Dr NK Tenai

Determined | Involved | Inquisitive | A Grateful Global Citizen | An Eternal Optimist

[Low Carb Down Under @lowcarb_aus]

Our latest release from 'Low Carb Brisbane 2025' - Dr. Deepa Mahananda provides an update on the important work of the Australasian Metabolic Health Society
#LowCarbBrisbane @AMHSorg @sydneylowcarb https://t.co/mtBaoHshw7

[Low Carb Down Under @lowcarb_aus]

Our latest release from 'Low Carb Brisbane 2025' - Prof. Caryn Zinn outlines the amazing progress her team is making to reverse Type 2 Diabetes in the land of the long white cloud @CarynZinn https://t.co/h1zgukF6XD

[Low Carb Down Under @lowcarb_aus]

Our latest release from 'Low Carb Brisbane 2025' - Prof. Grant Schofield looks at the science of Vitamin D and skin health @grantsnz
https://t.co/8XtVQZxFw6

[Dr NK Tenai @eNPire]

https://t.co/S71cQfhxRK

[Dr NK Tenai @eNPire]

https://t.co/hXobXXXhp7

[Dr NK Tenai @eNPire]

https://t.co/QXdiqf0IGW

[Dr David Unwin @lowcarbGP]

AT LAST UPDATED DIETARY GUIDANCE THAT MAKES SENSE !! Note the top line protein and green veg The bottom line starchy carbs. NOWHERE sugar or packets. Just eat real food. We have waited years for this HURRAH !

[Low Carb Down Under @lowcarb_aus]

Our latest release from 'Low Carb Brisbane 2025' - Beth McNally and Amy Rush present a guide to navigating insulin for protein & fat in Type 1 Diabetes when following therapeutic carbohydrate reduction #LowCarbBrisbane @T1DNutritionLC @Aimes_Rush https://t.co/fk0xkNWP3P

[Carolyn Rockey @CarolynWRockey]

The First Big Lie of Vaccinology: Antibody Production Is NOT Immunity, And It's Propping Up an Entire Industry Built on Deception
A damning new article just published by the Brownstone Institute on December 13, 2025, lays bare the single most pervasive deception in modern vaccine science.
Internal medicine physician Clayton J. Baker, MD, systematically dismantles the false claim that simply generating higher antibody levels in the body confers genuine, reliable immunity against disease.
This is the central pillar that has allowed pharmaceutical giants to market vaccines with flashy laboratory numbers while sidestepping the hard evidence of real-world protection.
For years, the public, physicians, and regulators have been sold the narrative that robust antibody responses equal safety from infection and severe outcomes.
Dr. Baker reveals this as a profound and dangerous oversimplification that exploits immune complexity for profit and perpetuates endless booster campaigns.
Here are the key points Dr. Baker drives home in his hard-hitting analysis:
1. The Core Lie: Equating Antibody Production with True Immunity
Vaccine companies aggressively promote the idea that stimulating antibodies equals disease protection. This false claim is pushed in clinical trials, press releases, and marketing to convince regulators, physicians, and the public that vaccines "work."
2. Antibody Metrics Are Misleading and Incomplete
Boasts of "4-fold increases in neutralizing antibodies"—like Pfizer's recent announcements for their LP.8.1-adapted COVID-19 shot—only prove the vaccine triggered antibody production. They say nothing about preventing infection, stopping spread, or reducing severe outcomes.
3. The Immune System Is Far More Complex Than Antibodies Alone
Antibodies are just one part (humoral immunity). True defense against viruses relies heavily on cellular immunity, including T-cells that destroy infected cells. Vaccine trials obsess over antibodies while ignoring this critical branch, oversimplifying and misrepresenting how immunity really works.
4. Targeted Antibodies Often Become Irrelevant Due to Viral Mutations
Rapidly mutating respiratory viruses like flu and SARS-CoV-2 evolve faster than vaccines can adapt. The specific antibodies induced quickly mismatch circulating strains, leaving people vulnerable despite vaccination—and setting the stage for perpetual "updated" boosters.
5. Reliance on Surrogate Markers Over Real Clinical Outcomes
Focusing on easy lab proxies like antibody titers speeds up approvals and fuels repeat sales, but it substitutes hype for hard evidence of disease prevention. This shortcut undermines trust and prioritizes profits over genuine public health.
6. Call for Rejection of This False Equivalency
Dr. Baker urges regulators, doctors, and citizens to reject antibody production as "proof" of efficacy and demand rigorous clinical outcomes—actual reductions in illness and death—instead.
This piece exposes how a single foundational falsehood has sustained an entire paradigm of vaccine development, approval, and promotion… one that treats the public as perpetual customers in a never-ending cycle of shots.
Read the full article here: https://t.co/Byx3dVCJAt
-Kari Bundy - Health Activist

