Is anyone else out there trying to control their b.p. w/o drugs? I am extremely drug sensitive... I had a protocol that worked, but over time I've found it does not work in a bunch of serious situations...namely during allergy seasons (which have lengthened for me since I turned 50), nor does it work following exercise (which RAISES my bp). In particular I find that allergies use up zinc (I can indeed breathe again if I take enough zinc - 100mg zinc picolinate (which is like 100% more absorbable - if not more - than other forms). So my theory is that allergies destroy nasal skin and it takes zinc to replace skin. (Although zinc lowers IgG, not sure how that figures in). But right or no, it is clear that in the presence of allergies I have insufficient zinc without major augmentation. However it ALSO takes zinc to make thyroxin. So my allergies use up all available zinc (AND POSSIBLY ADDITIONAL ELEMENTS) and my thyroid starts to go south. When that happens...well there are studies now showing a link between SUBCLINICAL hypothyroidism and low GFR (it slows the kidneys). Slowing the kidneys, raises BLOOD PRESSURE (at least in someone genetically disposed, such as me). So if my body makes too much aldosterone I can't get rid of it. Even if my body does not make too much, it adds up because I cannot get rid of it. ok, I get rid of it over night, but then I can't sleep for constantly getting up to pee and I have high blood pressure all day. I have not solved this yet and it's looking like I'm gonna have to go on drugs, but I am so sensitive to drugs I will not be able to stand my life from that moment forward. If anyone else has tried to control bp w/o drugs I'd like to know your experiences and I'd like to caution you to take your bp every day because there are things we are only discovering that can throw off the best protocol. You could think it pointless to measure as every day you are ok, ok, ok, but 6 months down the road there may be a day you'll find you are NOT ok and there is YET MORE TO BE LEARNED about blood pressure. SInce I am ACE +/+ I have the feeling this is what is going to kill me. My Dad died of his MTHFR 1298AC+/+. I am very leery of +/+. Just wondered if anyone has b.p. off drugs experiences and info to share. I find in some notes I took from a defunct holistic training url that vanadium is needed to make thyroxine - I will have to look into this as I am low on vanadium - a byproduct of being from a hereditary diabetic family. Maybe that's why zinc alone doesn't keep my thyroid normal...? Some studies: Volume 105, Issue 2, February 2005, Pages 127–149 Zinc metabolism in airway epithelium and airway inflammation: basic mechanisms and clinical targets. A review Peter D. Zalewski, Ai Q. Truong-Tran, Dion Grosser, Lata Jayaram, Chiara Murgia, Richard E. Ruffin In addition to basic housekeeping roles in metalloenzymes and transcription factors, dietary zinc (Zn) is an important immunoregulatory agent, growth cofactor, and cytoprotectant with anti-oxidant, anti-apoptotic, and anti-inflammatory roles. These properties of Zn are of particular importance in maintaining homeostasis of epithelial tissues which are at the front line of defense. This review is about the role of Zn in airway epithelium (AE). The first part focuses on the cellular biology of Zn, and what is known about its distribution and function in AE. The second part of the review considers evidence for altered Zn metabolism in asthma and other chronic diseases of airway inflammation. Important issues arise from a potential therapeutic perspective as to the optimal ways to monitor circulating and epithelial Zn levels in patients and the most effective means of supplementing these levels. Influence of Zinc and Selenium Deficiency on Parameters Relating to Thyroid Hormone Metabolism A. Kralik, K. Eder, M. Kirchgessner Institute of Nutrition Physiology, Technical University Munich, Freising-Weihenstephan, Germany 48 weaned male Sprague-Dawley rats with an initial average body weight of 41 g were divided into 4 groups of 12 animals (zinc-deficient; zinc-adequate, pair-fed with zinc-deficient group; selenium-deficient; selenium-adequate) for 40 days. All groups were fed a semisynthetic diet with casein being the source of protein. In the selenium-deficient