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Showing posts with label Goiter. Show all posts
Showing posts with label Goiter. Show all posts

Monday, 8 April 2019

When your thyroid gland goes into overdrive

Misdiagnosis in hyperthyroidism is quite common, because the key symptoms tend to overlap with other health conditions. Simply put, hyperthyroidism is an overactive thyroid gland that produces too much of thyroid hormones known as T3 and T4.

When your thyroid gland goes into overdrive
The thyroid gland, which produces thyroid hormones, is located at the front bottom part of your neck. — TNS

Located in the front section of your neck at the base, it helps to regulate body processes like metabolism, the nervous system, heart rate and body temperature, just to name a few.
Undetected or misdiagnosed hyperthyroidism puts a person at risk of damaging their thyroid gland.
This diminishing capacity to properly regulate important body processes can result in problems like the decline of energy, metabolic activity and mental function.
It even affects one’s mood, and subsequently, brings about depression.
Important test markers
Until recently, many health professionals were unaware of what to look for when testing for hyperthyroidism.
Most doctors would only glance at the numbers of hyperthyroidism tests, without truly understanding the meaning behind them.
As we now know better, here are key markers to examine when diagnosing hyperthyroidism.
Reverse T3: A body under intense stress will have high levels of the cortisol hormone.
Cortisol increases the levels of reverse T3, an inactive form of the T3 thyroid hormone. It mimics, but does not really perform the real functions of T3.
On this note, looking at total T3 and T4 levels alone do not tell you the whole story of what’s going on.
Only the free portion of T3 and T4 thyroid hormones are able to maximise their benefits on the body’s cells and those levels are important in helping to determine the health of your thyroid.
Vitamin D and magnesium: Patients with hyperthyroidism are very often found with low levels of vitamin D.
If you are found to be low in vitamin D, discuss a supplementation plan with your doctor.
Homocysteine: This amino acid is derived mainly from eating meat, but high levels of it complicate heart health and have been linked to the development of lung issues.
Studies also suggest that high levels of homocysteine is linked to patients with hyperthyroidism.
C reactive protein (CRP): The CRP-hs test gives patients and their doctors a better idea of the level of inflammation in the body.
T3 and T4 are less effective when inflammation is severe, and inflammation often plays a big role in thyroid problems.
Liver function: A substantial amount of thyroid hormones are processed in the liver.
Hence, a poorly functioning liver creates issues with metabolism, and alters the process of T3 and T4 conversion.
With a blood test, doctors can identify if liver enzymes are elevated and plan a corrective course of action.
Thyroid antibodies: Hyperthyroidism can be caused by autoimmune diseases, specifically Graves’ disease and Hashimoto’s thyroiditis.
Each of these diseases are linked to different types of antibodies that can be identified in tests, so it is important to test for antibodies.
Understanding if it is your liver function, a lack of critical nutrients or problems with the pituitary glands, is also necessary in order to plan a more accurate course of treatment.
With Graves’ disease, the test is known as either TSH binding inhibiting immunoglobin (TBII) or thyroid stimulating immunoglobin (TSI).
For Hashimoto’s thyroiditis, the condition is identified by testing the antibodies attached to thyroid tissues.
Causes and symptoms
Thyroid gland, hyperthyroidism, tremors, Star2.com
Tremors in your hands are one of the symptoms of hyperthyroidism. — 123rf.com
Women have to pay more attention to hyperthyroidism, as it is more prevalent in our gender.
If you are genetically prone to the condition, there’s a risk of developing it during pregnancy or within a year after delivery.
Overconsumption of iodine either from supplements, medicine or food, may also cause the thyroid to overproduce hormones.
Lumps in the thyroid glands are another culprit causing an overactive thyroid.
Those lumps are known as toxic nodular or multi-nodular goitre and encourage the production of excessive amounts of thyroid hormones.
Thyroiditis, which is inflammation of the thyroid gland, can occur when the immune system is weakened or the body is fighting off a virus.
This is temporary as long as you treat the problem and strengthen your immune system.
Finally, hyperthyroidism occurs due to the autoimmune diseases discussed above. Graves’ disease, which is hereditary, is the most common cause of hyperthyroidism.
In this condition, the body makes antibodies in order to combat viruses or bacteria, but these antibodies end up aggravating the thyroid instead, causing it to overproduce thyroid hormones.
Hyperthyroidism is tricky to diagnose, as its symptoms are very similar to that of other diseases. Pay extra attention to the following symptoms:
• Anxiety or nervousness
• Irregular heart beat
• Loss of weight
• Trouble falling asleep
• Fatigue
• Tremors in the hands
• Irregular periods
• Muscle weakness
• Changes in bowel movement
• Swelling in the neck
Treatment
Thyroid gland, hyperthyroidism, seafood, Star2.com
Seafood, which is high in iodine, is a no-no if you have hyperthyroidism. — Reuters
Most of the time, doctors will prescribe antithyroid medications to balance out excess activity.
Radiation or surgery are also options to consider in treating hyperthyroidism.
Before some of these treatments are carried out, a low iodine diet is prescribed and you’ll be advised to maintain a similar diet after completing your treatment.
Apart from low iodine, consuming more of the following foods calms the inflammation in your body and reduce chronic symptoms of hyperthyroidism:
• Vitamin D – cereals fortified with vitamin D, mushrooms, cow liver and fatty fish.
• Zinc – beef, cashew nuts, pumpkin seeds, cocoa powder and chickpeas.
• Iron – green leafy vegetables, red meat, chicken, turkey, lentils and whole grains.
• Healthy fats – oils from flaxseed, olive, avocado, sunflower, and unsalted nuts and seeds.
• Selenium – tea, Brazil nuts, couscous, mushrooms and chia seeds.
But there are also foods you should avoid or eat less of. They include:
• Foods that are high in iodine, such as seafood (prawns, lobster, squid etc), milk and dairy products, egg yolks, iodised water and iodised salt.
• Foods that contain nitrates, which makes the thyroid absorb iodine in large quantities, especially processed meat like pepperoni and other cold cuts, and even vegetables like turnips, carrots, cucumber, leeks, parsley, endives and beets.
• Foods containing gluten, which may cause inflammation.
• Soy, as research indicates it interferes with treatment of hyperthyroidism.
The bottom line on hyperthyroidism is that it is treatable.
Monitor your symptoms carefully if you suspect that you might be suffering from the condition, then seek your doctor’s help in getting tested and planning a treatment plan.

https://www.star2.com/health/2019/04/08/thyroid-gland-overdrive/

Tuesday, 10 September 2013

Thyroid Regulation - Life Extension

Health Concerns

Life Extension

Thyroid Regulation

Millions of Americans suffer from fatigue, weight gain, depression, and cognitive impairment. Many believe that they have no choice but to accept these seemingly “age-related” declines in quality of life.

Underactive thyroid (hypothyroidism) is often overlooked or misdiagnosed and can be the underlying cause of these symptoms. Patients and their doctors often disregard these common signs of thyroid hormone deficiency, mistaking them for normal aging.1

Overactive thyroid (hyperthyroidism) afflicts fewer people than hypothyroidism, yet the symptoms can be equally devastating. Subclinical hyperthyroidism, characterized by suppressed thyroid stimulating hormone (TSH) levels accompanied by normal thyroid hormones (T4 and T3) levels,2 has been associated with increased rates of cardiovascular disease; arrhythmia in particular.3 Overt hyperthyroidism compromises bone health,4 elevates blood glucose levels,5 and often causes anxiety.6

Fortunately, a simple blood test for TSH, T3 and T4 can reveal an underlying thyroid condition and help direct treatment to improve the symptoms.1, 2

In this protocol we will discuss the function and regulation of the thyroid gland, and the systemic implications of both hypothyroidism and hyperthyroidism. We will examine the importance of proper testing and interpretation of thyroid hormone levels and reveal natural approaches for maintaining optimal thyroid hormone levels.

Role of the Thyroid


The thyroid is a butterfly-shaped organ located just below the Adam’s apple in the neck. Made up of small sacs, this gland is filled with an iodine-rich protein called thyroglobulin along with the thyroid hormones thyroxine (T4) and small amounts of triiodothyronine (T3).

The primary function of these two hormones is to regulate metabolism by controlling the rate at which the body converts oxygen and calories to energy. In fact, the metabolic rate of every cell in the body is regulated by thyroid hormones, primarily T3.7

In healthy individuals the gland is imperceptible to the touch. A visibly enlarged thyroid gland is referred to as a goiter. Historically, goiter was most frequently caused by a lack of dietary iodine.8 However, in countries where salt is iodized, goiter of iodine deficiency is rare.

