We all know that inflammation is problem as it pertains to neurodegenerative disease, problems with healing from TBI and now it seems it alters appropriate hypothalamic function in weight control. Things to consider when looking at your weight.
1. Insulin resistance and c-peptide and glucose usage.
2. Thyroid function, free levels, bindings globulins and autoimmunity.
3. Gut function, inflammation and food sensitivities.
4. Mental and emotional aspects related to food.
5. Caloric intake and the quality of food.
6. The portions of food
7. Exercise amount and type.
8. Adrenal function.
9. Infectious disease that can create inflammation.
10. Optimal male and female hormones.
These are just some of the things that one needs consider when trying to shed some pounds.
Be watching for a book I will be releasing in the next year on the stories behind failed diets and what practitioners, patients and those afflicted are missing. Going Beyond the Fads!.
Preliminary clinical research suggests that vinpocetine might enhance memory in normal volunteer!
How many people suffer from poor blood flow or construction of crucial vasculature?
Orally, vinpocetine is used for enhancing memory, improving cerebral blood flow, improving cerebral oxygen and glucose utilization, protecting against age-related cognitive decline and Alzheimer's disease, treating cerebrovascular disease, preventing post-stroke morbidity and mortality, treating organic psychosyndromes, treating intractable tumoral calcinosis in people undergoing hemodialysis, decreasing stroke risk, treating menopausal symptoms, chronic fatigue syndrome (CFS), seizure disorders, and preventing motion sickness.
Dementia. Vinpocetine is used to treat cognitive impairment due to vascular disease, Alzheimer's disease, and other kinds of dementias. It might have a modest effect on cognitive impairment from various causes, but most studies have lasted 4 months or less. Also, most of the studies were published prior to 1990 and used a variety of terms and criteria for cognitive decline and dementia. It works, I have seen it clinically work but more empirical data needs to be generated over logistic logarithmic expansion.
Hemodialysis. Preliminary clinical research suggests that taking vinpocetine 15 mg daily for up to one year can eliminate calcium deposits in the soft tissue around joints (tumoral calcinosis) in renal failure patients undergoing hemodialysis
Memory. Preliminary clinical research suggests that vinpocetine might enhance memory in normal volunteer. Additionally, some clinical evidence shows that taking a combination product containing vinpocetine and ginkgo can improve short-terms memory in healthy adults.
Tinnitus. Some preliminary clinical evidence suggests that giving an intravenous infusion of a specific vinpocetine product (Cavinton) 20 mg in 250 mL of saline plus oral vinpocetine (Cavinton) 10 mg twice daily along with physiotherapy might improve tinnitus in patient with chronic tinnitus. However, giving this intravenous formulation of vinpocetine (Cavinton) 10 mg twice daily appears to be less effective than nicergoline for reducing tinnitus in patients with ringing in their ears due to recent acoustic trauma.
Urinary incontinence. Preliminary clinical evidence suggests that taking vipocetine 10 mg three times daily for 2 weeks might reduce daytime and nighttime frequency of urination in people with urinary incontinence.\
Antioxidant effects: According to a review, vinpocetine protects the nervous system from reactive oxygen species (ROS). In rat brain synaptosomes, vinpocetine inhibited the ascorbate/Fe2+ stimulated consumption of oxygen and thiobarbituric acid reactive substances (TBARS) accumulation in a concentration-dependent manner and significantly inhibited intrasynaptosomal reactive oxygen species (ROS) formation. In vitro, a relatively low concentration of vinpocetine inhibited the depolymerization of the high-molecular-weight hyaluronan caused by hydroxyl radicals. In vitro, a physiologically relevant concentration of vinpocetine exhibited significant scavenging activity, which was dose dependent.
Cerebral blood flow effects: Vinpocetine significantly enhanced cerebral blood flow, oxygen utilization, and metabolism in patients with cerebrovascular disorders, without significant alteration in parameters of systemic circulation. In chronic ischemic poststroke patients, vinpocetine infusion increased the regional cerebral blood flow, especially in the thalamus, basal ganglia, and visual cortex of the nonsymptomatic hemisphere, and decreased the flow in the symptomatic hemisphere. A different study found only that the regional cerebral blood flow of the ischemic lesion increased, while the mean cerebral blood flow did not change. In patients with cerebrovascular disorders who received 1mg/kg of vinpocetine infused intravenously over 25 minutes, the maximum increase of cerebral blood flow (25%) was measured at 32 minutes after the start of the infusion. In patients with cerebral circulatory disease, vinpocetine (5mg three times daily for two months) caused a decrease in cerebrovascular resistance. In humans, vinpocetine combined with hypotensive therapy significantly improved blood flow in cerebral vessels, as measured by an elevation of linear blood flow velocity, lowering of peripheral resistance, and increase of content of nitric oxide in blood serum.
