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Dihydrotestosterone – Wikipedia

Nov 16th, 2018
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This article is about dihydrotestosterone as a hormone. For its use as a medication, see Androstanolone.This article is about 5-dihydrotestosterone, an androgen. For the inactive 5 isomer, see 5-Dihydrotestosterone.DihydrotestosteroneNamesIUPAC name


DHT; 5-Dihydrotestosterone; 5-DHT; Androstanolone; Stanolone; 5-Androstan-17-ol-3-one


Dihydrotestosterone (DHT, 5-dihydrotestosterone, 5-DHT, androstanolone or stanolone) is an endogenous androgen sex steroid and hormone. The enzyme 5-reductase catalyzes the formation of DHT from testosterone in certain tissues including the prostate gland, seminal vesicles, epididymides, skin, hair follicles, liver, and brain. This enzyme mediates reduction of the C4-5 double bond of testosterone. Relative to testosterone, DHT is considerably more potent as an agonist of the androgen receptor (AR).

In addition to its role as a natural hormone, DHT has been used as a medication, for instance in the treatment of low testosterone levels in men; for information on DHT as a medication, see the androstanolone article.

DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body, and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from the less potent testosterone by the enzyme 5-reductase in select tissues, and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles.[2]

DHT signals mainly in an intracrine and paracrine manner in the tissues in which it is produced, playing only a minor role, if any, as a circulating endocrine hormone.[3][4][5] Circulating levels of DHT are 1/10th and 1/20th those of testosterone in terms of total and free concentrations, respectively,[6] whereas local DHT levels may be up to 10times those of testosterone in tissues with high 5-reductase expression such as the prostate gland.[7] In addition, unlike testosterone, DHT is inactivated by 3-hydroxysteroid dehydrogenase (3-HSD) into the very weak androgen 3-androstanediol in various tissues such as muscle, adipose, and liver among others,[5][8][9] and in relation to this, DHT has been reported to be a very poor anabolic agent when administered exogenously as a medication.[10]

In addition to normal biological functions, DHT also plays an important causative role in a number of androgen-dependent conditions including hair conditions like hirsutism (excessive facial/body hair growth) and pattern hair loss (androgenic alopecia or pattern baldness) and prostate diseases such as benign prostatic hyperplasia (BPH) and prostate cancer.[2] 5-Reductase inhibitors, which prevent DHT synthesis, are effective in the prevention and treatment of these conditions.[13][14][15][16]

Metabolites of DHT have been found to act as neurosteroids with their own AR-independent biological activity.[17] 3-Androstanediol is a potent positive allosteric modulator of the GABAA receptor, while 3-androstanediol is a potent and selective agonist of the estrogen receptor (ER) subtype ER.[17] These metabolites may play important roles in the central effects of DHT and by extension testosterone, including their antidepressant, anxiolytic, rewarding/hedonic, anti-stress, and pro-cognitive effects.[17][18]

Much of the biological role of DHT has been elucidated in studies of individuals with congenital 5-reductase type II deficiency, an intersex condition caused by a loss-of-function mutation in the gene encoding 5-reductase type II, the major enzyme responsible for the production of DHT in the body.[13][19][2] It is characterized by a defective and non-functional 5-reductase type II enzyme and a partial but majority loss of DHT production in the body.[13][19] In the condition, circulating testosterone levels are within or slightly above the normal male range, but DHT levels are low (around 30% of normal),[20][bettersourceneeded] and the ratio of circulating testosterone to DHT is greatly elevated (at about 3.5 to 5times higher than normal).[13]

Genetic males (46,XY) with 5-reductase type II deficiency are born with undervirilization including pseudohermaphroditism (ambiguous genitalia), pseudovaginal perineoscrotal hypospadias, and usually undescended testes. Their external genitalia are female-like, with micropenis (a small, clitoris-like phallus), a partially unfused, labia-like scrotum, and a blind-ending, shallow vaginal pouch.[13] Due to their lack of conspicuous male genitalia, genetic males with the condition are typically raised as girls.[19] At the time of puberty however, they develop striking phenotypically masculine secondary sexual characteristics including partial virilization of the genitals (enlargement of the phallus into a near-functional penis and descent of the testes), voice deepening, typical male musculoskeletal development,[12] and no menstruation, breast development, or other signs of feminization that occur during female puberty.[13][19][2] In addition, normal libido and spontaneous erections develop,[21] they usually show a sexual preference for females, and almost all develop a male gender identity.[13][22]

Nonetheless, males with 5-reductase type II deficiency exhibit signs of continued undervirilization in a number of domains. Facial hair was absent or sparse in a relatively large group of Dominican males with the condition. However, more facial hair has been observed in patients with the disorder from other parts of the world, although facial hair was still reduced relative to that of other men in the same communities. The divergent findings may reflect racial differences in androgen-dependent hair growth. A female pattern of androgenic hair growth, with terminal hair largely restricted to the axillae and lower pubic triangle, is observed in males with the condition. No temporal recession of the hairline or androgenic alopecia (pattern hair loss or baldness) has been observed in any of the cases of 5-reductase type II deficiency that have been reported, whereas this is normally seen to some degree in almost all Caucasian males.[13] Individuals with 5-reductase type II deficiency were initially reported to have no incidence of acne,[8][2] but subsequent research indicated normal sebum secretion and acne incidence.[12]