[Low Carb Down Under @lowcarb_aus]

Our latest release from 'Low Carb Brisbane 2025' - Dr. Andrew McIntyre reviews the uptake of low carb nutrition in gastroenterology #LowCarbBrisbane @akmcintyre
https://t.co/hMnyFsj0if

[Low Carb Down Under @lowcarb_aus]

Our latest release from 'Low Carb Brisbane 2025' - Dr. Paul Mason presents intriguing new evidence on the root cause of cardiovascular disease #LowCarbBrisbane @DrPaulMason https://t.co/VTIFlJWejQ

[Paul Mason MD @DrPaulMason]

If you have ever wondered about the real cause of coronary artery calcification and what to do about it, watch this lecture. https://t.co/pJ3PqZPu1d
@realDaveFeldman @siobhan_huggins @LDLSkeptic @ProfTimNoakes @malcolmken @nicknorwitz @MaryanneDemasi @DrEades @bigfatsurprise

[Dr David Unwin @lowcarbGP]

HURRAH! Our practice won a Royal College of GPs Practice Team Award tonight for our low carb work to help people with T2D 🥳 Just avoid the foods that put your blood sugar up 👍@DiabetesUK

[Robert Lufkin MD @robertlufkinmd]

Different types of calories have different effects on insulin
which determines fat storage and metabolic effects.

One has very different effects on our metabolism and health
compared to the other although
both have similar numbers of calories.

h/t @DoctorTro

[Paul Mason MD @DrPaulMason]

The prevention and treatment of autoimmune disease, including coeliac, MS, lupus and type 1 diabetes may well hinge on our understanding of the immune response to fungal infections. Molecular similarities between fungus and human tisssues can trick our immune system into friendly fire. This understanding also provides insight into how the carnivore and other low carb diets assists in autoimmune diseases. Improved immune system function, microbiome changes which suppress pathogenic fungii alongside their reduced nourishement of fungii (they tend to love carbs) results in suppression of fungal growth. Specific suppelments and medications may even be utilised. I believe that this understanding represents a paradigm shift in how we will consider and treat many modern diseases, potentially offering hope to millions for whom conventional treatment is failing.https://t.co/nHAtJDx64l

[American Diabetes Society @OfficialADSOrg]

Managing diabetes naturally through low-carb, nutrient-dense eating isn't just possible — it’s powerful. You can lower A1C, reduce insulin resistance, stabilize blood sugars, and feel energized again.

You have the power to change your story. #DiabetesAwareness

[American Diabetes Society @OfficialADSOrg]

A1C can lie.

@BenBikmanPhD explains why:

➡️ Long-lived red blood cells = falsely high A1C
➡️ Fragile red blood cells = falsely low A1C

Your A1C isn’t always about glucose. Don’t rely
on one number to measure your health. #metabolichealth #diabetesreversal

[Low Carb Down Under @lowcarb_aus]

Our first release from 'Low Carb Brisbane 2025'. Dr. Rod Tayler interviews Nina Teicholz on potential changes for the dietary guidelines, recognition of the dangers of seed oils and the rise of the carnivore diet #LowCarbBrisbane @bigfatsurprise
https://t.co/TyAPvMep0f

[Paul Mason MD @DrPaulMason]

My summary on thyroid disease did not include any information about how fluoride can compete with iodine (and cause mental retardation) or pesticides (for which evidence of causing thyroid disease is growing stronger). I have also included a much stronger focus on Hashimoto's disease itself.
Here is version 2.0.

