habit formation, movement, attention and goal-directed behaviour.

In addiction and alcohol use disorder, dopamine is important because it helps the brain learn that alcohol and alcohol-related cues are rewarding. People, places, times of day, stress states, music, social settings or even certain emotions can become linked with drinking.

The National Institute on Alcohol Abuse and Alcoholism describes dopamine as critical for learning to associate alcohol and related cues with rewarding effects. Over time, repeated drinking can strengthen these reward and habit pathways, making cravings feel automatic rather than purely conscious (NIAAA, 2024; Volkow et al., 2010).

This is one reason early recovery can feel flat. If the brain has been trained to expect a large dopamine-related reward from alcohol, normal rewards like exercise, food, work, hobbies, sunlight, music and connection may take time to feel satisfying again.

Dopamine primary functions

  • Motivation and drive
  • Reward learning
  • Pleasure and anticipation
  • Habit formation
  • Focus and goal-directed behaviour
  • Movement control
  • Reinforcement of cues and routines

Dopamine deficiency

Possible dopamine-related patterns may include addictive tendencies, tremors or restless legs, low libido, lacking motivation, depression, mental exhaustion, dull or boring dreams, forgetfulness, low reward, cravings or impulsive behaviour.

Again, this is not a diagnosis. It is a pattern to understand, especially in early sobriety when normal rewards may feel muted.

Dopamine excess

Possible dopamine excess or overactivation may be associated with agitation, aggression, impulsivity, risk-taking, insomnia or, in more complex clinical states, psychosis-like symptoms. Schizophrenia is sometimes discussed in relation to dopamine pathways, but it is a clinical diagnosis and not something to self-diagnose from a blog post.

If you have low dopamine production

Dopamine recovery is not about forcing constant stimulation. In fact, chasing stronger stimulation can keep the reward system stuck in the same loop.

Better foundations include consistent sleep, morning light, exercise, enough protein, meaningful goals, structured routines, small wins, reduced alcohol exposure, social connection and time away from high-intensity reward triggers.

Tyrosine is an amino acid involved in catecholamine production, including dopamine and noradrenaline. It may be worth considering in some cases, but supplements should be treated carefully, especially with medications, anxiety, blood pressure issues or mental health conditions. Food and routine come first.

GABA

GABA, or gamma-aminobutyric acid, is the calming force that resides in the body, and one of the main inhibitory neurotransmitters in the brain. GABA modulation is one pathway discussed in anxiety and nervous-system regulation research (Gauthier & Nuss, 2015).

In practical terms, GABA helps slow neuronal activity. It creates calm, relaxation, supports the part of the nervous system that allows us to rest and digest, and helps balance the more agitating neurotransmitters such as glutamate and noradrenaline.

Alcohol has a strong relationship with GABA. One of alcohol’s short-term effects is that it can enhance inhibitory GABA activity while also reducing excitatory glutamate activity. This is part of why alcohol can initially feel relaxing, sedating or anxiety-reducing.

The problem is what happens with repeated exposure. The brain adapts. Over time, the nervous system may compensate for alcohol’s sedating effect. When alcohol is removed, that adapted system can feel overexcited, anxious, shaky, irritable or unable to sleep. In some people, alcohol withdrawal can become dangerous and requires medical supervision (NIAAA, 2024; Dharavath et al., 2023).

GABA primary functions

  • Main inhibitory neurotransmitters
  • Calm and relaxation
  • Sleep support
  • Sleep maintenance
  • Stress regulation
  • Balancing excitatory neurotransmission
  • Reducing excessive neuronal firing

GABA deficiency

Possible GABA-related patterns may include feeling wired, moving fast, talking rapidly, feeling overstimulated, anxiety-like symptoms, panic attacks, alcohol cravings, insomnia or dwelling over stressful situations.

But symptoms like anxiety and insomnia can have many causes. They should not be treated as proof that someone needs a GABA supplement.

GABA excess

True GABA excess is not usually something people identify from symptoms alone. Too much sedative activity from alcohol, medications or other substances may cause drowsiness, poor coordination, slowed thinking or excessive sedation, which needs appropriate medical context.

If you have low GABA production

Foundational support includes alcohol reduction or abstinence where appropriate, consistent sleep timing, magnesium-rich foods, adequate protein, breathwork, gentle evening routines, less late caffeine, light exposure management, movement and nervous-system regulation practices.

Magnesium is still one of the first nutrients I think about here because it supports normal nerve and muscle function and is involved in nervous-system regulation. That does not make magnesium a direct cure for anxiety or withdrawal, but it can be part of the bigger picture. If alcohol withdrawal symptoms are significant, medical support matters.

Glutamate

Glutamate is almost the opposite of GABA. It is one of the main excitatory neurotransmitters in the body.

It is essential for attention, learning, memory, focus, cognition, sensory processing and normal brain function. You do not want no glutamate. You want glutamate activity to be properly regulated, because chronic glutamate toxicity and excitotoxicity have been discussed in neurodegenerative and neuronal-injury research (Lewerenz & Maher, 2015; Prentice et al., 2015).

GABA and glutamate work together like a balancing system. GABA helps slow things down. Glutamate helps activate and stimulate. The nervous system needs both.

Alcohol can suppress glutamate activity in the short term. With repeated heavy alcohol use, the brain may compensate in the opposite direction. During withdrawal, this can contribute to excessive excitatory activity, which helps explain symptoms such as agitation, poor sleep, anxiety-like feelings, tremor and, in severe withdrawal, seizure risk (NIAAA, 2024; Becker & Mulholland, 2014).

This is one of the reasons alcohol withdrawal should not be taken lightly. If someone has been drinking heavily or daily, stopping suddenly can be medically risky.

Glutamate primary functions

  • Main excitatory neurotransmitters
  • Learning and memory
  • Focus and attention
  • Motor function
  • Sensory processing
  • Executive function
  • Neuroplasticity

Glutamate deficiency

Low or disrupted glutamate signalling can affect cognition, learning, focus and memory, but glutamate deficiency is not something to casually self-diagnose.

Glutamate excess

Possible glutamate excess or excitatory overactivity may feel like agitation, irritability, overwhelming anxiety, shakiness, poor memory, poor focus, poor concentration, racing thoughts, poor sleep or sound and light sensitivity. In alcohol withdrawal, excessive excitatory activity can become medically serious.