In genetic males with 5-reductase type II deficiency, the prostate gland is rudimentary or absent, and if present, remains small, underdeveloped, and unpalpable throughout life.[8][4] In addition, neither BPH nor prostate cancer have been reported in these individuals.[14] Genetic males with the condition generally show oligozoospermia due to undescended testes, but spermatogenesis is reported to be normal in those with testes that have descended, and there are case instances of men with the condition successfully fathering children.[21][23]

Unlike males, genetic females with 5-reductase type II deficiency are phenotypically normal. However, similarly to genetic males with the condition, they show reduced body hair growth, including an absence of hair on the arms and legs, slightly decreased axillary hair, and moderately decreased pubic hair.[24][21] On the other hand, sebum production is normal.[24][25] This is in accordance with the fact that sebum secretion appears to be entirely under the control of 5-reductase type I.[25]

5-Reductase inhibitors like finasteride and dutasteride inhibit 5-reductase type II and/or other isoforms and are able to decrease circulating DHT levels by 65 to 98% depending on the 5-reductase inhibitor in question.[26][27][28][20] As such, similarly to the case of 5-reductase type II deficiency, they provide useful insights in the elucidation of the biological functions of DHT.[29] 5-Reductase inhibitors were developed and are used primarily for the treatment of BPH. The drugs are able to significantly reduce the size of the prostate gland and to alleviate symptoms of the condition.[14][30] Long-term treatment with 5-reductase inhibitors is also able to significantly reduce the overall risk of prostate cancer, although a simultaneous small increase in the risk of certain high-grade tumors has been observed.[15] In addition to prostate diseases, 5-reductase inhibitors have subsequently been developed and introduced for the treatment of pattern hair loss in men.[31] They are able to prevent further progression of hair loss in most men with the condition and to produce some recovery of hair in about two-thirds of men.[13] 5-Reductase inhibitors seem to be less effective for pattern hair loss in women on the other hand, although they do still show some effectiveness.[32] Aside from pattern hair loss, the drugs are also useful in the treatment of hirsutism and can greatly reduce facial and body hair growth in women with the condition.[33][16]

5-Reductase inhibitors are overall well-tolerated and show a low incidence of adverse effects.[34] Sexual dysfunction, including erectile dysfunction, loss of libido, and reduced ejaculate volume, may occur in 3.4 to 15.8% of men treated with finasteride or dutasteride.[34][35] A small increase in the risk of affective symptoms including depression, anxiety, and self-harm may be seen.[36][37][38] Both the sexual dysfunction and affective symptoms may be due partially or fully to prevention of the synthesis of neurosteroids like allopregnanolone rather necessarily than due to inhibition of DHT production.[36] A very small risk of gynecomastia has been associated with 5-reductase inhibitors (1.2 to 3.5%).[34][39] Based on reports of 5-reductase type II deficiency in males and the effectiveness of 5-reductase inhibitors for hirsutism in women, reduced body and/or facial hair growth is a likely potential side effect of these drugs in men.[13][16] There are very few studies evaluating the side effects of 5-reductase inhibitors in women. However, due to the known role of DHT in male sexual differentiation, 5-reductase inhibitors may cause birth defects such as ambiguous genitalia in the male fetuses of pregnant women. As such, they are not used in women during pregnancy.[34]

MK-386 is a selective 5-reductase type I inhibitor which was never marketed.[40] Whereas 5-reductase type II inhibitors achieve much higher reductions in circulating DHT production, MK-386 decreases circulating DHT levels by 20 to 30%.[41] Conversely, it was found to decrease sebum DHT levels by 55% in men versus a modest reduction of only 15% for finasteride.[42][43] However, MK-386 failed to show significant effectiveness in a subsequent clinical study for the treatment of acne.[44]

DHT is a potent agonist of the AR, and is in fact the most potent known endogenous ligand of the receptor. It has an affinity (Kd) of 0.25 to 0.5nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0nM)[45] and 1530times higher than that of adrenal androgens.[46] In addition, the dissociation rate of DHT from the AR is 5-fold slower than that of testosterone.[47] The EC50 of DHT for activation of the AR is 0.13nM, which is about 5-fold stronger than that of testosterone (EC50 = 0.66nM).[48] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[45]

The terminal half-life of DHT in the body (53minutes) is longer than that of testosterone (34minutes), and this may account for some of the difference in their potency.[49] A study of transdermal DHT and testosterone treatment reported terminal half-lives of 2.83hours and 1.29hours, respectively.[50]

Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase into an estrogen like estradiol. Therefore, it is frequently used in research settings to distinguish between the effects of testosterone caused by binding to the AR and those caused by testosterone’s conversion to estradiol and subsequent binding to and activation of ERs.[51] Although DHT cannot be aromatized, it is still transformed into metabolites with significant ER affinity and activity. These are 3-androstanediol and 3-androstanediol, which are predominant agonists of the ER.[17]