Hashimoto's disease and the Thyroid Gland: Function, Assessment, and Treatment 2.0
Understanding Hashimoto's Thyroiditis
Hashimoto's disease is an attack against the thyroid gland by your own immune system (autoimmune). It is typically diagnosed based on elevated levels of certain proteins produced by your immune system that can attack the thyroid gland. This typically includes thyroglobulin antibodies and thyroid peroxidase antibodies. The early phases of Hashimoto's disease may be typified by transient episodes of an overactive thyroid (such as anxiety, rapid heartbeat and tremors), due to destruction of the thyroid gland releasing stored thyroid hormone into the bloodstream. Over time (5–10+ years), the thyroid gland itself shrinks as it is progressively attacked and destroyed. Once a sufficient volume of the thyroid gland has been destroyed, it will no longer be able to secrete sufficient thyroid hormone to meet normal needs, and underactivity of the thyroid, or hypothyroidism, sets in. Therefore in early states, Hashimoto's disease may be typified by episodic periods of thyroid activity, which is eventially replaced by chronic (persistent) underactivity. This typically requires lifelong replacement of thyroid hormone as the thyroid gland cannot regenerate. Hashimoto's is quite common, being the most common autoimmune disease worldwide, with levothyroxine, a thyroid hormone replacement drug being the the second-most prescribed drug in the U.S.
Symptoms of Hyperthyroidism (overactive thyroid)
Hyperthyroidism causes an overactive metabolism leading to symptoms such as heat intolerance, sweating, tremor, anxiety, irritability, and rapid or irregular heartbeat. You may experience fatigue, muscle weakness, insomnia, frequent bowel movements, and menstrual irregularities.
Symptoms of Hypothyroidism (underactive thyroid)
Hypothyroidism (underactive thyroid) often presents with fatigue, unexplained weight gain, cold intolerance, dry skin and hair loss, constipation, muscle/joint pain, puffy face, elevated cholesterol levels, depression, and neck swelling from goiter.
Thyroid Hormone Regulation
The release of thyroid hormones is regulated by the pituitary gland, a small structure located on the underside of the brain. When the brain detects insufficient thyroid hormone levels, it signals the pituitary to secrete thyroid-stimulating hormone (TSH). TSH then stimulates the thyroid gland in the neck to produce and release two main forms of thyroid hormone: thyroxine (T4) and triiodothyronine (T3).
Impact of underactive thyroid on cognitive function
During growth, thyroid hormone is a critical regulator of numerous areas of brain development, including the formation of brain cells and connections between them. Thyroid hormone deficiency during critical phases of growth, including as a foetus, can result in permanent intellectual disability. This emphasises the increased importance of maintaining appropriate thyroid hormone activity during both preganancy and childhood.
In adulthood, thyroid hormones continue to support cognitive function. Hypothyroidism (low thyroid hormone) is associated with deficits in attention, memory (especially verbal and working memory), processing speed, executive function, and visuospatial abilities, often presenting as "brain fog" or mild cognitive impairment that is largely reversible with hormone replacement therapy. Low free T3 levels even when within the normal range are also tied to higher risks of cognitive impairment and poorer performance on global cognition tests, even with 'normal' TSH levels, in older adults.
Understanding T4 and T3
T4 is the primary hormone secreted by the thyroid gland (about 80–90% of total output) and serves as a precursor or "prohormone." It is largely inactive and must be converted to T3, the biologically active form, to exert effects on the body. The thyroid produces only 10–20% T3 directly; the majority (80%) is generated peripherally in tissues like the liver, kidneys, and muscles via deiodinase enzymes. All symptoms of hypothyroidism (underactive thyroid) stem from insufficient T3 activity, not T4 levels alone.
Factors Impairing T4 to T3 Conversion
Conversion relies on deiodinase enzymes (D1/D2), which can be inhibited, leading to low T3 despite a normal T4. Common factors which may be considered include:
Nutritional deficiencies: Selenium, zinc, or iodine** (cofactors for deiodinases).
Medications: Amiodarone, beta-blockers, corticosteroids.
Toxins: Heavy metals (e.g., mercury, lead, arsenic, cadmium), halognes (fluoride, chlorine, bromine) ***
Chronic inflammation: Linked to autoimmune diseases or infections; elevates reverse T3 (inactive form).
Sleep deprivation: Often tied to inflammation.