If you have high glutamate production

The biggest support is reducing the stressors that keep the nervous system overactivated. This can include alcohol support, sleep repair, consistent meals, blood sugar stability, magnesium-rich foods, calming routines, medical care where needed and gradual rebuilding of exercise tolerance.

If withdrawal symptoms are strong, professional help is not optional. It is the safer path.

Opioid and Endorphin System

The opioid system is a less commonly discussed one, but it is known for its ability to produce chemicals in the body called endorphins.

These are the body’s natural opioid-like chemicals, which are part of why you can feel good after a long run, a big exercise session, laughter, music, connection or meaningful achievement.

Opioid receptors are found across the nervous system and gastrointestinal tract and are involved in pain, reward, mood and gut function (Feng et al., 2012).

Alcohol can activate reward pathways involving opioid peptides and dopamine. This is one reason alcohol can feel reinforcing, especially when it is tied to relief, reward, social connection or emotional escape (NIAAA, 2024).

This system also helps explain why naltrexone, an opioid receptor antagonist, is used in alcohol use disorder treatment. It can reduce the pleasurable effects of alcohol by interfering with opioid-related reward activity. That does not mean everyone needs medication, but it does show how strongly reward chemistry is involved in alcohol behaviour.

Opioid and endorphin primary functions

  • Pain modulation
  • Pleasure and reward
  • Emotional comfort
  • Reward reinforcement
  • Social bonding
  • Exercise-related feel-good effects
  • Interaction with dopamine pathways

Opioid deficiency

Possible opioid or endorphin-system patterns may include low pain tolerance, addictive tendencies, carbohydrate cravings, anxiety-like feelings and tension, low mood, dwelling over major life situations, low pleasure or a strong desire for relief.

Again, these patterns are not diagnostic. They simply help explain why recovery can involve a period where life feels emotionally dull before natural rewards start to feel stronger again.

Opioid excess

Opioid-system excess is not usually a useful self-assessment category. In the context of opioid drugs or medications, excess opioid activity can be dangerous and may involve sedation, slowed breathing, confusion or loss of consciousness. That requires urgent medical support.

If you have low opioid or endorphin production

Helpful foundations include exercise at a tolerable level, sunlight, laughter, music, social connection, meaningful work, time in nature, physical affection where appropriate, cold or heat exposure if tolerated, and building routines that create natural reward without alcohol.

Noradrenaline

Noradrenaline, also called norepinephrine, are catecholamine-like neurotransmitters responsible for the body’s fight-or-flight stress response system.

It helps the body mobilise energy, increase heart rate, sharpen attention and respond to perceived threat. In the right amount, noradrenaline helps you wake up, focus and act. In excess or poor regulation, it can feel like stress, panic, tension or hypervigilance. Noradrenaline has also been discussed in stimulant addiction research and stress-related neurobiology (Sofuoglu & Sewell, 2009; Zhang et al., 2013).

In addiction science, noradrenaline is often discussed in relation to stress systems, withdrawal, negative emotional states and relapse risk. Newer reviews continue to explore noradrenergic mechanisms in alcohol use disorder, especially around stress, emotional pain and hyperkatifeia, which is a heightened negative emotional state linked with withdrawal and relapse vulnerability (NIAAA, 2024; Haass-Koffler et al., 2018; Varodayan et al., 2025).

Noradrenaline primary functions

  • Fight-or-flight response
  • Alertness and arousal
  • Focus and attention
  • Heart rate and blood pressure response
  • Stress adaptation
  • Memory formation around emotional events
  • Interaction with dopamine and serotonin systems

Noradrenaline deficiency

Possible noradrenaline-related deficiency patterns may include chronic stress, fatigue and pain, low mood, low blood pressure tendencies, blood sugar dips, exhaustion, short attention span, low pain tolerance or poor concentration.

Context matters, because the same person may swing between low arousal and overactivation depending on sleep, alcohol, caffeine, trauma, blood sugar and stress load.

Noradrenaline excess

Possible noradrenaline excess may feel like states of panic, panic attacks, racing heart, irritability, hypervigilance, poor stress tolerance, sleep disruption, tension or difficulty calming down after conflict.

If you have low noradrenaline production

Support starts with predictable routines, blood sugar stability, sleep repair, reducing alcohol and stimulant load, gentle movement, breathwork, therapy or coaching where appropriate, and building emotional regulation skills.

Because noradrenaline is made downstream from dopamine, the dopamine foundations above also matter. For some people, trauma, chronic stress or anxiety disorders are part of this picture and deserve proper support.

Endocannabinoid System

Our next neurotransmitter system is the endocannabinoid system, and to no surprise, it is closely tied with appetite, mood, pain, stress, inflammation, memory, reward and neurotransmitter release.

This is the system that gets activated in marijuana users, and it can often result in increased hunger, also known as the munchies.

The endocannabinoid system is commonly discussed through two receptor types, CB1 and CB2. CB1 receptors are found in high concentrations in the brain, especially in areas involved in emotion, memory, mood and sensory perception. CB2 receptors are often discussed in relation to immune signalling and inflammation, though the system is more complex than a simple brain-versus-immune split.

One interesting feature of the endocannabinoid system is that it can help regulate neurotransmitter release. In simple terms, it helps the nervous system modulate other signals rather than just pushing one direction all the time (Zou & Kumar, 2018). The endocannabinoid system has also been reviewed in relation to depression, reward and pain control (Huang et al., 2016).

Alcohol research has also explored endocannabinoid signalling in brain regions involved in stress and reward, including the amygdala and related circuits (Bedse et al., 2019).

Endocannabinoid primary functions

  • Regulation of feeding behaviour
  • Appetite
  • Energy metabolism
  • Learning and memory
  • Pain and inflammation
  • Mood and emotional regulation
  • Reward and motivation
  • Regulation of neurotransmitter release

Endocannabinoid deficiency

Possible endocannabinoid-related deficiency patterns may include low pain tolerance, excessive inflammation, treatment-resistant patterns, changes in appetite, poor stress tolerance, mood changes, poor sleep or feeling less able to experience natural reward.

This does not mean cannabis is automatically the answer. Cannabis can affect the same system, but it can also create problems for some people, especially when used heavily or relied on for sleep, appetite, stress or emotional regulation.

Endocannabinoid excess

Possible endocannabinoid overactivation may be associated with excessive food intake, increased obesity risk, lower motivation, altered memory, sedation or greater reliance on cannabis or other external inputs for regulation.