DHT is synthesized irreversibly from testosterone by the enzyme 5-reductase.[8][13] This occurs in various tissues including the genitals (penis, scrotum, clitoris, labia majora),[53] prostate gland, skin, hair follicles, liver, and brain.[8] Around 5 to 7% of testosterone undergoes 5-reduction into DHT,[54][55] and approximately 200 to 300g of DHT is synthesized in the body per day. Most DHT is produced in peripheral tissues like the skin and liver, whereas most circulating DHT originates specifically from the liver. The testes and prostate gland contribute relatively little to concentrations of DHT in circulation.[8]

There are two major isoforms of 5-reductase, SRD5A1 (type I) and SRD5A2 (type II), with the latter being the most biologically important isoenzyme.[8] There is also third 5-reductase: SRD5A3.[56] SRD5A2 is most highly expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles,[57][58] and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys. SRD5A1 is most highly expressed in non-genital skin/hair follicles, the liver, and certain brain areas, while lower levels are present in the prostate, epididymides, seminal vesicles, genital skin, testes, adrenal glands, and kidneys.[8] In the skin, 5-reductase is expressed in sebaceous glands, sweat glands, epidermal cells, and hair follicles.[57][58] Both isoenzymes are expressed in scalp hair follicles,[59] although SRD5A2 predominates in these cells.[58] The SRD5A2 subtype is the almost exclusive isoform expressed in the prostate gland.[60][20]

The plasma protein binding of DHT is more than 99%. In men, approximately 0.88% of DHT is unbound and hence free, while in premenopausal women, about 0.470.48% is unbound. In men, DHT is bound 49.7% to sex hormone-binding globulin (SHBG), 39.2% to albumin, and 0.22% to corticosteroid-binding globulin (CBG), while in premenopausal women, DHT is bound 78.178.4% to SHBG, 21.021.3% to albumin, and 0.12% to CBG. In late pregnancy, only 0.07% of DHT is unbound in women; 97.8% is bound to SHBG while 2.15% is bound to albumin and 0.04% is bound to CBG.[61][62] DHT has higher affinity for SHBG than does testosterone, estradiol, or any other steroid hormone.[63][62]

DHT is inactivated in the liver and extrahepatic tissues like the skin into 3-androstanediol and 3-androstanediol by the enzymes 3-hydroxysteroid dehydrogenase and 3-hydroxysteroid dehydrogenase, respectively.[8][64] These metabolites are in turn converted, respectively, into androsterone and epiandrosterone, then conjugated (via glucuronidation and/or sulfation), released into circulation, and excreted in urine.[8]

Unlike testosterone, DHT cannot be aromatized into an estrogen like estradiol, and for this reason, has no propensity for estrogenic effects.[65]

DHT is excreted in the urine as metabolites, such as conjugates of 3-androstanediol and androsterone.[66][8]

Serum DHT levels are about 10% of those of testosterone, but levels in the prostate gland are 5- to 10-fold higher than those of testosterone due to a more than 90% conversion of testosterone into DHT by locally expressed 5-reductase.[7] For this reason, and in addition to the fact that DHT is much more potent as an AR agonist than is testosterone,[45] DHT is considered to be the major androgen of the prostate gland.[7]

DHT is available in pharmaceutical formulations for medical use as an androgen or anabolicandrogenic steroid (AAS).[67] It is used mainly in the treatment of male hypogonadism.[68] When used as a medication, dihydrotestosterone is referred to as androstanolone (INN) or as stanolone (BAN),[67][69][70] and is sold under brand names such as Andractim among others.[67][69][70][68][71] The availability of pharmaceutical DHT is limited; it is not available in the United States or Canada,[72][73] but is available in certain European countries.[70][68] The available formulations of DHT include buccal or sublingual tablets, topical gels, and, as esters in oil, injectables like androstanolone propionate and androstanolone valerate.[67][68][71]

DHT, also known as 5-androstan-17-ol-3-one, is a naturally occurring androstane steroid with a ketone group at the C3 position and a hydroxyl group at the C17 position. It is the derivative of testosterone in which the double bond between the C4 and C5 positions has been reduced or hydrogenated.

DHT was first synthesized by Adolf Butenandt and his colleagues in 1935.[74][75] It was prepared via hydrogenation of testosterone,[75] which had been discovered earlier that year.[76] DHT was introduced for medical use as an AAS in 1953, and was noted to be more potent than testosterone but with reduced androgenicity.[77][78][79] It was not elucidated to be an endogenous substance until 1956, when it was shown to be formed from testosterone in rat liver homogenates.[75][80] In addition, the biological importance of DHT was not realized until the early 1960s, when it was found to be produced by 5-reductase from circulating testosterone in target tissues like the prostate gland and seminal vesicles and was found to be more potent than testosterone in bioassays.[81][82][83][84] The biological functions of DHT in humans became much more clearly defined upon the discovery and characterization of 5-reductase type II deficiency in 1974.[14] DHT was the last major sex hormone, the others being testosterone, estradiol, and progesterone, to be discovered, and is unique in that it is the only major sex hormone that functions principally as an intracrine and paracrine hormone rather than as an endocrine hormone.[85]

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Dihydrotestosterone – Wikipedia



Zinc – Scientific Review on Usage, Dosage, Side Effects …

Nov 16th, 2018
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Zinc is an essential mineral found in high levels in animal tissues and eggs, legumes, and fish; it is exceptionally high in shellfish such as oyster[2][3] and may also be fortified into cereal grains in developed countries.[4]

Zinc is most commonly touted to be important as it is a cofacter in over 300 enzymes involved in gene expression, cell proliferation and signal transduction[5][6][7] and deficiencies of zinc may reduce the activity of these enzymes.

