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If you drink green tea 24/7 you don't have to wonder if your thyroid is sluggish and your belly growing.

I've alluded to the anti-thyroid effects of green tea extracts in previous articles. That simply drinking green tea (albeit excessively) would trigger the exact same effects, though, is news. News I got from a very recent study from the Zagazig University Faculty of Medicine in Egypt.

The authors, Abulfadle K. A., Bakhaat G. A., Shaik R. and Tantry B. A., studied the effect of excessive green tea intake on body weight and serum thyroid hormones in male mice and compared their results to what happens if the rodents are fed only fluoride and caffeine.
To confirm the ill effects of excessive green tea intake on thyroid gland, the scientists measured both, the level of thyroid hormone and the weight of the thyroid of their 30 male albino mice who were divided into five groups.

• Control (C) group (6 mice) receiving distilled water. 
• Green tea (GT) treated group; 6 mice were given a 5 gm% tea hot water extract as their sole water supply (that's similar to you drinking 1-2 L or more). 
• Fluoride (FL) treated group, 6 mice were given fluorine excess solution as their only water supply. 
• Caffeine (Caf) treated group, 6 mice were treated with caffeine (6.25 mg/kg ip | that's only 0.51 mg/kg body weight for a human and thus not exactly much). 
• Propylthiouracil (PTU) treated group, a substance of which we know that it interferes with the synthesis of thyroid hormone, 6 mice were treated with PTU (10 mg/kg ip). 

Each of the five groups wass treated with the corresponding substance for 30 days, then sacrificed under ether anesthesia, blood was collected to study serum levels of T3 and T4.
As you can see in Figure 1, there was the expected significant decrease in serum T3 and T4 in the PTU treated group (T3 = 0.72±0.03). Similar, albeit less pronounced decreases were seen in the green tea (T3 = 0.96±0.04) and the fluoride (T3 = 0.93±0.04), but not in the caffeine group where only the T3 levels were significantly suppressed (T3 = 1.46±0.08) in comparison to the control group (T3 = 1.71±0.05).

Figure 1: Effect of green tea, fluoride & caffeine on final body weight, T3 and T4 | data is expressed in % of control; *P < 0.05 compared to control. ***P < 0.001 compared to control. #P > 0.05 compared to control (Abulfadle. 2015).

In conjunction with these significant decreases in T3 and T4, the scientists observed an increase of the rodents' final total body weight, but no change of the relative thyroid weight (that's in contrast to studies using purified green tea catechins, only, where the thyroid was sign. enlarged | Chandra. 2010) in comparison to the control group.
References:

• Abulfadle, Khaled Abdelfattah, et al. "Effect of Excessive Green Tea Versus Fluoride and Caffeine on Body Weight and Serum Thyroid Hormones in Male Mice." Journal of Physiology and Pharmacology Advances 5.2 (2015): 565-573.
• Chandra, Amar K., and Neela De. "Goitrogenic/antithyroidal potential of green tea extract in relation to catechin in rats." Food and Chemical Toxicology 48.8 (2010): 2304-2311.
• Chandra, Amar K., Neela De, and Shyamosree Roy Choudhury. "Effect of different doses of un-fractionated green and black tea extracts on thyroid physiology." Human & experimental toxicology 30.8 (2011): 884-896.
• Hase, Tadashi, et al. "Anti-obesity Effects of Tea Catechins in Humans [和文]." Journal of oleo science 50.7 (2001): 599-605.
• Kato, Kenji, et al. "(-)-Epigallocatechin gallate inhibits thyroid hormone‑stimulated osteocalcin synthesis in osteoblasts." Molecular medicine reports 4.2 (2011): 297-300.
• Sakamoto, Y., et al. "Goitrogenic effects of green tea extract catechins by dietary administration in rats." Archives of toxicology 75.10 (2001): 591-596.
• Wolfram, Swen, Ying Wang, and Frank Thielecke. "Anti‐obesity effects of green tea: From bedside to bench." Molecular nutrition & food research 50.2 (2006): 176-187.

Symptoms of hypo- and hypothyroidism (figure from youngstershub.com)

In previous articles about overtraining I've already touched on the possibility that training too much and eating to little can put you into a state where your TSH levels are low, even if the same goes for your free T3 and free T4 values.