Rischke, R. and Krieglstein, J. Effects of vinpocetine on local cerebral blood flow and glucose utilization seven days after forebrain ischemia in the rat. Pharmacology 1990;41(3):153-160.
Rischke, R. and Krieglstein, J. Protective effect of vinpocetine against brain damage caused by ischemia. Jpn J Pharmacol 1991;56(3):349-356.
Nevzorova, V. A., Zakharchuk, N. V., and Plotnikova, I. V. [The state of cerebral blood flow in hypertensive crises and possibilities of its correction]. Kardiologiia. 2007;47(12):20-23
Vaizova, O. E., Vengerovskii, A. I., and Alifirova, V. M. [An effect of vinpocetine (cavinton) on endothelium function in patients with chronic cerebral ischemia]. Zh.Nevrol.Psikhiatr.Im S S Korsakova 2006;Suppl 16:46-50.
Bagoly, E., Feher, G., and Szapary, L. [The role of vinpocetine in the treatment of cerebrovascular diseases based in human studies]. Orv.Hetil. 7-22-2007;148(29):1353-1358.
Hadjiev, D. Asymptomatic ischemic cerebrovascular disorders and neuroprotection with vinpocetine. Ideggyogy.Sz 5-20-2003;56(5-6):166-172.
Bonoczk, P., Panczel, G., and Nagy, Z. Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study. Eur.J.Ultrasound 2002;15(1-2):85-91.
Tamaki N, Kusunoki T, Matsumoto S. The effect of vinpocetine on cerebral blood flow in patients with cerebrovascular disorders. Ther Hung 1985;33:13-21
Mechanism of Action:
General: Selenium is a metallic substance that is available in a variety of chemical compounds. Often selenium is attached to an organic molecule as in selenocysteine, selenomethionine, and kappa-selenocarrageenan. In broccoli, garlic, onions, and other selenium-accumulating plants it is found as Se-methylselenocysteine or selenocystathionine. In dietary supplements selenium is commonly provided as selenomethionine or in a selenite or selenate salt form. Often selenium is given as selenized yeast, which is common brewer's yeast that has been grown in selenium-rich media. After ingestion as a selenate salt, selenite salt, or as one of the organic forms, selenium must be reduced or metabolized to form hydrogen selenide, an important intermediary form. Selenide is essential for the activity of selenoproteins, such as the glutathione peroxidase enzyme (GSH-Px). The primary organic forms of selenium are the amino acid-based selenocysteine and selenomethionine. Selenomethionine is incorporated directly into proteins, because RNA does not differentiate it from methionine. Selenomethionine serves as a storage form, releasing selenium as the proteins containing it are catabolized.
Antiaging effects: In vitro and in vivo research show that zinc is important for immune efficiency (both innate and adaptive), metabolic homeostasis (energy utilization and hormone turnover), and antioxidant activity (SOD enzyme). Selenium provokes zinc release by metallothioneins (MT), via reduction of glutathione peroxidase. Selenium in combination with other antioxidant micronutrients (lycopene, lutein, beta-carotene, alpha-tocopherol) has been shown to increase skin density and thickness in humans; however, the mechanism of action for this effect is unclear.
Anti-inflammatory effects: Both n vitro and in vivo experiments have shown that inhibition of the complement-neutrophil-reactive oxygen (ROS) activation feedback (CNAF) mechanism with sodium selenite and vitamin E could decrease reduced reactive oxygen (ROS) production and complement activation. This mechanism may modulate the inflammatory response in a variety of diseases, including vasculitis of the skin, lung, and liver.
Antineoplastic effects: Dietary selenium may be associated with lower rates of some forms of cancer. Selenocysteine is an essential component of thioredoxin reductase, the flavoenzyme that is responsible for the reduction of thioredoxin, a protein highly expressed in some human tumors. Selenium added to the culture medium increases thioredoxin reductase activity, due to an increase in thioredoxin reductase protein, but mostly due to an increase in the specific activity of the enzyme. Recent studies in a variety of model systems have increased the understanding of the anticarcinogenic mechanisms of selenium compounds. These include effects on gene expression, DNA damage and repair, signaling pathways, regulation of cell cycle and apoptosis, metastasis, and angiogenesis. These effects would appear to be related to the production of reactive oxygen species produced by the redox cycling, modification of protein-thiols, and methionine mimicry. Selenium may stimulate autophagy vacuolization, which may be either protumorigenic or antitumorigenic. Three principal selenium metabolites appear to execute these effects: hydrogen selenide, methylselenol, and selenomethionine.