If you have low endocannabinoid production

A good place to start here is a foundation that supports the body’s own endocannabinoid system: exercise, omega-3-rich foods, good sleep, stress regulation, social connection, time outdoors and reducing reliance on substances that override natural regulation.

Acetylcholine

Our last neurotransmitter is acetylcholine, which is vital for memory formation, memory recall and keeping our attention span sharp.

It is also relevant to nicotine and alcohol. Nicotine acts on nicotinic acetylcholine receptors, which are connected with dopamine reward pathways. Research has also explored how nicotinic acetylcholine receptors contribute to smoking, alcohol reward and dependence (Brunzell et al., 2015; Rahman et al., 2015; Tarren et al., 2016).

This helps explain why alcohol and smoking often become paired behaviours. The combination can amplify reward learning and make cues stronger.

Acetylcholine primary functions

  • Memory formation
  • Learning
  • Attention span
  • REM sleep
  • Parasympathetic nervous system function
  • Digestive secretions and motility
  • Muscle activation
  • Interaction with reward pathways

Acetylcholine deficiency

Possible acetylcholine-related patterns may include sympathetic dominance, short-term memory problems, age-related cognitive decline, impaired digestive function, being a light sleeper, poor sleep onset, tension in muscles, poor attention or strong nicotine-related cue patterns.

But again, those symptoms can have many causes. Sleep deprivation alone can affect memory, focus and emotional regulation.

Acetylcholine excess

Acetylcholine excess is not something to casually self-diagnose. In the wrong context, too much cholinergic activity can be associated with nausea, sweating, salivation, digestive upset, muscle twitching or other symptoms that need medical interpretation.

If you have low acetylcholine production

Choline-containing foods can support acetylcholine production. These include eggs, fish, chicken, beef, dairy, soy foods and some legumes.

Acetyl-l-carnitine is sometimes discussed in this space too, but I would still look at the bigger picture first: sleep, protein intake, nutrient density, alcohol reduction, nicotine support where needed, stress regulation and consistent routines.

What Supports Healthy Neurotransmitter Production?

It is tempting to jump straight to supplements, but neurotransmitters are not built in isolation. While the list of supporting neurotransmitters can be endless, below is a rather non-selective but good starting point. Most of these are foundational to our health and habits – I write more about Foundational Health Habits here, and how they support sobriety, recovery and resilience.

  • Enough protein intake – Sufficient protein intake is essential for healthy neurotransmitter production
  • B vitamins, Magnesium, zinc, iron and other minerals
  • Omega-3 fats help our nerves and neurons fire effectively
  • Good Sleep quality, Morning light and a balanced circadian rhythm – More on sleep hygiene here.
  • Exercise and movement
  • Stress regulation
  • Gut health
  • Reduced alcohol exposure and sustained abstinence.
  • And more.

If you are in alcohol recovery, this is the important part: feeling flat, anxious, unmotivated or emotionally sensitive does not mean you are broken. It may reflect a nervous system that is recalibrating after a long period of artificial reward, sedation, stimulation or stress relief.

The Takeaway

Hopefully, this gives you a fairly succinct and overall understanding of the many neurotransmitters found in the body, and why they matter so much in substance abuse, addiction recovery and sobriety.

Alcohol and substance use can affect multiple neurotransmitter systems at once. Dopamine, serotonin, GABA, glutamate, opioid peptides, noradrenaline, acetylcholine and the endocannabinoid system all play different roles in reward, relief, withdrawal, cravings, mood and nervous-system balance.

This is why early recovery can feel so physical and emotional. It is not simply a mindset issue. The brain and body are adapting.

The good news is that the brain is plastic. It can change. Research suggests that at least some alcohol-related brain and cognitive changes can improve with abstinence and the right support, although timelines vary from person to person (NIAAA, 2024; Powell et al., 2024).

The practical path is to build foundations: food, protein, sleep, morning light, movement, stress regulation, connection, medical support where needed and consistency.

If you are unsure what is driving your symptoms, Stephen can help you look at your diet, alcohol history, sleep, stress load, pathology, habits and supplement use in context.

FAQ

What neurotransmitters are involved in alcohol recovery?

Several neurotransmitter systems are involved in alcohol recovery, including dopamine, GABA, glutamate, serotonin, opioid peptides, noradrenaline, acetylcholine and the endocannabinoid system. These systems influence reward, motivation, stress, sleep, cravings, mood and nervous-system regulation.

Can low dopamine affect motivation after quitting alcohol?

Dopamine is involved in motivation, reward learning and habit formation. After repeated alcohol use, normal everyday rewards may feel less satisfying for a while. This can contribute to low motivation or feeling flat in early recovery. It does not mean dopamine is the only factor, but it is part of the picture.

Why do I feel anxious or wired after stopping alcohol?

Alcohol can affect the balance between GABA, which is inhibitory, and glutamate, which is excitatory. After repeated heavy drinking, stopping suddenly can leave the nervous system overexcited. This may contribute to anxiety-like symptoms, poor sleep, irritability or shakiness. Heavy or daily drinkers should seek medical advice before stopping suddenly because withdrawal can be dangerous.

How long does brain chemistry take to rebalance after alcohol?

There is no single timeline. Some people notice improvements within weeks, while other changes can take months or longer. Research suggests some cognitive and brain changes related to alcohol use disorder can improve with abstinence, but recovery depends on the person, drinking history, health status, sleep, nutrition, treatment and support.

What foods support neurotransmitter production?

Protein-rich foods provide amino acids used to make neurotransmitters. Examples include eggs, fish, meat, poultry, Greek yoghurt, legumes, tofu, tempeh, nuts and seeds. Nutrient-dense whole foods also provide B vitamins, magnesium, zinc, iron, omega-3 fats and other cofactors that support normal nervous-system function.

Are neurotransmitter symptoms enough to diagnose a deficiency?

No. Symptoms are not enough to diagnose a neurotransmitter deficiency. Low mood, anxiety, cravings, poor sleep, fatigue and brain fog can have many causes. Diet, blood sugar, sleep, stress, trauma, medications, alcohol history, mental health and pathology all need to be considered.

Can supplements fix neurotransmitters?

Supplements can sometimes help when there is a clear nutritional need, but they are not a shortcut for recovery and should not replace medical care. Some supplements can interact with medications or be unsuitable for certain conditions. Food, sleep, alcohol support, movement, mental health care and proper assessment come first.

