You have hypothyroidism.
You're taking your medication.
Your doctor tells you your TSH looks “great.”
Yet you're exhausted, freezing, constipated, foggy, losing your hair and gaining weight while eating less than everyone around you.
And then comes the advice every hypothyroid woman loves hearing:
“You just need to eat less and exercise more.”
Fantastic. Thanks.
Except many women with hypothyroidism have already been doing exactly that.
This is where I think conventional thyroid treatment has failed women for decades.
We have become very good at treating a laboratory number while sometimes forgetting to ask a much more important question:
Does the woman actually feel well?
Because if your TSH is sitting beautifully inside the reference range while you still have every symptom of low thyroid function, I don't consider that the end of the conversation.
Especially when it comes to weight.
Absolutely. Thyroid hormones help regulate metabolic rate, mitochondrial energy production, body temperature, heart rate, digestion, glucose metabolism and how efficiently your body uses energy. When thyroid hormone activity is inadequate at the cellular level, weight loss can become incredibly difficult.
And yes, hypothyroidism can contribute to considerably more weight gain than the tidy little “5 to 10 pounds” figure you often hear quoted.
That number gets repeated constantly.
But clinical reality can look very different.
I have worked with women who gained 20, 30, 40 pounds or more during the years their thyroid function deteriorated.
Does that mean every pound was caused directly by thyroid hormone deficiency?
No.
But that is also the wrong way to think about it.
Low thyroid function can influence:
resting energy expenditure
body temperature
spontaneous movement
fatigue and activity
insulin sensitivity
blood sugar regulation
digestion and constipation
fluid retention
sex hormones
appetite regulation
mitochondrial function
muscle function
cholesterol metabolism
So the thyroid may not simply “add 10 pounds.”
It can create a metabolic environment in which gaining fat becomes easier and losing it becomes much harder.
That distinction matters.
[INTERNAL LINK: hypothyroidism symptoms]
Here is where things get interesting.
Many women diagnosed with hypothyroidism are prescribed levothyroxine, Synthroid or another medication containing T4 only.
T4 is thyroxine.
And T4 matters.
But T4 is primarily a prohormone or storage form of thyroid hormone. Your body must convert T4 into the much more biologically active thyroid hormone T3.
T3 is the hormone interacting with thyroid receptors throughout your tissues.
That conversion step is the part of the story that women are rarely told about.
A healthy thyroid does not produce T4 alone.
The thyroid produces predominantly T4, but it also secretes T3 directly. The remainder of circulating T3 is generated when T4 is converted into T3 by deiodinase enzymes in tissues throughout the body.
So when we give someone T4-only medication, we are making an assumption:
We are assuming her body will efficiently convert enough of that T4 into T3.
Sometimes it does.
Sometimes it doesn't.
Women can technically be “on thyroid medication” yet still experience persistent symptoms if she isn't getting adequate T3 activity.
And this isn't just fringe conversation anymore.
Published thyroid literature now openly discusses the possibility that some levothyroxine-treated patients may experience inadequate tissue T3 signaling despite a normal TSH. Researchers have specifically questioned whether standard levothyroxine treatment fully restores thyroid hormone signaling in every patient.
Now we're getting somewhere.
This is one of the first things I want every woman with hypothyroidism to understand.
TSH is not thyroid hormone.
TSH stands for thyroid-stimulating hormone.
It is produced by your pituitary gland in your brain.
Its job is essentially to signal the thyroid gland.
So yes, TSH gives us useful information.
But I think we have made an enormous mistake by treating it as though it tells us everything happening throughout the thyroid system.
It doesn't.
A TSH test does not directly tell you:
how much free T3 you have
how much free T4 you have
how efficiently you convert T4 into T3
how much T4 is being converted into reverse T3
whether you have thyroid antibodies
how thyroid hormone is functioning within individual tissues
Yet women are still routinely told:
“Your TSH is normal. Your thyroid is fine.”
Meanwhile she is sitting there wearing a sweater in July, hasn't pooped since Tuesday, can't remember why she walked into the kitchen and has gained 25 pounds.
We need a better conversation.