Possible mechanisms of chemopreventive activity of selenium include a restoration of immune response. The results from studies in mice inoculated with SQCC cells expressing the receptor for interleukin-2 (IL-2) and supplemented with Se (2.00ppm) indicated that Se significantly retards the clinical appearance of tumors.
The group of genes significantly altered by selenium administration for potential chemopreventive effects includes cyclin D1, cdk5, cdk4, cdk2, cdc25A, and GADD 153. Selenium induces apoptosis by producing superoxide that activates p53.
Selenium may have effects on DNA methylation, resulting in chemoprotective effects,
Most potent chemopreventive effects have been attributed to compounds in which the Se moiety is methylated. These compounds are able to induce phase 2 enzymes, which are involved in the cellular defense system that is regulated by the Nrf2 transcription factor. Selenoproteins best studied in cancer development are members of the glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) family. In various cancer cells and tissues, GPx2, and/or TrxR1 are upregulated. Interestingly, both enzymes are targets of Nrf2. An enhanced expression of these enzymes may represent a mechanism to counteract carcinogenic pathways. They may, however, also provide a selective advantage for pre-existing tumor cells in guaranteeing survival and continuous proliferation.
In human research, selenium supplementation increased thrombocyte glutathione peroxidase (GPX) in women only, whereas no effects on phase 1 genes in leukocytes (GPX1), NAD(P)H:quinone oxidoreductase (NQO1), or aryl hydrocarbon receptor repressor (AhRR) gene expression were found. Furthermore, a significant downregulation of the expression of some phase 2 genes (GCLC, Fra1) was observed following Se supplementation, which may increase the risk of cancer.
Antioxidant effects: Selenium serves as a cofactor for glutathione peroxidase, an enzyme of the antioxidant defense system. Glutathione peroxidases (EC 188.8.131.52 and EC 184.108.40.206) catalyze the reduction of H(2)O(2) or organic hydroperoxides to water or corresponding alcohols using reduced glutathione. Selenium-containing glutathione peroxidase has been shown to catalyze peroxynitrite reduction, which may play a role in decreasing the incidence of disease, but its role in vivo is still a matter of debate.
Redox-protective peroxidases in the thyroid are peroxiredoxins, glutathione peroxidases, and catalase. Glutathione peroxidases are selenoenzymes, whereas selenium-independent peroxiredoxins are functionally linked to the selenoenzymes of the thioredoxin reductase family through their thioredoxin cofactors. Thus, selenium directly and indirectly affects protective enzymes in the thyroid, a link that has been supported by animal experiments and clinical observations.
Studies have shown that selenium supplementation for four weeks (150 mcg daily) did not have an effect on body antioxidative status (plasma alpha-tocopherol, retinol, uric acid, and whole blood glutathione). Selenium, when taken in combination with zinc, vitamin A, beta-carotene, vitamin E, and L-cysteine, did not show any pro-oxidant activity, although selenium may play an important role in the balance of antioxidant-pro-oxidant levels of cells.
The kidney accumulates the highest level of selenium (Se) in the organism and is the major source of plasma glutathione peroxidase (GSH-Px). Decreased blood Se levels and GSH-Px activity are common in chronic renal failure (CRF) patients. Erythropoietin (EPO) therapy with Se supplementation, but not EPO alone, has been shown to increase whole blood and plasma Se in hemodialysis (HD) patients, and to raise red cell GSH-Px activity, but not plasma GSH-Px activity, plasma superoxide dismutase, and plasma and red cell TBARS.
In human research, Se supplementation induced a 32% increase in blood glutathione (GSH) levels, which coincided with a 26% decrease in protein-bound GSH (bGSH) and a 44% decrease in bGSH:GSH ratios. These changes in GSH and bGSH were highly correlated with changes in plasma selenium concentrations and may reflect a decrease in oxidative stress.
Selenium, in combination with vitamin C, vitamin E, and beta-carotene, significantly diminishes oxidative damage to lipids when it is high initially and is effective in decreasing chromosomal instability in lymphocytes of middle-aged men. There was a significant decrease of malondialdehyde concentration in nonsmokers, while in smokers, the decrease of malondialdehyde concentration was not significant. Antioxidant supplementation did not affect the proportion of lymphocytes with micronuclei or the total number of micronuclei; however, there was a significant positive correlation between the malondialdehyde concentration at the beginning of the supplementation trial and the difference in the number of cells with micronuclei before and after the supplementation. Antioxidant supplementation (selenium, in combination with alpha-lipoic acid, coenzyme Q10, manganese, vitamin C, N-acetyl cysteine, and 400 IU of alpha-tocopherol) did not protect against exercise-induced DNA damage.
