Fatigue and Perimenopause: Why You're So Tired (Even When Your Blood Tests Are "Normal")
- Michaela Newsom
- Jul 29
- 19 min read
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TABLE OF CONTENTS
Why Am I So Tired During Perimenopause?
If you've reached your 40s and suddenly feel as though someone has turned down your energy levels, you're certainly not alone.
Many of the women I work with describe the same experience. They tell me they no longer feel like themselves. They wake feeling tired despite sleeping for eight hours, struggle to concentrate at work, rely on coffee just to get through the morning and feel completely drained by the end of the day. Exercise feels harder than it used to, and even the motivation to socialise can begin to disappear.
It's easy to assume this is simply what happens during perimenopause. After all, fatigue is one of the most commonly reported symptoms during the menopause transition. As hormone levels fluctuate, sleep can become disrupted, mood may change, and many women find themselves juggling careers, ageing parents, teenagers and an increasingly demanding mental load. It's hardly surprising that energy levels begin to suffer. But while hormonal changes certainly play a role, they rarely tell the whole story.
One of the things I love about functional medicine is that it encourages us to ask a different question.
Rather than asking, "Is fatigue normal during perimenopause?", we ask, "Why is this particular woman feeling so fatigued?"
Because tiredness isn't a diagnosis. It's a signal that somewhere in the body, the systems responsible for producing, transporting or using energy aren't working as efficiently as they could.
For some women, poor sleep is the biggest contributor. For others, it may be unstable blood sugar, chronic stress, an underactive thyroid or nutrient deficiencies that have gradually developed over many years. Digestive problems that affect nutrient absorption, chronic inflammation or changes in iron metabolism can also quietly reduce energy production long before disease develops.
This is why two women of exactly the same age can have completely different experiences of perimenopause. One continues to feel energetic and resilient, while the other feels as though she's constantly running on empty. Understanding the reason behind that difference is often where real progress begins.
Why "normal" blood tests don't always provide the full picture
One of the most common things I hear in clinic is:
"My GP said everything was normal."
For many women, those words are reassuring. But for others, they're deeply frustrating. How can everything be normal when you feel exhausted every single day? The answer lies partly in what standard blood tests are designed to do.
Routine NHS blood tests are incredibly valuable. They're excellent at identifying significant disease, diagnosing conditions such as anaemia, diabetes or severe thyroid dysfunction, and highlighting results that require urgent medical attention.
What they aren't always designed to do is identify the earlier nutritional and metabolic changes that may be affecting how well your body functions.
Think of it like servicing your car. A warning light on the dashboard tells you when something has gone seriously wrong. But an experienced mechanic will often spot worn brake pads, low oil levels or a failing battery long before that warning light appears.
Your body works in much the same way. Long before a nutrient deficiency becomes severe enough to meet the criteria for disease, it may already be affecting how efficiently your cells produce energy. Iron stores may be gradually declining after years of increasingly heavy periods. Vitamin B12 may be sitting comfortably within the laboratory reference range, yet may not be optimally available where your cells need it. Low-grade inflammation may be quietly altering the way your body handles iron. Individually, each result may appear perfectly acceptable. Together, they can begin to explain why you feel exhausted.
This is one of the reasons I rarely look at a single blood marker in isolation. Instead, I want to understand how different systems are interacting and whether the overall pattern reflects what you're experiencing.
Fatigue starts inside your cells
To understand why so many different factors can contribute to fatigue, it helps to step back and look at how your body actually creates energy.
Every thought you have, every heartbeat, every muscle contraction and every breath you take requires energy. Even while you're asleep, your body is incredibly busy. Cells are repairing damaged tissues, producing hormones, supporting your immune system, processing nutrients and maintaining thousands of chemical reactions that keep you alive.
The fuel for all of this work is a molecule called ATP (adenosine triphosphate).
You don't need to remember the name. What's important is that ATP is the form of energy every cell uses to function. Without it, nothing in the body works.
Most ATP is produced inside tiny structures called mitochondria. Their job is to take the food you eat and, using the oxygen you breathe, convert it into usable energy. It's a remarkably efficient process, but it's also hugely dependent on nutrients.
Your mitochondria need a constant supply of oxygen. They rely on iron to help transport that oxygen around the body. They depend on B vitamins, magnesium, copper and many other nutrients to keep the complex machinery of energy production running smoothly. If any part of that system starts to struggle, your cells simply become less efficient at producing energy.