In my practice, I want a much broader picture than TSH alone.
Depending on the woman and her history, that may include:
TSH
Free T4
Free T3
Reverse T3
TPO antibodies
Thyroglobulin antibodies
Sometimes total T3, iron status, ferritin, vitamin D, B12, glucose, insulin and sex hormones can add important context as well.
This does not mean one magic laboratory number diagnoses everything.
It means we stop pretending one pituitary hormone tells us the entire story.
Free T4 tells us how much unbound T4 is circulating and available for conversion.
Free T3 gives us information about the active thyroid hormone circulating in the blood.
This is particularly useful when a woman is taking plenty of T4 but still has a relatively low Free T3 and continues experiencing classic hypothyroid symptoms.
That should make you ask:
Where is the T4 going?
And this brings us to reverse T3.
Reverse T3, or rT3, is produced when T4 is converted down a different pathway.
T4 can become active T3.
Or T4 can become reverse T3.
Reverse T3 is biologically very different from T3.
Paul Robinson, author of The Thyroid Patient's Manual and Recovering With T3, describes reverse T3 as a useful marker when investigating poor conversion from T4 to active T3. He emphasizes one particularly important point:
T3 does not turn into reverse T3. Reverse T3 comes from T4.
Reverse T3 can rise during circumstances such as illness, calorie restriction and physiological stress.
If you want to understand this more deeply listen to the podcast episode I did with Elle Russ Author of The Paleo Thyroid Solution on Reverse T3
This is where thyroid medicine becomes controversial.
Conventional thyroid guidelines generally do not recommend routine reverse T3 testing because there isn't enough evidence showing that treating patients according to reverse T3 improves clinical outcomes.
Functional and thyroid-focused clinicians disagree.
Many of us find it useful in context, particularly when a woman has:
decent or high Free T4
lower Free T3
persistent hypothyroid symptoms
significant calorie restriction
chronic stress or illness
poor response to T4-only medication
I don't think reverse T3 should ever be interpreted by itself.
But I also don't think “the guidelines don't recommend it” automatically makes a physiological marker irrelevant.
Medicine evolves because somebody eventually asks questions that aren't in the guidelines yet.
Several factors can influence thyroid hormone metabolism and deiodinase activity.
These may include:
severe calorie restriction
illness
inflammation
nutrient deficiencies
certain medications
liver dysfunction
metabolic dysfunction
aging
physiological stress
genetic differences in deiodinase enzymes
Research has examined variants in genes such as DIO2, which codes for one of the enzymes involved in conversion of T4 to T3. Researchers are actively investigating whether these genetic differences may help explain why certain people respond differently to levothyroxine versus combination therapy.
We don't have all the answers yet.
But “we don't have every answer” is very different from saying:
“Your TSH is normal, therefore your symptoms can't possibly be thyroid-related.”
This is where my clinical experience differs sharply from the simple conventional thyroid model.
The overwhelming majority of women who come to me for thyroid help are already taking T4 medication.
They are not showing up because everything is going wonderfully.
They come because they're still:
exhausted
cold
constipated
gaining weight
losing hair
struggling with brain fog
depressed
unable to exercise normally
unable to lose weight
Now, there is an important selection bias here.
Women doing beautifully on levothyroxine aren't usually looking for me.
So I'm not going to claim that every woman taking T4-only medication needs T3.
But among the symptomatic women I see clinically?
T4-only treatment very often has not been enough.
And some research supports taking those women seriously.
In one randomized crossover trial involving women who continued to experience hypothyroid symptoms despite levothyroxine treatment, liothyronine treatment significantly improved multiple quality-of-life measures, particularly tiredness and cognitive complaints.
Other randomized trials have not consistently demonstrated superiority of combination treatment, which is why this remains controversial.
But here's a problem I think deserves much more attention:
Many older trials studied general hypothyroid populations rather than specifically recruiting people who were still symptomatic on T4.
More recent researchers have pointed out that patient selection, dosing, short-acting T3 preparations and study design may have obscured benefits in the subgroup we actually care about.
That's a pretty important distinction.