In studies in humans, selenium has been shown to inhibit oxidative stress during a second exposure to ultraviolet light .
Animal studies have shown that endotoxin injection results in lipid peroxide formation and membrane injury, causing decreased levels of free radical scavengers or quenchers, and that intracellular selenium levels may participate in the oxidative stress during endotoxemia.
Cardiovascular effects: Selenium is a central determinant of antioxidative glutathione peroxidase 1 (GPx-1) expression and activity. Sodium selenite and Se-methyl-selenocysteine hydrochloride increased GPx-1 protein and activity in coronary artery endothelial cells. Sodium selenite supplementation has been shown to increase glutathione peroxidase 1 (GPx-1) activity in endothelial cells and in coronary artery disease (CAD) patients. In type 2 diabetic patients, activation of NF-kappaB measured in peripheral blood monocytes can be reduced by selenium supplementation, confirming its importance in the prevention of cardiovascular diseases. In studies in animals, a supplement containing taurine, coenzyme Q10, carnitine, thiamine, creatine, vitamin E, vitamin C, and selenium given to cardiomyopathic hamsters during the late stages of the disease markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt, and -dp/dt.
Keshan disease is a cardiomyopathy restricted to the endemic areas of China and seen in residents having an extremely low selenium (Se) status. Prophylactic administration of sodium selenite has been shown to decrease significantly the incidence of acute and subacute cases. In human research, both forms of Se (selenite and organic Se-yeast) were equally effective in raising GSHPx activity, although Se-yeast provided a longer-lasting body pool of Se.
Fertility effects: In human research, dietary selenium supplementation resulted in changes in selenium concentrations in seminal plasma, but not in sperm; furthermore, serum androgen concentrations were unchanged. Serum triiodothyronine decreased and thyroid-stimulating hormone increased in the high-selenium group, suggesting that altered thyroid hormone metabolism may have affected sperm motility.
Hematological effects: In human research, although a diet rich in fish increased bleeding time and reduced serum triglyceride levels, selenium had no such effects. In children with thalassemic disease, selenium levels in red blood cells (RBC) appeared normal; however, GSH-Px activity was increased, and after vitamin E supplementation, these levels decreased. The authors noted that vitamin E and selenium have related functions in the prevention of RBC oxidation.
Hormonal effects: Higher levels of estrogens in females are protective against aging, by upregulating the expression of antioxidant, longevity-related genes, such as that of selenium-dependent glutathione peroxidase (GPx). Selenium is often combined with other macronutrients, and in one study, supplementation of a combination of vitamin E, selenium, vitamin C, and coenzyme-Q10 did not affect serum levels of PSA or hormone levels in patients with hormonally untreated carcinoma of the prostate.
Immune system effects: As a constituent of selenoproteins, selenium is needed for the proper functioning of neutrophils, macrophages, NK cells, T lymphocytes, and other immune mechanisms. Selenomethionine supplementation has been shown to produce transient and acute changes in lymphocyte, granulocyte, and platelet phospholipid-hydroperoxide glutathione peroxidase (GPx4) activity, possibly affecting the normal function of the cell.
Selenium may improve T lymphocyte responsiveness and thereby enhance primary immunity. Selenium may exert modulatory effects on keratinocyte-derived inflammatory cytokines. In human research, selenium supplementation has been shown to increase cytotoxic lymphocyte-mediated tumor cytotoxicity and natural killer cell activity. The authors speculated that these increased activities may have been related to the ability of selenium to enhance the expression of receptors for the growth regulatory lymphokine interleukin-2, and consequently, the rate of cell proliferation and differentiation into cytotoxic cells.
Correlations between plasma selenium concentrations and the numbers of CD4 lymphocytes have been observed in healthy elderly subjects. Also, selenium supplementation can increase proliferative responses to pokeweed mitogens in elderly subjects . An in vitro study has shown that selenium supplementation can influence both cellular and humoral immunity as measured by decreases in EG1 and EG2 epitopes on intracellular eosinophil cationic protein and eosinophil peroxidase, increases in relative numbers of CD3 HLADR+ T lymphocytes, decreases in responses of T lymphocytes to mitogenes PHA and ConcA in a lymphocyte blastogenesis test, decreases in activation of complement via complementary pathways (CP50) and alternate pathway (AP50), and finally, increases in IgG and IgA and decreases in IgE.
Selenium supplementation in corticoid-dependent asthmatics has been shown to affect the expression of adhesion molecules that are crucial in the inflammatory process, including decreases in adhesion molecules on peripheral blood mononuclear cells (PBMCs) (CD11a, CD11b, and CD62L), and decreases in those on cultured human umbilical vein endothelial cells (HUVEC) (VCAM-1, and P- and E-selectins).