Thyroid Regulation


The production of T4 and T3 in the thyroid gland is regulated by the hypothalamus and pituitary gland. To ensure stable levels of thyroid hormones, the hypothalamus monitors circulating thyroid hormone levels and responds to low levels by releasing thyrotropin-releasing hormone (TRH). This TRH then stimulates the pituitary to release thyroid stimulating hormone (TSH).9,10 When thyroid hormone levels increase, production of TSH decreases, which in turn slows the release of new hormone from the thyroid gland.

Cold temperatures can also increase TRH levels. This is thought to be an intrinsic mechanism that helps keep us warm in cold weather.11

Elevated levels of cortisol, as seen during stress and in conditions such as Cushing’s syndrome, lowers TRH, TSH and thyroid hormone levels as well.12,13

The thyroid gland needs iodine and the amino acid L-tyrosine to make T4 and T3. A diet deficient in iodine can limit how much T4 the thyroid gland can produce and lead to hypothyroidism.14

T3 is the biologically active form of thyroid hormone. The majority of T3 is produced in the peripheral tissues by conversion of T4 to T3 by a selenium-dependent enzyme. Various factors including nutrient deficiencies, drugs, and chemical toxicity may interfere with conversion of T4 to T3.15

Another related enzyme converts T4 to an inactive form of T3 called reverse T3 (rT3). Reverse T3 does not have thyroid hormone activity; instead it blocks the thyroid hormone receptors in the cell hindering action of regular T3.16

Ninety-nine percent of circulating thyroid hormones are bound to carrier proteins, rendering them metabolically inactive. The remaining “free” thyroid hormone, the majority of which is T3, binds to and activates thyroid hormone receptors, exerting biological activity.17 Very small changes in the amount of carrier proteins will affect the percentage of unbound hormones. Oral contraceptives, pregnancy, and conventional female hormone replacement therapy may increase thyroid carrier protein levels and, thereby, lower the amount of free thyroid hormone available.18

Thyroid Dysfunction

 

Hyperthyroidism


In hyperthyroidism, the thyroid gland produces too much thyroid hormone, which can significantly accelerate the body's metabolism. Typical symptoms of hyperthyroidism include sudden weight loss, a rapid heartbeat, sweating, nervousness or irritability. Hyperthyroidism affects about one percent of the population.19

Extreme hyperthyroidism, or thyrotoxicosis, can culminate in what’s referred to as “thyroid storm.”20 In this medical emergency, patients suffer from elevated heart rates and blood pressure, extreme exhaustion, and high fever. Thyroid storm sharply increases a patient’s risk for stroke and heart attack, and is fatal for up to 50% of patients, even with the best medical care.21

Hyperthyroidism: What you need to know

Hyperthyroidism is usually caused by Graves’ disease characterized by symptoms such as rapid heartbeat, sweating, nervousness, tremors, muscle weakness, sleep difficulties, increased appetite and sudden weight loss.22 Affected individuals can also experience thyroid storm—a potentially deadly medical emergency.23

Medical Treatment of Grave’s disease24
  • Anti-thyroid drugs, such as methimazole or propylthiouracil, inhibit the production of T3.
  • Radioactive iodine, which causes destruction of the overactive thyroid gland.
  • Surgical removal of the thyroid gland (thyroidectomy).
  • Βeta-blockers may be used to control the high blood pressure and increased heart rate associated with hyperthyroidism.

Nutritional Support of Hyperthyroidism
  • Increased thyroid activity increases loss of L-carnitine through the urine. Individuals suffering from hyperthyroidism may, therefore, require supplemental L-carnitine.25
  • L-carnitine supplementation helped prevent or reverse muscle weakness and other symptoms in individuals suffering from hyperthyroidism. Clinical trials have shown that doses of 2,000-4,000 mg/day of L-carnitine are helpful in individuals who suffer from hyperthyroidism.26
  • Passion flower (Passiflora incarnata ) and valerian (Valeriana officinalis) are botanicals that have a calming effect on the nervous system27,28 and thus may help control the symptoms of an overactive thyroid.

 

Hypothyroidism


Hypothyroidism is a condition in which the thyroid gland does not make enough thyroid hormones, characterized by a reduction in metabolic rate. The main symptoms of hypothyroidism are fatigue, weakness, increased sensitivity to cold, constipation, unexplained weight gain, dry skin, hair loss or coarse dry hair, muscle cramps and depression. However, most symptoms take years to develop. The slower the metabolism gets, the more obvious the signs and symptoms will become. If hypothyroidism goes untreated, the signs and symptoms could become severe, such as a swollen thyroid gland (goiter), slow thought processes, or dementia.29

Subclinical hypothyroidism, an often under-diagnosed thyroid disorder, manifests as elevated TSH, normal T4 and normal T3 levels.30 Individuals with subclinical hypothyroidism are at greater risk for developing overt hypothyroidism.31 An August 2010 study reported that 8.3% of women with no history of thyroid disease suffer from subclinical hypothyroidism.32 An article in the American Family Physician in 2005 estimated that about 20% of women over the age of 60 suffer from subclinical hypothyroidism.33

There is evidence that the standard blood TSH test reference range may cause many cases of hypothyroidism to be missed. Most physicians accept a reference range for TSH between 0.45 and 4.5 µIU/mL to indicate normal thyroid function. In reality, though, a TSH reading of more than 2.0 may indicate lower-than-optimal thyroid hormone levels.34

According to a study reported in Lancet, various TSH levels that fall within normal range are associated with adverse health outcomes.26
  • TSH greater than 2.0: increased 20-year risk of hypothyroidism and increased risk of thyroid autoimmune disease
  • TSH between 2.0 and 4.0: hypercholesterolemia and cholesterol levels decline in response to T4 therapy
  • TSH greater than 4.0: greater risk of heart disease

There is another and separate problem brought on by these overly broad normal ranges for TSH. People already diagnosed and being treated for hypothyroidism are often not taking correct doses of thyroid replacement hormone. A November 2010 study reported that about 37% of people being treated for hypothyroidism were taking incorrect doses, about half too much and another half too little hormone.35

Consequences of Hypothyroidism


Gastrointestinal problems. Hypothyroidism is a common cause of constipation. Constipation in hypothyroidism may result from diminished motility of the intestines. In some cases, this can lead to intestinal obstruction or abnormal enlargement of the colon.36 Hypothyroidism is also associated with decreased motility in the esophagus, which causes difficulty swallowing, heartburn, indigestion, nausea, or vomiting. Abdominal discomfort, flatulence, and bloating occur in those with small intestinal bacterial growth secondary to poor digestion.31

Depression and psychiatric disorders. Panic disorders, depression, and changes in cognition are frequently associated with thyroid disorders.37 Hypothyroidism is often misdiagnosed as depression.38 A study published in 2002 suggests that that thyroid function is especially important for bipolar patients: “Our results suggest that nearly three-quarters of patients with bipolar disorder have a thyroid profile that may be suboptimal for antidepressant response.”39

Cognitive decline. Patients with low thyroid function can suffer from slowed thinking, delayed processing of information, difficulty recalling names, etc.40 Patients with subclinical hypothyroidism show signs of decreased working memory,41 and decreased speed of sensory and cognitive processing. 42 An evaluation of thyroid hormones along with TSH may help avoid misdiagnosis as being depressed.43

Cardiovascular Disease. Hypothyroidism and subclinical hypothyroidism are associated with increased levels of blood cholesterol, increased blood pressure, and increased risk of cardiovascular disease.44 Even those with subclinical hypothyroidism were almost 3.4 times as likely to develop cardiovascular disease than those with healthy thyroid function.45

  • High blood pressure. Hypertension is relatively common among patients with hypothyroidism. In a 1983 study, 14.8% of patients with hypothyroidism had high blood pressure, compared with 5.5% of patients with normal thyroid function.46 “Hypothyroidism has been recognized as a cause of secondary hypertension. Previous studies … have demonstrated elevated blood pressure values. Increased peripheral vascular resistance and low cardiac output has been suggested to be the possible link between hypothyroidism and diastolic hypertension.”47
  • High cholesterol and atherosclerosis. “Overt hypothyroidism is characterized by hypercholesterolemia and a marked increase in low-density lipoproteins (LDL) and apolipoprotein B.”48 These changes accelerate atherosclerosis, which causes coronary artery disease.43 The risk of heart disease increases proportionally with increasing TSH, even in subclinical hypothyroidism.49 Hypothyroidism that is caused by autoimmune reactions is associated with stiffening of the blood vessels.50 Thyroid hormone replacement may slow the progression of coronary heart disease by inhibiting the progression of plaques.51,52
  • Homocysteine. Treating hypothyroid patients with thyroid hormone replacement might attenuate homocysteine levels, an independent risk factor for cardiovascular disease: “A strong inverse relationship between homocysteine and free thyroid hormones confirms the effect of thyroid hormones on homocysteine metabolism.”53
  • Elevated C-reactive protein. Overt and subclinical hypothyroidism are both associated with increased levels of low-grade inflammation, as indicated by elevated C-reactive protein (CRP). A 2003 clinic study observed that CRP values increased with progressive thyroid failure and suggested it may count as an additional risk factor for the development of coronary heart disease in hypothyroid patients.54