The result isn't usually dramatic. It doesn't happen overnight. Instead, energy gradually becomes harder to produce. You notice you need more caffeine than you used to. Afternoon slumps become more frequent. Exercise takes longer to recover from. Concentration becomes more difficult and your resilience to stress seems to disappear. These are often the early signs that your body's energy-producing systems are under pressure.
During perimenopause, that pressure can increase even further. Hormonal fluctuations affect mitochondrial function, sleep quality, blood sugar regulation and inflammation. At the same time, many women experience heavier menstrual bleeding, increasing the demand for iron just when the body needs it most. The good news is that once we understand how energy is produced, we can begin to understand where things may be going wrong. And one of the most important places to start is with iron.
Iron: So Much More Than a Haemoglobin Result
When most people think about iron, they think about anaemia. That's understandable. It's what we're often taught, and it's usually the point at which iron enters the conversation. Iron is the key component of haemoglobin which is the molecule that carries oxygen within red blood cells. If your haemoglobin falls below the laboratory reference range, you may be diagnosed with iron deficiency anaemia and offered iron supplements.
But iron's role in the body extends far beyond making red blood cells. In fact, one of the reasons iron deficiency can leave you feeling so exhausted is because iron is involved in almost every stage of the energy production process. It is essential for your mitochondria to generate the energy that powers every cell in your body. This is why iron deficiency doesn't simply affect how much oxygen you carry. It affects what your cells are able to do with that oxygen once it arrives. To understand why, it helps to follow the journey of oxygen through the body.
Oxygen: the missing ingredient in energy production
Imagine trying to light a fire without enough oxygen. You might have plenty of wood, but without oxygen the fire will never burn efficiently. Your cells work in much the same way. The food you eat provides the fuel, but oxygen allows your mitochondria to extract energy from that fuel and convert it into ATP.
Oxygen is carried around your body by haemoglobin, a protein found inside red blood cells. At the centre of every haemoglobin molecule sits iron. Without enough iron, your body simply can't produce enough healthy haemoglobin to transport oxygen efficiently. Less oxygen reaches your muscles, brain and other tissues, leaving you feeling fatigued, breathless or mentally sluggish.
But that's only half of the story.
Iron's hidden role inside your mitochondria
Once oxygen reaches your cells, another remarkable process begins. Inside your mitochondria, oxygen is used to release energy from the carbohydrates, fats and proteins you eat. This happens through a series of carefully coordinated biochemical reactions that ultimately generate ATP.
Iron plays an essential role here too. Several of the enzymes responsible for producing ATP contain iron. Without enough available iron, these enzymes become less efficient and the mitochondria simply can't produce energy at the same rate.
This is one of the reasons fatigue is often one of the earliest symptoms of iron deficiency.
Long before someone develops anaemia, their cells may already be struggling to generate energy efficiently. This is also why women with low iron often describe feeling as though they've "lost their spark." They're not just carrying less oxygen.
Their cells are also finding it harder to produce energy from the oxygen they do have.
Why perimenopause increases your risk of iron deficiency
One of the biggest contributors to iron deficiency during perimenopause is changing menstrual patterns. Although periods eventually stop, the years leading up to menopause are often characterised by hormonal fluctuations that can make periods heavier, longer or more frequent.
For some women, this change happens gradually and almost goes unnoticed. Others suddenly find themselves needing to change sanitary protection far more often than they used to or experience flooding that significantly affects daily life.
Every menstrual cycle involves some blood loss. The heavier the bleeding, the greater the loss of iron. Over months and years, those losses can begin to exceed the amount of iron being absorbed from the diet.
At first, the body quietly compensates by drawing on its iron stores. Eventually, however, those stores begin to run low. The challenge is that this process often develops slowly. Many women adapt to feeling increasingly tired without realising anything has changed until everyday activities begin to feel unexpectedly difficult.
You don't have to be anaemic to feel exhausted
This is one of the most important messages I hope you take away from this article.
Iron deficiency and iron deficiency anaemia are not the same thing.
Iron deficiency develops gradually. Before haemoglobin falls, your body first begins using the iron stored in tissues such as the liver and bone marrow. During this stage, your haemoglobin may remain completely normal, even though your available iron reserves are becoming depleted.
From a medical perspective, you may not meet the criteria for anaemia.
From your perspective, however, you may already be noticing the consequences.
Many women experience:
Persistent fatigue
Reduced stamina during exercise
Difficulty concentrating
Brain fog
Feeling cold more easily
Hair shedding
Restless legs
Reduced resilience to stress
Breathlessness during physical activity
Several clinical studies have shown that women with iron deficiency but without anaemia can still experience significant fatigue, and that appropriate iron treatment, when clinically indicated, may improve symptoms.
