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Most physiological reactions to dietary supplements diverge into two categories:
- A reaction to the purity of the supplement.
- A reaction to the effects of a supplement.
As of 2017, most supplements source from China, a country not exactly favored for its quality controls.
It’s often necessary to measure an individual’s reaction to a supplement by keeping most other variables constant including intake of other accompanying supplements. High levels of work-stress can exacerbate reactions to foods, medications, supplements, or hormones, and hypothyroidism tends to increase individual sensitivity to environmental insults by similar mechanisms.
Hypothyroidism features high levels of inflammation. Small amounts of caffeine (as in coffee) can attenuate the inflammation, but due to caffeine’s tendency to both flush fat from the liver into the blood stream, and also due to its tendency to lower GABA, caffeine can provoke anxiety and even panic attacks hypothyroid individuals.
Raymond Peat, PhD has commented on the benefits of small doses of caffeine in optimizing energy production. In his blog, Edward J. Edmonds mentions a study wherein caffeine utilized as an adjunct therapy yielded superior benefits than its use in isolation.
Corticotropin-releasing hormone (CRH) increases anxiety levels and interferes with normal learning processes. CRH itself increases the level of ACTH, and in the presence of serotonin, ACTH will produce excess cortisol. Estrogen increases the activity of CRH, whereas progesterone counters the effect, partly responsible for progesterone’s efficacy in alleviating anxiety. Aspirin, which opposes estrogen’s effects lowers anxiety and improves learning. Caffeine can increase sertoonin Edmonds also mentions a case of exaggerated aspirin toxicity (for the GI tract) in the case of magnesium deficiency.
Dr. Peat offers insight into the occurrence in his article Aspirin, brain, and cancer:
“(By activating T3, aspirin can sometimes increase the temperature and pulse rate.) Magnesium, niacinamide, and other nerve protective substances work together.”
As hyperthyroidism increases the need for all nutrients, aspirin particularly increases requirements for neuroprotective agents. In addition, aspirin restores insulin sensitivity, which promotes healthy sugar metabolism. Like caffeine, niacinamide, and most other pro-metabolic substances, aspirin will lower blood sugar, and as many as several hundred grams of sugar will be required, and individual cravings will self-regulate intake.
If in a “water-logged” hypo-osmolar state, intake of caffeine and aspirin can raise the temperature set point and increase water evaporation, and therefore increase the tolerability of liquids. Except in the context of larger amounts of caffeine and aspirin, or instead sufficient amounts of thyroid hormone, pregnenolone, or progesterone (along with other pro-metabolic substances), a solid, salty meal with low-water content can oppose the hypo-osmolartiy and restore water balance to a person’s cells.
Chronic intake of liquids, particularly without adequate salts can lead to chronic hypo-osmolarity, and the poor regulation of cellular water in hypothyroidism often precipitates such a state. An excess of liquids paired with hypothyroidism can lead to dangerous electrolyte imbalances and overproduction of aldosterone, which contributes to kidney damage.
Minerals should be obtained via food and never supplementation, as mineral supplements act as potent allergens.
For calcium, egg shell and oyster shell serve as high-quality sources in descending quality. Bone meal from cattle or other ruminants should not be used due to contamination with heavy metals. Citric acid and citrate salts tend to promote the excretion of minerals, particularly calcium in the urine and should be avoided, as with calcium citrate, magnesium citrate and so forth.
Magnesium can be obtained by boiling kale leaves and drinking the leftover broth. Fruits tend to have high amounts of magnesium, whereas nuts, seeds and grains should be avoided. Magnesium hydroxide (milk of magnesia) mixed with seltzer water offers a bioavailable form of magnesium, as does magnesium sulfate (Epsom salts) added to bathwater.
With good thyroid function, potassium needs increase, and large amounts of potassium can be found in most fruits and cooked vegetables.
Sodium needs tend to decrease with increasing thyroid function, and in hypothyroidism, larger amounts of sodium can promote energy efficiency and deter hypothyroid symptoms. Salt cravings regulate intake effectively. Iodized table salt contains too much iodine, and Himalayan pink salt contains heavy metals. Pickling and canning salt without added iodine offers superior purity. Salt should never be taken on its own, as it may irritate the stomach. Salty, delicious meals promote a high metabolic rate and make life worthwhile.
Copper, although needed in larger amounts appears in abundance with a nutritious diet including fruits, dairy, and particularly shellfish. Copper has a higher degree of toxicity when supplemented above 5 mg per day, and even this amount does not seem necessary.
Zinc, like copper appears in shellfish as well as in meat. Oysters offer very high concentrations of zinc, and many benefit from zinc rather than copper supplementation. An amount of 10-50 mg per day seems safe, but depending on the diet, any added zinc can become toxic over time.
References
Ottoboni, F., & Ottoboni, M. A. (2002). The Modern Nutritional Diseases: Heart Disease, Stroke, Type-2 Diabetes, Obesity, Cancer : and how to Prevent Them. amazon.com, 63.
Raymond Peat, PhD. (2006). Aspirin, brain, and cancer. Retrieved October 23, 2017, from http://raypeat.com/articles/aging/aspirin-brain-cancer.shtml
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Bale, T. L., Picetti, R., Contarino, A., Koob, G. F., Vale, W. W., & Lee, K.-F. (2002). Mice deficient for both corticotropin-releasing factor receptor 1 (CRFR1) and CRFR2 have an impaired stress response and display sexually dichotomous anxiety-like behavior.