Metabolic Syndrome. In a study of more than 1500 subjects, researchers found that those with metabolic syndrome had statistically significantly higher TSH levels (meaning lower thyroid hormone output) than healthy control subjects. Subclinical hypothyroidism was also correlated with elevated triglyceride levels and increased blood pressure. Slight increases in TSH may put people at higher risk for metabolic syndrome.55

Reproductive system problems. In women, hypothyroidism is associated with menstrual irregularities and infertility.56 Proper treatment can restore a normal menstrual cycle and improve fertility.57

Fatigue and weakness. The well-known and common symptoms of hypothyroidism, such as chilliness, weight gain, paresthesia (tingling or crawling sensation in the skin) and cramps are often absent in elderly patients compared with younger patients, fatigue and weakness are common in hypothyroid patients.58

 

Testing Thyroid Function


Thyroid stimulating hormone (TSH). TSH level is the most common test for screening for thyroid dysfunction. In the last decade the diagnostic strategy for using TSH measurements has changed as a result of the sensitivity improvements in these assays. It is now recognized that the TSH measurement is a more sensitive test than T4 for detecting both hypo- and hyperthyroidism.59 As a result, some countries now promote a TSH-first strategy for diagnosing thyroid dysfunction in patients.60

In 2008 many labs adopted the reference range for TSH, 0.45 to 4.50 μIU/mL, recommended by both the Endocrine Society and the American Medical Association. Although this range is an improvement over the previous 0.45-5.5 mIU/L, it is still considered too broad by many clinicians.59,60,61

The American Association of Clinical Endocrinologists now recommends an upper limit of 3.0 mIU/L.61 The guidelines for diagnosing thyroid disease from The National Academy of Clinical Biochemistry point out that "more than 95% of normal individuals have TSH levels below 2.5 [µIU/mL]."62 This panel suggests that the upper limit of TSH should be reduced to 2.5 µIU/mL.63
On the other hand, current studies also suggest that TSH values below the normal range may represent thyroid hormone excess and, in elderly patients, might be associated with an increased risk of death due to cardiovascular disease.64,65

Life Extension suggests an optimal level of TSH between 1.0 and 2.0 µIU/mL, as some studies have noted that a TSH above 2.0 may be associated with adverse cardiovascular risk factors.26 In addition, a TSH between 1.0 and 2.0 µIU/mL has been associated with the lowest subsequent incidence of abnormal thyroid function.66

However, while a measure of TSH alone is a useful screening tool in assessing thyroid function, Life Extension advocates additional testing, including Free T3 and T4 levels, to provide a more complete evaluation of the thyroid.

Note: TSH values do fluctuate with time of day, infection, and various other factors. In a 2007 survey published in the Archives of Internal Medicine, values spontaneously returned to normal in more than 50% of patients with abnormal TSH levels when the test was repeated at a later date.67 No single measurement of TSH should be considered diagnostic.

Basal Body Temperature. An alternative method for assessing thyroid status that was widely used in the past, before the development of accurate thyroid function blood tests, is the basal body temperature test. The temperature is taken when the body is at complete rest, immediately after waking and before beginning any activity. The normal basal temperature is 97.6-98.2 ºF, and some alternative practitioners believe that a 5-day consecutive temperature reading below 97.6 ºF is indicative of hypothyroidism. One study showed a significant correlation between the basal body temperature and low thyroid function in whiplash patients. The authors of this study conclude that basal body temperature “seems to be a sensitive screening test, in combination with laboratory analysis, for the hypothyroidism seen after whiplash trauma.”68 However, there are many reasons for alteration of basal body temperature, a thyroid panel blood test should be taken to accurately evaluate the thyroid function.

Tests for T4 and T3. Thyroid hormones can be tested in both their free and protein-bound forms. Tests for the protein-bound forms and unbound form of T4 or T3 are generally referred to as Total T4 or Total T3 respectively; unbound forms are called Free T4 and Free T3. Each of these tests gives information about how the body is making, activating, and responding to thyroid hormone. Levels of free T3 and T4 will be below normal in clinical hypothyroidism. In subclinical hypothyroidism the TSH will be elevated while the thyroid hormone levels are still in the normal reference range.

Reverse T3. Certain individuals with apparently normal T4 and T3 hormone levels still display the classic symptoms of hypothyroidism. This may be due to an excessive production of reverseT3 (rT3). rT3 is inactive and may interfere with the action of T3 in the body. Stress and extreme exercise may play a role in lowering thyroid hormone action by suppressing production of TSH and T3 and elevating rT3 levels.69,70

Autoimmune antibodies. When evaluating the thyroid it is also important to consider that the most common cause of overt hypothyroidism in the United States is an autoimmune disorder known as Hashimoto’s thyroiditis.71 In this condition the body produces antibodies to the thyroid gland and damage the gland. Hashimoto’s thyroiditis is diagnosed by standard thyroid testing in conjunction with testing for the presence of these antibodies called antithyroglobulin antibodies (AgAb) and thyroperoxidase antibodies (TPOAb). Some people with celiac disease or sensitivity to gluten are at increased risk for developing autoimmune thyroid disease and should be evaluated.72

Elevated thyroid antibodies are often associated with chronic urticaria, also called hives. Studies report that as many as 57.4% of patients with hives have the presence of anti-thyroid antibodies.73,74 An August 2010 paper suggests that treatment with T4 improves the itching associated with urticaria, but did not advise treatment with T4 unless the patient was hypothyroid.75

Additional testing. Sometimes biopsy or enzymatic studies are required to establish a definite diagnosis for thyroid dysfunction. Major abnormalities of the thyroid gland detected in physical exam can be further assessed by ultrasound or a procedure known as scintigraphy.

Hypothalamic pituitary axis (HPA). There is an intimate relationship between the thyroid, the adrenal glands and the sex hormones.76 If hypothyroidism is suspected, an evaluation of the adrenal glands as well as the sex hormones is suggested.

Hypothyroidism: What you need to know

  • Thyroid diseases occur about five times more frequently in women than in men. As many as 20% of women over 60 years old have subclinical hypothyroidism.77
  • If untreated, chronic hypothyroidism can result in myxedema coma, a rare, life-threatening condition. Mental dysfunction, stupor, cardiovascular collapse, and coma can develop after the worsening of chronic hypothyroidism as well.78
  • An autoimmune disease called Hashimoto’s thyroiditis is the most common cause of low thyroid function in the United States. The body’s immune system mistakenly attacks the thyroid tissue impairing the ability to make hormones.79 Hypothyroidism caused by Hashimoto's disease is treated with thyroid hormone replacement agents.
  • Hashimoto’s disease usually causes hypothyroidism, but may also trigger hyperthyroid symptoms.80
  • Hyperthyroidism is usually caused by Graves’ disease, in which antibodies are produced that bind to TSH receptors in the thyroid gland, stimulating excess thyroid hormone production.20
  • The distinction between Hashimoto’s thyroiditis and Graves’ disease may not be as important as once thought. In 2009 researchers wrote that, “Hashimoto's and Graves' disease are different expressions of a basically similar autoimmune process, and the clinical appearance reflects the spectrum of the immune response in a particular patient.” 81 The two diseases can overlap causing both thyroid gland stimulation and destruction simultaneously or in sequence.82 Some clinicians consider the two conditions different presentations of the same disease.83 About 4% of patients with Graves’ disease displayed some symptoms of Hashimoto’s thyroiditis during childhood.84
  • Pregnant women are especially at risk for hypothyroidism. During pregnancy, the thyroid gland produces more thyroid hormone than when a woman is not pregnant,85 and the gland may increase in size slightly.
  • Uncontrolled thyroid dysfunction during pregnancy can lead to preterm birth, mental retardation, and hemorrhage in the postpartum period.86 It is important to work closely with a physician to monitor thyroid function during pregnancy.
  • Tests to diagnose and monitor hypothyroidism include: Thyroid Stimulating Hormone (TSH), Total T4, Total T3, Free T4 (fT4), Free T3 (fT3), Reverse T3 (rT3), Thyroid peroxidase antibody (TPOAb), Thyroglobulin antibody (TgAb)
                 

Thyroid Hormone Replacement


The most common treatment for low thyroid hormone levels consists of thyroid hormone replacement therapy. The goal of thyroid hormone replacement is to relieve symptoms and to provide sufficient thyroid hormone to decrease elevated TSH levels to within the normal range.87

Conventional treatment almost always begins with synthetic T4 (levothyroxine) preparations like Synthroid® or Levoxyl®. Low doses are usually used at first because a rapid increase in thyroid hormone may result in cardiac damage.88

Sometimes hypothyroid symptoms persist despite T4 treatment. In a 2001 study, T4 therapy was no more effective than placebo in improving cognitive function and psychological well-being in patients with symptoms of hypothyroidism, despite improvement in free T3 levels.89 A December 2010 study compared the T3 and T4 levels of hypothyroid patients treated with T4 alone against the levels found in healthy people and reported that T4 supplementation alone did not increase T3 to the same level as found in healthy people.90 As you will read later, deficiencies in nutrients like selenium can disable the body from converting T4 to biologically active T3.