***Halogens are a family of chemicals that are very reactive. In addition to iodine, they include fluoride (may be added to drinking water), chlorine (in bleach and pools), bromine (flame retardents and some spas). Due to their chemical similarity with iodine, these other halogens may 'compete' with iodine blocking its entry into the thyroid gland. These halogens may then take the place of iodine in key enzymes, impairing the production of thyroid hormone. An increased intake of iodine may partially compensate for these other halogen exposures. (The importance of thyroid hormone in brain development explains why excessive intakes of fluoride via drinking water have been found to be associated with developmental mental retardation).
** While iodine is necessary for thyroid function, high iodine intake can paradoxically induce hypothyroidism through a protective mechanism called the Wolff-Chaikoff effect. Excess iodide inhibits thyroid peroxidase (TPO), an enzyme involved in the production of thyroid hormones (T4 and T3). In healthy individuals, this is usually only transient (24-48 hours), however in some patients, symptoms of underactive thyroid may last for 2-3 weeks. The risk of this occurring is increased in those with autoimmune thyroid conditions like Hashimoto’s disease.The recommended upper limit of intake for iodine is 1,100mcg, which is a little less than ½ a drop of Lugol’s 2% iodine. Doses may need to be higher in those with absorption issues, which are commonly associated with thyroid disease, or in those with halogen exposure (fluoride, chlorine, bromide) which competes with iodine for biological effect. Urine iodine testing is the most accurate way of assessing iodine levels. Skin patch testing is unreliable and not recommended.
Assessing Thyroid Function: The Limitations of TSH
Most clinicians rely on TSH as the primary screening tool for thyroid function, with a low TSH generally thought to indicate adequate thyroid hormone activity. -Elevated TSH indicates the pituitary is compensating for low thyroid hormone output, signaling hypothyroidism. However, a common misconception is that high TSH reflects high thyroid activity—it does not; it signifies inadequate hormone production or action.
-Reference ranges for TSH (typically 0.4–4.0 mIU/L) are somewhat arbitrary and often overlap with subclinical hypothyroidism. These TSH ranges have also been used to set T3 + T4 cutoffs, limiting the clinical utility of their reference intervals.
-Problems higher up in the brain (hypothalamus) or within the pituitary can both cause low TSH, making TSH alone unable to detect these disorders.
-Impaired T4-to-T3 conversion may yield normal/low TSH (as T4 may communicate to the hypothalamus and pituitary that thyroid hormone levels are sufficient, despite T4 being biologically inactive). Thus TSH may be inappropriately lowered, even though T3 is deficient.
-Treatment with thyroid hormone tends to result in increased suppression of TSH levels compared to thyroid hormone effectiveness. That is, symptoms of an underactive thyroid are still common even though TSH suggests sufficient thyroid activity. This suppression of TSH may be moderated through the use of sustained release T3, which results in more stable levels with reduced peak levels.
-Research supports serum free T3 as the single most reliable marker of thyroid activity.
The Role of Cortisol
Cortisol influences thyroid function bidirectionally.:
Low cortisol: Common in Hashimoto's/Graves'; impairs T3 receptor binding (thyroid resistance), reducing response to therapy.
T3 supplementation can boost ACTH leading to increased cortisol release.
Preliminary testing via ACTH/cortisol; trial hydrocortisone if symptoms persist on T3.
Initiating thyroid therapy may accelerate cortisol metabolism, leading to a paradoxical deficiency. Consider this if there is an increase in symptoms on initiating thyroid hormone therapy.
High cortisol: Inhibits deiodinases, impairing activation of T4 to T3 (favours production of rT3 -inactive T3).
Thyroid Hormone Supplementation
Supplementation options include:
-T4 monotherapy (e.g., levothyroxine): Most common; long half-life (~7 days) allows daily or weekly dosing. However, unreliable conversion to T3 can limit efficacy.
-T3 supplementation (e.g., liothyronine): Short half-life (~1 day) requires twice daily doses; consideration may be given to sustained release preparations if ongoing symptoms or cardiac risk factors, ~3.5 times more potent than T4.
-Combination therapy (T4 + T3): May be synthetic or bio-identical (natural desiccated thyroid NDT from porcine glands) provide a fixed ratio (~4:1 of T4:T3), while combinations of synthetic T4 +T3 may be given in ratios of approximately 15:1 which better approximates normal human levels (for example 75mcg T4 + 5mcg T3).
A key study comparing levothyroxine (synthetic T4) monotherapy, combined synthetic T4 + T3, and natural desiccated thyroid (NDT, a natural T4 + T3 extract) found largely equivalent biochemical responses across the three options. However, patient preferences varied significantly: 45% favored NDT, 32% preferred the synthetic T4 + T3 combination, and only 23% chose T4 alone.Notably, about one-third of patients who remained symptomatic on T4 monotherapy experienced significant symptom improvement when switching to either NDT or the T4 + T3 combination. This supports a practical clinical approach of starting with affordable, easy-to-dose T4 monotherapy, then trialling NDT or T4 + T3 if symptoms persist.
Target Blood Levels
Recommend adjusting thyroid hormone dosing for symptom relief and optimal ranges of T3, not just TSH. Suggested targets:
-Free T4: 1.0–1.6 ng/dL (or total T4: 5.0–12.0 μg/dL).
-Free T3: 2.5–4.3 pg/mL (or total T3: 80–220 ng/dL).
-TSH: 0.04–2.5 mIU/L (avoid <0.04 mIU/L to minimise cardiac risks).
Adequate dosing of thyroid hormone often suppresses TSH below the standard reference interval. It is recommended to titrate doses based on symptoms and T3 levels, while ensuring TSH does not fall below 0.04 mIU/L.