This is an important distinction because haemoglobin is often the only iron-related marker many people are familiar with. If haemoglobin is normal, it's easy to conclude that iron isn't the issue. In reality, haemoglobin is often one of the last markers to change.
Why ferritin doesn't always tell the whole story
If you've ever had your iron levels checked, there's a good chance you've also had a ferritin test. Ferritin is a protein that stores iron inside your cells, and measuring ferritin in the blood gives us a useful indication of your iron reserves. In many cases, ferritin is an excellent place to start. Low ferritin almost always tells us that iron stores are becoming depleted.
However, like all blood markers, ferritin needs to be interpreted in context. This is because ferritin is also what we call an acute phase protein. In simple terms, it rises during inflammation. Why does this matter?
Imagine two women both have a ferritin level of 80 µg/L. The first is healthy, active and has no evidence of inflammation. The second has chronic inflammatory bowel disease or an ongoing inflammatory condition. Although their ferritin levels look identical on paper, they may not represent the same iron status. Inflammation changes the way the body handles iron. Rather than allowing iron to circulate freely, the immune system deliberately begins storing more of it inside cells. This is thought to be a protective mechanism because many bacteria rely on iron to grow. By locking iron away, the body attempts to limit its availability to invading pathogens.
While this response can be helpful during an acute infection, persistent low-grade inflammation can sometimes make iron less available for normal physiological processes, including energy production.
It's one of the reasons I do not look at ferritin on its own. Instead, I like to understand the wider picture by considering markers such as serum iron, transferrin, transferrin saturation, a full blood count and, where appropriate, inflammatory markers such as high-sensitivity C-reactive protein (hs-CRP). Looking at these markers together often provides a much clearer understanding of how well iron is actually being transported and utilised.
And this is where the story becomes even more interesting.
Because having enough stored iron doesn't necessarily mean your body is able to move it to where it's needed. To understand why, we need to introduce a protein that most people have never heard of, yet plays a remarkably important role in iron metabolism: ceruloplasmin.
Ceruloplasmin: The Missing Piece of the Iron Puzzle
If you've never heard of ceruloplasmin, you're certainly not alone. It's not a marker that's routinely included in standard blood tests, and it's rarely discussed outside specialist areas of medicine. Yet from a functional medicine perspective, it can sometimes provide valuable insight into why someone continues to experience fatigue despite apparently "normal" iron results.
To understand why, we first need to look at what happens after iron has been absorbed. Iron doesn't simply circulate around the body on its own. It has to be carefully stored, transported and delivered to the tissues that need it. This process is tightly controlled because both too little and too much iron can be harmful.
Think of your body's iron as a delivery network. Ferritin acts like a warehouse, safely storing iron until it's needed. Transferrin is the delivery vehicle, transporting iron through the bloodstream to organs and tissues.
For that system to work efficiently, however, iron first has to leave its storage sites and be loaded onto transferrin. This is where ceruloplasmin comes in.
Why ceruloplasmin matters
Ceruloplasmin is a protein produced primarily by the liver that carries much of the copper found in your bloodstream. While it's often described as a copper transport protein, one of its most important jobs is actually helping your body handle iron.
When iron leaves storage cells, it isn't quite in the right chemical form to attach to transferrin. Ceruloplasmin acts as an enzyme that converts iron into the form transferrin can recognise and carry around the body. In other words, it helps prepare iron for transport. Without this step, iron may not move as efficiently from storage to the tissues that need it.
This doesn't mean that every person with low energy has low ceruloplasmin, nor does it mean ceruloplasmin should be measured routinely in everyone experiencing fatigue. But in the right clinical context, it can help explain why someone appears to have adequate iron stores, yet still shows signs that their tissues aren't receiving or using iron as efficiently as they should. Like every blood marker, ceruloplasmin needs to be interpreted alongside the wider clinical picture rather than in isolation.
Iron isn't just about how much you have
One of the biggest shifts in thinking that functional medicine encourages is moving away from asking:
"Do you have enough of a nutrient?"
Towards asking:
"Is your body able to use that nutrient effectively?"
Those are two very different questions.
You can have sufficient iron in storage but still struggle to make that iron available where it's needed. Likewise, you can have an adequate intake of vitamin B12 but absorb it poorly, or have sufficient vitamin D but reduced activation because of liver or kidney dysfunction. The body is remarkably interconnected. This is why I rarely think about nutrients in isolation. Instead, I look at the systems responsible for absorbing, transporting, activating and recycling them. Ultimately, it's not how much of a nutrient is sitting in your bloodstream that matters most. It's whether your cells can actually use it.