In an animal study, rats with the thyroid gland removed were treated with T4 alone. The researchers found that no single dose restored normal concentrations of TSH, T4, and T3 in the blood, tissues and organs.91 The following year the same authors reported that a combination of T4 and T3 was able to normalize hormone levels in both blood and tissues.92 Other studies have failed to demonstrate any advantage of the combination therapy, although the results do suggest the possibility of a subset of hypothyroid patients who would benefit from combination therapy.93,94

One combination option is a drug called Thyrolar, which combines synthetic T3 and T4 in a fixed 1:4 ratio. Caution should be used, however, in administering T3 to older individuals because excess T3 may cause adverse cardiac events in this population.95

Another T3 option is a drug called Cytomel®, which is a synthetic form of T3. This can be used in combination with T4.

Desiccated Thyroid. Armour thyroid, Nature-throid, and Westhroid are prescription medications that contain desiccated porcine thyroid gland. Natural thyroid extracts have been used since 1892 and were approved by the Food and Drug Administration in 1939. Armour thyroid and most other natural glandular preparations are made to standards approved by the United States Pharmacopoeia.

Armour thyroid is preferred by some clinicians because it may achieve results in patients that fail to respond to levothyroxine alone. Patients with hypothyroidism show greater improvements in mood and brain function if they receive treatment with Armour thyroid rather than Synthroid®.96 One argument favoring natural hormones is that other naturally occurring hormones and chemicals found in these preparations may buffer or enhance the effect of the active hormones.87,92

Ultimately, there may not be a single correct approach to low thyroid hormone levels. Instead, the best option may be to monitor thyroid levels through regular blood testing and systematically try various protocols to see what yields the best resolution of symptoms. Some people may prefer to begin with desiccated thyroid, while others may find it preferable to begin with T4 supplementation then move to a combination T3-T4 therapy if they experience no improvement from T4 alone.

Absorption of Thyroid Hormone Medications. Coffee,97 aluminum antacids,98 ferrous sulfate (iron),99 calcium carbonate,100 soy101 and possibly grapefruit juice102 can all decrease the absorption of thyroid hormone prescriptions. Most doctors simply advise patients to take thyroid hormone away from any food or medication.

While most people take thyroid hormone in the morning, a December 2010 paper suggests that it is more effective to take thyroid medication just before bed.103

 

Nutrients to Support Thyroid Function


Iodine. The body needs iodine to make thyroid hormone. As of the late 1990s, thirty-two European countries were still affected by iodine deficiency.104 In 2007 the WHO estimated that over 30% of the world’s population (2 billion people) has insufficient iodine intake as measured by urinary iodine excretion below 100 µg/L.105 Iodized salt has proven to be effective at preventing iodine deficiency. The Morton Salt Company began selling iodized salt in the United States in 1924.106

Hypothyroidism in the unborn child, congenital hypothyroidism or cretinism, is frequently caused by iodine deficiency. In industrialized countries the incidence is about 1 case in 4500 live births. Yet, the incidence of cretinism can increase to as much as 1 case in 20 live births in areas that have iodine deficiency.107 Because of this, iodine deficiency remains one of the leading causes of mental retardation.108

During pregnancy T4 production doubles, causing increases in daily iodine requirements.109 Iodine deficient pregnant women cannot produce the thyroid hormones that are needed for proper neurological development of their growing babies, and are at high risk of giving birth to infants with cognitive impairment and learning delay. Even moderate iodine deficiency in a pregnant woman can lower her infant’s IQ from 8 to 16 points.110, 111

People who avoid iodized salt or adhere to a salt-restricted diet may become iodine deficient.112 Vegetarians are also at risk of developing iodine deficiency, especially if they eat food grown in low iodine soil.113 Vegans that avoid sea vegetables, are also at higher risk.114

Diets both low and high in iodine are associated with hypothyroidism. This is supported by studies that have shown that both low and high urinary iodine excretion are associated with hypothyroidism.115 High intake of iodine also increases the risk of Hashimoto’s thyroiditis.116

Iodine or foods high in iodine, such as seaweed, are thought useful in treating hypothyroidism but this is probably only true for people who are iodine deficient.113, 114 The upper intake level (UL) of iodine for adults is 1.1mg per day. However, iodine ingestion above this amount is generally well tolerated.117

The amount of supplemental iodine needed for an individual varies widely based on the factors previously listed. It is important to test thyroid function when supplementing with iodine since both low and excessively high intake can contribute to thyroid dysfunction.

Selenium. After iodine, selenium is probably the next most important mineral affecting thyroid function. The thyroid contains more selenium by weight than any other organ.118 Selenium is a necessary component of the enzymes that remove iodine molecules from T4 converting it into T3; without selenium there would be no activation of thyroid hormone. When patients suffering from various forms of thyroid disease were tested for selenium levels, all were found to be lower than normal healthy people.119 Some researchers suggest that selenium supplementation will improve conversion of T4 to T3.120 Selenium also plays a role in protecting the thyroid gland itself. The cells of the thyroid generate hydrogen peroxide and use it to make thyroid hormone. Selenium protects the thyroid gland from the oxidative damage caused by these reactions. Without adequate selenium, high iodine levels lead to destruction of the thyroid gland cells.121,122

People living in areas with low soil selenium content are more likely to develop Hashimoto's disease.123 This may be because a selenium deficiency makes the enzyme glutathione peroxidase less effective.124 Thus selenium supplementation has been suggested for treating Hashimoto’s disease.125

In a placebo controlled study published in 2002, researchers in Germany reported on an experiment in which they gave 200 mcg of sodium selenite daily to patients with Hashimoto's disease and high levels of thyroid peroxidase antibodies. After three months, the thyroid peroxidase antibody levels of the patients taking selenium were decreased by 66.4% compared to their pre-treatment values, and antibody levels returned to normal in nine of the selenium treated patients.126 Austrian researchers reported in 2008 that they were unable to duplicate the results of the earlier study when they did not limit the study population to those with high levels of thyroid peroxidase antibodies. They suggest that selenium supplementation might be of greater benefit to patients with higher disease activity.127

Selenium deficiency is also common in celiac disease, and this may be the tie-in to increased frequency of thyroid problems with celiac disease.128

During severe or prolonged infection, blood levels of selenium, T4, T3 and TSH decrease and the conversion of T4 to T3 slows, inducing a hypothyroid state.129 Because the enzymes that moderate this conversion require selenium, it has been hypothesized that supplementing extra selenium might prevent this decrease in T3 during illness. Supplying extra selenium may decrease mortality from infection, but it does not normalize thyroid hormone levels.130 It seems that the suppression of T3 during sickness is mediated by cytokines, in particular interleukin-6 (IL-6).131 It may be that IL-6 and other cytokines, generated by the infection, limit production of the selenium-enzymes and interfere with hormone production.

Zinc. Zinc may be helpful in patients with low T3 and may contribute to conversion of T4 to T3. In animal studies, zinc deficiency lowered T3 and free T4 concentrations by approximately 30%. Levels of total T4 were not affected by zinc deficiency.132 In a group of patients with low levels of free T3 and normal T4, but elevated rT3 and mild to moderate Zn deficiency, taking oral zinc supplements for 12 months, normalized the serum free T3 and total T3 levels, decreased the rT3 and normalized TSH levels.133

On the other hand, like iodine, too much zinc may suppress thyroid function.134 Very high doses of zinc interfere with copper absorption and can lead to serious and potentially fatal copper deficiency.135,136,137 Thus it is advised to take copper when supplementing with zinc.

Iron. Iron deficiency hinders manufacture of thyroid hormone by reducing activity of the enzyme thyroid peroxidase. In one study 15.7% of women with subclinical hypothyroidism were iron deficient, compared to only 9.8 % of the control group.138 Iron-deficiency anemia decreases, and iron supplementation improves, the beneficial effects of iodine supplementation.139 Treating iron deficient hypothyroid patients with levothyroxine (T4) along with iron improves their iron deficiency anemia more than treatment with iron alone.140

Copper. An August 2010 study revealed that copper is important for normal brain development and its deficiency leaves the hypothalamus unable to regulate thyroid hormone effectively. Copper deficient pregnant rats give birth to infant rats that produce 48% less T3 than those born from healthy mothers.141

Vitamin E. Vitamin E may reduce the oxidative stress caused by hypothyroidism. In one animal study, vitamin E was shown to protect animals from increased oxidation and thyroid cell damage.142 In another study, vitamin E reduced the amount of thyroid cell replication in animals with induced hypothyroidism.143

Vitamin D. Deficiency of vitamin D may increase risk of autoimmune thyroid disease. When adjusted for age, presence of thyroid antibodies was inversely correlated with vitamin D levels in a group of 642 participants (244 males and 398 females) in New Delhi, India.144 Moreover, other evidence suggests that vitamin D deficiency is more common among individuals with thyroid cancer or thyroid nodules, compared to the general population.145 Given the many benefits of adequate vitamin D, it makes sense to supplement if needed.