We're not asking whether every person with hypothyroidism needs T3.
We're asking:
What do we do with the woman who has been taking T4 for six years, has a “normal” TSH, feels awful and still can't lose weight?
Telling her everything looks fine clearly isn't working.
Depending on the individual, thyroid treatment may involve several approaches.
Some clinicians combine levothyroxine with liothyronine, providing both T4 and T3.
This can reduce complete dependence on the body's ability to convert T4 into T3.
Even mainstream UK guidance now acknowledges that a monitored trial of T4/T3 combination treatment may be appropriate in certain people with confirmed hypothyroidism who remain symptomatic despite optimized levothyroxine treatment.
That is quite a shift from the old:
“T3 is dangerous. Never use it.”
Natural desiccated thyroid, commonly called NDT, contains both T4 and T3 along with other thyroid-derived compounds.
Some patients prefer NDT because it provides direct T3 rather than relying solely on conversion.
Stop the Thyroid Madness has been one of the longest-running patient communities advocating for NDT, T4/T3 and appropriately managed T3 therapy based largely on decades of patient experiences.
T3-only treatment is a more specialized approach.
Paul Robinson has written extensively about the use of T3-only therapy in patients who have significant difficulty utilizing T4-based treatment.
It isn't appropriate for everyone.
But it should not automatically be treated as some terrifying fringe therapy either.
Liothyronine is simply synthetic T3, a hormone your body naturally uses every day.
The issue is not whether T3 is inherently “good” or “bad.”
The issue is choosing the correct patient, dose, timing and monitoring.
Read more about reverse T3 by Paul Robinson "Current Diagnosis and Treatment of Hypothyroidism are Both Fundamentally Flawed by Paul Robinson"
Here's the part women care about.
Why can your thyroid make fat loss so damn difficult?
Because thyroid hormone influences much more than the number on your scale.
T3 helps regulate energy expenditure.
When thyroid signaling drops, your body can become extraordinarily efficient at conserving energy.
That sounds lovely if you're stranded on a deserted island.
Less lovely when you're trying to lose 30 pounds.
When you're tired, achy and cold, you move less.
Not because you're lazy.
Because your body feels like someone unplugged it.
Those hundreds of tiny daily movements matter for total energy expenditure.
Thyroid hormones interact closely with glucose and lipid metabolism.
This becomes particularly important for women in perimenopause and menopause, when insulin resistance may already be increasing.
You cannot tell an exhausted woman to simply “exercise harder” when she barely has enough cellular energy to make it through the afternoon.
Optimizing the physiology often makes healthy behaviours easier.
That is very different from shaming her into doing more.
This one makes me crazy.
A woman can't lose weight.
So she drops her calories.
Nothing happens.
So she drops them again.
Then she adds fasting.
Then cardio.
Then more cardio.
Soon she's eating 1,100 calories and wondering why her body seems determined to hang onto every ounce.
Severe calorie restriction itself can influence thyroid hormone metabolism and reduce T3 as part of the body's energy-conservation response.
That makes complete evolutionary sense.
Your body does not know you're trying to fit into your jeans.
It interprets prolonged low energy availability as:
Apparently food has disappeared. Conserve resources.
This is one reason I repeatedly caution hypothyroid patients against chronic aggressive calorie restriction, particularly when T3 is already struggling.
Instead, I want women focusing on:
adequate protein
building muscle
resistance training
appropriate calories
insulin sensitivity
thyroid optimization
sleep
recovery
You cannot punish a struggling metabolism into becoming healthier.
Hashimoto's thyroiditis is an autoimmune disease in which the immune system attacks thyroid tissue.
That means simply replacing thyroid hormone addresses the hormone deficiency, but it doesn't necessarily address why the thyroid became dysfunctional in the first place.
This is where I do think we should look more broadly.
Possible areas worth assessing include:
gut health
celiac disease
food sensitivities when clinically relevant
nutrient deficiencies
vitamin D
iron and ferritin
selenium
iodine status
chronic inflammation
metabolic health
I do not think every woman needs a massive elimination diet.
But I also don't agree with dismissing nutrition simply because levothyroxine lowered the TSH.