Zinc’s main role in the body is as a prosthetic group for several enzymes called metalloproteins, one of which is the Superoxide Dismustase enzyme; an endogenous anti-oxidant involving both zinc and copper.[8][9][10] Zinc is also involved in regulating the immune system.[11][12]

The RDA values for zinc are an Estimated Average Requirement (EAR) of 6.5mg for females, 8.5-10mg for pregnant or lactating females, and 12mg a day for men. The Recommended Daily Intake (RDI) values are 8mg for females, 10-12mg for pregnant or lactating females, and 14-15mg for males, and the Tolerable Upper intake Limit (TUL) is in the range of 35-40mg for adults of both genders (all numbers daily requirements).[13][14]

A deficiency in zinc is related to delayed growth in youth and hypogonadism in adult males[15] as well as general mental lethargy and skin abnormalities.[16]

When looking at zinc deficiency rates, it has been noted that around 10% of persons (USA) have a dietary intake of less than half the RDA of zinc[17][18] while global deficiency rates are over 50% (due to high deficiency rates in third world countries).[18] It has been reported (WHO, 2002) to be a major factor contributing to 1.4% deaths worldwide associated with severe zinc deficiency in childhood[19] although this magnitude of deficiency is almost never observed in first-world countries.[20]

Zinc is lost during sweat and exercise[21][22] and may be a contributing factor to why testosterone levels seem to be depressed after exhaustive exercise.[23][24]

In diabetic individuals (following information seems to apply equally to type I and type II diabetics), urinary zinc excretion rates are increased[25][26][27] and although serum zinc concentrations are unreliably influenced (increased,[25][28] decreased,[29][30][31] or not different from non-diabetic controls[32]) cellular concentrations of zinc as measured in immune cells (mononuclear cells, granulocytes, lymphocytes and leucocytes) tend to be reduced relative to nondiabetic controls.[29][33][30]

Zinc Citrate, at 50mg elemental Zinc (146mg) daily for 4 weeks is associated with a maintenance of Zinc status while placebo declines over time (told to maintain a low Zinc diet, estimated between 10-12mg).[34]

Zinc Gluconate, at 50mg elemental Zinc (385mg), appears to be slightly more effective than Zinc Citrate (nonsignificant) and can increase serum and erythrocytic stores of Zinc in apparently healthy persons over a period of 4 weeks.[34]

Zinc Picolinate (bound to picolinic acid, a metabolite of tryptophan), at 50mg elemental Zinc (144mg) in healthy persons appears to increase urinary and serum levels greater than placebo and the other two forms tested (Citrate, Gluconate).[34]

Zinc carnosine (ZnC) is a synthetic molecule where zinc and carnosine are linked together in a 1:1 ratio, forming a polymer-structure. The compound has been used for some time in Japan as a treatment for gastritis and gastric ulcers, and studies have shown that ZnC is up to 3 times more effective at promoting gastric integrity than either zinc or carnosine alone.[35] When the integrity of gastrointestinal (GI) tract becomes compromised, intestinal permeability increases which may allow the passage of harmful substances into the blood stream. This can cause an immune response, leading to systemic inflammation. Although not an official medical term, conditions associated with increased intestinal permeability have been termed leaky gut syndrome, which can be caused by food allergies, certain medications and inflammatory bowel disease.[36]

While ZnC is known to protect against increases in intestinal permeability, the mechanisms at work are not entirely clear. One study employed several in vitro and in vivo models to examine the mechanisms behind ZnC protection of the GI tract.[37] To examine the effects of ZnC on wound healing mechanisms that may be important in the context of leaky guy syndrome, HT129 colonic cells were grown to form a cell monolayer covering the entire surface cell culture plates. An artificial wound was then induced by scraping a line through the entire cell monolayer, removing all cells within the scratch. The ability of the cells to migrate back into the scratch, healing the cell monolayer was then tested in the presence or absence of ZnC. ZnC increased cell migration by approximately 100% compared to the vehicle control, suggesting that it may promote gastric healing in part by increasing epithelial cell migration in injured regions of the GI tract.[37] ZnC also induced a dose-dependent increase on cell proliferation, with a maximal response at 100M.[37]

To examine the ability of ZnC to promote gastric healing in vivo, researchers also examined the effects of ZnC in a rat model for gastric damage. Rats were given ZnC (1 or 5 mg/mL) or a placebo prior to 20 mg/kg indomethacin, a non-steroidal anti-inflammatory drug (NSAID) that causes gastric damage. ZnC substantially decreased markers for gastric damage at both 1 and 5 mg/ml, with the 5 mg/ml dose being more effective.[37]

The ability of ZnC to prevent small intestinal damage by indomethacin was also evaluated in mice. In control mice that received indomethacin alone, substantial shortening of intestinal villi were noted, along with decreased intestinal weight, both indicators of damage. In contrast, ZnC treatment reduced indomethacin-induced villus-shortening and increased intestinal weight, indicating a protective effect.