Vitamin B12. Hypothyroid patients are often vitamin B12 deficient. In a 2008 paper, Pakistani doctors reported that of 116 hypothyroid patients tested for vitamin B12, approximately 40% were deficient.146 It is not clear what the link between B12 deficiency and low thyroid function is, nor if thyroid function will improve with B12 supplementation.147 But, since low B12 causes serious neurologic damage, all hypothyroid patients should be tested.

DHEA and Pregnenolone. Japanese researchers reported that concentrations of DHEA, DHEA-sulfate, and pregnenolone-sulfate are significantly lower in hypothyroid patients compared to age and sex matched healthy controls.148

Turmeric (Curcuma longa) Extract. A 2002 study, using rats, found that treatment with turmeric extract reduced the impact of chemically induced hypothyroidism in terms of thyroid weight, T4, T3 and cholesterol levels.149 Results of a similar trial on rats treated with vitamin E and curcumin, a component found in turmeric, showed that treatment prevented a decline in basal body temperature and protected the liver.150

Rhodiola rosea. Given the fact that stress can influence thyroid status, it may be beneficial for some individuals with hypothyroidism to consider adaptogenic herbs such as Rhodiola.151,152 Adaptogenic herbs support the adrenal glands and can improve the body’s response to stress.153

Dietary Recommendations


Some foods contain goitrogenic substances that reduce the utilization of iodine. These foods include canola oil, vegetables from the Brassica family (eg, cabbage,154 brussels sprouts,155 cassava,156 and millet157). The actual content of goitrogens in these foods is relatively low, however, and cooking significantly reduces the impact of these goitrogens on thyroid function.158

Studies show conflicting information concerning the impact of soy on the thyroid. Isoflavone molecules in soy do inhibit an enzyme involved in thyroid hormone synthesis,159,160 but that has not translated into poor thyroid function in otherwise healthy individuals with adequate iodine intake.161,162,163

For those with hypothyroidism, raw goitrogenic foods and soy foods that have not undergone fermentation and/ or food processing should be consumed in moderation and discontinued if symptoms should appear.

Life Extension Suggestions


Thyroid hormone supplementation: If hormones are necessary, work with an experienced medical provider to find a hormone supplement that works best for you.

The following suggestions may support thyroid hormone production.
  • Iodine: Up to 1150 mcg daily. Intake above this amount is generally well tolerated. The exact dosage to be taken should be determined by thyroid function testing and the advice of a health care professional.
  • Selenium: 200 – 400 mcg daily
  • Zinc: 30 – 80 mg daily
  • Copper: 1 – 2 mg daily
  • Curcumin (as highly absorbed BCM-95®): 400 – 800 mg daily
  • Natural Vitamin E: 400 IU alpha-tocopherol and 200 mg gamma-tocopherol
  • Vitamin C: 1000 – 2000 mg daily
  • Iron: Check for deficiency and correct if low
  • Vitamin B12 (as methylcobalamin): 1000 – 2000 mcg daily
  • DHEA: The exact dosage to be taken should be determined by blood testing and the advice of a physician. Typical dosages range from 15 – 75 mg daily taken in the morning. DHEA serum blood tests are suggested 3 – 6 weeks after initiating DHEA replacement therapy to optimize individual dosing.
  • Pregnenolone: Check for deficiencies and correct if low. Typical dosages are 50 – 100 mg daily. A complete hormone profile is suggested when supplementing with pregnenolone as it may affect levels of other hormones, such as progesterone, estrogen, testosterone and/or DHEA.
  • Rhodiola, standardized extract: 250 – 500 mg daily
  • L-tyrosine: 500 – 1000 mg daily

In addition, the following blood testing resources may be helpful:

 

Disclaimer and Safety Information


This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the therapies discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. Life Extension has not performed independent verification of the data contained in the referenced materials, and expressly disclaims responsibility for any error in the literature.

http://www.lef.org/protocols/metabolic_health/thyroid_regulation_01.htm

The Silent Epidemic of Iodine Deficiency

Life Extension Magazine October 2011

Report
By Nancy Piccone
 
The Silent Epidemic of Iodine Deficiency
In 2008, researchers concerned about the growing threat of iodine deficiency analyzed 88 samples1 of iodized table salt—the main supply of this critical micronutrient for most people.2

Less than half of those tested contained amounts of iodine sufficient for optimal health.

Coupled with the trend of reduced salt consumption, rates of iodine deficiency are now reaching epidemic levels.

In the developed world, iodine deficiency has increased more than fourfold over the past 40 years. Nearly 74% of normal, “healthy” adults may no longer consume enough iodine.3,4

In this article, the latest data on this dangerous trend are presented. You will learn of iodine deficiency’s profound impact on overall health. You will discover iodine’s vital role in thyroid function and its link to obesity, cognitive impairment, heart disease, psychiatric disorders, and various forms of cancer. You will also find out how iodine can help ward off breast cancer and fibrocystic breast disease.

Unknowingly Robbing Our Bodies


In nature, iodine is a relatively rare element. It’s found in abundance in the ocean. Its presence in soil, on the other hand, is very low in many places around the world, including the United States.
Iodine is essential to life and especially crucial for brain development in children, making its deficiency the number one cause of preventable mental retardation worldwide.

It also plays a central role in healthy function of your thyroid gland. This is why the most visible symptom of iodine deficiency is goiter—the unsightly, painful enlargement of the thyroid gland that manifests as an enormous swelling around the neck and larynx.

Unknowingly Robbing Our Bodies
While goiter was relatively common a few generations ago, most middle age and younger Americans have never seen it. This is largely due to the industry practice of salt iodization in this country, first implemented in the 1920s after the effects of iodine deficiency were recognized and since emulated around the world.2,5,6 (The Morton company was the first to add iodine to salt in 1924, after a successful public health campaign.)7 Unfortunately, as evidenced by recent FDA findings, many table salt makers are now failing to add iodine in quantities sufficient to support optimal health.

Other consequences of iodine deficiency, so-called iodine deficiency disorders (IDD), are subtle and may inflict greater damage.6,8 It is estimated that IDDs affect between 800 million and 2 billion people worldwide; reduction in salt intake is likely to drive those numbers still higher.2,9-11

The health benefits of reducing salt intake have been well established.9,12,13 Millions of Americans are slashing their use of salt to protect themselves against high blood pressure and cardiovascular disease.

But by cutting our salt intake we are also cutting our iodine intake, which is why mean urinary iodine levels (a measure of iodine sufficiency) plummeted by more than half over a 20-year period.4,14 Additional, otherwise healthy behaviors have also contributed to inadequate iodine intake. (See Table 1.)

The danger of low dietary iodine is further compounded by your body’s decreased ability to utilize it, the result of contamination by a ubiquitous environmental toxin called perchlorate.

Originally developed for explosives and rocket fuel,18 perchlorate now pervades ground water and food supplies throughout the US. It’s even used as a flavor-enhancer in certain foods.19-21 Perchlorate blocks the thyroid gland’s ability to absorb and utilize dietary iodine, an effect that is of concern when iodine intake drops off.18,22

The US recommended dietary allowance (RDA) for iodine is 150-290 micrograms (mcg) for adults, while the Food and Nutrition Board of the Institute of Medicine has set the tolerable upper limit at 1,100 mcg.18,23,24

Your Thyroid Gland and the Role of Iodine
These guidelines may be inadequate to address certain health conditions.

They were first established as sufficient only to prevent goiter. Daily doses for optimal health of 3,000-6,000 mcg have been used without side effects in studies of people with other iodine deficiency-related health conditions such as polycystic breast disease.18

By way of comparison, the average daily Japanese consumption of iodine ranges from 5,280 to 13,800 mcg of iodine, with no harmful effects and a host of benefits.18,25,26 The Japanese experience is shedding new light on the importance of iodine, not only for thyroid health, but on other body functions as well. In particular, compelling evidence is emerging about the role of iodine in maintaining breast health, a major concern for millions of American women.

Since thyroid function is a puzzle to many people, we’ll begin with a brief overview of that important gland and its requirements for iodine. Then we’ll turn to the role of iodine in maintaining breast health, particularly in preventing breast cancer and fibrocystic breast disease.

