Category Archives: Iodine and selenium - Page 2

Micronutrient Deficiencies: An Underappreciated Cause of Hypothyroidism

Posted by on December 3, 2010 72 comments

A significant number of our readers have hypothyroidism with normal T4 but low T3. For instance, Kratos:

I followed a strict low carb diet with around 50g of carb per day for over 1 year and I think I have developed hypothyroidism …

TSH 3.4 (0.3-4.0)

FT3 2.2 (2.1-4.9)

FT4 11.4 (6.8-18.0)

This situation can have many causes. Our last post discussed how shift work and disrupted circadian rhythms can cause hypothyroidism. Another often-overlooked cause of hypothyroidism is nutrient deficiencies.

As noted in the book, selenium and iodine deficiencies are classic causes of hypothyroidism. Here I want to look at a few other possiblities.

Copper and Iron Deficiency

Copper deficiency, iron deficiency, and iodine deficiency during pregnancy or infancy generate similar neurological defects, and during adulthood generate similar hypothyroid symptoms:

Cu, Fe, and iodine/TH deficiencies result in similar defects in rodent brain development, including hypomyelination of axons, aberrant hippocampal structure and function, altered brain energy metabolism, and altered neuronal signaling (8–13). In addition, the behavioral and neurochemical abnormalities associated with perinatal Cu, Fe, and iodine/TH deficiencies are irreversible and persist into adulthood (14–16). These similarities suggest that there may be a common underlying mechanism associated with all three deficiencies contributing to the observed neurodevelopmental defects.

Several studies in postweanling rodents show that Cuand Fe deficiencies impair thyroid metabolism. Fe deficiency reduces circulating thyroxine (T4) and triiodothyronine (T3) concentrations (17–20), peripheral conversion of T4 to T3 (18, 19), TSH response to TRH (19), and thyroid peroxidase (TPO) activity (20). Cu deficiency also reduces circulating T4 andT3 concentrations and peripheral conversion of T4 to T3  (21, 22). In addition, Cu deficiency reduces serum and brain Fe levels, which may contribute to the Cu-dependent effect on thyroidal status (23). [1]

In infant rats, deficiencies of either copper or iron cause hypothyroidism:

Cu deficiency reduced serum total T(3) by 48%, serum total T(4) by 21%, and whole-brain T(3) by 10% at P12. Fe deficiency reduced serum total T(3) by 43%, serum total T(4) by 67%, and whole-brain T(3) by 25% at P12. [1]

Note that copper deficiency hypothyroidism reduces serum T3 levels more strongly than T4 levels, the same pattern that Kratos displays.

While We’re On the Topic of Micronutrients and Hypothyroidism …

Hypothyroidism induces the symptoms of riboflavin deficiency. This is because thyroid hormone is needed for production of the enzyme flavin kinase, which is in turn needed to generate flavin adenine dinucleotide (FAD). Riboflavin deficiency and thyroid hormone deficiency lead to the same low FAD levels in both rats and humans. [2]

This suggests that hypothyroid persons may wish to supplement with riboflavin, so that extra riboflavin may help make up for deficient flavin kinase.

Conclusion

I believe that those with health problems should strive to “overnourish” themselves. Micronutrient deficiencies can have insidious disabling effects, yet be impossible to diagnose. In disease conditions, needs for many micronutrients are increased. Many micronutrients are non-toxic up to fairly large doses and can be safely supplemented.

An effort to eat micronutritious foods and supplement micronutrients into their “plateau ranges” to eliminate deficiencies might generate startling health improvements.

Minerals like copper, selenium, and iodine are among the most important nutrients – they are among our eight essential supplements – yet also among the most widely deficient. Most supplementers neglect key minerals; but optimizing their intake can pay large health dividends.

References

[1] Bastian TW et al. Perinatal iron and copper deficiencies alter neonatal rat circulating and brain thyroid hormone concentrations. Endocrinology. 2010 Aug;151(8):4055-65. http://pmid.us/20573724.

[2] Cimino JA et al. Riboflavin metabolism in the hypothyroid newborn. Am J Clin Nutr. 1988 Mar;47(3):481-3. http://pmid.us/3348160.

