Iodine is one of the most misunderstood, and arguably most clinically neglected, micronutrients in modern practice.
Contemporary research, much of it pioneered by the late Dr. Guy E. Abraham MD, and then popularised by Dr David Brownstein MD, suggests that iodine is a pleiotropic nutrient with critical roles far beyond thyroid hormone production, particularly in breast and ovarian tissue, and that modern environmental exposures may be actively displacing iodine from the body.
With the launch of our new liposomal iodine (13,000 mcg per 1 ml), it is timely to revisit iodine physiology, halide competition, and how this fits into a broader clinical framework for women’s health and indeed everyones endocrine health.
Iodine and the Thyroid the classic story
At its most basic level, iodine is required for the synthesis of thyroid hormones T4 (thyroxine) and T3 (triiodothyronine).
In fact, the number in T4/T3 is the number of iodines in the tyrosine amino acid.
The thyroid actively transports iodide from the bloodstream via the sodium-iodide symporter (NIS), incorporates it into the enzyme thyroglobulin, and ultimately produces thyroid hormones that regulate basal metabolic rate, mitochondrial function, thermogenesis, lipid metabolism, and neuro-development (the last one is why undetected low thyroid in pregnancy can give cretinism in babies).
When iodine intake is insufficient, the thyroid cannot produce adequate T4 and T3, which can lead to elevated TSH, goitre, hypothyroid symptoms, and, in severe cases, cretinism in infants.
However, what is often missed in conventional teaching is that the recommended daily intake (RDI) of iodine, around 150 mcg for adults, is designed primarily to prevent goitre, not to optimise whole-body iodine sufficiency and health.
Dr. Abraham argued that this “anti-goitre dose” may be far below what many tissues actually utilise.
Remember also, the standard NHS test for thyroid is TSH, or thyroid stimulating hormone.
This is an indirect marker for thyroid function produced by the anterior pituitary when thyroid production is lower than demand from the cells.
Unfortunately, it is quite insensitive and the NHS ranges are extremely wide, leading to very high levels of TSH being considered normal. But not necessarily optimum and often with significant levels of symptoms that do correlate with hypothyroidism.
0.3 – 5 mU/L is common, though there is some variation.
In functional lab analysis we like to see TSH under 3 (ish).
Beyond the thyroid: iodine in breast and ovarian tissue
One of Abraham’s most important contributions was demonstrating that iodine is concentrated not only in the thyroid, but also in extra-thyroidal tissues, particularly the breast, ovaries, stomach, salivary glands, and immune cells.
Breast tissue expresses the sodium-iodide symporter and actively takes up iodine. Experimental and clinical data suggest that iodine plays a role in:
- Modulating oestrogen sensitivity in breast tissue
- Supporting normal breast cell differentiation
- Reducing proliferative signalling
- Acting as an antioxidant within glandular tissue
Abraham and colleagues published work showing that iodine supplementation was associated with reduced fibrocystic breast changes in many women, a condition thought to be driven by oestrogen dominance, oxidative stress, and altered tissue signalling.
The implication is that iodine may act as a local modulator of breast tissue health, not merely as a thyroid nutrient.
Similarly, ovarian tissue also utilises iodine, and there is growing interest in its role in ovarian physiology, steroidogenesis, and oxidative balance.
This broader perspective is critical for clinicians: iodine is not just “for the thyroid,” but a multi-organ nutrient with implications for women’s health, endocrine balance, and tissue resilience.
Halides: the hidden iodine antagonists
A central pillar of Abraham’s work, and one that is increasingly relevant today, is the concept of halide competition.
Iodine belongs to a family of elements known as halides, which also includes:
- Fluoride
- Chloride
- Bromide
IMPORTANT: These elements compete with iodine for transport into tissues via the sodium-iodide symporter.
Over the past century, human exposure to non-iodine halides has increased dramatically:
- Fluoride is widely added to toothpaste and, in some regions, to water.
- Chlorine is commonly used in drinking water and swimming pools.
- Bromine (and brominated compounds) is used as a flame retardant in furniture, mattresses, and some plastics, and historically in some food products.
The fluoride and chlorine can be avoided with fluoride free toothpaste and a good quality water filter for your home.
However, bromine is unavoidable and is surrounding you wherever you go and competing for your iodine transporter.
Abraham proposed that chronic exposure to these competing halides could displace iodine from tissues, effectively creating a “functional iodine deficiency” even when dietary intake appears adequate.
In practical terms, this means that many individuals may have sufficient iodine in their diet but still have suboptimal iodine saturation in key tissues, particularly the breast and thyroid, due to halide competition.
This concept helps explain why some patients with apparently “normal” iodine intake still exhibit thyroid dysfunction, fibrocystic breast changes, or other iodine-responsive conditions.
Why higher doses may be clinically relevant
One of the most controversial aspects of Abraham’s work was his advocacy for what he termed “iodine sufficiency,” which involved doses far higher than the RDI, often in the milligram (mg) range rather than microgram (mcg) range.