To validate the results obtained with in vitro cell culture studies and animal models, 10 healthy human volunteers were recruited in a double-blind, randomized and placebo controlled study. To assess the effects of ZnC on indomethacin-induced increases in intestinal permeability, participants drank a sugar solution containing a mixture of mono-and disaccharides. Since disaccharides are larger and are not easily absorbed in the GI tract by passive diffusion, an increase in urine disaccharide to monosaccharide ratio indicates increased intestinal permeability due to damage. Subjects took either ZnC (37.5 mg twice daily) or a placebo for seven days, with indomethacin for the last 5 days. When taking a placebo, subjects showed a 3x increase in disaccharide ratio, indicating a substantial increase in intestinal permeability from the indomethacin-induced injury. In contrast, subjects taking ZnC showed no significant increase in disaccharide ratio, indicating a strong protective effect on the gut mucosa.[37]

The regulation of bodily zinc levels tends to occur at the level of the intestines secondary to regulated absorption and fecal excretion[38][39] and in instances of zinc deficiency intestinal absorption can near 100%.[38] This has been replicated in humans where zinc absorption during instances of deficiency and is attenuated with sufficiency.[40][41][42]

At least one animal study has suggested that dysregulation occurs with intestinal zinc absorption during aging, and adequate dietary intake may in turn be metabolically insufficient due to poorer absorption.[43]

Absorption of zinc tends to be regulated, with higher oral intakes being associated with lower bioavailability and approximately 5mg absorbed in postmenopausal women regardless of dietary or supplemental intake.[44]

In otherwise healthy men supplemented with zinc, fasting plasma concentrations can increase within five days of supplementation regardless of baseline zinc status.[45] 10mg and 20mg elemental zinc (syrup) were equivalent in their ability to heighten plasma zinc levels, and were normalized two weeks after zinc supplementation.[45]

Zinc, as a trace mineral, is present in the cerebral cortex, pineal gland, and hippocampus where it acts as an atypical neuromodulator.[46][47][48] In the hippocampus, particularly the vesicles of mossy fibers, zinc can reach concentrations of 220-300M which is around 8% of total brain zinc[49] (concentrations of free zinc are more modest at 1-20M[50][51]) and is sensitive to prolonged (but not acute) zinc deficiency,[52] while in the pineal gland it may regulate the response of this organ to leptin.[53]

Similar to most neuromodulators, zinc is released from the synapse upon action potentials.[54]

The cell can take up zinc via ion channels such as the AMPK/kainate calcium channel (in neurons)[55] where it is then taken up by the cell’s mitochondria.[55][56]

The zinc ion has been noted to possess moderate potency NMDA receptor inhibitory actions in the range of 100-1,000M without affecting basal currents, while the activity of 10M was weak and the IC50 value placed near 100M;[57] the effects on NMDA receptor agonists appeared to be similar to magnesium.[57]

Zinc may also activate neuronal potassium channels and reduce glutamate release into the synapse.[58]

In the corpus callosum (commissure between brain hemispheres, function appears to be altered in depression[59][60] and serotonin uptake may be hindered by antidepressants fluoxetine and imipramine[61]), elemental zinc and zinc sulfate can enhance uptake at a relevant concentration of 1M by 45%.[62] This increase in uptake was also noted the cingulate cortex (58%) and Raphe nucleus (65%), concentrations of zinc between 10-100nM were ineffective, and the hindering effects of antidepressants on this function was negated with 1M zinc.[62]

Brain-derived neurotrophic factor (BDNF) is a protein found in both serum and brain (serum concentrations thought to be reflective of brain concentrations[63]) which is involved in regulating neuronal growth and plasticity;[64] BDNF signalling is implicated in both depression and memory function.[65] Zinc is known to be involved with BDNF as a deficiency of zinc seems to reduce the ability of BDNF in activating its receptors[66] and zinc itself can form a complex with the BDNF protein,[67] although it is primarily thought that via activating some metalloprotein enzymes (MMP-2 and MMP-9) which has been noted with oral zinc in mice[68] that zinc helps cleave the inactive form of BDNF (pro-BDNF) into ‘mature’ or active BDNF.[69]

High levels of dietary zinc in mice (30ppm via diet with 60ppm via supplemented drinking water) has been noted to reduce the actions of BDNF in the brain and impair memory, which was noted to be associated with a zinc deficiency in the hippocampus.[70] Zinc injections directly increase BDNF,[70] and the reason why high oral intake led to a reduction in hippocampal zinc is not known.