Both things can matter.
Read Reversing Autoimmune Disease Symptoms in 8 steps
This needs nuance.
There is a clear relationship between celiac disease and autoimmune thyroid disease.
For anyone with celiac disease, gluten avoidance is obviously necessary.
For Hashimoto's without celiac disease, the research on gluten-free diets is mixed and limited. A recent systematic review concluded that the evidence is still too uncertain to say that every person with Hashimoto's benefits from gluten avoidance.
That does not mean individual women never improve without gluten.
Some absolutely report that they do.
It means:
Don't confuse “we don't have strong population-level evidence” with “no individual could possibly benefit.”
Those are two very different statements.
I am a big believer in testing, tracking symptoms and individualizing rather than creating religious food rules.
I would not tell most women with hypothyroidism to eliminate cruciferous vegetables.
Broccoli did not cause your thyroid problem.
Foods such as broccoli, cabbage, cauliflower and kale contain compounds that can affect iodine utilization under certain circumstances, particularly in very large amounts or when iodine status is poor.
Cooking also reduces much of the goitrogenic activity.
Normal servings of these nutrient-dense foods are rarely the thing keeping a woman hypothyroid.
Please do not fear kale while ignoring the fact that your Free T3 is sitting on the floor.
Priorities.
The gut-thyroid relationship deserves attention, particularly in autoimmune thyroid disease.
Your gastrointestinal system plays a role in:
nutrient absorption
immune regulation
medication absorption
estrogen metabolism
inflammation
And hypothyroidism itself can slow gastrointestinal motility, contributing to constipation and sometimes increasing susceptibility to digestive problems.
So the relationship can travel both directions.
I consider investigating gut health when symptoms warrant it, especially persistent:
bloating
constipation
diarrhea
reflux
nutrient deficiencies
abdominal discomfort
food intolerance
Could SIBO, celiac disease or another gastrointestinal condition be contributing?
Possibly.
But again, test intelligently.
We do not need to diagnose every woman on Instagram with Candida, parasites, leaky gut and three forms of mold toxicity before breakfast.
Stress matters enormously.
But I want to update the language from the old idea that your adrenal glands simply “burn out.”
The physiology is more complicated than that.
Chronic stress can alter the hypothalamic-pituitary-adrenal axis, sleep, blood glucose, appetite, inflammation and thyroid hormone metabolism.
Illness and physiological stress can also shift thyroid hormone metabolism away from active T3 and toward inactive metabolites such as reverse T3.
Paul Robinson's work has focused extensively on the intersection between cortisol regulation and the ability of some patients to tolerate and utilize thyroid hormone appropriately.
So yes, stress absolutely belongs in the conversation.
But I don't want “reduce stress” to become another lazy answer to a woman whose thyroid treatment is clearly inadequate.
Sometimes she doesn't need another meditation app.
She needs somebody to actually look at her thyroid.
Now add perimenopause to this picture.
Because apparently midlife needed another plot twist.
Estrogen, progesterone, thyroid hormone, insulin and cortisol do not exist in separate little boxes.
Women may simultaneously experience:
declining or fluctuating estrogen
declining progesterone
sleep disruption
loss of muscle
increasing insulin resistance
changes in body-fat distribution
thyroid dysfunction
And the symptoms overlap almost perfectly.
Brain fog.
Fatigue.
Weight gain.
Hair loss.
Anxiety.
Depression.
Poor sleep.
Low libido.
Cold intolerance.
Constipation.
This is why the 45-year-old woman saying “I don't feel like myself anymore” needs more than a TSH test.
She needs someone willing to look at the whole hormonal and metabolic picture.
[INTERNAL LINK: perimenopause and thyroid]
[INTERNAL LINK: HRT and thyroid]
I would stop asking only:
“Is my TSH normal?”
And start asking:
“Is my thyroid treatment actually restoring thyroid function well enough that I feel and function normally?”
I would want to understand:
What does my TSH look like?
What is my Free T4?
What is my Free T3?
Is Reverse T3 relevant in my situation?
Have thyroid antibodies been checked?