Nutritional support effects: In humans with low selenium intake, selenium supplementation significantly altered the retention of radiolabeled Se in the plasma, but not in the erythrocytes or platelets. Supplementation resulted in relatively more isotope being retained in a medium molecular mass protein considered to be albumin, and relatively less in another fraction considered to be selenoprotein P. The authors suggest that supplemental Se was not being used to replete critical pools of Se, and this may have been due to an adaptation to low Se intake.
In patients with end-stage renal disease on hemodialysis, selenium supplementation has been shown to maintain selenium concentrations within normal range and, in fact, could increase plasma selenium levels. Supplementation with a preparation containing selenium and vitamins with antioxidant properties (Protecton Zellaktiv from Smith Kline Naturarznei-Germany) has been shown to increase glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) activities .
Physical endurance effects: The link between selenium supplementation and endurance training adaptations at the mitochondrial level appear to be contradictory. One study has shown that selenium supplementation failed to show any effects on endurance training adaptations, as indicated by a lack of effect on total oxygen uptake during a running test, mitochondrial activity of succinate dehydrogenase (SDH) and cytochrome c oxidase (Cyt Ox), and myosin heavy-chain (MHC) expression in muscle fibers. However, another study suggests that selenium supplementation may dampen mitochondria changes during both chronic and acute exercise, although the mechanism behind this action in unclear.
Platelet aggregation effects: In human research, selenium supplementation increased platelet GSH-Px activity; however, no effects were observed on platelet aggregation.
Protection against toxicity: Zinc and selenium have been shown to exert protective effects against mercury toxicity, most likely mediated by induction of the metal-binding proteins metallothionein and selenoprotein P. Selenium also alters carcinogen metabolism, resulting in the production of inactive compounds.
Skin effects: Selenium supplementation increased C-reactive protein (CRP) and soluble tumor necrosis factor-alpha receptor type 1 (sTNF-R1) in patients with psoriasis receiving narrow-band ultraviolet B therapy and selenomethionine supplementation. The authors concluded that supplementation with selenomethionine is inefficacious as adjuvant therapy in patients with psoriasis.
Thyroid effects: Thyroid function depends on the essential trace mineral selenium, which is at the active center of the iodothyronine deiodinase enzymes that catalyze the conversion of the prohormone thyroxine (T(4)) to the active form of thyroid hormone, triiodothyronine (T(3)). However, no evidence of any effect of selenium supplementation on thyroid hormone function (T(4)-to-T(3) conversion) was observed in elderly volunteers or in healthy men.
Vascular effects: In animal research, selenoprotein P binds to endothelial cells in the rat, and plasma levels of the protein correlate with prevention of diquat-induced lipid peroxidation and hepatic endothelial cell injury.
PharmacokineticsAbsorption: Diet is the major source of selenium, and approximately 80% of dietary Se is absorbed, depending on the type of food consumed. Selenium compounds in yeast are available for absorption and further metabolism . L-selenomethionine has been shown to be absorbed more efficiently than parselenium. One pharmacokinetic study suggests that selenomethionine is rapidly absorbed. Volunteers taking one dose of selenomethionine 200 mcg showed increased serum selenium levels at 2 hours, peak serum selenium levels at 4 hours, and abundant amounts of selenium in the serum 24-hours post consumption.
Bioavailability: Selenium bioavailability varies according to the Se source and nutritional status of the subject, being significantly higher for organic forms of Se. Different forms of organic selenium elicit widely different responses when administered to a relatively selenium-replete population, and the explanation for this must be sought at the metabolic level. Se-yeast is capable of increasing the activity of the selenoenzymes, and its bioavailability has been found to be higher than that of inorganic Se sources. Seleno-methionine (SeMet) is a naturally occurring toxic amino acid, but at the same time represents the major nutritional source of selenium for higher animals and humans and had nearly twice the bioavailability of selenium as selenite. The ability of selenomethionine (SeMet) to be incorporated into the body proteins in place of methionine furthermore provides a means of reversible Se storage in organs and tissues. This property is not shared by any other naturally occurring selenoamino acids and thus could be associated with a specific physiological function of SeMet.
Distribution: The kidney accumulates the highest level of selenium (Se) in the organism and is the major source of plasma glutathione peroxidase (GSH-Px). It has been proposed that dietary bioactive compounds, such as selenium, must pass down the gastrointestinal tract, cross the intestinal barrier, reach the blood circulation, and then be distributed to the different tissues of the body, including the skin, which allows for selenium to be metabolized and presented to the entire tissue, potentially in an active form.