The antidepressive effects of zinc are thought to be mediated by an increase in BDNF, which has been noted in the serum of depressed humans given 30mg elemental zinc over the course of 12 weeks compared to placebo.[71] This study noted that baseline BDNF in serum, 15.37+/-8.28ng/mL, was increased 42% to reach 21.84+/-6.87ng/mL despite no change in placebo and this occurred alongside a 41% increase in serum zinc concentrations.[71]

Such an increase in BDNF has failed to occur elsewhere when 25mg was given as adjuvant over the same time length to depressed persons already on SSRI therapy despite zinc bettering symptoms of depression.[72]

Despite its importance in the brain, high concentrations of zinc can be excitotoxic[73] and this is sometimes seen in ischemic injury where an excess amount of zinc is released from the synapse and mediates cell death[73][74] and infarctions.[75] This is why zinc chelators are therapeutic in instances of stroke rehabilitation.[76]

Obsessive compulsive disorder is known to at least be associated with glutaminergic abnormalities, particular an excessive level of synaptic glutamate and signalling thereof[77][78] which positively correlates with symptom severity.[79] As glutamate antagonists have been previously implicated in treating OCD[80] and zinc has the potential to be anti-glutaminergic, it is investigated for possible benefits.

The addition of zinc (220mg twice daily) to fluoxetine therapy (20mg) for obsessive compulsive disorder is able to reduce symptoms of OCD as assessed by the Y-BOCS rating scale, although the benefits were present at weeks two and eight but not 4-6.[81]

A deficiency of zinc is known to be a cause of anorexia (reduction of appetite, not the same as anorexia nervosa), and is usually the first symptom of a zinc deficiency[82] and is shortly followed by depressive symptoms and anhedonia.[83]

In rats, orally supplemented zinc (19mcg/kg) appears to stimulate food intake and this effect was not observed with other bivalent cations.[84] Injections of zinc seem ineffective,[84] even in deficient rats.[85]

Oral zinc appears to stimulate the vagal nerve (effects abolished by vagotomy[84]) which then increase mRNA translation of the two appetite stimulating neural factors orexin and neuropeptide Y (also abolished by antagonists of these receptors[84]). Zinc is known to activate the GPR39 receptor (a Ghrelin receptor)[86] and since ghrelin is known to stimulate these two neural fators via the vagus nerve[87][88] it is thought that this receptor is the molecular target of zinc.

In children with ADHD, 30mg elemental zinc daily for 13 weeks (final five weeks used alongside D-amphetamine) was able to reduce the amount of D-amphetamine that was needed by 37% and reduced affective blunting from 21% (placebo with amphetamine) to 11%; however, zinc supplementation inherently failed to benefit symptoms of ADHD.[89]

Depressed patients appear to have reduced circulating zinc concentrations in serum[90] which is further reduced in treatment resistant persons relative to treatment non-resistant (treatment being imipramine)[91] and the magnitude of zinc deficiency correlating with severity of depression.[92][93] Overall, persons with depression seem to usually have lower zinc concentrations in serum and the worse the symptoms of depression the lower the zinc concentration tends to be.

At least in rats, the depressive[94] and behavioural symptoms (increased susceptability to stress[95]) that are seen with two weeks of zinc deprivation are normalized upon supplemetnation of zinc. Interestingly, deprivation of zinc causes rats to be resistant to fluoxetine (SSRI) therapy.[94]

In patients with major depression given zinc therapy (25mg elemental zinc) alongside their antidepressant medication (SSRIs) noted that supplementation had an adjuvant role by reducing depressive symptoms over 12 weeks when compared to SSRI paired with placebo;[72] monotherapy alone at 30mg elemental zinc in overweight/obese depressed persons appears to also reduce depressive symptoms (assessed by BDI II) over 12 weeks when compared to placebo.[71]

Zinc has been reported to noncompetitively inhibit glycogen synthase kinase-3 (GSK3) with an IC50 of 15M.[96] As GSK3 is a molecular target of mood disorders[97] and mood disorders being associated with alterations in zinc metabolism[98] supplementation is thought to have a potential role in its treatment.[17]

In otherwise healthy young women given 7mg of elemental zinc in a multivitamin format (placebo given the same multivitamin), depressive and aggressive symptoms were modestly but significantly reduced relative to placebo.[99] This modest benefit to mood has failed to occur in healthy elderly perosns (70-87yrs) given 15-30mg zinc as assessed by POMS.[100]

In persons given imipramine but were resistant to treatment, supplementation of 25mg elemental zinc for twelve weeks is able to reduce depressive symptoms relative to placebo to the levels seen with non-resistant persons as assessed by BDI, HAMD, and CGI.[101]

Zinc is known to be highly concentrated in the hippocampus[46][49] and a deficiency of zinc is associated with both mood disorders as well as impaired memory formation.[102] While a dietary insufficiency of zinc is known to cause a corresponding decrease in hippocampal zinc (attenuated with supplemental zinc[102]), high oral intakes in mice (additional 60ppm to drinking water) have also been noted to paradoxically reduce zinc concentrations in the hippocampus[70] which is not seem with mild elevations in rats (10ppm).[103]