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience,
22(1), 193–199.
Corticotropin-releasing factor (CRF) and its family of peptides are critical coordinators of homeostasis whose actions are mediated through their receptors, CRF receptor 1 (CRFR1) and CRFR2, found throughout the CNS and periphery. The phenotypes of mice deficient in either CRFR1 or CRFR2 demonstrate the critical role these receptors play. CRFR1-mutant mice have an impaired stress response and display decreased anxiety-like behavior, whereas CRFR2-mutant mice are hypersensitive to stress and display increased anxiety-like behavior. To further elucidate the roles of both CRF receptors and determine their interaction in behaviors, we have generated mice deficient in both CRFR1 and CRFR2. The behavioral phenotype of these mice demonstrates a novel role of the mother’s genotype on development of pup anxiety. We have found that although the female double-mutant mice display anxiolytic-like behavior, the male double-mutant mice show significantly more anxiety-like behavior compared with the females. We have also determined that the dam’s CRFR2 genotype affects the anxiety-like behavior of the male mice, such that a pup born to a heterozygous or mutant dam displays significantly more anxiety-like behavior regardless of that pup’s genotype. Double-mutant mice also display an even greater impairment of their hypothalamic-pituitary-adrenal axis response to stress than that of the CRFR1-mutant mice. CRF mRNA levels are elevated in CRFR1- and double-mutant mice, and urocortin III and vasopressin mRNA levels are increased in CRFR2- and double-mutant mice. These results indicate that both CRFR1 and CRFR2 have critical roles in gene regulation and the maintenance of homeostasis in response to stress.
d
Bale, T. L., Picetti, R., Contarino, A., Koob, G. F., Vale, W. W., & Lee, K.-F. (2002). Mice deficient for both corticotropin-releasing factor receptor 1 (CRFR1) and CRFR2 have an impaired stress response and display sexually dichotomous anxiety-like behavior.
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience,
22(1), 193–199.
Corticotropin-releasing factor (CRF) and its family of peptides are critical coordinators of homeostasis whose actions are mediated through their receptors, CRF receptor 1 (CRFR1) and CRFR2, found throughout the CNS and periphery. The phenotypes of mice deficient in either CRFR1 or CRFR2 demonstrate the critical role these receptors play. CRFR1-mutant mice have an impaired stress response and display decreased anxiety-like behavior, whereas CRFR2-mutant mice are hypersensitive to stress and display increased anxiety-like behavior. To further elucidate the roles of both CRF receptors and determine their interaction in behaviors, we have generated mice deficient in both CRFR1 and CRFR2. The behavioral phenotype of these mice demonstrates a novel role of the mother’s genotype on development of pup anxiety. We have found that although the female double-mutant mice display anxiolytic-like behavior, the male double-mutant mice show significantly more anxiety-like behavior compared with the females. We have also determined that the dam’s CRFR2 genotype affects the anxiety-like behavior of the male mice, such that a pup born to a heterozygous or mutant dam displays significantly more anxiety-like behavior regardless of that pup’s genotype. Double-mutant mice also display an even greater impairment of their hypothalamic-pituitary-adrenal axis response to stress than that of the CRFR1-mutant mice. CRF mRNA levels are elevated in CRFR1- and double-mutant mice, and urocortin III and vasopressin mRNA levels are increased in CRFR2- and double-mutant mice. These results indicate that both CRFR1 and CRFR2 have critical roles in gene regulation and the maintenance of homeostasis in response to stress.
d
Steckler, T., & Holsboer, F. (2001). Interaction between the cholinergic system and CRH in the modulation of spatial discrimination learning in mice.
Brain Research,
906(1–2), 46–59.
Both cholinergic and CRH systems have been linked to cognitive processes such as learning and memory, and neuroanatomical as well as neurochemical evidence suggests important interactions between these two systems. Moreover, recent reports of pro-mnestic effects of CRH open the possibility that CRH could have beneficial effects in animals with cholinergic dysfunction. In a first experiment, spatial discrimination of C57BL/6 mice treated with various doses of scopolamine (0.5–2.0 mg/kg IP) was tested in a two-choice water maze task. Scopolamine, but not methylscopolamine, impaired accuracy and decreased responsivity. In contrast, similar doses of the nicotinic antagonist mecamylamine had no effect on choice accuracy but altered responsivity, as indicated by increased errors of omission and a reduction in swim speed during early experimental stages. ICV CRH (0.5–1.0 microg) also failed to significantly affect accuracy, but a strong tendency was observed to impair percentage correct responses. Measures of responsivity, such as errors of omission, choice latency and distance traveled, and of thigmotaxis were not significantly affected by CRH. However, initial swim speed was reduced by the peptide. Combined treatment with scopolamine (0.5 mg/kg IP) and CRH (0.5 microg ICV) had only mild, and primarily independent, effects, but overall suggested that concomitant blockade of muscarinic receptors and activation of the CRH system would rather act synergistically to disrupt spatial discrimination learning. Synergistic effects were also observed when animals receiving a combination of mecamylamine (2.0 mg/kg IP) and CRH (0.5 microg ICV) were tested, both in terms of responsivity and thigmotaxis, and there was limited evidence that part of these effects were potentiating. Thus, the cholinergic and CRH systems interact in the modulation of learning, but CRH, contrary to prediction, worsens the impairment caused by cholinergic blockade.
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