These observations and those of gel filtration studies of erythrocytes and plasma proteins reported elsewhere are consistent with the incorporation of Se from selenomethionine into a general tissue protein pool while selenate is directly available for GSHPx synthesis, and explain the poorer correlation between Se and GSHPx in individuals with higher Se status. However, selenate raised platelet GSHPx activities to a greater extent than did selenomethionine suggesting some other effect of selenate on platelets that needs further investigation. A response of GSHPx activity in New Zealand subjects indicates that their dietary Se intake is insufficient to meet recommended intakes based on the criterion of saturation of GSHPx activity, and could reflect a marginal Se status. The level of blood Se necessary for saturation of GSHPx of about 100ng of Se/mL of whole blood confirms observations in earlier studies.
Metabolism: The metabolism of selenium by the brain differs from other organs in that at times of deficiency, the brain retains selenium to a greater extent.
Excretion: Plasma and urinary Se have been shown to be the most sensitive indices to Se exposure. In human research, Se in plasma has been shown to increase steadily, whereas urinary Se reached a plateau between 30 and 60 days following exposure. By contrast, erythrocyte Se only changed after 45 days. Enzyme in plasma and erythrocytes did not respond, whereas platelet GSH Px did. The plateau of activity that was observed after 15 days for plasma Se in the range 1.40-1.50mcM/L could mean that the Se status is insufficient for an optimal function of GSH Px, and implies that dietary intake in Belgium (less than 50-60 mcg of Se daily) is not adequate. Organic Se forms (Se-yeast, selenomethionine, and food Se) increased blood Se more concentration rapidly and to a greater extent than inorganic forms (selenite and selenate). However, no significant difference in the response of both plasma and erythrocyte GSH-Px activity could be observed.
In human research, supplementation with high-selenium yeast, the form used in most supplements (300 mcg daily, 3.8mcM daily) for 48 weeks more than doubled urinary selenium excretion, from 69 to 160 mcg daily (876 to 2,032nM daily). Urinary excretion was correlated with recent selenium intake. After 48 weeks of supplementation, plasma selenium was increased 60%, from 142 to 228 mcg/L (1.8 to 2.9mcM/L) and erythrocyte selenium was approximately doubled, from 261 to 524 mcg/L (3.3 to 6.6mcM/L). Selenium concentrations increased more modestly in hair (56%) and platelets (42%). Platelets were the only blood component in which glutathione peroxidase activity was significantly related to selenium content. Selenium levels decreased rapidly after the end of supplementation, and there were no significant differences in selenium status indicators between groups by week 96. The absorption, distribution, and excretion of selenium from high-Se yeast were similar to selenium in foods.
Urinary selenium excretion has been shown to be greater after selenomethionine than after selenite, with excretion after yeast being intermediate and not significantly different from either of the other two. Selenoprotein P turns over rapidly in rat plasma, with the consequence that approximately 25% of the amount of whole-body selenium passes through it each day. In human research, following supplementation with Se-rich bread (providing 100, 200, and 300 mcg of Se daily) for six weeks, about 50% of the Se intake was excreted in the urine by week 6, compared with 67% before the intervention started.
Clinical research shows that taking selenium 200 mcg daily in combination with levothyroxine significantly reduces thyroid peroxidase antibodies by about 6% to 30% more than placebo in adult patients with thyroiditis after 3-12 months of treatment. Selenium also seems to improve measures of quality of life such as feelings of well-being and mood.
Duntas, L. H. Environmental factors and autoimmune thyroiditis. Nat.Clin.Pract Endocrinol.Metab 2008;4(8):454-460.
Hawkes, W. C., Keim, N. L., Diane, Richter B., Gustafson, M. B., Gale, B., Mackey, B. E., and Bonnel, E. L. High-selenium yeast supplementation in free-living North American men: no effect on thyroid hormone metabolism or body composition. J Trace Elem.Med Biol. 2008;22(2):131-142
Negro, R., Greco, G., Mangieri, T., Pezzarossa, A., Dazzi, D., and Hassan, H. The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies. J Clin Endocrinol.Metab 2007;92(4):1263-1268.
Toulis KA, Anastasilakis AD, Tzellos TG, et al. Selenium supplementation in the treatment of Hashimoto's thyroiditis: A systematic review and a meta-analysis. Thyroid 2010;20:1163-73.
Mazokopakis EE, Papadakis JA, Papadomanolaki MG, et al. Effects of 12 months treatment with L-selenomethionine on serum anti-TPO levels in patients with Hashimoto's thyroiditis. Thyroid 2007;17:609-12.
Turker O, Kumanlioglu K, Karapolat I, Dogan I. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. J Endocrinol 2006;190:151-6.
