FFN Root Cause Guide to Low T3 in Active Women

You can do everything “right” – exercise regularly, fuel intentionally, manage stress levels – and still end up with confusing thyroid labs. Active women are uniquely prone to low T3, the active form of thyroid hormone. Their bodies are constantly trying to balance high physical demands with energy availability, recovery, and stress signaling.

Underfueling, intense training, and chronic stress can all push the body out of balance and into conservation mode, diverting thyroid hormone away from active T3 and toward inactive reverse T3. At the same time, immune activation, inadequate recovery, and common nutrient deficiencies impair thyroid hormone production and conversion, further lowering free T3 levels. 

In many cases, low T3 isn’t a thyroid failure, but a protective metabolic adaptation to perceived stress and insufficient resources. At Functional Fueling, we take a root cause approach to thyroid dysfunction and low T3 levels. Together let’s explore the 4 most common root causes of low T3 levels in active women, and what you can do about it.

 

What Is T3 & Why It’s So Important

Thyroid Activity and T3 Explained

We know that the thyroid is responsible for supporting energy, metabolism, mood, and hormone production, but it’s more specifically the role of active thyroid hormones (aka Free T3). 

The thyroid gland produces T4 (tetraiodothyronine, or thyroxine), an inactive precursor hormone. T4 must be converted into T3 (triiodothyronine), the active thyroid hormone, in order to exert its effects throughout the body. This conversion happens largely in the liver and gut, using enzymes called deiodinases, which are heavily dependent on thyroid-supportive nutrients like selenium.

In this blog we will be referring to Free T3 as simply T3, not to be confused with Total T3, a different measure of thyroid hormones that doesn’t reflect available T3 hormones). 

T3 is the hormone that actually does the work. It influences the speed of nearly every process in the body – from metabolism, digestion, brain function, and cellular energy production, to temperature regulation, menstrual cycles, ovulation, and implantation. When T3 levels are functionally optimal (not just within the conventional lab reference ranges), the body runs efficiently. When T3 is low, everything slows down. 

 

How Thyroid Dysfunction Manifests

In this blog we will discuss why T4 doesn’t always convert into active T3. In most cases, the downregulation of thyroid hormone conversion is actually a protective mechanism. Our body does this as a way to conserve energy during perceived threats, but when this shift becomes chronic, symptoms quickly follow. 

Some of the most common symptoms we see among our clients that are linked to low T3 levels include:

• Persistent fatigue and brain fog
• Constipation
• Irregular and/or anovulatory cycles
• Impaired recovery from workouts or poor exercise tolerance
• Difficulty losing weight, or uncontrollably gaining weight
• Recurrent bloating or SIBO
• Elevated cholesterol levels
• Fertility challenges

A helpful way to understand T3 activity and how thyroid dysfunction manifests is to think of a thermostat in your house. 

If your house is cold and the thermostat reads a low temperature, your first instinct might be to put on a jacket. Adding more thyroid hormones when T3 is low through thyroid hormone replacement works in the same way – like putting a jacket on. This may temporarily relieve symptoms, but it doesn’t explain why the house is cold. 

If the windows and doors are open, letting cold air rush in, it’s no surprise it’s still cold inside. This is why many women continue to feel symptomatic even while taking thyroid medications like levothyroxine (T4) or Cytomel (T3). 

It’s like putting a jacket on while cold air still blows in, or turning up the thermostat while the open windows prevent your home from actually warming up.

To effectively improve thyroid function and raise low T3 levels, we have to address the root causes and close those open windows and doors!

 

Not Sure of Your T3 Levels?

Unfortunately, many women have no idea their T3 levels may be low. Standard thyroid testing typically stops at TSH (thyroid stimulating hormone), which does not reflect active thyroid hormone availability. To assess true thyroid function, we must look at thyroid hormones themselves, especially Free T3, not just Total T3 or TSH. If you have no idea what your T3 levels are, take our free quiz here to better understand if low T3 levels could be contributing to your symptoms. 

Now that we understand why T3 is so critical, let’s dive into the most common root causes driving low T3 in active women.

 

Root Cause #1 — Low Energy Availability

Low energy availability is one of the most common, and most overlooked, drivers of low T3 in active women. While it’s often described as “energy intake minus energy expenditure from exercise,” this definition is incomplete. Energy availability isn’t just about how much you eat versus how much you train, it’s about whether your body has enough usable energy left over to support reproductive health, nervous system activity, thyroid function, and more.