The negative effects of low zinc concentrations in the hippocampus seem to be related to spatial memory,[102] and spatial memory is known to be associated with brain-derived neurotrophic factor (BDNF) signalling;[104] accordingly, injections of zinc into the rat brain cause dose-dependent increases in BDNF signalling and protein content[70] and a deficiency results in decreased BDNF signalling although the elevated protein content suggests insensitivity of the TrkB receptor.[66]

In general and in studies on how zinc influences spatial memory formation, low dose zinc in drinking water (10ppm) has been associated with beneficial,[68][105] adverse,[103] and no significant alterations.[70] Greater elevations (60ppm) have been noted to force a reduction in spatial learning associated with reduced hippocampal zinc and BDNF,[70] although at least one study noted impairments in memory at 10ppm alongside an increase in brain zinc concentrations.[103] This negative effect of zinc on spatial memory has been noted in one rat study to be significantly reduced with coadministration of copper (at approximately 2.5% the dose of zinc).[106]

In persons who experienced subacute stroke and had suboptimal dietary intake of zinc (6.6mg or less), supplementation of 10mg elemental zinc was associated with greater improvements than placebo on cognition as assessed by the NIH stroke scale after 30 days.[107]

Zinc is thought to be an anti-artherogenic agent[108] and in particular a zinc deficiency is thought to be a risk factor for artherogenesis with supplementation alleviating this risk.[109] Dietary zinc intake is known to be inversely associated with artherosclerotic buildup in arteries.[110]

In otherwise healthy elderly persons (higher risk of zinc deficiency), supplementation of 45mg elemental zinc daily (as gluconate) daily for six months is associated with reductions in cell adhesion factors (ICAM-1 and vCAM-1) and inflammatory cytokines including C-reactive protein, IL-6, and MCP-1.[111]

Supplementation of 20mg elemental zinc in obese insulin resistant children over eight weeks is associated with a reduction in total cholesterol and LDL-C.[112]

Oxidized LDL-C appears to be reduced when insulin resistant children are given 20mg elemental zinc for eight weeks, possibly secondary to reducing the state of insulin resistance.[112]

20M zinc has been noted to, in vitro in liver cells, to increase the activity of glycogen synthase 2-fold secondary to its inhibition of GSK-3 (IC50 15M).[96]

Zinc has been reported to act via the insulin receptor[113] and phosphorylate Akt in vitro, which is downstream of the insulin receptor.[30] The inhibition of glycogen synthase kinase-3 (GSK3) that occurs with zinc[96] is able to preserve insulin signalling, as GSK3 is a negative regulator of insulin signalling via IRS-1.[114] Zinc can augment uptake of glucose into cells that express insulin-sensitive GLUT4, but not other GLUT transporters.[96]

In diabetic individuals (following information seems to apply equally to type I and type II diabetics), urinary zinc excretion rates are increased[25][26][27] and although serum zinc concentrations are unreliably influenced (increased,[25][28] decreased,[29][30][31] or not different from non-diabetic controls[32]) cellular concentrations of zinc as measured in immune cells (mononuclear cells, granulocytes, lymphocytes and leucocytes) tend to be reduced relative to nondiabetic controls.[29][33][30]

Beyond measuring zinc concentrations themselves (as serum markers are not thought to be overly reliable for subclinical deficiencies[115]), a sensitive biomarker for zinc deficiency (Ecto 5′ nucleotidase[116]) is also known to be reduced in diabetic persons relative to control.[117]

Three weeks of supplementation with 30mg elemental zinc (glycine chelation) appears to be sufficient to at least partially restore a zinc deficiency in diabetics.[117]

In obese insulin resistant children (who were likely deficient in zinc) given 20mg elemental zinc for eight weeks supplementation was associated with a betterment of all biomarkers of glucose metabolism including blood glucose (7% reduction), fasting insulin (23% reduction), and insulin sensitivity as assessed by HOMA-IR (31% improvement)[112] which has been reported elsewhere in a replication.[118]

In diabetics who have been confirmed to have adequate stores of zinc, further supplementation of high dose zinc (240mg elemental zinc as gluconate) for three months has failed to have any appreciable benefit.[119]

Tumor necrosis factor alpha (TNF-) is a cytokine that is reduced in states of zinc deficiency (restored upon zinc replenishment[120]).