Is alcohol withdrawal dangerous?

It can be. People who drink heavily or daily should not assume they can stop suddenly without risk. Alcohol withdrawal can involve serious symptoms, including seizures in some cases. Medical support is important if there is any concern.

References

Brunzell, D. H., Stafford, A. M., & Dixon, C. I. (2015). Nicotinic receptor contributions to smoking: Insights from human studies and animal models. Current Addiction Reports, 2(1), 33-46. https://doi.org/10.1007/s40429-015-0042-2

Feng, Y., He, X., Yang, Y., Chao, D., Lazarus, L. H., & Xia, Y. (2012). Current research on opioid receptor function. Current Drug Targets, 13(2), 230-246. https://doi.org/10.2174/138945012799201612

Gauthier, I., & Nuss, P. (2015). Anxiety disorders and GABA neurotransmission: A disturbance of modulation. Neuropsychiatric Disease and Treatment, 11, 165-175. https://doi.org/10.2147/NDT.S58841

Huang, W., Chen, W., & Zhang, X. (2016). Endocannabinoid system: Role in depression, reward and pain control. Molecular Medicine Reports, 14(4), 2899-2903. https://doi.org/10.3892/mmr.2016.5585

Lewerenz, J., & Maher, P. (2015). Chronic glutamate toxicity in neurodegenerative diseases: What is the evidence? Frontiers in Neuroscience, 9, 469. https://doi.org/10.3389/fnins.2015.00469

Nordquist, N., & Oreland, L. (2010). Serotonin, genetic variability, behaviour, and psychiatric disorders: A review. Upsala Journal of Medical Sciences, 115(1), 2-10. https://doi.org/10.3109/03009730903573246

Prentice, H., Modi, J. P., & Wu, J. Y. (2015). Mechanisms of neuronal protection against excitotoxicity, endoplasmic reticulum stress, and mitochondrial dysfunction in stroke and neurodegenerative diseases. Oxidative Medicine and Cellular Longevity, 2015, 964518. https://doi.org/10.1155/2015/964518

Sofuoglu, M., & Sewell, R. A. (2009). Norepinephrine and stimulant addiction. Addiction Biology, 14(2), 119-129. https://doi.org/10.1111/j.1369-1600.2008.00138.x

Tarren, J. R., Shariff, M., Holgate, J., & Bartlett, S. E. (2016). Effects of alcohol on nicotinic acetylcholine receptors and impact on addiction. In Neuropathology of Drug Addictions and Substance Misuse (pp. 411-419). https://doi.org/10.1016/B978-0-12-800213-1.00038-9

Volkow, N. D., Wang, G. J., Fowler, J. S., Tomasi, D., Telang, F., & Baler, R. (2010). Addiction: Decreased reward sensitivity and increased expectation sensitivity conspire to overwhelm the brain’s control circuit. BioEssays, 32(9), 748-755. https://doi.org/10.1002/bies.201000042

Zhang, G., Gao, Z., Guan, S., Zhu, Y., & Wang, J. (2013). Upregulation of excitatory neurons and downregulation of inhibitory neurons in barrel cortex are associated with loss of whisker inputs. Molecular Brain, 6, 2. https://doi.org/10.1186/1756-6606-6-2

Dharavath, R. N., Pina-Leblanc, C., Tang, V. M., Sloan, M. E., Nikolova, Y. S., Pangarov, P., Ruocco, A. C., Shield, K., Voineskos, D., Blumberger, D. M., Boileau, I., Bozinoff, N., Gerretsen, P., Vieira, E., Melamed, O. C., Sibille, E., Quilty, L. C., & Prevot, T. D. (2023). GABAergic signaling in alcohol use disorder and withdrawal: Pathological involvement and therapeutic potential. Frontiers in Neural Circuits, 17, 1218737. https://www.frontiersin.org/journals/neural-circuits/articles/10.3389/fncir.2023.1218737/full

Varodayan, F. P., Erikson, C. M., Scroger, M. V., & Roberto, M. (2025). Noradrenergic mechanisms and circuitry of hyperkatifeia in alcohol use disorder. Biological Psychiatry, 97(6), 580-589. https://pmc.ncbi.nlm.nih.gov/articles/PMC11839382/

Yang, W., Singla, R., Maheshwari, O., Fontaine, C. J., & Gil-Mohapel, J. (2022). Alcohol use disorder: Neurobiology and therapeutics. Biomedicines, 10(5), 1192. https://pmc.ncbi.nlm.nih.gov/articles/PMC9139063/

Haass-Koffler, C. L., et al. (2018). Noradrenergic targets for the treatment of alcohol use disorder. Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/29460163/

Lovinger, D. M. (1997). Serotonin’s role in alcohol’s effects on the brain. Alcohol Health and Research World. https://pmc.ncbi.nlm.nih.gov/articles/PMC6826824/

Marcinkiewcz, C. A. (2015). Serotonergic neuroplasticity in alcohol addiction. ACS Chemical Neuroscience. https://pmc.ncbi.nlm.nih.gov/articles/PMC5928559/

National Institute on Alcohol Abuse and Alcoholism. (2024). Neuroscience: The brain in addiction and recovery. https://www.niaaa.nih.gov/health-professionals-communities/core-resource-on-alcohol/neuroscience-brain-addiction-and-recovery

Powell, A., Sumnall, H., Smith, J., Kuiper, R., & Montgomery, C. (2024). Recovery of neuropsychological function following abstinence from alcohol in adults diagnosed with an alcohol use disorder: Systematic review of longitudinal studies. PLOS ONE. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0296043

Rahman, S., Engleman, E. A., & Bell, R. L. (2015). Nicotinic receptor modulation to treat alcohol and drug dependence. Frontiers in Neuroscience, 8, 426. https://pmc.ncbi.nlm.nih.gov/articles/PMC4754113/

Becker, H. C., & Mulholland, P. J. (2014). Neurochemical mechanisms of alcohol withdrawal. Handbook of Clinical Neurology, 125, 133-156. https://pmc.ncbi.nlm.nih.gov/articles/PMC6943828/

Bedse, G., Centanni, S. W., Winder, D. G., & Patel, S. (2019). Endocannabinoid signaling in the central amygdala and bed nucleus of the stria terminalis: Implications for the pathophysiology and treatment of alcohol use disorder. Alcoholism: Clinical and Experimental Research, 43(10), 2014-2027. https://pmc.ncbi.nlm.nih.gov/articles/PMC6779484/

Zou, S., & Kumar, U. (2018). Cannabinoid receptors and the endocannabinoid system: Signaling and function in the central nervous system. International Journal of Molecular Sciences, 19(3), 833. https://doi.org/10.3390/ijms19030833

Magnesium: Why This Mineral Matters for Energy, Stress, Sleep and the Nervous System

Posted on by Stephen Brumwell

Magnesium is one of those nutrients that can sound simple on the surface. It gets mentioned for cramps, sleep, stress and muscle relaxation, so it is easy to think of it as a basic supplement you take when you feel tight, tired or wired.