Energy balance is tightly controlled in order for our bodies to function optimally. The hypothalamus plays a central role here, acting as a control center that senses energy availability and coordinates multiple hormone cascades. These include the hypothalamic-pituitary-thyroid (HPT) axis, hypothalamic-pituitary-adrenal (HPA) axis, and hypothalamic-pituitary-ovarian (HPO) axis. When energy availability drops too low, the hypothalamus prioritizes survival over other functions like reproduction, and shifts metabolism to conservation mode.

We know that low energy availability directly induces a low T3 state in women. Importantly, this isn’t simply about “not eating enough.” It’s about chronic underfueling relative to total physiological demand. This includes the energy your body needs for training, recovery, immune activity, digestion, stress adaptation, and reproductive function. When energy is scarce, the body downshifts thyroid hormone activity to conserve resources.

 

Impacts of Low Energy Availability and Who Is Affected

Low energy availability can result from high training volume or intensity, inadequate overall intake, low carbohydrate intake, or digestive issues that impair nutrient absorption. While often discussed among female athletes, low energy availability affects a wide range of women. This includes those who exercise recreationally, those in chronic dieting cycles, women navigating high-stress life seasons, and active moms. 

Over time, this energy mismatch shifts the body into conservation mode. Thyroid suppression is one of the earliest adaptations to low energy availability, particularly decreased conversion from inactive T4 to active T3, resulting in low T3 levels as a protective mechanism. 

Metabolism slows, digestion becomes impaired, cortisol signaling becomes dysregulated, bone mineral density decreases, and reproductive function declines. This leads to fatigue, poor recovery, frequent injuries or stress fractures, fertility challenges, menstrual irregularities, and conditions such as hypothalamic amenorrhea (HA).

In sports medicine, this pattern is often described as Relative Energy Deficiency in Sport (RED-S), a framework that highlights how multiple systems, including the thyroid, are affected by insufficient energy availability. While RED-S is commonly associated with competitive athletes, the same physiology applies to women engaging in high-intensity or endurance training (ex. CrossFit or marathon running), especially when fueling and recovery are not adequately supported.

Assessing energy availability requires more than tracking calories. Food and exercise logs paired functional metrics such as resting heart rate, heart rate variability, sleep quality, and perceived recovery also offer valuable insight.

Restoring thyroid function in this context means restoring energy safely and strategically. Refueling with adequate carbohydrate intake is especially critical, as carbohydrates help suppress excess cortisol, support T4-to-T3 conversion, and replenish glycogen needed for recovery. Periodized fueling around training, intentional refeeding days, and adjusting training based on recovery status are often necessary steps. When energy availability improves, thyroid hormone activity often follows.

 

Root Cause #2 — Allostatic Load: An Overflowing Stress Bucket

Our bodies are remarkably adaptive. In the short term, stress is not only normal, but it’s necessary. Training stress builds strength, metabolic stress drives adaptation, and acute mental stress helps us respond to challenges. The problems arise when stress is no longer temporary. Our bodies were never designed to be exposed to constant stress without adequate recovery. When stress becomes chronic and cumulative, it increases what’s known as allostatic load – the total burden of stress placed on the body over time.

Allostatic load goes far beyond mental or emotional stress. It includes biological and physical stressors such as overtraining, chronic low energy availability, blood sugar dysregulation, inflammation, poor sleep, gut microbiome imbalances, illness, and even unresolved life stressors. Each stressor adds to the same physiological “stress bucket.” When that bucket overflows, the body shifts from adaptation into conservation or protection.

Overtraining is one of the most common contributors to high allostatic load in active women. Importantly, overtraining is not defined by training volume alone. Rather, it’s a chronic imbalance between training load and recovery capacity, which is influenced by systemic (whole-body) stress. This means overtraining can occur even when calorie intake seems adequate. If recovery, sleep, nervous system regulation, or overall stress resilience are insufficient, the body still perceives threat because that stress bucket is likely overflowing.

 

Downstream Effects of Chronic Stress & What To Do About It

When stress accumulates, the hypothalamic-pituitary-adrenal (HPA) axis becomes chronically activated, leading to elevated cortisol production. Cortisol is an essential hormone, but persistently high levels keep the body locked into the sympathetic nervous system state of “fight, flight, or freeze.” This puts us in survival and energy conservation mode. 

One key adaptation in this state is a downshift in thyroid hormone activation, or the conversion of T4 into active T3. This effectively suppresses thyroid hormone activity at the cellular level. Over time, this stress-driven pattern drives hypothyroid symptoms. Common signs that low T3 may be driven by high allostatic load and HPA axis dysfunction include: 

• Feeling “tired but wired” at night
• Reliance on caffeine to function
• Mood changes, including depression and anxiety
• Plateaued or declining performance
• Frequent injuries
• Poor sleep quality
• Difficulty recovering between training sessions

Appetite hormones like ghrelin and leptin may also become dysregulated, further complicating fueling, hunger cues, and metabolic stability. Leptin not only signals fullness, but also plays an essential role in regulating reproductive hormone production, menstrual cycles, and thyroid activity.