Your Thyroid Gland and the Role of Iodine

What You Need to Know: Iodine Deficiency

Your thyroid gland is located in the front of your neck, just below your voice box. The thyroid produces two forms of thyroid hormone, both of which are derived from the amino acid tyrosine and several atoms of iodine. Thyroid hormones control your body’s metabolism, regulating everything from body temperature and heart rate to glucose consumption and even blood lipid levels.27-29

Too much thyroid hormone (hyperthyroidism) results in an excessively high metabolic rate. People with this condition have rapid heart rates and often palpitations,29 excessive sweating, and may feel much warmer than other people do, even in a cool room. In extreme cases they may lose weight and experience muscle weakness.

Too little thyroid hormone (hypothyroidism) results in just the opposite set of symptoms: a slower than normal heart rate,29 a chronic feeling of being cold, constipation, unexplained weight gain, dry skin, hair loss or coarse dry hair, weakness, muscle aches, depression, and fatigue.30,31 In extreme cases, people with low thyroid function experience cognitive decline,32 and babies born to mothers with inadequate iodine levels are at high risk for a unique form of mental retardation known as cretinism. Cognitive impairment caused by low thyroid function is reversible with iodine or thyroid hormone supplementation.32,33

Both over- and under-production of thyroid hormone are associated with the thyroid gland swelling known as goiter. In hyperthyroidism, the goiter is the result of inflammation of the gland as it is under attack by an overactive immune system.

What You Need to Know: Iodine Deficiency
  • Iodized salt is the chief source of iodine in the industrialized world.
  • Rates of iodine deficiency have reached epidemic levels, increasing fourfold over the past 40 years.
  • Recent scientific analysis reveals that many commercial table salt brands now contain inadequate amounts of iodine.
  • Iodine is critical to healthy thyroid function.
  • Inadequate iodine intake causes weight gain, low energy, depression, cardiovascular disease, cognitive decline, and a variety of cancers.
  • Iodine is vital to breast health in older women, with low intake correlated to increased risks for breast cancer and fibrocystic breast disease.

In hypothyroidism, the goiter develops as the thyroid attempts to make more thyroid hormone in the absence of sufficient dietary iodine.

Iodine deficiency is the most common cause of goiter, and since it causes hypothyroidism, is also the most common endocrine (glandular) problem in the world.18 Iodine deficiency is most prevalent in people who live far inland, away from the oceans that provide our best source of iodine. Those areas are commonly referred to as “goiter belts,” because of the high rates of impaired thyroid function.5

Why Health-Conscious Americans Suffer From Iodine Deficiency
Iodine deficiency disorders can produce symptoms of low thyroid function (hypothyroidism) even without abnormalities in measured thyroid hormone levels.34 Recent evidence suggests, for example, that iodine deficiency is linked to obesity, cognitive impairment, psychiatric disorders, fibromyalgia, and a variety of cancers.34

Paradoxically, another major consequence of mild-to-moderate iodine deficiency in older adults is hyperthyroidism (excessive thyroid function), especially in women.35 This is the result of rapidly growing thyroid gland nodules that over-produce thyroid hormone; it can trigger cardiac arrhythmias, osteoporosis, and muscle wasting.35

Among those negative consequences is the impact of iodine deficiency on breast health. Compelling data are emerging that link iodine deficiency to breast cancers and high rates of fibrocystic breast disease, two of the greatest concerns of older women in the US. It’s worth exploring those data here; including evidence that iodine supplementation can promote healthy breast tissue.

Fortunately, all iodine deficiency disorders and related health dangers can be prevented by adequate intake of iodine.8

Table 1. Why Health-Conscious Americans Suffer From Iodine Deficiency
Healthy Action
Unintended Reduction in Iodine Consumption
 
Are you using less salt overall?Iodized salt is a major source of iodine in America; using less salt means you’re getting less iodine2
Are you putting less salt on your food directly?
Salt used in cooking loses up to 62.4% of its iodine content15
 
Are you using Kosher or sea salt?These forms of salt contain little or no iodine
Are you eating more vegetables and less meat?
Foods of plant origin have lower iodine content than foods of animal origin16
Are you exercising regularly?
A substantial amount of iodine is lost in sweating during regular exercise regimens17

 

The Emerging Role of Iodine in Breast Health


Iodine deficiency is rapidly emerging as a major risk factor for breast cancer.
Human breast tissue and breast milk contain higher concentrations of iodine than the thyroid gland itself, which contains just 30% of the body’s iodine stores.18,36,370 Breast tissue is rich in the same iodine-transporting proteins used by the thyroid gland to take up iodine from the blood.18,38 The evolutionary reasons for this are clear: iodine is essential to the developing newborn brain, so the mother’s body must have a direct means of supplying iodine to the nursing infant.18,39

The Emerging Role of Iodine in Breast Health
Iodine plays an important role in the health of women’s breast tissue.40 In the presence of chemicals and enzymes found in breast tissue, iodine has been shown to exert a powerful antioxidant effect equivalent to vitamin C.18,41 Iodine-deficient breast tissue exhibits chemical markers of elevated lipid peroxidation, one of the earliest factors in cancer development.18,42-45

Iodine-deficient breast tissue also shows alterations in DNA and increases in estrogen receptor proteins.40 Coupled with iodine deficiency-induced increases in circulating estrogen levels, these changes can substantially increase the risk of breast cancer in women with low iodine levels.44

Iodine also helps regulate levels of the stress hormone cortisol and contributes to normal immune function.46,47 Abnormal cortisol levels and deficient immune function are significant contributors to the risks of breast cancer; women with fibrocystic breast disease may also suffer from elevated cortisol levels.48-51

Taken together, these biological factors explain the well-known link between iodine deficiency and thyroid disease, thyroid cancer, and breast cancer, all of which predominate in postmenopausal women.42,52,53

The link between iodine consumption and breast cancer is most evident when you compare the Japanese and Western diets against cancer incidence.

Japanese women consume a diet high in iodine-rich seaweed, which provides them with an iodine intake 25 times higher than the average American woman’s.54 Japanese women also have breast cancer rates roughly one-third of those found in American women, a difference that disappears in Japanese women who immigrate to the US, where they consume considerably less seaweed.18,52,55

Prevalence of Iodine Deficiency in Australia
Studies of iodine therapy for breast cancer prevention are encouraging. Continuous iodine given to cancer-prone rats cut mammary tumor rates nearly 2.5-fold.56 Breast cancer cells avidly absorb iodine, which in turn suppresses tumor growth and causes cancer cell death.57,58

Added dietary iodine reduces the size of both benign and malignant breast tumors, an effect credited in part to iodine’s direct reduction of lipid peroxidation levels.54,56 Although the doses of iodine used in these studies are substantial, equivalent to 5,000 mcg daily, no toxic effects of iodine were observed, either on thyroid function or in other tissues.18,54,56 Further benefits may be obtained by supplementing with selenium in addition to iodine; selenium is an essential cofactor in the enzymes used in thyroid and breast tissue to make optimal use of dietary iodine.4,11,25

In addition to its obvious role in preventing breast cancer, increased iodine intake may be important in mitigating another common, if less lethal, breast disorder—fibrocystic breast disease or FBD.

While harmless, fibrocystic breast disease is extremely common. It is found in at least 9% of all women who undergo biopsies, though the actual rate is probably much higher.18,59 Animal studies have shown that fibrocystic breast disease can be induced by depriving breast tissue of iodine.11,40,60 These changes can be reversed by iodine doses equivalent to 5,000 mcg per day in humans.18,61

Women with fibrocystic breast disease obtain substantial relief from oral administration of iodine at doses of 3,000-6,000 mcg, with 65% achieving improvements according to their own and their physicians’ assessments.62 In those studies, only 33% of placebo recipients reported any benefit. No side effects were detected at any of the doses used.18

It is becoming increasingly clear that iodine deficiency interferes with optimum breast health, and intake of levels far higher than the recommended dietary allowance of 150-290 mcg is required to achieve benefits. Daily amounts of 3,000-6,000 mcg may help relieve the symptoms of fibrocystic breast disease.18

Table 2. Prevalence of Iodine Deficiency in Australia3
Group% With Mild Deficiency% With Moderate to Severe DeficiencyTotal % Deficient
Pregnant Women29.619.849.4
Postpartum Women34.619.253.8
Diabetic Patients37.834.171.9
Normal Volunteers47.426.373.7

 

The Role of Iodine in Cardiovascular Health


Iodine and iodine-rich foods enjoy a long history as natural therapies for hypertension and cardiovascular disease.4 Even when no overt symptoms are evident, hypothyroidism can contribute to heart disease and stroke, and it increases the risk of death from these conditions.63-65

Thyroid dysfunction creates unfavorable disturbances in lipid profiles, elevating low-density lipoprotein (LDL) and total cholesterol levels and raising the risk of atherosclerosis.27,28,66

Hypothyroidism also weakens the heart muscle, causing it to “squeeze” less firmly with each contraction; it can cause cardiac arrhythmias as well.29,63,67 These effects may not be evident at rest, but become important during moderate exercise.63 Low thyroid function is also associated with higher waist-to-hip ratios, an obesity-related risk factor for cardiovascular disease.68

Restoring normal thyroid function helps reverse multiple cardiovascular risk factors, most notably adverse lipid profiles.27 Yet mainstream medicine has traditionally used thyroid hormone treatment, which may be dangerous if it over-drives an already weakened heart.69

Iodine therapy shows promise in safely and effectively modulating these health concerns.