Lifestyle recommendations for autoimmune thyroid disease:
Lifestyle interventions show promise for both slowing progression of Hashimoto's disease, while also reducing thyroid hormone replacement needs by enhancing thyroid receptor sensitivity.
-Strict gluten (and likely dairy-free diets) to reduce autoimmunity.
-Treating gut dysbiosis including bacterial and fungal overgrowth
-Eliminating seed oils/sugar for better insulin/thyroid receptor function
-avoiding pesticides (consume organic plant foods)
-reverse osmosis water filtration (to reduce fluoride exposure)
-adequate intake of selenium, zinc and iodine
-review of need for medications including amiodarone and beta blockers (both used to lower blood pressure)
-Persistent symptoms despite treatment may warrant consideration of surgical removal of the thyroid (thyroidectomy) which may reduce antibody levels and improve symptoms.
Pesticides and autoimmune thyroid disease
Evidence indicates that both insecticides and herbicide exposure is associated with an increased risk of thyroid disease. This includes a large cohort study of U.S. pesticide applicators (over 50,000 participants) who were followed for more than 20 years, and studies in farmers who use glyphosate finding altered thyroid hormone levels when compared to lower exposure groups. Experimental animal studies support these findings, with rodent studies finding glyphosate-based herbicide exposure can reduce T3/T4 levels, elevate TSH and lead to microscopic changes within the thyroid gland. Lab based studies indicate direct toxicity to thyroid tissue, as evidenced by reduced thyroid cell viability in association with increased reactive oxygen species.
Risks and Considerations of thyroid hormone treatment
Heart attack, stroke and blood clotting risk
There has previously been some concern regarding an increased risk of heart attack, stroke and blood clotting due to high levels of thyroid hormone. This research was based on patients with thyroid disease where their own thyroid gland secreted excessive levels of thyroid hormone. Research indicates no increased risk in patients treated with thyroid hormone therapy where the TSH remains >0.04 IU/l (which is 10 times lower than the standard reference interval). Overtreatment resulting in a TSH of <0.04 IU/l should be avoided).
Risk of atrial fibrillation, a problem with excessively rapid contraction of the heart is increased with thyroid hormone therapy. This should be considered in any patient with a history of atrial fibrillation. Furthermore, if a patient experiences any symptoms that may suggest atrial fibrillation, including a sense of palpitations (a pounding or racing heart or a sense of skipping beats), sense of excessive fatigue or breathlessness especially with exercise or chest discomfort, they should immediately seek medical attention. The risk of atrial fibrillation may be reduced by replacing immediate release T3 with sustained release T3.
Bone health - at normal levels, T3 appears to exert anabolic, or building effects on bone. At high levels however, it may become catabolic, increasing bone breakdown. It is likely that nutrition plays a key role, as bone breakdown and formation are typically tightly linked. In a setting of deficient nutrient availability, such as may be caused by a poor diet or malabsorption due to gastrointestinal pathology, bone formation may be impaired even in the presence of appropriate hormonal stimulus. It is likely that T3 will augment the state of anabolism or catabolism, whichever is dominant. Clinical assessment of bone turnover may be made with serum procollagen type 1 N-terminal propeptide (P1NP) which directly reflects bone building activity, and C-terminal telopeptide (CTX) which measures bone resorption or breakdown. In summary, thyroid hormone may both enhance or impair bone health, which is dependent on other underlying factors.
Muscle health - muscle pain and fatigue is a common symptom of an underactive thyroid gland. This is because thyroid hormone has a supportive or anabolic effect on muscle, and deficiency of thyroid hormone can result in breakdown of muscle. This can be detected by an elevated level of an enzyme typically located inside muscle cells, creatine kinase (CK), which can 'leak' into the blood when muscle cells are damaged. Accordingly, consideration should be given to assessing thyroid health if CK is detected in the blood at an elevated level.
Red blood cells / macrocytic anaemia -deficiency of thyroid hormone may impair the ability of the bone marrow to make red blood cells. This can lead to a deficiency of red blood cells, with the red blood cells often having a large size (macrocytic anaemia). Macrocytic anaemia is typically associated with low B12 or folate levels - an underactive thyroid should be considered in cases of macrocytic anaemia where B12 and folate levels are appropriate.
References
https://t.co/kxKHC79i9E
https://t.co/nlIKTmUsq0
https://t.co/CnCoKdz83G
https://t.co/jJDd93WFpv
https://t.co/6ENAIURw7t
https://t.co/qaQb6lmTv8
https://t.co/xG0ojmMo6b
https://t.co/W5IseqPbgm
https://t.co/NxMHPUkSwy
https://t.co/fNWfCIsOxA
https://t.co/WzyIImab4L
https://t.co/i88XhXeNmW
https://t.co/1VNcvL0W1i
https://t.co/oBKfA0YAjF
https://t.co/zcwyC1FHBb