Normally, your hypothalamus should correct low levels of the two active thyroid hormone T3 and T4 by increasing TSH. This physiological up-and-down is what doctors use to diagnose hypo- and hyperthyroidism by measuring TSH and in many cases only TSH - text-book practice, but still questionable against the background of the latest science.
Yes, even though everybody knows that you cannot judge the speed of a car by measuring how far its driver pushed the gas pedal into the floor, TSH remains the most commonly used endocrine test in clinical practice, when it comes to testing thyroid function; and this is despite the fact that more and more scientists are questioning the use of TSH, in general, and the reference ranges in particular.

Figure 1: Prevalence of thyroid antibodies across TSH intervals in women (top) and men (Spencer. 2007).

Speaking of reference ranger, if your TSH level is within the 1-1.5 mU/L range, you're considered "normal" (Biondi. 2013; Fontes. 2014; Vadiveloo. 2013). If your TSH is above 4.2-4.5 mU/L doctors believe this would indicate that your free T3 and free T4 levels were low, i.e. that your thyroid is not producing enough thyroid hormones and you're diagnosed hypothyroid - and this is where the problems begin.

After all, there is also an argument that a highly significant number of patients (up to 30%) with TSH above 3.0 mU/L have an occult autoimmune thyroid disease that may remain undiagnosed (Spencer. 2007 | see Figure 1). The same goes for people with subclinical hypothyrodism, simply because textbooks still say that TSH was all you need to test the health of your patients' thyroid.

Figure 2: High(er) rates of thyroid antibodies in non-frail vs. frail elderly women are suggestive of a protective effect of thyroid antibodies (Wang. 2010).

In contrast to young people, in whom thyroid diseases (esp. hypothyroidism and autoimmune diseases) will often remain undiagosed if doctors rely on TSH, only.

Elderly patients (i.e. 70 plus years), on the other hand, may be falsely diagnosed with hypothyroidism due to age-related increase in TSH ranging to up to 6.0 mU/L - and that despite the fact that that there are no or irrelevantly small changes in free T3 and free T4. This is particularly important, because ill health effects as they are seen in young individuals are rare or non-existent in elderly patients with autoimmune thyroid diseases nor hypothyroidism.

Rather than being detrimental, a 2010 study by Wang et al., which found that elderly subjects with raised titres of thyroid autoantibodies are less frail than age-matched peers (see Figure 2), suggests that having anti-thyroid antibodies in the blood can actually protect older women from the age-induced loss of muscle mass and function - surprising, isn't it? In view of the fact that the TSH levels of elderly patients usually have to rise above 6-7 mU/L before there is an actual decline in T4 below the normal range, the upper limit for TSH in the elderly should be increased (Hadlow. 2013).
References:

• Biondi, Bernadette. "The normal TSH reference range: what has changed in the last decade?." The Journal of clinical endocrinology and metabolism 98.9 (2013): 3584.
• Fontes, Rosita, et al. "Reference interval of thyroid stimulating hormone and free thyroxine in a reference population over 60 years old and in very old subjects (over 80 years): comparison to young subjects." Thyroid research 6.1 (2013): 1-8.
• Hadlow, Narelle C., et al. "The relationship between TSH and free T4 in a large population is complex and nonlinear and differs by age and sex." The Journal of Clinical Endocrinology & Metabolism 98.7 (2013): 2936-2943.
• Lewandowski, Krzysztof. "Reference ranges for TSH and thyroid hormones." Thyroid Research 8.Suppl 1 (2015): A17.
• Rodondi, Nicolas, et al. "Subclinical hypothyroidism and the risk of coronary heart disease: a meta-analysis." The American journal of medicine 119.7 (2006): 541-551.
• Spencer, C. A., et al. "National Health and Nutrition Examination Survey III thyroid-stimulating hormone (TSH)-thyroperoxidase antibody relationships demonstrate that TSH upper reference limits may be skewed by occult thyroid dysfunction." The Journal of Clinical Endocrinology & Metabolism 92.11 (2007): 4236-4240.
• Vadiveloo, Thenmalar, et al. "Age-and gender-specific TSH reference intervals in people with no obvious thyroid disease in Tayside, Scotland: the Thyroid Epidemiology, Audit, and Research Study (TEARS)." The Journal of Clinical Endocrinology & Metabolism 98.3 (2013): 1147-1153.
• Wang, George C., et al. "Thyroid autoantibodies are associated with a reduced prevalence of frailty in community-dwelling older women." The Journal of Clinical Endocrinology & Metabolism 95.3 (2010): 1161-1168.