Iodine Protects Against Stomach Cancer

Iodine From The Sea: The Most Effective Natural Form

The thyroid gland, breast tissue, and portions of the digestive tract share similarities in that all of them contain a rich concentration of iodine.42,70 Stomach lining cells in particular concentrate iodine, capitalizing on its antioxidant effects.71

This has led medical researchers to investigate whether iodine deficiency plays a role in cancers of the digestive tract.

They found that people living in iodine-deficient areas of the world are not only prone to iodine-deficiency goiters, but also have higher rates of stomach cancers.71 Stomach cancer patients in a landlocked area of Iran were 2.5 times as likely to have severe iodine deficiency than control patients.72 Gastric cancer is the most common cancer in parts of northeastern Turkey where iodine deficiency is common, and iodine levels in gastric cancer tissue were markedly lower than those in surrounding healthy tissue.73

Increased iodine intake has been strongly correlated with a reduction in stomach cancer rates in recent years.74

Iodine From The Sea: The Most Effective Natural Form

Earth’s oceans are the main repository of iodine on the planet, and nowhere is iodine as highly concentrated as in seaweed. In particular, seaweeds such as kelp and bladderwrack are capable of concentrating and storing iodine at astonishingly high levels. Scientists speculate that these primitive plants accumulate iodine to protect themselves from oxidative stress in the open ocean.75 Humans can reap the benefits of this natural process, because the iodine in these seaweeds is in the most biologically available forms, making it ideal for consumption.
 

 

Summary


Iodine is critical to healthy thyroid function. Its deficiency can cause weight gain, low energy, depression, cardiovascular disease, cognitive decline, and a variety of cancers.

Yet rates of iodine deficiency have reached epidemic levels, increasing fourfold over the past 40 years. A startling 74% of normal, “healthy” adults may no longer be consuming sufficient quantities.

Recent scientific analysis reveals that many commercial table salt brands now contain inadequate amounts of iodine. Emerging evidence points to the severe impact of low iodine on a wide range of health issues, including increased risks of breast cancer and fibrocystic breast diseases.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.
 