Thanks for reading this far. Now its time for me to get back to writing my lectures for next weekends conference on the actual causes of heart disease.
https://t.co/bslwHq0vnz

[Paul Mason MD @DrPaulMason]

Here is my updated my patient information handout on thyroid disorders, including considerations for optimal treatment.

The Thyroid Gland: Function, Assessment, and Treatment
Thyroid Hormone Regulation
The release of thyroid hormones is regulated by the pituitary gland, a small structure located on the underside of the brain. When the brain detects insufficient thyroid hormone levels, it signals the pituitary to secrete thyroid-stimulating hormone (TSH). TSH then stimulates the thyroid gland in the neck to produce and release two main forms of thyroid hormone: thyroxine (T4) and triiodothyronine (T3).
Symptoms of Hypothyroidism
Hypothyroidism (underactive thyroid) often presents with fatigue, unexplained weight gain, cold intolerance, dry skin and hair loss, constipation, muscle/joint pain, puffy face, elevated cholesterol levels, depression, and neck swelling from goiter.
Symptoms of Hashimoto's Thyroiditis
Hashimoto's, an autoimmune cause of hypothyroidism, shares these symptoms but may include transient hyperthyroid phases (anxiety, rapid heartbeat, tremors) early on, as the immune attack releases stored hormones before gland destruction sets in.
Understanding T3 and T4
T4 is the primary hormone secreted by the thyroid gland (about 80-90% of total output) and serves as a precursor or "prohormone." It is largely inactive and must be converted to T3, the biologically active form, to exert effects on the body. The thyroid produces only 10-20% T3 directly; the majority (80%) is generated peripherally in tissues like the liver, kidneys, and muscles via deiodinase enzymes. All symptoms of hypothyroidism (underactive thyroid) stem from insufficient T3 activity, not T4 levels alone.
Factors Impairing T4 to T3 Conversion
Conversion relies on deiodinase enzymes (D1/D2), which can be inhibited, leading to low T3 despite a normal T4. Common factors which may be considered include:
Nutritional deficiencies: Selenium, zinc, or iodine** (cofactors for deiodinases).
Medications: Amiodarone, beta-blockers, corticosteroids.
Toxins: Heavy metals (e.g., mercury, lead, arsenic, cadmium).
Chronic inflammation: Linked to autoimmune diseases or infections; elevates reverse T3 (inactive form).
Sleep deprivation: Often tied to inflammation.
** While iodine is necessary for thyroid function, high iodine intake can paradoxically induce hypothyroidism through a protective mechanism called the Wolff-Chaikoff effect. Excess iodide inhibits thyroid peroxidase (TPO), an enzyme involved in the production of thyroid hormones (T4 and T3). In healthy individuals, this is usually only transient (24-48 hours), however in some patients, symptoms of underactive thyroid may last for 2-3 weeks. The risk of this occurring is increased in those with autoimmune thyroid conditions like Hashimoto’s disease.The recommended upper limit of intake for iodine is 1,100mcg, which is a little less than ½ a drop of Lugol’s 2% iodine. Doses may need to be higher in those with absorption issues, which are commonly associated with thyroid disease. Urine iodine testing is the most accurate way of assessing iodine levels. Skin patch testing is unreliable and not recommended.
Assessing Thyroid Function: The Limitations of TSH
Many clinicians rely soley on TSH as the primary screening tool for thyroid function, with a low TSH generally thought to indicate adequate thyroid hormone activity. Elevated TSH indicates the pituitary is compensating for low thyroid hormone output, signaling hypothyroidism (many people incorrectly a low TSH indicates an underactive thyroid gland).