But magnesium is much deeper than that, and in this article, we’ll unpack magnesium from various angles.

Magnesium is an essential mineral involved in more than 300 enzymatic reactions in the body. It supports energy production, protein synthesis, nerve communication, muscle contraction and relaxation, blood glucose regulation, blood pressure regulation, DNA function, electrolyte balance and normal cellular signalling (Kirkland et al., 2018; DiNicolantonio et al., 2018).

That is why magnesium is not just a sleep nutrient, a cramp nutrient or a recovery nutrient. It is a foundational mineral for normal physiology.

Magnesium becomes especially relevant when the body has been under pressure. Poor diet, heavy alcohol use, chronic stress, hard training, inconsistent meals, digestive issues and poor sleep can all increase the need to pay attention to magnesium intake and status.

Whether someone is rebuilding after alcohol use, dealing with long-term stress, training hard, eating inconsistently, struggling with sleep or simply trying to understand their nutrition better, magnesium is worth understanding properly.

What To Know (Snapshot Takeaway)

  • Magnesium is an essential mineral and cofactor in hundreds of enzymatic reactions.
  • It plays a major role in ATP production, nerve signalling, muscle relaxation, blood glucose regulation, blood pressure regulation, DNA stability and neurotransmission.
  • Magnesium is especially relevant to the nervous system because it helps regulate excitatory signalling, including pathways involving glutamate and NMDA receptors (Kirkland et al., 2018; Gillessen et al., 2000-2013).
  • Low magnesium intake is not rare. Older Australian Health Survey data found inadequate magnesium intake was common in younger Australians (Australian Bureau of Statistics, 2015). More recent ABS data also suggests inadequate magnesium intake remains common across the population (Australian Bureau of Statistics, 2026).
  • Alcohol, poor dietary intake, digestive issues, diuretics, high stress, diabetes, diarrhoea and some medications can all increase the likelihood that magnesium status needs attention.
  • Food should come first where possible, but supplement form matters. Magnesium glycinate, citrate, oxide, malate, taurate, threonate, chloride and orotate are not the same.
  • Do not treat symptoms alone as proof of deficiency. Magnesium assessment should consider diet, symptoms, medications, health conditions and testing where appropriate.

What Is Magnesium?

Magnesium, or Mg, is an essential mineral. Your body cannot make it, so it has to come from food, fluids and, in some cases, supplements.

Most magnesium is stored in bone and muscle. Only a small amount circulates in the blood, which is one reason magnesium deficiency can be difficult to assess from a standard blood test alone. This does not mean testing is pointless. It means the result needs to be interpreted with the broader clinical picture.

Magnesium is involved in protein synthesis, cellular energy production, glucose metabolism, blood pressure regulation, neuromuscular function and nervous-system signalling (DiNicolantonio et al., 2018; Kirkland et al., 2018).

One of the deeper reasons magnesium matters is its relationship with the nervous system.

Magnesium helps regulate excitatory signalling in the brain and nervous system, particularly through its influence on NMDA receptors and glutamate pathways (Kirkland et al., 2018). Glutamate is an important excitatory neurotransmitter. We need it for normal brain function, but excessive excitatory activity is not something we want running unchecked.

In more technical terms, high excitatory amino acid activity can contribute to neurotoxicity when the system is pushed beyond its normal range (Gillessen et al., 2000-2013). In more practical language: magnesium is one of the nutrients involved in keeping nerve signaling from becoming too overexcited.

That does not mean magnesium is a treatment for anxiety, addiction, insomnia or neurological disease. It means magnesium sits right in the middle of many systems that matter when someone feels stressed, depleted, wired, tense, crampy, sleep-deprived or under-recovered.

The Role of Magnesium in the Body

Magnesium serves many purposes in the body. The list can get long very quickly, but the main roles are worth understanding.

One key role is ATP production. ATP, or adenosine triphosphate, is the main energy currency your cells use to do work. Magnesium is required for normal ATP function, so when we talk about cellular energy, magnesium is part of that conversation (DiNicolantonio et al., 2018).

Magnesium also supports:

  • Protein synthesis: Magnesium acts as a cofactor for enzymes involved in RNA, DNA and protein synthesis.
  • Muscle contraction and relaxation: Magnesium interacts with calcium signalling, which helps muscles contract and relax appropriately.
  • Neurons and nerve function: Magnesium is involved in neurotransmitter release and normal nerve communication (Kirkland et al., 2018).
  • Blood glucose control: Magnesium plays a role in insulin action and glucose metabolism (DiNicolantonio et al., 2018).
  • Blood pressure regulation: Magnesium can influence vascular tone and calcium-channel activity, which is relevant to blood pressure physiology.
  • Hormone receptor signalling: Magnesium helps support normal cellular signalling processes.
  • Calcium-channel gating: Magnesium influences calcium movement across membranes, which matters for nerve and muscle function.
  • DNA support: Magnesium contributes to DNA stability, repair and replication.
  • Glycolysis: Magnesium is involved in enzymes that help break down glucose for energy.

So when someone says magnesium is important, they are not exaggerating. It is woven through normal body function.

The practical takeaway is this: if your diet has been poor, your stress has been high, your sleep has been rough, you have been drinking heavily, your digestion is compromised or you are relying on ultra-processed foods, magnesium is one of the first nutrients worth bringing back into the conversation.

Magnesium, Alcohol and Nutrient Depletion

Although this article is not focused on alcohol and addiction, it’s part of my past experience, and deserves it’s own section due to many ways alcohol can impact magnesium status.

Alcohol can contribute to magnesium depletion through several direct and indirect mechanisms.

Reduced absorption

Chronic alcohol intake can affect the gastrointestinal tract and may impair normal nutrient absorption. Magnesium is absorbed mainly in the small intestine, so gut integrity and digestive function matter.

