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4x fail - if you look at the latest cold-water immersion science.

There are proven acute regenerative benefits of both cold water immersion and cold / ice application after exercise... cool? Not so cool, no. Two recent studies demonstrate: In the long run both will impair your gains.

The studies from Japan (Yamane. 2015) and Norway + Australia (Roberts. 2015) were conducted independently and published almost simultaneously in the International Journal of Sports Medicine and the Journal of Physiology, respectively. Therefore, I'd like to discuss them one after the other, before I finally tie the knots between the studies in a conclusion some of you are not going to like.
"Does Regular Post-exercise Cold Application Attenuate Trained Muscle Adaptation?" that's not only the title, but also the central question in a recent study by Yamane et al. (2015). In the corresponding experiment, 14 male subjects did 5 sets of 8 wrist-flexion exercises at workloads of 70–80% of the single repetition maximum, 3 times a week for 6 weeks. Of the total of 14 male subjects,

• 7 subjects immersed their experimental forearms in cold water (10± 1°C) for 20min after wrist-flexion exercises (cooled group), while
• the other 7 who served as control subjects (noncooled group) refrained from putting their forearms into the 10°C cold water

At the end of the 6-week training period, the wrist-flexor thickness, brachial-artery diameter, maximal muscle strength, and local muscle endurance were measured in upper extremities.

Figure 1: Rel. changes (%) of forearm diameter (muscle size), muscle strength (of the wrist flexors), brachial-artery diameter (vascular adapation) and local muscle endurance (Yamane. 2015).

The results in Figure 1 may come as a nasty surprise to some of you: The wrist-flexor thicknesses of the experimental arms increased after training in both groups, but the extent of each increase was significantly less in the cooled group compared with the non-cooled group.

That this is not a question of post-exercising swelling, only, can be inferred from the fact that the maximal muscle strength and brachial-artery diameter did not increase in the cooled group, either. That's much in contrast to the non-cooled group where both variables as well as the local muscle endurance increased significantly. If we assume that similar effects occur for other muscle parts, it would thus not be a good idea to join Peer Mertesacker in the ice-tub that made him world-famous after the quarter-finals of the soccer world cup, last year.
Now, with just one study investigating only one muscle group, you may well argue that this could be an outlier and eventually it's thus not a problem or even beneficial if you use cold water application or cold water immersion after every workout.

If we add the results Llion A. Roberts et al. present in their accepted article in the The Journal of Physiology, however, it does no longer look like any of the findings were coincidental. After all, Roberts et al. conducted not one but two studies to investigate whether and why "regular cold water immersion influences muscle adaptations to strength" (Roberts. 2015). More specifically, the two experiments the researchers from Norway and Australia conducted were...

• Table 1: Overview of the RT-program in study 1 (Robert. 2015)

  study 1 - 21 physically active men strength trained for 12 weeks (2 d/wk), with either 10 min of CWI or active recovery (ACT) after each training session. The sessions involved mainly the lower body. Training sessions were performed twice a week, separated by 72 h. The loads were set to 8-rep, 10-rep and 12-repetition maximum (RM), and weights corresponding to a proportion of each participant’s body mass.
  
  Strength training was progressive, and included 45° leg press, knee extension, knee flexion, walking lunges and plyometrics exercises. The plyometric component comprised countermovement drop jumps, slow eccentric squat jumps, split lunge jumps and countermovement box jumps. All strength training was supervised and was performed at normal room temperature (23–25°C). 
• study 2 - 9 active men performed a bout of single-leg strength exercises on separate days, followed by CWI or ACT to elucidate the acute effects and potential mechanisms that explain the reduced gains in the chronic training study

The cold water immersion (CWI) itself was performed within 5 min after each training session. The procedure is described as follows: "Participants in the cold water immersion group sat in an inflatable bath (iCool iBody, iCool, Miami, Australia) for 10 min with both legs immersed in water up to the waist. Water was circulated continuously and maintained at 10.1 ± 0.3°C using a circulatory cooling unit (iCool LITE, iCool)" (Roberts. 2015). In contrast, the active recovery group performed 10 min active recovery at a self-selected low intensity on a stationary cycle ergometer (Wattbike, Nottingham, United Kingdom) at a really light mean intensity level of 59.5 ± 9.4 W.

Figure 2: Training-induced changes in type II fiber count and size (left, top), myonucle per fiber (left, bottom), leg press strength (A), knee extension strength (B), isometric torque (C) and RFD impulse (D | Roberts. 2015).

Just as it was the case in the much smaller wrist muscles in the Yamane study, the strength and muscle mass increases in the legs of the subjects in the Roberts study were blunted by the application of cold water (CWI). Practically speaking this means that the isokinetic work (19%), type II muscle fibre cross-sectional area (17%) and the number of myonuclei per fibre (26%) increased in the ACT group (all P<0.05) but not the CWI group.