Reference ranges for TSH (typically 0.4-4.0 mIU/L) are somewhat arbitrary and often overlap with subclinical hypothyroidism. These TSH ranges have also been used to set T3 + T4 cutoffs, limiting the clinical utility of these reference intervals.
-Problems higher up in the brain (hypothalamus) or within the pituitary can both cause low TSH, making TSH alone unable to detect these disorders.
-Impaired T4 to T3 conversion may yield normal/low TSH (as T4 can signal to the hypothalamus/pituitary that thyroid hormone levels are sufficient). Thus T4 can lower TSH even when not being adequately converted into T3.
-Treatment with thyroid hormone tends to result in increased suppression of TSH levels compared to actual thyroid hormone activity. That is, symptoms of an underactive thyroid are still common even though TSH levels may suggest sufficient thyroid activity. This suppression of TSH may be moderated through the use of sustained release T3, which results in more stable levels with reduced peak levels.
Research supports serum free T3 as the single most reliable marker of thyroid activity.
The Role of Cortisol
Cortisol influences thyroid function bidirectionally.:
Low cortisol: Common in Hashimoto's/Graves'; impairs T3 receptor binding (thyroid resistance), reducing response to therapy.
-T3 supplementation can boost ACTH leading to increased cortisol release.
-Preliminary testing via ACTH/cortisol; trial hydrocortisone if symptoms persist on T3.
-Initiating thyroid therapy may accelerate cortisol metabolism, leading to a paradoxical deficiency. Consider this if there is an increase in symptoms on initiating thyroid hormone therapy.
High cortisol: Inhibits deiodinases, impairing activation of T4 to T3 (favours production of rT3 -inactive T3).
Thyroid Hormone Supplementation
Supplementation options include:
-T4 monotherapy (such as levothyroxine): Most common; long half-life (~7 days) allows daily or weekly dosing. However, unreliable conversion to T3 can limit efficacy.
-T3 supplementation (such as liothyronine): Short half-life (~1 day) requires twice daily dosing; consideration may be given to sustained release preparations if ongoing symptoms or cardiac risk factors. T3 is ~3.5 times more potent than T4.
-Combination therapy (T4 + T3): May be synthetic or bio-identical (natural desiccated thyroid NDT from porcine glands) provide a fixed ratio (~4:1 of T4/T3). When given in synthetic form, ratios of T4/T3 tend to be closer to 15:1 which better approximates normal human levels (for example 75mcg T4 + 5mcg T3).
A key study comparing levothyroxine (synthetic T4) monotherapy, combined synthetic T4 + T3, and natural desiccated thyroid (NDT, a natural T4 + T3 extract) found largely equivalent biochemical responses across the three options. However, patient preferences varied significantly: 45% favored NDT, 32% preferred the synthetic T4 + T3 combination, and only 23% chose T4 alone.Notably, about one-third of patients who remained symptomatic on T4 monotherapy experienced significant symptom improvement when switching to either NDT or the T4 + T3 combination.This supports a practical clinical approach of starting with affordable, easy-to-dose T4 monotherapy, then trialling NDT or T4 + T3 if symptoms persist.
Target Serum Levels
Recommend adjusting to symptom relief and normal ranges of T3, not just TSH. Suggested targets:
-Free T4: 1.0–1.6 ng/dL (or total T4: 5.0–12.0 μg/dL).
-Free T3: 2.5–4.3 pg/mL (or total T3: 80–220 ng/dL).
-TSH: 0.04–2.5 mIU/L (avoid <0.04 mIU/L to minimise cardiac risks).
Adequate dosing of thyroid hormone often suppresses TSH below the standard reference interval. It is recommended to titrate doses based on symptoms and T3 levels, while ensuring TSH does not fall below 0.04 mIU/L.
Hashimoto's Disease