Increased loss

Alcohol can have a diuretic effect, increasing urine production and potentially increasing the loss of minerals and electrolytes. Magnesium can be lost this way, particularly when alcohol intake is frequent or heavy.

Poor dietary habits

Alcohol often displaces food. Some people skip meals, under-eat, rely on takeaway, crave refined carbohydrates or lose the routine of balanced eating. That can mean fewer magnesium-rich foods such as nuts, seeds, legumes, leafy greens, whole grains and quality protein meals.

Wider metabolic stress

Alcohol can also affect liver function, hormones, sleep, blood sugar and appetite regulation. These do not all mean magnesium deficiency is guaranteed, but they do increase the relevance of nutrition assessment.

This is why magnesium can matter in alcohol reduction or recovery. Not because magnesium fixes recovery, but because the body may need better nutritional foundations after a long period of depletion.

How Do I Know If I Am Low in Magnesium?

It’s a good question, one that is asked frequently. Magnesium deficiency can be hard to identify from symptoms alone.

As mentioned earlier, most magnesium is stored in bone and muscle, with only a small amount in the blood. That can make standard blood testing an incomplete picture. Urine testing, red blood cell magnesium, hair mineral analysis or broader metabolic testing may be considered in some clinical contexts, but no single test should be treated as perfect.

The better approach is to look at the whole picture:

  • What does your diet look like?
  • Are you eating magnesium-rich foods regularly?
  • Do you drink alcohol frequently or heavily?
  • Are you under high stress?
  • Do you have digestive symptoms?
  • Are you taking medications that may affect magnesium?
  • Are there signs of electrolyte disturbance?
  • Are symptoms ongoing, severe or unexplained?

Older Australian Health Survey data found inadequate magnesium intake was common, especially among younger Australians (Australian Bureau of Statistics, 2015). More recent data from the ABS also shows inadequate magnesium intake remains a meaningful issue in Australia (Australian Bureau of Statistics, 2026).

That does not mean everyone needs a supplement. It does mean magnesium intake deserves more attention than it usually gets.

Common Factors That Can Increase Magnesium Risk

Several factors can increase the chance that magnesium intake, absorption or retention may be compromised.

These include:

  • Excessive use of diuretics (Caffeine, stimulants, etc): Increases urinary excretion, leading to loss of magnesium.
  • Alcohol: Impairs absorption and increases excretion of magnesium.
  • Hypochlorhydria (low stomach acid): Reduces magnesium absorption efficiency.
  • Antacids: Bind to and reduce absorption of magnesium.
  • Vitamin D (due to its role in Calcium absorption): Alters calcium and magnesium balance, potentially decreasing magnesium levels.
  • Coeliac disease: Damages the intestinal lining, hindering magnesium absorption.
  • Chronic stress (emotional or psychological – overactive sympathetic nervous system): Elevates stress hormones, increasing magnesium excretion.
  • Crohn’s disease: Causes malabsorption of nutrients, including magnesium.
  • Type 1 and 2 Diabetes: Increases urinary loss of magnesium.
  • Diarrhoea / Laxatives: Leads to rapid loss of fluids and electrolytes, including magnesium.
  • Diets high in sugar: Require more magnesium for processing, depleting body stores.
  • Excessive menstruation: Can lead to increased loss of magnesium.
  • High phosphorus in the diet (inorganic phosphates found in inactive processed food ingredients): Competes with and reduces magnesium absorption.
  • Insulin resistance: Linked to lower magnesium levels in the body.
  • Low salt intake: May affect magnesium levels due to the interconnected balance of electrolytes.
  • Low selenium intake: Selenium deficiency can affect magnesium status and metabolism.
  • Vitamin B6 (pyridoxine) deficiency: Essential for magnesium absorption and utilisation in the body.

Don’t use this list as gospel, but if you notice you tick off some of these, magnesium intake might be something to consider.

If someone has poor magnesium intake, multiple risk factors plus symptoms, magnesium is worth assessing properly.

Potential Signs of Magnesium Deficiency

Signs of magnesium deficiency can vary. Some can be vague. Some can be serious. Many overlap with other conditions.

One clinical clue to consider is unexplained hypokalaemia, or low potassium, and hypocalcaemia, or low calcium. These can sometimes point toward significant magnesium depletion. Neuromuscular irritability, including signs such as the Trousseau sign, may also be relevant in more significant depletion states (Pokan et al., 2006).

Possible signs associated with low magnesium or altered magnesium status can include:

  • Muscle cramps
  • Muscle weakness
  • Twitching or fasciculations
  • Tremors
  • Irritability
  • Anxiety-like symptoms
  • Poor sleep
  • Fatigue
  • Neuromuscular irritability
  • Tinnitus
  • Disorientation in more significant cases
  • Abnormal heart rhythm in more severe deficiency states
  • Low calcium or low potassium on testing

More severe deficiency states can be associated with more serious features such as arrhythmias, convulsions or marked neuromuscular symptoms. These require medical assessment, not supplement guessing.

Important to remember that symptoms are not always proof, and investigations are always recommended to confirm as well.

Choosing the Correct Magnesium Supplement

Not all magnesium supplements are created equal.

If a product has magnesium written on the front label, that does not tell you the full story. The form of magnesium matters. The dose of elemental magnesium matters. The person’s digestion, goal, medication use and tolerance all matter.

On a slightly more technical level, magnesium is bound to another compound in supplement form. That companion compound affects absorption, tolerance and how the supplement behaves in the gut.

This is why magnesium citrate is different from magnesium oxide, magnesium glycinate is different from magnesium malate, and magnesium threonate is different again.

Magnesium glycinate

Magnesium glycinate is magnesium bound to glycine. It is often chosen when sleep, nervous-system support or bowel tolerance are priorities.

Research comparing magnesium diglycinate with magnesium oxide in people with ileal resection found that magnesium diglycinate showed better bioavailability in that specific clinical setting (Schuette et al., 1994).

Glycine itself has also been studied for sleep quality. This does not prove magnesium glycinate is a sleep cure, but it helps explain why this form is commonly discussed in sleep and calming contexts (Yamadera et al., 2007).

Magnesium oxide

Magnesium oxide is common, cheap and high in elemental magnesium, but it is generally less bioavailable than some other forms. Because more of it may stay in the gut, it can have a stronger laxative effect for some people (Schuchardt & Hahn, 2017).