If you want to know something about the reasons of these statistically significant and practically highly relevant difference are concerned, I suggest you take a closer look at the red box - it may also help you to fully understand the bottom line.
References:

• Roberts, et al. "Post-exercise cold water immersion attenuates acute anabolic signalling and long-term adaptations in muscle to strength training." The Journal of Physiology (2015): Accepted article.
• Yamane, M., N. Ohnishi, and T. Matsumoto. "Does Regular Post-exercise Cold Application Attenuate Trained Muscle Adaptation?." International journal of sports medicine (2015).

Seafood is an excellent source of iodine, but many people get most of their iodine from iodized table salt.

I assume you would have expected me to forget that I promised to do my very best to turn the "too much of a good thing" article on selenium I wrote a week ago into a series, right? Well, you obviously don't know me well enough, then, because here's installment #2 of this new series. One that is closely related to #1, but was significantly more difficult to write.

Why's that? Well, if you took a look at the literature discussing the effects of iodine supplementation on thyroid function, you'd know why it was ... well, "complicated" and not exactly unambigous to say the least.
In view of the fact that it would go beyond the scope of any single article to discuss the detailed effects of iodine and iodine supplements in the various thyroid disease states, I will focus solely on the beneficial and detrimental effects of iodine in more or less healthy individuals. Furthermore, I will not go into details as far as...

• Table 1: The spectrum of iodine deficiency disorders - click to see all (Delange. 1994)

  the important role of iodine in brain and general physical development and the ~30% increase in iodine requirements in pregnant women (Delange. 2000; Zimmermann. 2004 & 2011),
• the role of iodine in psychiatric disease (Hetzel. 2000), and
• the influence of (inorganic) iodine in the environment on human / general mammalian health (Fuge. 1987)

are concerned. What I would like to mention, at least, is the often-cited role of iodine in breast cancer, because the purported protective effect of iodine from supplements or food (Cann. 2000; Funahashi. 2001) is one of the reasons many women consume iodine supplements in dosages that could be more of a threat than a blessing for their health. That's bad news in view of the fact that the "evidence" of breast cancer protective effects is still in the hypothetical state and "rigorous retrospective and prospective studies are needed to confirm this hypothesis" (Cann. 2000).
Things we can say about iodine that are above all relevant for both, men and women, is that it is essential for normal thyroid function. Just as it is the case for selenium (discussed in the last installment of this series), though, the effects of supplemental iodine on thyroid function are far from being conclusive. While a lack of iodine will force the thyroid to increase it's efficacy by - eventually - developing goiterous growth, the dietary and even more so the supplemental ingestion of copious amounts of iodine (>1mg) do something most people won't expect: They reduce the function of the thyroid glands.

Figure 1: On a population-based study, high(er) iodine intakes are associated with higher TSH levels and thus reduced thyroid function, while high intakes are associated with increased TSH and reduced thyroid fct. (Laurberg. 1998).

It is thus not surprising that populations with low and high iodine intake tend to develop opposite thyroid disorders with

• goiter and thyroid hyperfunction being more prevalent among populations with low(er) iodine intakes, and 
• impaired thyroid function (=subclinical and clinical hypothyroidism) being more prevalent among populations with relatively high iodine intakes (Lauerberg. 1998). 

This does not mean, that "half-deficient" intakes were best, even though there's evidence that a mild = non-goitrogenic iodine deficiency partly protects against autoimmune thyroid disease (Laurberg. 1998). In that US scientists warn that it is not sure, in how many cases the iodine induced reduction in thyroid function "may result from the adverse effect of excess iodine on thyroid function in persons with underlying thyroid disease such as Hashimoto’s thyroiditis, history of subacute thyroiditis, or silent postpartum lymphocytic thyroiditis" (Hollowell. 2002).
It is thus all the more important to take the little experimental evidence there is into consideration. In that, the often-seen drops in thyroid function in response to the ingestion of large quantities of iodine are often ascribed to the so-called Wolff-Chaikoff which is supposed to reduce the thyroid function for no longer than a few a days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns (Markou. 2001). Now, the problem is: The phenomenon is not always as short-lived as it is supposed to be

Table 2: Taking high amounts of iodine can significantly reduce thyroid function or induce goiter. Specifically in the subgroups of the population mentioed above (Roti. 2000)

"in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with autoimmune thyroiditis, and Graves' disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues [and may require temporary or permanent treatment with thyroid medications]" (Markou. 2001). 

Even if you believe you know you don't suffer from any of the aforementioned thyroid problems taking 10mg or more of iodine may be likened to Russian Thyroid Roulette, because it always entails the risk of iodide-induced hypothyroidism. Usually the hypothyroidism is transient and regresses within 2-3 weeks after iodide withdrawal, but as Markou et al. highlight there's a small subgroup of patients who develop transient iodine-induced hypothyroidism that must be followed long term thereafter because many will develop permanent primary hypothyroidism.

Figure 2: People with a previous history of painful subacute thyroiditis (SAT) are highly susceptible to the hypothyroid effects of 300mg/day iodine compared to people who had surgery for benign thyroid nodules (Roti. 1990).