Reducing allostatic load requires both lowering total stress input and increasing recovery capacity. Check out two of our favorite LOdown episodes of the Strength in Hormones Podcast for more insight on supporting a healthy cortisol response to workouts (linked here), and how to control inflammation around workouts (linked here). 

Equally nutrition and lifestyle foundations include stabilizing blood sugar, prioritizing sleep, and ensuring adequate carbohydrate intake to support healthy cortisol rhythms and T3 production. Recovery modalities such as active recovery days, massage, breathwork, meditation, and nervous system regulation are additional helpful tools to balance allostatic load. When allostatic load decreases, the thyroid no longer needs to slow metabolism for protection, allowing T3 levels to recover naturally.

 

Root Cause #3 — Chronic Immune Activation

The immune system and thyroid are deeply interconnected. When immune activity increases, either acutely or chronically, thyroid hormone production and activation shift in response. This is not a malfunction, but yet another protective adaptation designed to conserve energy during times of perceived danger.

During acute immune stress, such as infection, injury, or significant inflammation, the body initiates a survival response. One hallmark of this response is altered thyroid hormone conversion: instead of converting T4 into active T3, the body diverts it down the pathway of Reverse T3 instead. Reverse T3 is not only inactive, but it blocks thyroid receptors, preventing available Free T3 from being utilized. This effectively slows metabolism to conserve energy.

This temporary shift helps conserve energy so resources can be redirected toward healing and immune defenses. In the short term, this is a perfectly normal response. However, issues arise when immune activation becomes frequent or chronic, reinforcing this low T3 state and diversion to Reverse T3. 

When assessing thyroid labs, it’s important to consider Reverse T3 levels alongside Free T4 and Free T3 to gather a full picture of thyroid hormone activity. In our practice, we typically see low Free T3 paired with high Reverse T3, normal TSH, and normal or subclinically low Free T4 levels. This pattern, commonly referred to as euthyroid sick syndrome, often reflects a stress adaptation as opposed to an issue with the thyroid gland itself. 

Chronic immune activation keeps this stress response turned on. Common drivers of chronic immune activation include:

• Persistent low-grade inflammation from gut dysbiosis and intestinal permeability (leaky gut)
• Environmental toxin exposures and endocrine disrupting chemicals
• Mold exposure and mold illness
• Parasitic infections and latent viral infections (ex. Epstein-Barr Virus (EBV), responsible for mononucleosis infections, Herpes Simplex Virus (HSV), and tickborne illnesses such as Lyme disease)

 

Importance of Addressing Chronic Stressors & How to Evaluate Your Immune Status

Over time, these signals continually tell the body it’s not safe, suppressing T3 production and conversion, and even leading to more serious immune system dysfunction and possibly the development of autoimmune conditions like Hashimoto’s thyroiditis. In conditions like Hashimoto’s, immune attacks gradually disrupt thyroid tissue and hormone regulation. 

It’s important to note that autoimmune activity does not begin as a low thyroid hormone problem. Antibody production (Anti-TPO or Anti-TG) typically precedes changes in TSH, T4, or T3 levels by years. This means many women experience symptoms long before conventional labs flag a thyroid issue. Learn more about the development of Hashimoto’s here. 

Addressing unresolved or excessive inflammation and chronic immune triggers as potential drivers of low T3 starts with proper assessment. This may include evaluating thyroid antibodies, inflammatory markers like high-sensitivity CRP (hs-CRP), metabolic markers, gut health status, and viral infection markers. These can be insidious hidden drivers of long-lasting thyroid symptoms.

In order to best address both acute and chronic immune system stressors, treatment strategies should focus on reducing immune burden while restoring balance. This includes nutrition and lifestyle interventions, often alongside complementary therapeutic modalities such as Micro-immunotherapy to actually modulate and restore the immune system.

If you already have basic labs but aren’t sure what they mean, our Thyroid Inflammation Lab Decoder Guide can help connect the dots. With this guide you’ll learn how to interpret key markers, including hs-CRP, thyroid hormones, metabolic markers, and reproductive hormones based on optimal reference ranges. Use this insight to identify hidden inflammation and understand what your results mean and what to do next.