That does not make it useless. It means it is often better suited to bowel-related use than to correcting low magnesium status quickly.

Magnesium citrate

Magnesium citrate is commonly used and generally better absorbed than oxide. It may also loosen stools, so dose and tolerance matter.

One trial has looked at oral magnesium for pregnancy-induced leg cramps (Supakatisant & Phupong, 2012). This is useful context, but it should not be stretched into a blanket claim that magnesium citrate fixes all cramping.

Magnesium chloride

Magnesium chloride is another form used in supplements and topical products. It may be considered where digestion, absorption or tolerance are priorities, although the quality of the product and the dose still matter.

Magnesium malate

Magnesium malate is magnesium bound to malic acid. Malate is involved in energy metabolism, which is why this form is often marketed around energy and muscle pain.

Malate-related cellular energy research helps explain why malate is discussed in energy-metabolism contexts (Scheibe, 2004). That reference is not direct proof that magnesium malate treats fatigue, but it gives useful biochemical context.

Magnesium taurate

Magnesium taurate is magnesium bound to taurine. Taurine has been studied in relation to cardiovascular function and cellular regulation (Zulli, 2011).

This form is often positioned as calming or heart-supportive, but claims should be kept sensible. It may be a useful option for some people, but it is not automatically the best magnesium for everyone.

Magnesium threonate

Magnesium threonate is often marketed around brain health because of interest in brain magnesium levels, memory and cognition.

Animal research has shown that elevating brain magnesium could affect synaptic loss and cognitive deficits in an Alzheimer’s disease mouse model (Li et al., 2014). NMDA receptor research in neuropathic pain contexts also helps explain why magnesium and excitatory signalling are often discussed together (Wu & Zhuo, 2009).

This is interesting, but it needs careful wording. Mouse studies and mechanistic papers are not the same as proving a human supplement outcome. Magnesium threonate may be worth watching, but it should not be oversold.

Magnesium sulfate

Magnesium sulfate is better known as Epsom salts. It is commonly used externally in baths. I would not frame it as a detox product, because that language often runs ahead of the evidence. If used, it is better discussed around relaxation rituals, muscle comfort and bath use rather than internal supplementation.

Magnesium orotate

Magnesium orotate is often discussed in cardiovascular and performance contexts. Research on oral magnesium therapy in coronary artery disease patients has looked at exercise heart rate, exercise tolerance and myocardial function (Pokan et al., 2006).

This is not a reason to self-prescribe magnesium for heart disease. It is a reason to respect magnesium’s role in cardiovascular physiology and seek proper guidance when heart health is involved.

Magnesium carbonate

Magnesium carbonate is often used for its antacid properties. Research on an aluminium- and magnesium-containing antacid has shown that magnesium-containing products can affect drug bioavailability in some contexts (Krishna et al., 2007).

This is a reminder that magnesium-containing antacids and medications can interact with absorption and medication timing. If you use medications, especially antibiotics or other timing-sensitive medicines, check with your practitioner or pharmacist.

Forms I am more cautious with

I am cautious about making blanket statements that a form is bad for everyone, but there are some forms I would approach carefully.

Magnesium hydroxide is commonly used as a laxative or antacid form and is not usually the form I would reach for when the goal is broader magnesium repletion.

Magnesium aspartate and magnesium pidolate can raise questions because they are bound to excitatory amino acid-related compounds. Excitatory amino acid neurotoxicity research gives some context for that caution (Gillessen et al., 2000-2013). The cautious framing is this: if someone already feels wired, over-stimulated or neurologically sensitive, I would usually choose a better-tolerated form first rather than defaulting to these.

Food Sources of Magnesium

Food should always be part of the magnesium conversation. While we can’t always get it from diet, a food first is generally always recommended to support foundational nutrient status.

Supplementation can be useful when there is a clear reason, but a food-first approach usually gives you more than magnesium. You also get fibre, potassium, polyphenols, healthy fats, protein, B vitamins and other minerals.

Good magnesium-rich foods include:

  • Pumpkin Seeds – 535mg
  • Raw Cacao – 507mg (Cacao nibs anyone?)
  • Flax Seeds – 392mg
  • Brazil Nuts – 350mg (also super high in selenium)
  • Sesame Seeds – 340mg
  • Chia Seeds – 335mg
  • Almonds – 260mg
  • Cashews – 250mg
  • Buckwheat – 221mg
  • Peanuts – 160mg
  • Walnuts – 150mg
  • Dark Chocolate (70%+) – 120mg (The darker the higher the Magnesium content)
  • Tofu – 74mg
  • Spinach – 74mg
  • Sardines– 39mg
  • Kale – 33mg
  • Avocado – 27mg
  • Whole Oats – 24mg

These foods are often compared per 100 g, which is useful for nutrient tables, but it is also worth being practical. You are probably not eating 100 g of pumpkin seeds in one sitting. A better way to use this list is to build magnesium-rich foods into daily meals.

For example:

  • Add chia seeds or flax seeds to oats.
  • Use pumpkin seeds over salads or yoghurt bowls.
  • Eat almonds, cashews or walnuts as a snack.
  • Include tofu, legumes or buckwheat in meals.
  • Use spinach or kale in eggs, smoothies, soups or stir-fries.
  • Choose dark chocolate as a magnesium-containing treat rather than a daily main source.

One important note: some plant foods contain phytates, also called phytic acid. Phytates can bind minerals and reduce absorption. This does not make nuts, seeds, legumes or grains bad. It simply means soaking, sprouting, fermenting, cooking and eating a varied diet can help improve overall mineral availability.

Correct Dosing for Magnesium Deficiency

Magnesium dosing needs care.

It depends on the person, the form, the reason for using it, the dose of elemental magnesium, bowel tolerance, kidney function, medications, pregnancy status and whether there is a confirmed or suspected deficiency.

DiNicolantonio et al. discuss magnesium deficiency and higher weight-based intake considerations in the context of subclinical deficiency and cardiovascular risk (DiNicolantonio et al., 2018). That is useful context, but it should not be turned into a general public dosing instruction.

When supplementing Magnesium, the general guidance is to:

  • Check the elemental magnesium amount on the label.
  • The average daily supplementation of elemental magnesium is 400-600 mg daily.
  • Do not assume a higher dose is better.
  • Be careful if magnesium causes loose stools, nausea or cramping.
  • Avoid high-dose supplementation without guidance if you have kidney disease, heart rhythm issues, significant medical conditions or multiple medications.
  • If pregnancy is involved, dosing should be discussed with a qualified practitioner.
  • If a true deficiency is suspected, assess properly rather than guessing.