Why inflammation can change iron metabolism
Another important player in iron metabolism is inflammation. Whenever the immune system detects infection or inflammation, it responds by increasing production of a hormone called hepcidin. Hepcidin acts a little like a gatekeeper. One of its jobs is to reduce the amount of iron entering the circulation by blocking a protein called ferroportin, which normally allows iron to leave storage cells. This is thought to be an evolutionary defence mechanism. Many bacteria rely on iron to survive, so temporarily reducing the amount of freely circulating iron helps protect us during infection.
The problem arises when inflammation becomes chronic. Persistently raised hepcidin can block the transport of iron into circulation, making less iron available for everyday physiological functions, including red blood cell production and cellular energy generation. It's one of the reasons someone may have a ferritin result that appears reassuring while still showing signs of reduced iron availability. Again, this highlights why interpreting iron studies requires looking at the whole pattern rather than focusing on a single number.
Homocysteine: Another Marker That Can Tell Us More
Iron isn't the only nutrient that influences energy production. Another blood marker I often find helpful when investigating persistent fatigue is homocysteine.
Like ceruloplasmin, homocysteine isn't routinely measured in standard NHS blood tests. Yet it can provide valuable information about how efficiently several important nutritional pathways are functioning.
Homocysteine is a naturally occurring amino acid produced during the metabolism of methionine, one of the amino acids found in protein-rich foods. Under healthy circumstances, homocysteine doesn't remain in the bloodstream for very long. Instead, it's continually recycled through a network of biochemical reactions known as one-carbon metabolism or methylation. These reactions rely on several key nutrients, particularly vitamin B12, folate, vitamin B6 and riboflavin (B2). If one or more of these nutrients is lacking—or isn't being used efficiently—homocysteine may begin to rise.
Why vitamin B12 is so important for energy
Vitamin B12 is often marketed as an "energy vitamin." While that's a simplification, there's a good reason why low B12 can leave people feeling exhausted.
B12 is involved in two fundamental processes that influence energy production.
The first is the production of healthy red blood cells. Without adequate vitamin B12, red blood cells become larger and less efficient at transporting oxygen around the body. Over time, this can lead to megaloblastic anaemia, another well-recognised cause of fatigue.
The second role is less widely appreciated. Inside the mitochondria, vitamin B12 helps convert nutrients from the food you eat into compounds that feed directly into the Krebs cycle—the series of reactions responsible for generating much of your cellular energy. In other words, vitamin B12 supports the machinery that allows your cells to produce ATP. If that machinery isn't working efficiently, it's hardly surprising that energy levels begin to suffer.
Why a "normal" B12 result doesn't always tell the whole story
One of the most common questions I'm asked is:
"My B12 was normal, so that can't be the problem… can it?"
The answer is: not necessarily. A standard serum B12 test measures the amount of vitamin B12 circulating in your blood. It doesn't always tell us how much is actually reaching your cells or whether those cells are able to use it effectively.
This is where functional markers can sometimes provide additional insight.
An elevated homocysteine result may suggest that B12, folate or vitamin B6-dependent pathways aren't functioning optimally.
Another marker, methylmalonic acid (MMA), is considered more specific for vitamin B12 deficiency because it reflects one of the enzyme reactions that depends directly on B12.
Neither marker is perfect. Both need to be interpreted alongside symptoms, dietary intake, medication use and the rest of the blood picture. But together, they can often reveal patterns that a serum B12 result alone might miss.
Looking at the Bigger Picture
One of the things I love most about functional medicine is that it encourages us to think in systems rather than isolated symptoms.
Fatigue is a perfect example. Rarely is there a single explanation. Instead, it's often the result of several small changes gradually adding up over time.
Perhaps your sleep has become lighter because of fluctuating progesterone.
Your periods have become heavier, slowly reducing your iron stores.
Years of digestive symptoms have affected your absorption of vitamin B12.
Increasing insulin resistance is making blood sugar less stable, leaving you reaching for caffeine and sugary snacks just to get through the afternoon.
Individually, each of these factors may seem relatively minor. Together, however, they place increasing pressure on the body's ability to produce energy efficiently. This is why a functional medicine consultation isn't simply about identifying deficiencies.
