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Poultry is high in tryptophan and so is spirulina, cod, soy beans, parmesan and pork. They all have higher tryptophan contents than turkey. So, it doesn't always have to be poultry ;-)

As a waredownloadsoft reader you know that "[n]utrition plays a key role in the maintenance of muscle and bone mass, and dietary protein deficiency has in particular been associated with catabolism of both muscle and bone tissue" (Dukes. 2015). You will also be aware that leucine and some other amino acids play a particularly important role in the accrual and maintenance of muscle mass.

Until today, l-tryptophan, the amino acid the "happy neurotransmitter" serotonin is not among the usual suspects when it comes to building muscle. If the results of a recent study from the Georgia Regents Univ. translate into practic-ally relevant research, this may change soon (Dukes. 2015).
The aim of said study was to test the hypothesis that the essential amino acid tryptophan, and its metabolite kynurenine, might directly affect muscle metabolism in the setting of protein deficiency. To this ends, adult mice (12 mo) were fed a normal diet (18% protein), as well as diets with low protein (8%) supplemented with increasing concentrations (50, 100, and 200 uM) of kynurenine (Kyn) or tryptophan (Trp; 1.5 mM) for 8 weeks.

Table 1: Dietary formulations for the different groups in the study | Kyn, kynurenine; Trp, tryptophan (Dukes. 2015).

To be able to elucidate the exact mechanisms that made the mice that received Trp supplementation on top of the low protein diet leaner and more muscular than any other group, the scientists conducted an additional study on myoprogenitor cells which were also treated with Trp and Kyn in to determine their effects on cell proliferation and expression of myogenic differentiation markers.

Figure 1: Body composition (% body fat and % lean mass) of the rodents on the different diets (Dukes. 2015).

Ok, I have to admit the differences of the body composition of the rodents is not extremely impressive, but if you take into account that the changes were driven by significant differences in some of the most important drivers of skeletal muscle hypertrophy, you will probably understand why they still made the waredownloadsoft news.

Figure 2: An anlysis of muscle samples revealed significant increases in the myostatin suppressing protein follistatin, IGF-1 and leptin, as well as slight decreases in myostatin (Dukes. 2015).

The enzyme-linked immunosorbent assays the scientists conducted show significant increases in skeletal muscle insulin-like growth factor-1, leptin, and the myostatin antagonist follistatin with Trp supplementation. The corresponding mRNA microarray and gene pathway analysis that were performed on muscle samples of the rodents demonstrate that the pro-anabolic mTor/eif4/p70s6k pathway molecules were significantly upregulated in muscles from mice on Kyn and Trp supplementation. Increases in myoprogenitor cell activity, were yet only seen with tryptophan (not shown in Figure 2). Its metabolite kynurenine, however, didn't have any effect on MyoD, myogenin & myosin heavy chain.
References:

• Dukes, Amy, et al. "The aromatic amino acid tryptophan stimulates skeletal muscle IGF1/p70s6k/mTor signaling in vivo and the expression of myogenic genes in vitro." Nutrition (2015).
• Lin, Frank D., Trevor K. Smith, and Henry S. Bayley. "A role for tryptophan in regulation of protein synthesis in porcine muscle." The Journal of nutrition 118.4 (1988): 445-449.
• Musumeci, Giuseppe, et al. "Importance of serotonin (5-HT) and its precursor l-tryptophan for homeostasis and function of skeletal muscle in rats. A morphological and endocrinological study." Acta histochemica 117.3 (2015): 267-274.
• Sanfilippo, S., R. M. Imbesi, and S. Sanfilippo Jr. "Effects of a tryptophan deficient diet on the morphology of skeletal muscle fibers of the rat. Preliminary observations at neuroendocrinological and submicroscopical levels." Italian journal of anatomy and embryology= Archivio italiano di anatomia ed embriologia 100 (1994): 131-141.

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.