The phrase elemental magnesium matters. It refers to the true amount of magnesium in the supplement, not the total weight of the compound.

For example, 1000 mg of magnesium glycinate does not mean 1000 mg of elemental magnesium. The label should tell you the elemental magnesium per serve.

How To Choose a Magnesium Product

There are many magnesium products on the market, and some are much better formulated than others.

Rather than listing products here, I would focus on what to look for:

  • Clear elemental magnesium amount per serve
  • A form that matches the goal and digestive tolerance
  • Minimal unnecessary fillers
  • A dose that does not cause bowel irritation
  • Practitioner guidance if you are using it for a specific condition
  • No exaggerated claims around detox, cure-all effects or guaranteed sleep outcomes

A good product should make the dose and form clear. If you cannot tell what form of magnesium is being used, or how much elemental magnesium you are getting, I would be cautious.

The Takeaway

Magnesium is a critical mineral for normal human function. It is involved in energy production, nerve communication, muscle relaxation, glucose metabolism, DNA support, blood pressure physiology, electrolyte balance and nervous-system regulation.

It becomes especially relevant when someone has been under long-term stress, eating poorly, drinking heavily, sleeping badly, training hard, using diuretics or dealing with digestive issues.

The big picture is simple: magnesium matters because it supports the systems that help you feel steady, energised, relaxed, coordinated and resilient.

Start with food. Build meals around magnesium-rich ingredients such as nuts, seeds, leafy greens, legumes, tofu, whole grains, oats, cacao and quality whole foods. If supplementation is needed, choose the form carefully, pay attention to elemental magnesium and avoid assuming more is better.

If you are unsure whether magnesium is relevant for you, Stephen can help you look at your diet, symptoms, alcohol intake, stress load, sleep, training, pathology and supplement options in context.

FAQ

What does magnesium do in the body?

Magnesium supports hundreds of enzymatic reactions, including energy production, protein synthesis, nerve function, muscle contraction and relaxation, glucose metabolism, blood pressure regulation and DNA stability.

Why is magnesium important for the nervous system?

Magnesium helps regulate nerve signaling and excitatory pathways, including mechanisms involving glutamate and NMDA receptors (Kirkland et al., 2018). This is one reason it is often discussed in relation to stress, sleep, tension and nervous-system regulation.

Can alcohol lower magnesium?

Alcohol can contribute to low magnesium status through poor dietary intake, impaired absorption, increased urinary loss and wider metabolic stress. This is especially relevant with frequent or heavy alcohol intake.

How do I know if I am magnesium-deficient?

You cannot confirm magnesium deficiency from symptoms alone. Diet, symptoms, alcohol intake, digestive health, medications, pathology and sometimes additional testing need to be considered together.

What are signs of low magnesium?

Possible signs include cramps, twitching, fatigue, muscle weakness, irritability, poor sleep, tremors, neuromuscular irritability and, in more serious cases, abnormal heart rhythm or electrolyte disturbances. These signs can have many causes, so they should be assessed properly.

What is the best form of magnesium?

There is no single best form for everyone. Glycinate is often used for tolerance and sleep-focused support, citrate is common but can loosen stools, oxide is cheaper but generally less bioavailable, malate is often discussed around energy, and threonate is marketed around brain health. The best option depends on the person.

What does elemental magnesium mean?

Elemental magnesium is the actual amount of magnesium in the supplement. The total compound weight is different from the elemental magnesium dose, so always check the label.

Should I take magnesium every day?

Some people benefit from daily magnesium supplementation, but it is not automatically needed. Food intake, symptoms, health conditions, medications and dose all matter. If you are unsure, get individual guidance.

References

Australian Bureau of Statistics. (2015). Australian Health Survey: Usual nutrient intakes, 2011-12 financial year. https://www.abs.gov.au/statistics/health/health-conditions-and-risks/australian-health-survey-usual-nutrient-intakes/latest-release

Australian Bureau of Statistics. (2026). Usual nutrient intakes, 2023. https://www.abs.gov.au/statistics/health/health-conditions-and-risks/usual-nutrient-intakes/latest-release

DiNicolantonio, J. J., O’Keefe, J. H., & Wilson, W. (2018). Subclinical magnesium deficiency: A principal driver of cardiovascular disease and a public health crisis. Open Heart, 5(1), e000668. https://doi.org/10.1136/openhrt-2017-000668

Gillessen, T., Budd, S. L., & Lipton, S. A. (2000-2013). Excitatory amino acid neurotoxicity. In Madame Curie Bioscience Database. Landes Bioscience. https://www.ncbi.nlm.nih.gov/books/NBK6108/

Kirkland, A. E., Sarlo, G. L., & Holton, K. F. (2018). The role of magnesium in neurological disorders. Nutrients, 10(6), 730. https://doi.org/10.3390/nu10060730

Krishna, G., Kisicki, J. C., Olsen, S., Grasela, D. M., & Wang, Z. (2007). Effect of an aluminum- and magnesium-containing antacid on the bioavailability of garenoxacin in healthy volunteers. Pharmacotherapy, 27(7), 963-969. https://doi.org/10.1592/phco.27.7.963

Li, W., Yu, J., Liu, Y., Huang, X., Abumaria, N., Zhu, Y., Huang, X., Xiong, W., Ren, C., Liu, X., Chui, D., & Liu, G. (2014). Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer’s disease mouse model. Molecular Brain, 7, 65. https://doi.org/10.1186/s13041-014-0065-y

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Schuchardt, J. P., & Hahn, A. (2017). Intestinal absorption and factors influencing bioavailability of magnesium: An update. Current Nutrition & Food Science, 13(4), 260-278. https://doi.org/10.2174/1573401313666170427162740

Schuette, S. A., Lashner, B. A., & Janghorbani, M. (1994). Bioavailability of magnesium diglycinate vs magnesium oxide in patients with ileal resection. Journal of Parenteral and Enteral Nutrition, 18(5), 430-435. https://doi.org/10.1177/0148607194018005430

Supakatisant, C., & Phupong, V. (2012). Oral magnesium for relief in pregnancy-induced leg cramps: A randomised controlled trial. Maternal & Child Nutrition, 11(2), 139-145. https://doi.org/10.1111/j.1740-8709.2012.00440.x

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