It's about understanding how different systems influence one another and asking what might be preventing your body from functioning at its best. When we support those systems appropriately, many women notice improvements not only in their energy levels, but also in their concentration, mood, exercise tolerance, resilience and overall sense of wellbeing.
A Functional Medicine Approach to Investigating Fatigue
When someone comes to see me with persistent fatigue, I want to understand whether your cells have everything they need to produce energy efficiently and whether there are any barriers preventing that from happening.
Depending on your symptoms and medical history, this may include looking at:
A comprehensive iron panel, including ferritin, serum iron, transferrin and transferrin saturation.
A full blood count to assess red blood cell health.
Vitamin B12, folate and, where appropriate, homocysteine or methylmalonic acid.
Vitamin D status.
Thyroid function, including a more comprehensive thyroid assessment where clinically indicated.
Markers of inflammation such as high-sensitivity C-reactive protein (hs-CRP).
Blood glucose, HbA1c and fasting insulin to assess metabolic health.
Liver and kidney function, which both influence nutrient metabolism.
In selected cases, copper and ceruloplasmin to provide additional insight into iron handling.
No single blood test can explain every symptom. But when we bring together your history, symptoms, lifestyle and carefully interpreted blood markers, we can often begin to understand why your body has been struggling.
Frequently Asked Questions
Is fatigue normal during perimenopause?
Fatigue is commonly reported during the menopause transition. Hormonal fluctuations can affect sleep, thermoregulation, mood and metabolic function.
However, persistent or significant fatigue should not automatically be attributed to perimenopause.
Iron deficiency, thyroid dysfunction, vitamin B12 or folate deficiency, sleep apnoea, metabolic dysfunction, chronic infection, inflammatory disease and other medical conditions can also cause fatigue.
New, severe or worsening fatigue should always be medically assessed.
Can I be iron deficient if my haemoglobin is normal?
Yes.
Iron deficiency can occur without anaemia.
Ferritin may fall before haemoglobin drops below the diagnostic threshold for anaemia.
Research suggests that iron deficiency without anaemia can contribute to fatigue in some women.
This is why ferritin and, where appropriate, a complete iron panel may provide more information than haemoglobin alone.
What blood tests should I ask for if I am tired in perimenopause?
The appropriate tests depend on your symptoms and medical history.
A clinician may consider a full blood count, ferritin, iron studies, thyroid markers, B12, folate, vitamin D, liver function, kidney function, glucose markers and inflammatory markers.
In selected cases, homocysteine, methylmalonic acid, active B12, fasting insulin, soluble transferrin receptor, copper and ceruloplasmin may provide additional information.
More testing is not always better.
Testing should be clinically justified and interpreted as a pattern.
What is ceruloplasmin?
Ceruloplasmin is a copper-containing protein produced mainly by the liver.
It carries a substantial proportion of circulating copper and also acts as a ferroxidase.
Its ferroxidase activity helps convert Fe2+ to Fe3+, supporting the loading of iron onto transferrin and normal iron transport.
Ceruloplasmin is not routinely required in every fatigue investigation but may provide useful additional information in selected clinical situations.
Does low ceruloplasmin cause fatigue?
Low ceruloplasmin should not automatically be assumed to be the cause of fatigue.
Significantly low ceruloplasmin can occur in disorders of copper metabolism and may be associated with abnormal iron handling.
However, ceruloplasmin is influenced by several factors and should be interpreted alongside copper markers, iron studies, inflammatory markers, liver function and clinical history.
Can low copper affect iron metabolism?
Yes.
Copper-dependent enzymes are involved in normal iron transport.
Ceruloplasmin and hephaestin are copper-containing ferroxidases that help facilitate iron export and oxidation.
Severe copper deficiency can impair iron metabolism and contribute to haematological abnormalities.
However, copper supplementation should not be started simply because ferritin is low or fatigue is present. Excess copper can also be harmful.
Is homocysteine a marker of vitamin B12 deficiency?
Homocysteine can rise in vitamin B12 deficiency, but it is not specific to B12.
Folate deficiency, vitamin B6 status, kidney function, thyroid function, genetics and certain medications can also influence homocysteine.
Methylmalonic acid is generally considered a more specific functional marker of B12 status.
Why does vitamin B12 affect energy?
Vitamin B12 is required for normal red blood cell production and neurological function.
It is also a cofactor for methylmalonyl-CoA mutase, a mitochondrial enzyme involved in converting methylmalonyl-CoA to succinyl-CoA.
Succinyl-CoA can enter the TCA cycle, a central pathway in cellular energy metabolism.
Should I take iron if I am tired?