References
1. Dasgupta PK, Liu Y, Dyke JV. Iodine nutrition: iodine content of iodized salt in the United States. Environ Sci Technol. 2008 Feb 15;42(4):1315-23.
2. Dasgupta PK, Liu Y, Dyke JV. Iodine nutrition: iodine content of iodized salt in the United States. Environ Sci Technol. 2008 Feb 15;42(4):1315-23.
3. Gunton JE, Hams G, Fiegert M, McElduff A. Iodine deficiency in ambulatory participants at a Sydney teaching hospital: is Australia truly iodine replete? Med J Aust. 1999 Nov 1;171(9):467-70.
4. Hoption Cann SA. Hypothesis: dietary iodine intake in the etiology of cardiovascular disease. J Am Coll Nutr. 2006 Feb;25(1):1-11.
5. Kapil U, Sharma TD, Singh P, Dwivedi SN, Kaur S. Thirty years of a ban on the sale of noniodized salt: impact on iodine nutrition in children in Himachal Pradesh, India. Food Nutr Bull. 2005 Sep;26(3):255-8.
6. Dunn JT. Seven deadly sins in confronting endemic iodine deficiency, and how to avoid them. J Clin Endocrinol Metab. 1996 Apr;81(4):1332-5.
7. McClure RD. Goiter prophylaxis with iodized salt. Science. 1935 Oct 18;82(2129):370–1.
8. Darcan S, Goksen D. Consequences of iodine deficiency and preventive measures. Pediatr Endocrinol Rev. 2003 Dec;1 Suppl 2:162-8; discussion 68-9.
9. Szybinski Z, Jarosz M, Hubalewska-Dydejczyk A, et al. Iodine-deficiency prophylaxis and the restriction of salt consumption - a 21st century challenge. Endokrynol Pol. 2010 Jan-Feb;61(1):135-40.
10. Zimmermann MB. Iodine deficiency. Endocr Rev. 2009 Jun;30(4):376-408.
11. Triggiani V, Tafaro E, Giagulli VA, et al. Role of iodine, selenium and other micronutrients in thyroid function and disorders. Endocr Metab Immune Disord Drug Targets. 2009 Sep;9(3):277-94.
12. Bibbins-Domingo K, Chertow GM, Coxson PG, et al. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med. 2010 Feb 18;362(7):590-9.
13. Titze J, Ritz E. Salt and its effect on blood pressure and target organ damage: new pieces in an old puzzle. J Nephrol. 2009 Mar-Apr;22(2):177-89.
14. Caldwell KL, Jones R, Hollowell JG. Urinary iodine concentration: United States National Health And Nutrition Examination Survey 2001-2002. Thyroid. 2005 Jul;15(7):692-9.
15. Wang GY, Zhou RH, Wang Z, Shi L, Sun M. Effects of storage and cooking on the iodine content in iodized salt and study on monitoring iodine content in iodized salt. Biomed Environ Sci. 1999 Mar;12(1):1-9.
16. Krajcovicova-Kudlackova M, Buckova K, Klimes I, Sebokova E. Iodine deficiency in vegetarians and vegans. Ann Nutr Metab. 2003;47(5):183-5.
17. Smyth PP, Duntas LH. Iodine uptake and loss-can frequent strenuous exercise induce iodine deficiency? Horm Metab Res. 2005 Sep;37(9):555-8.
18. Patrick L. Iodine: deficiency and therapeutic considerations. Altern Med Rev. 2008 Jun;13(2):116-27.
19. Baier-Anderson C, Blount BC, Lakind JS, Naiman DQ, Wilbur SB, Tan S. Estimates of exposures to perchlorate from consumption of human milk, dairy milk, and water, and comparison to current reference dose. J Toxicol Environ Health A. 2006 Feb;69(3-4):319-30.
20. Sanchez CA, Krieger RI, Khandaker N, Moore RC, Holts KC, Neidel LL. Accumulation and perchlorate exposure potential of lettuce produced in the Lower Colorado River region. J Agric Food Chem. 2005 Jun 29;53(13):5479-86.
21. Snyder SA, Pleus RC, Vanderford BJ, Holady JC. Perchlorate and chlorate in dietary supplements and flavor enhancing ingredients. Anal Chim Acta. 2006 May 10;567(1):26-32.
22. Greer MA, Goodman G, Pleus RC, Greer SE. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Environ Health Perspect. 2002 Sep;110(9):927-37.
23. Available at: http://lpi.oregonstate.edu/infocenter/minerals/iodine/. Accessed July 18, 2011.
24. Available at: http://emedicine.medscape.com/article/122714-overview. Accessed July 18, 2011.
25. Cann SA, van Netten JP, van Netten C. Hypothesis: iodine, selenium and the development of breast cancer. Cancer Causes Control. 2000 Feb;11(2):121-7.
26. Nagataki S, Shizume K, Nakao K. Thyroid function in chronic excess iodide ingestion: comparison of thyroidal absolute iodine uptake and degradation of thyroxine in euthyroid Japanese subjects. J Clin Endocrinol Metab. 1967 May;27(5):638-47.
27. Canturk Z, Cetinarslan B, Tarkun I, Canturk NZ, Ozden M. Lipid profile and lipoprotein (a) as a risk factor for cardiovascular disease in women with subclinical hypothyroidism. Endocr Res. 2003 Aug;29(3):307-16.
28. Iqbal A, Jorde R, Figenschau Y. Serum lipid levels in relation to serum thyroid-stimulating hormone and the effect of thyroxine treatment on serum lipid levels in subjects with subclinical hypothyroidism: the Tromso Study. J Intern Med. 2006 Jul;260(1):53-61.
29. Fazio S, Palmieri EA, Lombardi G, Biondi B. Effects of thyroid hormone on the cardiovascular system. Recent Prog Horm Res. 2004;59:31-50.
30. Canaris GJ, Steiner JF, Ridgway EC. Do traditional symptoms of hypothyroidism correlate with biochemical disease? J Gen Intern Med. 1997 Sep;12(9):544-50.
31. Wartofsky L. Management of subclinical hyperthyroidism. J Clin Endocrinol Metab. 2011 Jan;96(1):59-61.
32. Kramer CK, Von Muhlen D, Kritz-Silverstein D, Barrett-Connor E. Treated hypothyroidism, depressed mood, and cognitive function in old age: the Rancho Bernardo Study. Eur J Endocrinol. 2009 Dec; 161(6):917-21
33. Zimmermann MB. Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. Am J Clin Nutr. 2009 Feb;89(2):668S-72S.
34. Verheesen RH, Schweitzer CM. Iodine deficiency, more than cretinism and goiter. Med Hypotheses. 2008 Nov;71(5):645-8.
35. Laurberg P, Nohr SB, Pedersen KM, et al. Thyroid disorders in mild iodine deficiency. Thyroid. 2000 Nov;10(11):951-63.
36. Bretthauer EW, Mullen AL, Moghissi AA. Milk transfer comparisons of different chemical forms of radioiodine. Health Phys. 1972 Mar;22(3):257-60.
37. Spitzweg C, Harrington KJ, Pinke LA, Vile JG, Morris JC. Clinical review 132: the sodium iodide symporter and its potential role in cancer therapy. J Clin Endocrinol Metab 2001 Jul;86(7):3327-35.
38. Kilbane MT, Ajjan RA, Weetman AP, et al. Tissue iodine content and serum-mediated 125I uptake-blocking activity in breast cancer. J Clin Endocrinol Metab. 2000 Mar;85(3):1245-50.
39. Topper YJ, Freeman CS. Multiple hormone interactions in the developmental biology of the mammary gland. Physiol Rev 1980 Oct;60(4):1049-106
40. Eskin BA. Iodine and mammary cancer. Adv Exp Med Biol. 1977;91:293-304.
41. Smyth PP. Role of iodine in antioxidant defence in thyroid and breast disease. Biofactors. 2003;19(3-4):121-30.
42. Venturi S, Donati FM, Venturi A, Venturi M, Grossi L, Guidi A. Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach. Adv Clin Path. 2000 Jan;4(1):11-7.
43. Venturi S. Is there a role for iodine in breast diseases? Breast. 2001 Oct;10(5):379-82.
44. Stadel BV. Dietary iodine and risk of breast, endometrial, and ovarian cancer. Lancet. 1976 Apr 24;1(7965):890-1.
45. Many MC, Papadopolos C, Martin I, et al. Iodine induced cell damage in mouse hyperplastic thyroid is associated with lipid peroxidation. In: Gordon A, Gross J, Hennemann G, eds. Progress in Thyroid Research. New York, NY: Routledge; 1991:213-5.
46. Nolan LA, Windle RJ, Wood SA, et al. Chronic iodine deprivation attenuates stress-induced and diurnal variation in corticosterone secretion in female Wistar rats. J Neuroendocrinol. 2000 Dec;12(12):1149-59.
47. Stolc V. Stimulation of iodoproteins and thyroxine formation in human leukocytes by phagocytosis. Biochem Biophys Res Commun. 1971 Oct 1;45(1):159-66.
48. Cohen M, Klein E, Kuten A, Fried G, Zinder O, Pollack S. Increased emotional distress in daughters of breast cancer patients is associated with decreased natural cytotoxic activity, elevated levels of stress hormones and decreased secretion of Th1 cytokines. Int J Cancer. 2002 Jul 20;100(3):347-54.
49. Inaudi P, Bernabei A, Gioffre W, et al. Plasma and cyst fluid levels of delta 5 and delta 4 steroid hormones in women with gross cystic breast disease. Clin Endocrinol (Oxf). 1987 Dec;27(6):643-8.
50. James GD, Gastrich HJ, Valdimarsdottir HB, Bovbjerg DH. The rate of urinary cortisol excretion at work is persistently elevated in women at familial risk for breast cancer. Am J Hum Biol. 2008 Jul-Aug;20(4):478-80.
51. Thornton LM, Andersen BL, Carson WE, 3rd. Immune, endocrine, and behavioral precursors to breast cancer recurrence: a case-control analysis. Cancer Immunol Immunother. 2008 Oct;57(10):1471-81.
52. Smyth PP. The thyroid, iodine and breast cancer. Breast Cancer Res. 2003;5(5):235-8.
53. Smyth PP. Thyroid disease and breast cancer. J Endocrinol Invest. 1993 May;16(5):396-401.
54. Aceves C, Anguiano B, Delgado G. Is iodine a gatekeeper of the integrity of the mammary gland? J Mammary Gland Biol Neoplasia. 2005 Apr;10(2):189-96.
55. Ziegler RG, Hoover RN, Pike MC, et al. Migration patterns and breast cancer risk in Asian-American women. J Natl Cancer Inst. 1993 Nov 17;85(22):1819-27.
56. Garcia-Solis P, Alfaro Y, Anguiano B, et al. Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion. Mol Cell Endocrinol. 2005 May 31;236(1-2):49-57.
57. Funahashi H, Imai T, Tanaka Y, et al. Suppressive effect of iodine on DMBA-induced breast tumor growth in the rat. J Surg Oncol. 1996 Mar;61(3):209-13.
58. Shrivastava A, Tiwari M, Sinha RA, et al. Molecular iodine induces caspase-independent apoptosis in human breast carcinoma cells involving the mitochondria-mediated pathway. J Biol Chem. 2006 Jul 14;281(28):19762-71.
59. Goehring C, Morabia A. Epidemiology of benign breast disease, with special attention to histologic types. Epidemiol Rev. 1997;19(2):310-27.
60. Krouse TB, Eskin BA, Mobini J. Age-related changes resembling fibrocystic disease in iodine-blocked rat breasts. Arch Pathol Lab Med. 1979 Nov;103(12):631-4.
61. Eskin BA, Grotkowski CE, Connolly CP, Ghent WR. Different tissue responses for iodine and iodide in rat thyroid and mammary glands. Biol Trace Elem Res. 1995 Jul;49(1):9-19.
62. Ghent WR, Eskin BA, Low DA, Hill LP. Iodine replacement in fibrocystic disease of the breast. Can J Surg. 1993 Oct;36(5):453-60.
63. Kahaly GJ. Cardiovascular and atherogenic aspects of subclinical hypothyroidism. Thyroid. 2000 Aug;10(8):665-79.
64. Park YJ, Lee YJ, Choi SI, Chun EJ, Jang HC, Chang HJ. Impact of subclinical hypothyroidism on the coronary artery disease in apparently healthy subjects. Eur J Endocrinol. 2011 Jul;165(1):115-21.
65. Haentjens P, Van Meerhaeghe A, Poppe K, Velkeniers B. Subclinical thyroid dysfunction and mortality: An estimate of relative and absolute excess all-cause mortality based on time-to-event data from cohort studies. Eur J Endocrinol. 2008 Sep;159(3):329-41.
66. Rizos CV, Elisaf MS, Liberopoulos EN. Effects of thyroid dysfunction on lipid profile. Open Cardiovasc Med J. 2011;5:76-84.
67. Molnar I, Magyari M, Stief L. Iodine deficiency in cardiovascular diseases. Orv Hetil. 1998 Aug 30;139(35):2071-3.
68. Jung CH, Sung KC, Shin HS, et al. Thyroid dysfunction and their relation to cardiovascular risk factors such as lipid profile, hsCRP, and waist hip ratio in Korea. Korean J Intern Med. 2003 Sep;18(3):146-53.
69. Mariotti S, Cambuli VM. Cardiovascular risk in elderly hypothyroid patients. Thyroid. 2007 Nov;17(11):1067-73.
70. Venturi S, Venturi M. Iodine in evolution of salivary glands and in oral health. Nutr Health. 2009;20(2):119-34.
71. Abnet CC, Fan JH, Kamangar F, et al. Self-reported goiter is associated with a significantly increased risk of gastric noncardia adenocarcinoma in a large population-based Chinese cohort. Int J Cancer. 2006 Sep 15;119(6):1508-10.
72. Behrouzian R, Aghdami N. Urinary iodine/creatinine ratio in patients with stomach cancer in Urmia, Islamic Republic of Iran. East Mediterr Health J. 2004 Nov;10(6):921-4.
73. Gulaboglu M, Yildiz L, Celebi F, Gul M, Peker K. Comparison of iodine contents in gastric cancer and surrounding normal tissues. Clin Chem Lab Med. 2005;43(6):581-4.
74. Golkowski F, Szybinski Z, Rachtan J, et al. Iodine prophylaxis—the protective factor against stomach cancer in iodine deficient areas. Eur J Nutr. 2007 Aug;46(5):251-6.
75. Kupper FC, Carpenter LJ, McFiggans GB, et al. Iodide accumulation provides kelp with an inorganic antioxidant impacting atmospheric chemistry. Proc Natl Acad Sci U S A. 2008 May 13;105(19):6954-8.

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