diet, there was a selenium concentration of 0.038 mg/kg. The other diets were supplemented with Na-selenite in order to adjust the selenium concentration to 0.3 mg/kg. In the zinc-deficient diet, there was a zinc concentration of 4.1 mg/kg. The zinc concentrations in the other diets were adjusted to 45 mg/kg by the addition of zinc-sulfate heptahydrate. Zinc-deficient rats were characterized by a markedly reduced alkaline phosphatase activity in their serum, whilst selenium-deficient rats showed a markedly reduced glutathione peroxidase in serum proving their respective zinc-deficient and selenium-deficient states. Zinc deficiency decreased concentrations of triiodothyronine (T3) and free thyroxine (fT4) in serum by approximately 30% when compared with zinc-adequate controls. The concentration of thyroxine (T4) in serum was not affected by zinc deficiency. Selenium-deficient animals had lower concentrations of T3and T4 than selenium-adequate animals. The concentration of fT4 in serum was not affected by selenium deficiency. The activity of hepatic type I 5′deiodinase was decreased by 67% by zinc deficiency and by 47% by selenium deficiency compared to adequate controls. The study data show that both zinc and selenium deficiency affect the metabolism of thyroid hormones. American Journal of the Medical Sciences: October 1999 - Volume 318 - Issue 4 - p 277 Original Articles Blood Volumes and Renal Function in Overt and Subclinical Primary Hypothyroidism VILLABONA, CARLES MD; SAHUN, MANUEL MD; ROCA, MANUEL PhD; MORA, JAUME MD; GÓMEZ, NÚRIA MD; GÓMEZ, JOSÉ M. MD; PUCHAL, RAFAEL PhD; SOLER, JOAN MD Abstract Introduction: Thyroid dysfunction is associated with marked alterations in cardiovascular and renal functions. In hypothyroidism, myocardial contractility, cardiac output, and oxygen consumption are decreased, whereas peripheral resistance is increased. Methods: We assessed blood volumes and effective renal plasma blood flow (ERPF) and glomerular filtration rate (GFR) in 17 patients with overt primary hypothyroidism and in 15 of these patients when in euthyroid state after substitutive therapy. We performed the same measurements in eight patients with subclinical hypothyroidism. Results: In the hypothyroid state, the plasma volume measured by dilution of 125I-albumin (APV) was higher than the calculated plasma volume (CPV) from packed red cell mass, suggesting an extravascular escape of albumin. After substitutive therapy, the CPV showed a statistical increase (P< 0.05), whereas APV remained unchanged. Both ERPF and GFR increased after thyroxine therapy (p< 0.05). In the subclinical group, blood volumes and renal function were similar to those found in the other group of patients when in the euthyroid state. Conclusions: We conclude that in primary hypothyroidism, ERPF and GFR are low, but that these values improve with substitutive therapy. CPV is a better index of the current plasma volume than APV. The difference between these two parameters suggests that the escape of albumin into the extravascular space in primary hypothyroidism is terminated by treatment. There are no clear abnormalities either in blood volumes or in renal function in subclinical hypothyroidism. Consistent Reversible Elevations of Serum Creatinine Levels in Severe Hypothyroidism FREE Stuart H. Kreisman, MDCM; James V. Hennessey, MD Arch Intern Med. 1999;159(1):79-82. doi:10.1001/archinte.159.1.79. Background Changes in routine clinical chemical indicators of renal function in the hypothyroid state are not well characterized, and are infrequently discussed in standard internal medicine or subspeciality textbooks. Patients and Methods We evaluated 24 consecutive patients with iatrogenic hypothyroidism induced prior to radioiodine scanning for monitoring of thyroid carcinoma. Serum creatinine and thyroid function tests were measured prior to, during, and subsequent to the period of induced hypothyroidism. Results Among 29 episodes with paired prior euthyroid and hypothyroid serum creatinine values, the hypothyroid value was greater in 26 (89.7%), and equal in 3 (10.3%), less in none; the mean hypothyroid value was significantly greater (103 vs 76 µmol/L [1.17 vs 0.87 mg/dL]) (P<.001). Among 36 episodes with paired hypothyroid and subsequent euthyroid serum creatinine values, the hypothyroid value was greater in 33 (91.7%), equal in 2 (5.6%), and less in 1 (2.8%); the mean hypothyroid value was again significantly greater (102 vs 75 µmol/L [1.15 vs 0.85 mg/dL]) (P<.001). There was no significant difference between prior and subsequent euthyroid serum creatinine values. Serum creatinine values above the stated normal range occurred in 6 of 36 hypothyroid episodes. Conclusions There is a consistent and reversible elevation of serum creatinine values in the hypothyroid state. Frankly abnormal serum creatinine levels will occur in some cases. J Clin Invest. 