Overall, it should be noted, though that the human body is pretty good at managing high intakes of iodine. While iodine-induced hypothyroidism was also reported in patients with no apparent thyroid disease the number of scientifically verified reports like the mild reversible hypothyroidism that was observed in elderly patients consuming iodinated glycerol by Drinka et al. (1998) or the two Japanese patients with anorexia nervosa developed iodine-induced hypothyroidism after they had consumped of large quantities of OshaberiKombu, a Japanese food that is extensively consumed on lowe energy diets and contains approximately 13.4 mg of iodine per 100g (Matsubayashi. 1998).

All in all the aforementioned examples are yet the exception to the rule. A rule which is evidenced in studies like Markou et al. (2000), in which the authors administered 80 mg potassium iodide (which is also the form of "iodine" in Lugol's solution) to 30 normal children 8 to 14 years old for 3 months and found that none developed overt or subclinical hypothyroidism. That does not mean that the iodine was without effect, but what the scientists observed was the expected transient elevation in serum TSH values (5–8 mU/L) as a result of the Wolff-Chaikoff effect. An effect that abated without further medical intervention on part of the researchers after 3-4 weeks when the TSH returned to normal levels despite the continuation of iodide treatment (Markou. 2000).
References:

• Cann, Stephen A., Johannes P. van Netten, and Christiaan van Netten. "Hypothesis: iodine, selenium and the development of breast cancer." Cancer Causes & Control 11.2 (2000): 121-127.
• Caldwell, Kathleen L., et al. "Iodine status of the US population, National Health and Nutrition Examination Survey, 2005–2006 and 2007–2008." Thyroid 21.4 (2011): 419-427.
• Delange, François. "The disorders induced by iodine deficiency." Thyroid 4.1 (1994): 107-128.
• Delange, Francois. "The role of iodine in brain development." Proceedings of the nutrition society 59.01 (2000): 75-79.
• Denef, Jean-François, Marie-Christine Many, and M. F. van Den Hove. "Iodine-induced thyroid inhibition and cell necrosis: two consequences of the same free-radical mediated mechanism?." Molecular and cellular endocrinology 121.1 (1996): 101-103.
• Drinka, Paul J., and Wolfram E. Nolten. "Effects of iodinated glycerol on thyroid function studies in elderly nursing home residents." Journal of the American Geriatrics Society 36.10 (1988): 911-913.
• Fuge, R. "Iodine in the environment: its distribution and relationship to human health." Trace substances in environmental health-XXI. 1987.
• Funahashi, Hiroomi, et al. "Seaweed prevents breast cancer?." Cancer Science 92.5 (2001): 483-487.
• Hetzel, Basil S. "Iodine and neuropsychological development." The Journal of nutrition 130.2 (2000): 493S-495S.
• Hollowell, Joseph G., et al. "Serum TSH, T4, and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III)." The Journal of Clinical Endocrinology & Metabolism 87.2 (2002): 489-499.
• Laurberg, Peter, et al. "Iodine intake and the pattern of thyroid disorders: a comparative epidemiological study of thyroid abnormalities in the elderly in Iceland and in Jutland, Denmark." The Journal of Clinical Endocrinology & Metabolism 83.3 (1998): 765-769.
• Many, Marie-Christine, et al. "In vitro study of acute toxic effects of high iodide doses in human thyroid follicles." Endocrinology 131.2 (1992): 621-630.
• Matsubayashi, Sunao, et al. "Iodine-induced hypothyroidism as a result of excessive intake of confectionery made with tangle weed, Kombu, used as a low calorie food during a bulimic period in a patient with anorexia nervosa." Eating and Weight Disorders-Studies on Anorexia, Bulimia and Obesity 3.1 (1998): 50-52.
• Markou, K., et al. "Effects of chronic iodide administration in thyroid function in children and adolescents with a history of transient congenital hypothyroidism." 27th Annual Meeting, Greek Endocrine Association, Nicosia Cyprus. Vol. 82. 2000.
• Roti, Elio, et al. "Iodine-Induced Hypothyroidism in Euthyroid Subjects with a Previous Episode of Subacute Thyroiditis*." The Journal of Clinical Endocrinology & Metabolism 70.6 (1990): 1581-1585.
• Roti, E., and A. G. Vagenakis. "Effect of excess iodide: clinical aspects." Werner and Ingbar’s The Thyroid–Braverman LE and Utiger RD. Ed, Lippincott (2000): 316-329.
• Sang, Zhongna, et al. "Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial." The American journal of clinical nutrition 95.2 (2012): 367-373.
• Zanzonico, Pat B., and David V. Becker. "Effects of time of administration and dietary iodine levels on potassium iodide (KI) blockade of thyroid irradiation by 131I from radioactive fallout." Health Physics 78.6 (2000): 660-667.
• Zimmermann, M., and F. Delange. "Iodine supplementation of pregnant women in Europe: a review and recommendations." European Journal of Clinical Nutrition 58.7 (2004): 979-984.
• Zimmermann, Michael B. "The role of iodine in human growth and development." Seminars in cell & developmental biology. Vol. 22. No. 6. Academic Press, 2011.

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.