 

Root Cause #4 — Low Thyroid-Supportive Nutrients

Thyroid hormone production and activation depend on a tightly coordinated network of nutrients, especially minerals, that act as both structural building blocks and biochemical catalysts. Even when stress, energy availability, and training load are well managed, nutrient insufficiencies alone can significantly impair T3 levels, particularly in active women. 

 

Iron & Selenium

Iron plays a foundational role at the very first step of thyroid hormone production. It is required for thyroid peroxidase (TPO), the enzyme responsible for creating and synthesizing thyroid hormones. Its job is to bind iodine to the amino acid tyrosine in order to form the T4 hormone. When iron stores are low, reflected by low ferritin levels, thyroid hormone production slows down. The thyroid becomes less efficient, triggering an increase in brain-to-thyroid signaling, resulting in an elevation in TSH. It doesn’t take long for low T4 levels to contribute to low T3 levels downstream. 

Because menstruating women lose iron monthly, and active individuals have increased iron turnover, iron deficiency is an extremely common contributor to thyroid dysfunction in active women in their reproductive years.

Selenium is equally critical, playing a pivotal role at the level of thyroid hormone activation. Selenium-dependent deiodinase enzymes convert inactive T4 into active T3 throughout the body, especially within the liver and gut. Without adequate selenium, this conversion becomes inefficient, increasing the likelihood of low T3 or diversion toward Reverse T3 during times of stress. 

Selenium also is a powerful antioxidant, protecting the thyroid gland from oxidative stress generated during hormone synthesis. This protective role is especially important in the presence of inflammation, chronic immune activation, and high training stress, when oxidative stress is significantly elevated.

 

Iodine & Other Key Nutrients

Iodine provides the structural backbone of thyroid hormones. Both T4 and T3 are composed of iodine molecules bound to tyrosine, an amino acid, which create the framework for hormone formation. However, iodine requires a delicate balance. Too little iodine limits hormone production, while too much can drive oxidative stress, inflammation, and thyroid dysfunction. Because of this, it’s important to know your iodine levels before supplementing, to ensure we are supporting proper iodine balance.

Your body also relies on additional nutrients like zinc and magnesium to support essential thyroid activities. Zinc supports thyroid hormone receptor function and cellular responsiveness to T3. Magnesium supports enzyme activity and energy production within the mitochondria, where thyroid hormones exert their metabolic impacts.

Without adequate nutrient availability, the thyroid simply lacks the raw materials it needs to function optimally, from hormone production to hormone activation, regardless of how well other systems are supported. Active women are especially vulnerable to mineral deficiencies due to menstrual blood loss, dietary restrictions, and increased nutrient demands from training and stress exposure. Symptoms often extend beyond thyroid concerns and may include hair loss, fatigue, cold intolerance, reduced endurance, poor workout recovery, and increased injury risk.

Addressing nutrient insufficiencies begins with proper assessment to determine the most appropriate replenishment strategies. In our 1:1 coaching program, we use personalized functional testing to guide your individualized treatment plan and targeted nutrient replenishment through nutrition and supplementation. When nutrients are restored to optimal levels, along with adequate energy intake and recovery, thyroid hormone production and conversion can begin to improve naturally.

 

Your Next Steps Toward Thyroid Healing

Low T3 is not an inevitable consequence of being an active woman, and it is absolutely treatable when the root causes are identified and addressed. Fatigue, poor recovery, stalled metabolism, irregular cycles, and brain fog are not normal symptoms you need to live with, or signs that your body is failing you. They are signals that your system is under-resourced or under stress.

As you’ve seen throughout this guide, low T3 rarely has a single cause. Low energy availability, elevated allostatic load, chronic immune activation, and nutrient deficiencies often interact. One stressor compounds another – low energy availability increases cortisol, cortisol drives reverse T3, inflammation impairs conversion, and nutrient gaps limit hormone production. Like an overflowing stress bucket, these pressures add up until the body shifts into conservation mode and downregulates thyroid activity to protect itself.

The good news? When the right stressors are removed and the right supports are put in place, the thyroid can recover. With proper assessment, comprehensive testing, and personalized guidance, thyroid hormone production and activation can normalize without simply adding more medication.

If you’re unsure whether low T3 may be contributing to your symptoms, start with our free quiz (linked here). If you already have labs, whether basic or comprehensive, but don’t know what they mean, download our Thyroid Inflammation Lab Decoder Guide to learn how to interpret key markers using optimal ranges.

And if you’re ready for deeper, personalized support, our 1:1 coaching program helps identify your unique root causes, guide comprehensive testing, and build an evolving plan tailored to your body, lifestyle, and goals. Apply to work with us today!

 

 

Written by Romana Brennan, MS, RDN