Not without appropriate assessment.
Iron deficiency can cause fatigue, but excess iron can be harmful.
Iron supplementation should ideally be guided by blood tests and clinical advice, particularly if fatigue is persistent or unexplained.
It is also important to understand why iron is low.
In perimenopausal women, heavy menstrual bleeding is a common cause, but gastrointestinal blood loss, coeliac disease, poor absorption and other medical conditions may also need to be considered.
My blood tests are normal. Why am I still exhausted?
There are many possible reasons.
Standard blood tests may not include a complete iron panel, homocysteine, methylmalonic acid or other markers relevant to your individual symptoms.
Equally, fatigue may be driven by poor sleep, sleep apnoea, insulin resistance, chronic stress, inadequate energy intake, medication effects, inflammation or another medical condition.
The next step is not necessarily “more supplements”.
It is a more detailed assessment of your symptoms, history and existing blood results.
Medical disclaimer
The information in this article is for educational purposes only and is not intended to diagnose, treat or replace individual medical advice. Fatigue can be associated with a wide range of medical conditions. If you are experiencing persistent, severe or unexplained fatigue, please speak to your GP or another appropriately qualified healthcare professional. Nutritional supplements, particularly iron and copper, should not be taken solely on the basis of symptoms and should be guided by appropriate testing and professional advice.
References & Further Reading
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Collins JF, Prohaska JR, Knutson MD. Metabolic crossroads of iron and copper. Nutrition Reviews. 2010;68(3):133–147.
Duan G, Li C, Liu Y, et al. Mitochondrial iron metabolism: the crucial actors in diseases. Molecules. 2023;28(1):29.
Hoes MF, Grote Beverborg N, Kijlstra JD, et al. Iron deficiency impairs contractility of human cardiomyocytes through decreased mitochondrial function. European Journal of Heart Failure. 2018;20(5):910–919.
Houston BL, Hurrie D, Graham J, et al. Efficacy of iron supplementation on fatigue and physical capacity in non-anaemic iron-deficient adults: a systematic review of randomised controlled trials. BMJ Open. 2018;8.
Kocaoz S, Cirpan R, Degirmencioglu AZ. The prevalence and impacts heavy menstrual bleeding on anemia, fatigue and quality of life in women of reproductive age. Pakistan Journal of Medical Sciences. 2019;35(2):365–370.
Mucha P, et al. Vitamin B12 metabolism: a network of multi-protein mediated processes. International Journal of Molecular Sciences. 2024.
Munro MG, Mast AE, Powers JM, et al. The relationship between heavy menstrual bleeding, iron deficiency, and iron deficiency anemia. American Journal of Obstetrics and Gynecology. 2023;229(1):1–9.
Musci G, Polticelli F, Bonaccorsi di Patti MC. Ceruloplasmin-ferroportin system of iron traffic in vertebrates. World Journal of Biological Chemistry. 2014;5(2):204–215.
Nolfi-Donegan D, Braganza A, Shiva S. Mitochondrial electron transport chain: oxidative phosphorylation, oxidant production, and methods of measurement. Redox Biology. 2020;37:101674.
Read AD, Bentley RE, Archer SL, Dunham-Snary KJ. Mitochondrial iron-sulfur clusters: structure, function, and an emerging role in vascular biology. Redox Biology. 2021;47:102164.
Takahashi-Iñiguez T, García-Hernandez E, Arreguín-Espinosa R, Flores ME. Role of vitamin B12 on methylmalonyl-CoA mutase activity. Journal of Zhejiang University Science B. 2012;13(6):423–437.
Vashi P, Edwin P, Popiel B, Lammersfeld C, Gupta D. Methylmalonic acid and homocysteine as indicators of vitamin B-12 deficiency in cancer. PLoS ONE. 2016;11(1).
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Verdon F, Burnand B, Fallab Stubi CL, et al. Iron supplementation for unexplained fatigue in non-anaemic women: double blind randomised placebo controlled trial. BMJ. 2003;326:1124.
About The Author
Michaela Newsom
Registered Nutritional Therapist, mBANT, rCNHC
Michaela is a women’s health expert with a specialist interest in the impact of menopause on the female brain. Her mission is to empower women to optimise their cognitive function and mental wellbeing throughout life with a special focus on the challenges that take place during perimenopause, menopause and beyond.
With a Postgraduate qualification in Personalised Nutrition and advanced Functional medicine training with IFM and the Kharrizian Institute Michaela has expertise spanning hormones, brain health, cognitive function and mood disorders.
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