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Antioxidants are Required for Healthy Thyroid Function

Most people do not realize that the natural process of making and activating thyroid hormone is highly oxidative, meaning a lot of free radicals are made even when the thyroid is running normally.  Once the thyroid starts to struggle the increase in free radicals and related inflammatory signals (like TNFa and IL6) is significant.

Free radicals are neutralized by antioxidants.  Once your antioxidant reserves are depleted your thyroid function must slow down otherwise there will be too much metabolic friction and health-deteriorating inflammation.  Unfortunately, the modern diet is lacking in antioxidants and other nutrients needed to support thyroid health.  Factors like stress, pollution, and obesity further deplete antioxidant reserves, invariably setting the stage for the wear and tear that falls into a pattern of sluggish thyroid symptoms.

Selenium

Selenium is highly concentrated in the thyroid gland, more so than in any other organ in the human body, indicating its vital need in normal thyroid function.  It acts as an antioxidant that protects the thyroid gland, a cofactor nutrient that facilitates the production of thyroid hormone, and as a nutrient that is required to facilitate the conversion of T4 to T3 (triiodothyronine, active thyroid hormone that works inside cells to set the pace of metabolism).

Selenium combines with the sulfur-containing amino acid cysteine to make a special protein known as selenocysteine, a selenoprotein. There are 30 selenoproteins that are currently identified, mostly involving the antioxidant defense system and thyroid function.

The selenium-containing antioxidant enzymes are known as glutathione peroxidases (GSH).  Six different GSH enzymes have now been identified; helping to protect the inside of cells, the GI tract, the reproductive system, and operating in fluids between cells.  GSH enzymes are vital to maintaining normal health.  They are now proven to protect the thyroid gland during thyroid hormone formation.

The formation of thyroid hormone occurs on cell membranes of thyroid cells known as thyrocytes.  This process requires selenium as a cofactor nutrient.  During this process the enzyme thyroid peroxidase (TPO) prepares iodine for attachment to tyrosine to form thyroid hormone.  The normal activity of TPO generates tremendous numbers of free radicals within the thyroid gland in the form of H2O2 and lipid peroxides.  These must be deactivated by GSH enzymes, otherwise the production of thyroid hormone stresses and inflames the thyroid gland.  This can easily result in a reduced rate of thyroid hormone formation.  It’s like trying to run on a sprained ankle, except it is a sprained thyroid. 

Selenoproteins also act in various ways to change T4 into T3 (active thyroid hormone) and reverseT3 (which inactivates T3).  Three main selenoproteins activate and inactivate thyroid hormone, known as D1, D2, and D3. 

D1 is the primary activator of thyroid hormone for your body, working mostly in the liver and to some degree in the kidneys.  D2 is active in the thyroid gland, brain, nerves, and heart.  It plays the primary role in thyroid activation in the brain under normal conditions, and produces thyroid hormone for the rest of the body under stressed conditions.  D3 is mostly a brake on thyroid hormone activity, turning off active hormone.

When the body starts to run low on selenium the activation of thyroid hormone by D1 may drop by 90%.  The body compensates by turning on the back up system, using the D2 enzyme to maintain active thyroid hormone.  The problem with this back up system running for any great length of time is that is causes significantly increased production of free radicals.  Even worse, the lack of selenium already handicapped the primary antioxidant that protects the thyroid gland and liver, GSH.  Thus, selenium deficiency forces the body into a very uncomfortable metabolic coping strategy that eventually leads to slower metabolism, increased oxidative stress, and wear and tear to the thyroid gland and liver. 

Manganese

Manganese has long been known as the anti-pear nutrient, helping to reduce weight gain on the hips and thighs.  New science is showing the vital role of manganese in liver function, fat metabolism, and liver anti-oxidant status.  This relates to thyroid hormone activation, as most activation (conversion of T4 to T3) occurs on cell membranes in the liver.  If the liver is suffering from excessive free radical stress, then cell membranes are not as functional and the activation of thyroid hormone may become distressed.

Manganese is a mineral that is required to form a special antioxidant enzyme called manganese-dependent superoxide dismutase (MnSOD).  It is a key part of the cell engine’s antioxidant defense system that enables cellular engines (mitochondria) to produce energy and heat efficiently.  Poor function of this enzyme reduces the ability of cells to make energy efficiently. 

MnSOD is now found to be a primary protector of thyroid hormone activity in the liver.  This enzyme naturally rises as thyroid hormone activity is increased, acting as a protective buffer to support increased metabolic rate.  If this enzyme, or the selenium-dependent GSH are lacking, then activation of thyroid hormone generates friction and stress in the form of excessive free radicals.  This results in wear and tear to the thyroid gland, liver, and nerves.  A lack of manganese is now clearly associated with reduced function of thyroid hormone in the body.

New science has shown that as free radical stress increases due to lacking GSH and MnSOD activity, fat begins to accumulate in the liver, generating further free radical stress in the form of damaged fats, known as lipid peroxides.  This makes a stressed metabolic situation worse.  Once this happens a person is more likely to gain weight around the midsection. 

Comments

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Posted by mapril  on  07/21  at  10:24 AM

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Posted by mapril  on  07/21  at  10:31 AM

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