Rayman MP, Thompson AJ, Bekaert B, et al. Randomized controlled trial of the effect of selenium supplementation on thyroid function in the elderly in the United Kingdom. Am J Clin Nutr 2008;87:370-8.
Duntas LH, Mantzou E, Koutras DA. Effects of a six month treatment with selenomethionine in patients with autoimmune throiditis. Eur J Endocrinol 2003;148:389-93.
Gartner R, Gasinier BC. Selenium in the treatment of autoimmune thyroiditis. Biofactors 2003;19:165-70.
What is Changing:
It seems that the Obama administration has really been pushing hard to have drug control across the country, illegal and legal. I mean we all know that those pesky Hyrdrocodones and Percocets and Oxys are really killing folks, and to be fair and balanced, they are with abusers, but so are a lot of other drugs. Make no mistake, these drugs are beyond dangerous and have killed people, created massive addiction, but saved a lot of people from dying from pain when used correctlyy. I for one do not write schedule II drugs, but I see the impact of these meds everyday.
There is however a very scary separate point that is being overlooked here. In the last two years, some of the most powerful prescription drugs have left as a schedule III drug status (most codeine based), which could be given by all doctors, even midlevel provides like NPs with a DEA number and is now have gone to level II categorization, which is out of reach of most providers because schedule two drugs have a whole other set of rules as a controlled substance and most will not prescribe them. Many codeine based products got pulled down to schedule two from schedule three. Various administrators thought that having it moved to a cat II drug would really change the massive pain drug addiction epidemic. Yeah.....lets all go celebrate, not as many drug users on the street -- huh. NOT SO FAST, there is still going to be drug users, just less getting meds from controlled sources and the lack of them in the office has the potential to push these people to the streets, where there is no quality assurance on the product itself. Someone with real pain might easily turn to heroin now, and it is showing up, story after story. Now doctors are having to turn to other medications to help their desperate patients, some not designed for pain and, and some are not FDA approved drugs for various types of pain and then there is the topical pain cream debacle that is costing insurance companies for the time being, billions because they are compounded with multiple ingredients. Ten grand for a tube of cream that has some muscle relaxers in it is a joke. Sorry!
Something to now consider:
What we have left is drugs like tramadol for example. This is NOT a drug typically used as an acute pain medication. It is made for fibro patients with things like associated depression and seasonal affective disorder and is a compilation of medications that work on different neurological pathways for a certain condition. Some of these medications may not be good or work well for a patient that just had a small procedure and really hurt afterwards. It has three drugs, an SSRI, an SNRI and a synthetic opiate. Most people think that this drug is no big deal, until they have to come off of it after long use.
The average hydrocodone user comes off of it and goes into withdrawal and about a week later, the hell is over, because it is a ONE substance medications. With drugs like Tramadol, you have to take more to get the same effect so it is not as strong, so you get used to the transmitter changes from usage, the opiate still changes things and when you ever come off, multiple withdrawals can occur upon is stoppage if usage had a long duration, at the same time. This patient has the potential for drug discontinuation syndrome from losing the serotonin (which gives them the whirlies) , loss of attention span from the loss of the SNRI and then narcotic withdrawal from the synthetic Mu receptor manipulator for pain, which will give them flulike symptoms. It is a three in one withdrawal and some people are NEVER able to escape and it can be terrible. Imagine getting this because you had to take it because another more simple drug was not available that you could have taken for a few days while you were going through your pain.
In the end, drugs are drugs. When the decision is made to use them, there is almost always a consequence. The final example left is Tylenol with codeine which is left as a schedule III drug also. Again, just like Tramadol, another good drug, but when used long term, the tylenol will have the potential to do super damage to your liver, alter biotransformation and detoxification capacity is altered, and you still have the pain medication in it so you likely WILL NOT biotransform the med you are taking very well. Why is this still ok? It is not stigmatized because it is not as abused, but the physiological implications from multiple drugs in one pill is overlooked which can be more dangerous. Some people start taking WAY to much of this to compensate for their pain and the Acetaminophen can do SERIOUS harm. Debatably more harm than the codeine in it.
So I ask the question, do I want a drug that works, and easier to get off of at times, or do I want a weaker drug that creates less of a desired effect and has potentially way more issues when coming off or has a greater impact on normal physiology? Do we want to just get rid of medications that have been stigmatized as abusive, or do we need to look at all of them that we know actually causes the most physiological damage and make them classified as more dangerous due to side effects, not just from their misuse profile. I believe the classification systems or categories of medications should be based off of the physiological complications that are possible, not just the affinity for misuse. These are just thoughts and there are lots of angles to this. One to ponder over for sure.