1974 October; 54(4): 926–934. doi: 10.1172/JCI107833 PMCID: PMC301633 Mechanism of Impaired Water Excretion in the Hypothyroid Rat Dimitrios S. Emmanouel, Marshall D. Lindheimer, and Adrian I. Katz The ability to excrete an oral water load and the renal diluting mechanism were studied in hypothyroid rats and in age-matched euthyroid controls. Hypothyroid animals excreted a significantly smaller fraction of a 50-ml/kg oral water load than controls, demonstrating the same limited ability to excrete free water as thyroid-deficient man. During hypotonic (0.45%) saline infusion, absolute sodium delivery to the diluting segment and free water clearance were markedly lower in hypothyroid rats. However, both fractional distal sodium delivery and fractional free water clearance were similar in hypothyroid and control animals, suggesting that the reduced absolute free water formation in hypothyroid rats was due to decreased net distal delivery. In support of this hypothesis was the observation that fractional distal sodium reabsorption was equal or higher in thyroid-deficient rats, which indicates that the sodium reabsorptive capacity of the diluting segment was preserved in these animals. The results cannot be attributed to incomplete suppression of antidiuretic hormone (ADH) since they were identical in diabetes insipidus rats, nor to different rates of non-ADH-dependent backflux of filtrate since tissue osmolality and solute concentrations in the cortex, medulla, and papilla were similar in hypothyroid and control rats of both Sprague-Dawley and Brattleboro strains. The functional integrity of the diluting segment in hypothyroid rats was further demonstrated in experiments in which distal delivery was increased by contralateral nephrectomy or by administration of carbonic anhydrase inhibitors which decrease proximal sodium reabsorption. In both studies, fractional free water clearance increased markedly reaching levels significantly greater than in euthyroid controls. These results demonstrate that the impaired ability of the hypothyroid rat to excrete a water load is not due to incomplete suppression of ADH or decreased reabsorptive capacity of the diluting segment but results from decreased filtrate delivery to this site secondary to reduced GFR. Correlation between severity of thyroid dysfunction and renal function Den Hollander, J. G., Wulkan, R. W., Mantel, M. J. and Berghout, A. (2005), Correlation between severity of thyroid dysfunction and renal function. Clinical Endocrinology, 62: 423–427. doi: 10.1111/j.1365-2265.2005.02236.x Objective Renal function is profoundly influenced by thyroid status; however, this has not been studied in detail in human subjects. The purpose of the present study was to determine the relationship between renal function and thyroid status before and after treatment for hypothyroidism and hyperthyroidism, respectively. Design and patients In 37 consecutive hypothyroid and 14 hyperthyroid patients renal function as measured by plasma creatinine and glomerular filtration rate (GFR) [based on the modification of diet in renal disease (MDRD) formula] was determined before treatment and after regaining euthyroidism. Results Renal function improved significantly during treatment of hypothyroidism and decreased during treatment of hyperthyroidism. There was a strong correlation between the change in thyroid status determined as the ratio log10(fT4 post-treatment/fT4 pretreatment) and the change in renal function as a result of therapy expressed as serum creatinine (r2 = 0·81, P < 0·0001) and estimated GFR (0·69, P < 0·0001). Conclusion The kidney is an important target of thyroid hormone action.