Three things make this study special #1 it's human study, #2 it was conducted in a metabolic ward and #3 it didn't use potentially toxic Se supplements

If you ask around about how you can accelerate your metabolism, selenium and iodine, which are both important players in the concert of thyroid hormones, are usually among the first supplements to be mentioned. The bad news is: If you are not deficient in one of them, taking copious amounts of either of them may well slow down your metabolism significantly.

In view of the fact that the mechanism that triggers this side effect for selenium is a bit more straight forward than it is for iodine, I would like to start this new series with the initially mentioned essential trace element.
Now, from previous waredownloadsoft posts on things like zinc or chromium (both may worsen your insulin sensitivity in high doses), you will be well aware that despite being "essential", i.e. it being absolutely necessary to have them in your diet, consuming too much of these "essentials" can and usually will backfire.

In the case of selenium the consequences became most obvious in a 2003 study from the U.S. Department of Agriculture (USDA). In said study (Hawkes. 2003b), which was conducted by researchers from the Western Human Nutrition Research Center and Department of Nutrition in Davis, CA, the scientists didn't even have to use copious amounts of supplemental selenium to slow down their subjects' thyroid and have them gain weight.

Table 1: Sample meal plan for one week. I've taken this from a previous paper by the same researchers (Hawkes. 2003), in which they used the protocol for the first time - albeit for a different purpose..

Rather than that, Wayne Chris Hawkes and Nancy L. Keim fed healthy men foods which were either naturally high or low in selenium for 120 days. What's so great about this study is that it was conducted in a well-controlled manner with all subjects being confined to a metabolic research unit for the whole study period.Thus, the scientists were able to ensure that the selenium intake for all subjects was 47 μg/d (595 nmol/d | almost the RDA) for the first 21 d, before they were randomly assigned to consume diets containing either 14 µg/day (n = 6 | 25% of the RDA) or 297 (n = 5) μg/day (177 nmol/d or 3.8 μmol/d | 5.4x the RDA) for the remaining 99 days, which was long enough to cause significant changes in blood selenium and glutathione peroxidase and more.
In contrast to what you may have expected based on "broscience" the levels of the active thyroid hormone 3,3′,5-triiodothyronine (T3) in the subjects blood decreased in the high selenium group, increased in the low selenium group, and was significantly different between groups from day 45 onward.

Figure 1: Changes in relevant markers of thyroid and lipid metabolism (left | p < 0.05 for inter-group differences), as well as changes in lean and fat mass (right | only the reduction in body fat in the low selenium group was statistically sign.)

In spite of a compensatory increase of thyrotropin (TSH) in the high selenium group, the T3 levels of the subjects in the high selenium group kept declining, while those of the subjects on the low selenium diets kept increasing (the T4 levels didn't change significantly in either group).

Against that background, it's not really surprising that the high selenium group began to gain while the low selenium group began to lose weight by day 64 (the weight gain is not reflected in in the data in Figure 1, because taken on it's own, the 700g the subjects gained were not significantly; that's in contrast to the inter-group difference with p = 0,001). It did thus take no more than 6 weeks on the high vs. low selenium diet to trigger measurable effects not just on the subjects' metabolism, but also on their body weight; and by day 92, the weight gain / loss in the high vs. low selenium groups was pronounced and uniform enough to be statistically significant.
References:

• Berry, Marla J., and P. Reed Larsen. "The Role of Selenium in Thyroid Hormone Action*." Endocrine reviews 13.2 (1992): 207-219.
• Hawkes, Wayne Chris, Fulya Zeynep Alkan, and Lynn Oehler. "Absorption, distribution and excretion of selenium from beef and rice in healthy North American men." The Journal of nutrition 133.11 (2003a): 3434-3442.
• Hawkes, Wayne Chris, and Nancy L. Keim. "Dietary selenium intake modulates thyroid hormone and energy metabolism in men." The Journal of nutrition 133.11 (2003b): 3443-3448.
• Hawkes, Wayne Chris, et al. "High-selenium yeast supplementation in free-living North American men: no effect on thyroid hormone metabolism or body composition." Journal of trace elements in medicine and biology 22.2 (2008): 131-142.
• Kenfield, Stacey A., et al. "Selenium Supplementation and Prostate Cancer Mortality." Journal of the National Cancer Institute 107.1 (2015): dju360.
• Köhrle, J. "Thyroid hormone deiodination in target tissues--a regulatory role for the trace element selenium?." Experimental and clinical endocrinology 102.2 (1993): 63-89.