NZ Man Left for Dead by Doctors, Cured by Vitamin C

Posted by on August 26, 2010 23 comments

Modern doctors are often deeply over-invested in the use of drugs, and amazingly ignorant of the power of the human immune system, when supported by a healthy diet and optimal nutrition, to defeat disease.

They sometimes exhaust their repertoire of drugs without ever considering using nutritional supplements to support the patient’s immune defense.

An extraordinary illustration comes from New Zealand. It began when Alan Smith, a New Zealand farmer, contracted swine flu:

He caught the Swine Flu (probably while on a fishing trip in Fiji), so badly that his lungs had “white out”, which is to say they were so full of fluid that they didn’t show up on an x-ray. The doctors also said he had got leukemia and he ended up being put on a life support machine.

The doctors told the family the machine should be turned off … [1]

The diagnosis of leukemia is suspicious. Both infections and leukemia lead to “leukocytosis” or a very high white blood cell count. In one case the white blood cells are multiplying to fight the infection, in the other a malignant population is multiplying. The difference is that in leukemia the population is monoclonal, i.e. all the new white blood cells are genetically identical, while in normal people with infections the white blood cells are created with genetic diversity. (Keywords for those who wish to investigate: T-cell antigen repertoire and B-cell immunoglobulin repertoire.)

As subsequent events showed, the leukemia “diagnosis” was mistaken. I wonder if it was made just for “family management” – in order to help persuade the family his case was hopeless and support the recommendation to end life support.

… but the family asked that he be given high dosages of Vitamin C. After a fight (one of many), one of the doctors agreed. Alan began getting better; his lungs showed pockets of air. Then he began to get worse and the family found out the doctors had stopped the Vit C.

Many more fights ensued, the patient getting better while having the Vit C, and getting worse when he was taken off. Alan’s wife describes one of the doctors sitting back in his chair, arms folded, rolling his eyes, looking at the ceiling, telling her that no way could the vitamin C be helping. The family hired a lawyer, forcing the doctors to continue the vit C treatment (albeit in slow dosage, until he got better enough to eat and his wife brought along sachets of large dosage herself for him to take).

Eventually Alan fully recovered, no trace of leukemia even. [1]

He should have been given high doses of vitamin D and iodine as well. Iodine supports leukocyte respiratory bursts of reactive oxygen species which destroy pathogens; vitamin C supports respiratory bursts by recycling glutathione and providing antioxidant protection for leukocytes against their own respiratory bursts, and also supports anti-viral immunity; vitamin D creates antimicrobial peptides that kill many pathogens.

Other possibly beneficial supplements in cases of elevated leukocyte counts due to infection: selenium, to support both glutathione and iodine/thyroid function; iron, for myeloperoxidase (respiratory burst enzyme) and catalase (antioxidant defense); N-acetyl cysteine (for glutathione production) and glutathione; zinc and copper (for the anti-oxidant zinc-copper superoxide dismutase).

Thank goodness the family had the sense to try vitamin C, and that that was enough for him to recover. It would have been a shame if he died for lack of vitamin D and iodine.

New Zealand was a pioneer of socialized medicine in the English-speaking world. Economists say that people respond to incentives; one wonders if the doctors were more motivated to tend to the interests of the bureaucrats who controlled their budgets, than to the health of the family and patient who weren’t paying them. Perhaps “free” medical care has unexpected costs.

References

[1] “Indictment of Our Medical Profession,” New Zealand Conservative, http://nzconservative.blogspot.com/2010/08/indictment-of-our-medical-profession.html; hat tip to Jewel at http://health.groups.yahoo.com/group/infection-cortisol/message/1760.

Thyroid: More Evidence That “Normal” is Unhealthy

Posted by on July 30, 2010 114 comments

Two inexpensive blood tests should be done routinely, but often aren’t: Vitamin D levels (by serum 25-hydroxyvitamin D) and thyroid stimulating hormone levels (TSH). There are few easier ways to substantially improve health than to normalize levels of these hormones.

One difficulty, however, is disagreement over what “normal” levels are. The standard “normal” range for TSH on lab tests is about 0.5 to 4.6 mIU/L. This range originally encompassed two standard deviations about the US mean, meaning that 95% of the population fell in the “normal” range. Unfortunately, evidence that TSH values in this range were healthy has always been lacking.  In fact, many people with “normal” TSH live with symptoms of hypothyroidism.