Hashimoto's thyroiditis is an autoimmune attack on the thyroid, leading to fluctuating or progressive dysfunction. The gland stores preformed hormones; initial attacks release them en masse, causing transient hyperthyroidism which is often experienced as episodic anxiety. Over 5-10+ years, destruction results in permanent hypothyroidism, often requiring lifelong replacement (levothyroxine is the second-most prescribed drug in the U.S.). Regeneration is unlikely once destroyed, but lifestyle interventions can slow progression and reduce replacement needs by enhancing thyroid receptor sensitivity.
Evidence supports:
-Strict gluten (and likely dairy-free diets) to reduce autoimmunity.
-Treating gut dysbiosis including bacterial and fungal overgrowth
-Eliminating seed oils/sugar for better insulin/thyroid receptor function.
-Persistent symptoms despite treatment may warrant consideration of surgical removal of the thyroid (thyroidectomy) which may reduce antibody levels and improve symptoms.
Risks and Considerations
Heart attack, stroke and blood clotting risk
There has previously been some concern regarding an increased risk of heart attack, stroke and blood clotting due to high levels of thyroid hormone. This research was based on patients with thyroid disease where their own thyroid gland secreted excessive levels of thyroid hormone. Research indicates no increased risk in patients treated with thyroid hormone therapy where the TSH remains >0.04 IU/l (which is 10 times lower than the standard reference interval). Overtreatment resulting in a TSH of <0.04 IU/l should be avoided).
Risk of atrial fibrillation, a problem with excessively rapid contraction of the heart is increased with thyroid hormone therapy. This should be considered in any patient with a history of atrial fibrillation. Furthermore, if a patient experiences any symptoms that may suggest atrial fibrillation, including a sense of palpitations (a pounding or racing heart or a sense of skipping beats), sense of excessive fatigue or breathlessness especially with exercise or chest discomfort, they should immediately seek medical attention. The risk of atrial fibrillation may be reduced by replacing immediate release T3 with sustained release T3.
Bone health - at normal levels, T3 appears to exert anabolic, or building effects on bone. At high levels however, it may become catabolic, increasing bone breakdown. It is likely that nutrition plays a key role, as bone breakdown and formation are typically tightly linked. In a setting of deficient nutrient availability, such as may be caused by a poor diet or malabsorption due to gastrointestinal pathology, bone formation may be impaired even in the presence of appropriate hormonal stimulus. It is likely that T3 will augment the state of anabolism or catabolism, whichever is dominant. Clinical assessment of bone turnover may be made with serum procollagen type 1 N-terminal propeptide (P1NP) which directly reflects bone building activity, and C-terminal telopeptide (CTX) which measures bone resorption or breakdown.
Muscle health - muscle pain and fatigue is a common symptom of an underactive thyroid gland. This is because thyroid hormone has a supportive or anabolic effect on muscle, and deficiency of thyroid hormone can result in breakdown of muscle. This can be detected by an elevated level of an enzyme typically located inside muscle cells, creatine kinase (CK), which can 'leak' into the blood when muscle cells are damaged. Accordingly, consideration should be given to assessing thyroid health if CK is detected in the blood at an elevated level.
Red blood cells / macrocytic anaemia -deficiency of thyroid hormone may impair the ability of the bone marrow to make red blood cells. This can lead to a deficiency of red blood cells, with the red blood cells often having a large size (macrocytic anaemia). Macrocytic anaemia is typically associated with low B12 or folate levels - an underactive thyroid should be considered in cases of macrocytic anaemia where B12 and folate levels are appropriate.
References
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