He argued that the body’s true iodine requirement, particularly in the context of high halide exposure, may be closer to 12.5 mg (12,500 mcg) per day, a dose he commonly used in clinical protocols.
This is where our new liposomal iodine product becomes relevant.
At 13,000 mcg (13.0 mg) per 1 ml, it aligns closely with the dosing framework Abraham frequently referenced, while offering superior absorption and tolerability via a liposomal delivery system.
Note, we often use doses up to 50 mg (50,000 mcg), slowly titrated up from 0.5-1 ml which is 6.5 – 13 mg (6,500-13,000 mcg).
Liposomal encapsulation helps enhance cellular uptake
This is a crucial and easily missed point in clinical outcomes. Getting into the blood is good, but we want it in the cell, doing the work.
Liposomes go from blood through the cell membrane made of a fatty phospholipid bilayer, because liposome are a fatty phospholipid molecule around iodine in this case.
With our liposomal manufacturing partners, we have developed INtraCell – Delivery System (DS) to take the iodine from the mouth/gut into the blood and directly into the cells.
For clinicians working with patients who have thyroid symptoms, fibrocystic breasts, oestrogen dominance, or high environmental halide exposure (I could argue that is everyone), this presents a practical, modern way to implement an iodine sufficiency approach.
Iodine, oestrogen, and endocrine balance
A key insight from Abraham’s work is that iodine interacts with oestrogen signalling in breast tissue.
High oestrogen states, whether from endogenous production, contraceptives, HRT, or xenoestrogens, can increase oxidative stress and proliferative signalling in breast tissue.
Iodine appears to exert a protective, differentiating effect, helping to normalise tissue responses.
This does not mean iodine is a “treatment” for breast disease, but it does suggest that adequate iodine status is a foundational aspect of healthy breast physiology.
From a functional perspective, this fits neatly into a broader clinical framework that includes:
- Supporting liver clearance of oestrogens
- Optimising gut microbiome and enterohepatic circulation
- Ensuring adequate magnesium, selenium, and B vitamins for thyroid function
- Minimising exposure to endocrine disruptors where possible
Selenium — the essential partner nutrient
It is important to emphasise that iodine does not work in isolation. Selenium is required for the conversion of T4 to the active hormone T3 and for protecting the thyroid from oxidative damage during hormone synthesis.
This is important as T3 is x4-5 more potent than T4 and so for optimal thyroid metabolism, you need the conversion to occur.
Brazil nuts are the easiest source of selenium, 68-96 mcg per nut, some people find they are better absorbed covered in dark chocolate……😙
Some clinicians who have concerns about higher-dose iodine are primarily worried about the risk of triggering or worsening autoimmune thyroid conditions such as Hashimoto’s.
While this is a nuanced topic, ensuring adequate selenium status is widely considered best practice when supporting iodine intake.
Clinical application for chiropractors and functional practitioners
As chiropractors working in a nutrition-informed model, you are uniquely placed to educate patients about environmental factors, lifestyle exposures, and foundational micronutrients.
In practice, iodine assessment can be approached via:
- Symptom pattern (fatigue, cold intolerance, hair loss, breast tenderness, carpal tunnel syndrome bilaterally)
- Thyroid labs (TSH, free T4, free T3, TPO antibodies)
- Existing known hypothyroid patients
Note we are now running www.optimaltesting.co.uk our UK functional blood testing facility, but only with CCCN members until we have ironed out all the wrinkles in the platform. But hopefully in the next few weeks we will be live for all of you to test thyroid function.
For patients who are good candidates, liposomal iodine offers a convenient, precise, and clinically meaningful way to deliver higher-dose iodine in a controlled manner.
Why liposomal iodine matters
Traditional iodine supplements (e.g., Lugol’s solution or potassium iodide) can be harsh, unpalatable, and inconsistent in absorption.
A liposomal format helps ensure that iodine is carried into cells more effectively, potentially improving tissue saturation, particularly in extra-thyroidal sites such as the breast.
At 13,000 mcg per 1 ml, dosing can be tailored to the individual, allowing for gradual titration rather than a blunt, one-size-fits-all approach. Going up to 50,000 mcg to saturate tissue adn push out the other halides, then drop down again to a maintenance dose of 6,500 – 13,000 mcg (0.5 – 1 ml).
In summary, iodine should be viewed not merely as a thyroid nutrient, but as a systemic micronutrient with roles in:
- Thyroid hormone production
- Breast and ovarian tissue health
- Antioxidant defence
- Cellular differentiation
- Endocrine balance
- Immune system function
At the same time, we must recognise that modern environmental exposure to competing halides, fluoride, chlorine, and bromine, may be pushing many individuals toward a state of functional iodine deficiency.
Dr. Guy Abraham’s work challenges us to think beyond the RDI and consider what true iodine sufficiency might look like in a world very different from that in which our nutritional guidelines were originally established.
Our new liposomal iodine is designed to support this broader, more nuanced understanding of iodine physiology, offering a practical, clinically relevant tool for practitioners committed to evidence-informed, functional care.