As awareness has grown of the biological significance of thyroid hormone, researchers have looked more closely into the correlation of TSH levels with health.  This research is revealing is that many people are thyroid-deficient and that improving thyroid status can dramatically improve health.

The best research has been conducted in Europe:

  • The HUNT study of 25,000 healthy Norwegians found that their prospects were substantially affected by thyroid function. Those with a TSH level of 1.5 to 2.4 were 41% more likely to die over the next 8 years than those with TSH below 1.5; those with TSH 2.5-3.4 were 69% more likely to die. [1]
  • An Italian study showed that pregnant women with TSH between 2.5 and 5.0 had a miscarriage rate 70% higher than women with TSH below 2.5. [2]

Now, a Dutch study shows that the likelihood of breech birth rises monotonically with the mother’s TSH levels at gestational week 36. [3] Breech birth is a significant hazard:  it commonly requires a Caesarean section delivery, and both mother and infant are more likely to die or otherwise suffer damaged health if the baby presents in the breech position. The Dutch study found that:

  • Pregnant women with a TSH of 0.5 or less had NO breech births at all, and those between 0.51 and 0.71 had only a 1% chance of a breech birth.
  • Pregnant women with a TSH between 0.71 and 2.49 had about a 5% chance of breech birth.
  • Pregnant women with TSH of 2.50 to 2.89 had an 11% chance of breech birth, while those with TSH above 2.89 had a 14% chance of breech birth.

The authors didn’t provide a detailed breakdown of breech rates for TSH levels in the middle range, but it is a safe bet that TSH levels of 1.5 to 2.49 were much more dangerous than TSH levels of 0.72 to 1.0.

What these studies are telling us is that:

  1. People with the healthiest thyroid status have very low TSH. A TSH level below 0.5 can indicate either hyperthyroidism (too much thyroid hormone) or perfect health. Any TSH above 0.5 is suggestive of, at a minimum, a slight deficiency of either iodine or selenium.
  2. You can have impaired thyroid status with normal free T4 hormone levels. This study and others have found that TSH levels, not free thyroid hormone levels, are the best indicator of health.
  3. Health becomes significantly impaired above TSH levels of about 1.5. Any TSH above 1.5 should be addressed, if only through iodine and selenium supplementation (or abundant seaweed consumption with ~3 Brazil nuts per day.) Since a TSH of 1.5 is about the population mean, it’s a fair inference that most Americans are needlessly suffering impaired health due to impaired thyroid status.
  4. Especially during pregnancy, thyroid and iodine status are critical. Breech birth and miscarriage are far from the only negative consequences of impaired thyroid status. An elevated TSH usually indicates an iodine deficiency, and “even a mild iodine deficiency during pregnancy and during the first years of life adversely affects brain development.” [4] Iodine deficiency is the most common worldwide cause of mental retardation (cretinism), and elevated TSH during pregnancy can be expected to reduce the IQ of the child by up to 10 points and to produce other neurological deficits, including “visuomotor, memory, attention and posture” deficits. [5]

So, if your doctor doesn’t do it routinely, ask for TSH and vitamin D measurements at your next physical. There are few easier ways to improve your health than fixing thyroid and vitamin D status.

[1] Asvold BO et al. Thyrotropin levels and risk of fatal coronary heart disease: the HUNT study. Arch Intern Med. 2008 Apr 28;168(8):855-60. http://pmid.us/18443261.

[2] Negro R et al. Increased Pregnancy Loss Rate in Thyroid Antibody Negative Women with TSH Levels between 2.5 and 5.0 in the First Trimester of Pregnancy. J Clin Endocrinol Metab. 2010 Jun 9. [Epub ahead of print] http://pmid.us/20534758.

[3] Kuppens SM et al. Maternal thyroid function during gestation is related to breech presentation at term. Clin Endocrinol (Oxf). 2010 Jun;72(6):820-4. http://pmid.us/19832853.

[4] Remer T et al. Iodine deficiency in infancy – a risk for cognitive development. Dtsch Med Wochenschr. 2010 Aug;135(31/32):1551-1556. http://pmid.us/20665419.

[5] Joseph R. Neuro-developmental deficits in early-treated congenital hypothyroidism. Ann Acad Med Singapore. 2008 Dec;37(12 Suppl):42-3. http://pmid.us/19904446.