Am I efficiently converting T4 into T3?
Am I still symptomatic despite medication?
Do my symptoms fit hypothyroidism?
Is insulin resistance contributing?
Am I eating enough protein?
Am I maintaining muscle?
Is perimenopause or menopause adding another metabolic layer?
Are iron, ferritin or other nutrients low?
Is my thyroid medication being absorbed properly?
And perhaps the biggest question:
Why am I still suffering if everyone keeps telling me my treatment is working?
That question deserves an answer.
For decades, thyroid care has revolved heavily around TSH and T4-only treatment.
That approach works beautifully for some people.
But there is also a very real population of women who remain symptomatic.
That doesn't make them difficult.
It doesn't mean they're eating too much.
It doesn't automatically mean they need an antidepressant.
And it certainly doesn't mean the symptoms are all in their heads.
Thyroid physiology is more complicated than one laboratory marker.
T4 matters.
T3 matters.
Conversion matters.
Metabolic health matters.
Insulin matters.
Nutrition matters.
Muscle matters.
Sex hormones matter.
And most importantly, how the woman actually feels matters.
The goal of thyroid treatment should not simply be to create a laboratory report that says NORMAL.
The goal should be to help the woman sitting in front of us feel normal again.
That is a very different standard of care.
Yes. Hypothyroidism can contribute to weight gain both directly and indirectly by affecting metabolic rate, energy expenditure, movement, fluid balance, insulin sensitivity and other metabolic systems. The amount of weight associated with thyroid dysfunction varies considerably between individuals.
Levothyroxine provides T4, which must be converted into active T3. Some people may continue to experience low-thyroid symptoms despite T4 treatment, particularly when T3 availability is inadequate or other metabolic factors such as insulin resistance, menopause, muscle loss or aggressive calorie restriction are present.
Yes. Some levothyroxine-treated patients continue to experience fatigue, cognitive problems and other hypothyroid symptoms despite a TSH within the laboratory reference range. Research continues to investigate differences in T3 availability and thyroid hormone signaling that may help explain this phenomenon.
Free T3 can provide additional information about circulating T3, particularly in symptomatic patients. Conventional guidelines rely heavily on TSH and Free T4, while many thyroid-focused and functional clinicians also evaluate Free T3 as part of a more complete thyroid picture.
Reverse T3 is an inactive metabolite produced from T4. Levels can change during illness, fasting and physiological stress. Its role in routine thyroid management remains controversial, but some clinicians use it alongside Free T4, Free T3, symptoms and clinical history when investigating possible impaired T4-to-T3 conversion.
T3 is a naturally occurring thyroid hormone, and liothyronine is a prescription form of T3. Like any thyroid hormone, excessive doses can cause problems, which is why dosing and monitoring matter. Current medical guidance increasingly recognizes that selected patients with persistent symptoms may be candidates for supervised T3-containing therapy.
Not universally. Some patients report feeling significantly better on natural desiccated thyroid or T4/T3 combination treatment, while others do well with levothyroxine. The better question is whether the treatment adequately controls symptoms and restores thyroid hormone status for that individual.
Prolonged caloric restriction can reduce T3 production as part of the body's adaptation to lower energy availability. For women already struggling with hypothyroidism, repeatedly slashing calories can therefore become counterproductive.
If you are taking thyroid medication and still feel hypothyroid, don't let one “normal” laboratory value end the conversation.
Ask better questions.
Look at the full thyroid picture.
Look at T4.
Look at T3.
Look at conversion.
Look at antibodies.
Look at insulin.
Look at muscle.
Look at menopause.
Look at nutrition.
And above all, look at the woman.
Because thyroid treatment should not be about making a lab slip happy.
It should be about getting you back.
Karen Martel is a Certified Hormone Specialist and Transformational Nutrition Coach who founded Karen Martel Midlife Solutions to close the gap in women's midlife healthcare. She specializes in personalized bioidentical hormone therapy, perimenopause and menopause support, and root-cause hormone optimization. Karen and her all-female clinical team work with health-conscious women in their 40s, 50s, and beyond who are ready for real answers and a care plan built around their specific biology.
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