I have to start out by saying that most folks get over a concussion or a mild traumatic brain injury. They seem ok at a certain point, and then everyone moves on. We also know that about sixth grade, athletes are a bit more prone for injuries it seems and when it comes to concussion, there is really no accepted gold standard of treatment. There are only the thoughts of individual doctors or groups, but no really solidified best practice measures that are researched by multiple groups, various angles and given a consensus of agreement. I saw it today during a very high profile meeting, you get a group of brain researchers together and virtually everyone has a different opinion. The giant question is, who is right, and how does the outcome of real research and good data impact playing a lot of contact sports?
You have all seen it, mainly on Sunday with the NFL. We should make rules, make guidelines regarding how certain sports are played, and the folks that look at these injuries in younger people have to be able to do more than a levels of consciousness exam. I'm sorry but the quality of exams done are at times terrible and just because you can comment or have a degree that allows you to, does not mean you SHOULD comment. I HAVE SEEN neuro exams done by multiple pediatricians and even neurologists and other clinicians that are board certified practitioners by various organizations. These practitioners are very good with certain conditions, but when you put them in a neurological environment that relates to subtle head injuries and forced to determine present time function, neurological fatigue, fragility and possible inevitable complications, there is typically incomplete information to make such determinations. We are finding that at times, a basic exam is not enough and sometimes instrumentation has to be used to measure true function and make a safe determination.
Some of these aforementioned practitioners are the gate keepers of return to play and they report the data that drives policy and sets the "tone" of the overall problem and even the tone on what research questions need to be answered-----thus we have the articles and papers that you see with a myriad of opinions. Many generalists will make neurological decisions based upon what the patient is saying (subjective) and not based upon adequate exam (objective) data; so MANY cases get marginalized. This sets the patient up for possible glial cell ramification development, degeneration that will not show up for multiple years or worse. By the time the issue becomes clinical, it is way down the road. I have seriously questioned many practitioners capacity to determine true level of function or return to play capacity with what they did during their patient encounter to make such decisions. No cerebellar exam, no ocular movement exam, no cranial nerves, no instrumentation, no cognitive testing, no vestibular examination or common tests such as an IMPACT, and then when you ask them about the cranial nerves for example, they cannot even name them, or if you ask them the function of a particular region like the cerebellum, they cannot tell you about it, how to diagnose a lesion there or any form of stimulation that might change or enhance the Hebbian process of plasticity there.
I hate to be the horn tooter, but do not let credentials be a cover that suggests all general practitioners either adult or pediatric are doing adequate neurological exams, or that they even understand the nervous system or the exam that the do. This can compromise patients, screw up reliable gathering of data and more. We have seen that indeed, most head injuries in youth sports do heal, but there are genotypes, those with underlying co-morbidities and multiplicity of trauma that changes the rules. It is a small percentage, but many patients that are told they are ok, have very microscopic symptoms that are missed which later point to very serious and blooming compromise and they are returned to play or an adult back to work or even back into schoolwork way to early, and then they are set up for another episode that could really allow them to have a neurological trigger occur that can allow physiology to spiral in the direction of neurodegeneration or ongoing symptoms.
This is the basis of the CTE epidemic in the NFL. Time of playing plus repetitive head contact equals microglial ramification, neurological inflammation and brain compromise that keeps going, even when contact stops. In the end I would say this and it is clear......PARENTS, if your child is using their head as a weapon in any sport or it is used as part of the sport......be concerned, be aware and be cautious and when your kid is injured, think about a 2 to 4 week break, even if they have ZERO symptoms and know that most should be better by at least three months, or something is going on that needs to be determined. The beast of head injury is the physiological deception that you cannot see, and you may get better in a few days, but the silent fire that is sparked from aberrant neurological physiology may show up so much later, that connecting the possible future symptoms may be so far from the head injury that the connections is NOT made.
Sometimes the patient does not even include the head injury in their past medical history down the road. This is the danger and can lead to false stats and create the sense of false security and the NOTION, that parents are making this overblown! We are talking about the brain folks!!!!! Don't screw yours up, because if you do, life is no longer any fun! It may not be tomorrow or right after the head injury, but when depression, insomnia, forgetfulness or something else creeps in out of nowhere ten or so years later, do NOT be surprised. We have to research more to know who is really at risk and how do we identify them? How do we truly determine prognosis with treatment? Which treatments work, which ones do not? What technology coming out is inspiring and which ones are crap which is being made merely by exploiting the fears of the public over this topic. There are a lot of questions. What I can say is this, until we know more, watch out and keep your head safe, don't get into hurries to return to activity, see a qualified practitioner with experience, not just someone with a degree and see practitioners that can offer treatment