Ex vivo production of TNF from macrophages in elderly persons who supplemented 45mg elemental zinc for a year appears to be reduced.[121]

IL-2 is known to be decreased with zinc deficiency[120] and restored upon replenishment.[120]

Ex vivo production of IL-2 (assessed by the induction of IL-2 mRNA from stimulated immune cells) is increased with supplementation of zinc at 45mg for a year, despite basal concentrations of IL-2 being unaffected.[121]

Zinc deficiency is known to lead to a reduced count of T-cells and subsequently depressed humoral and cell-mediated immunity.[122]

A meta-analysis of 15 trials including 1360 persons overall noted that zinc, in the form of lozenges (gluconate) or syrup (sulfate), was associated with less duration and severity of the common cold when taken within 24 hours of onset that, after a week, had an odds ratio of 0.45 (less than half the risk).[123]

Supplementation of 45mg zinc in elderly persons (with lower zinc concentrations in serum relative to young controls) for a year is associated with a reduced rate of upper respiratory tract infections (50% reduction that failed to be significant) and general infections (88% occurrence reduced to 29%).[121]

Prolonged supplementation of zinc over five months is associated with a reduced incidence of sickness (RR 0.64) although with a high variability.[123]

In children with acute pneumonia, 10-20mg elemental zinc (as acetate syrup) over two weeks failed to outperform placebo in reducing the length of sickness.[124]

Supplementation of zinc at 20mg as adjuvant therapy (alongside antibiotics) was effective in further reducing recovery time in children under two years old with very severe pneumonia, but due to having no effect in severe pneumonia and the benefit in very severe being lost when controlling for underweight children the authors concluded no significant overall effect of treatment.[125] Other studies using the same dose that differentiate between severe and nonsevere pneumonia note a failure of zinc therapy outright relative to placebo[126][127][128] or that the beneficial effects were insignificant (statistically and clinically).[129] Although most evidence suggests a lack of efficacy, there is some counter evidence with the same protocol noting efficacy in reducing the length of sickness for severe pneumonia[130] and a study that noted a failure overall with zinc supplementation did report reduced mortality with severe pneumonia (which mostly protected children with HIV).[128]

The usage of zinc as a preventative for two weeks (10-20mg elemental zinc daily) was unable to influence the occurrence of pneumonia in children measured over the following six months.[131]

Adults with diagnosed HIV appear to be at greater relative risk for zinc deficiencies at up to 50%[132][133][134] and those who are deficient seem to have faster disease progression[135][136] and mortality;[137] a dietary surplus of zinc also appears to be associated with negative effects in this cohort, specifically an increased disease progression rate to AIDS.[138]

In HIV positive adults with confirmed low plasma zinc concentrations (0.75g/mL or less) given 12-15mg elemental zinc daily for 18 months, zinc supplementation was associated with a four-fold reduced risk of immunological failure relative to placebo without affecting viral load[139] and has elsewhere been associated with significantly less opportunistic infections regardless of whether or not subjects were on antiretroviral therapy.[140]

In children diagnosed with HIV who also experience severe pneumonia, supplementation of zinc appears to be effective in reducing mortality (7 deaths in control and none noted with zinc at 20mg daily for seven days).[128]

In a study dividing athletes and sedentary persons into a zinc supplement (5mg/kg zinc sulfate daily), both athletic and sedentary persons given zinc experienced a reduction in levels of lipid peroxidation relative to placebo and an increase in levels of the enzymes glutathione peroxidase and SOD.[141]

Bodily zinc stores are positively associated with serum testosterone[142][143] and increased urinary excretion negatively associated (as well as magnesium).[144]

Zinc deficiency is also associated with an impairment of converting cholesterol and lipid precursors into sex hormones despite testicular cell uptake being unaffected[145] and other side-effects associated with zinc deficiency include the population of androgen receptors being reduced overall (59% of control)[146] and in male sex organs (36% of control);[147] this may be related to how the androgen receptors have a zinc binding site,[148] and their functionality is impaired without adequate zinc.

When looking at rat studies that are not models of deficiency, zinc supplementation is able to increase circulating testosterone and free testosterone when injected at 3mg/kg[149] and oral intake of 20mg/kg zinc chloride has increased testosterone to levels higher than baseline in rats.[150]

In human studies of zinc deficiency supplementation of zinc is able to increase circulating testosterone concentrations, with this study noting that 250mg zinc sulfate for six weeks is able to increase testosterone by 84% (1.55nM/dL to 2.96nM/dL) in persons on hemodialysis.[151]

Infertile men who also have low testosterone (less than 4.8ng/mL) experience an increase in testosterone following zinc supplementation, but this is not observed in men with normal testosterone levels.[152]

Supplementation of ZMA in persons with an adequate zinc intake in the diet (11.9-23.2mg) failed to significantly increase circulating testosterone or free testosterone[1] and this failure to increase basal testosterone concentrations is also seen with 15mg elemental zinc in cyclists[153] and 3mg/kg zinc sulfate in elite wrestlers.[154]

When measuring testosterone acutely following exercise, there is a slight increase in free testosterone associated with zinc supplementation at 15mg in men who are not otherwise deficient[153] and the decrease in testosterone and free testosterone that may occur with exhaustive exercise is attenuated with zinc sulphate supplementation at 3mg/kg in elite wrestlers[154] and in sedentary men subject to cycling.[155]

Zinc is thought to reduce DHT secondary to inhibition of 5-reductase (converts testosterone to DHT) in the 3-15mM range (up to 98% inhibition), although concentrations as low as 500M are minimially effective (30%).[156] It is synergistic with vitamin B6 in this regard despite B6 not possessing any inherent inhibitory properties, which may explain the formulation of ZMA.

Injections of 10-20mg zinc (gluconate and arginine included in the weights here) into the prostate of rats has noted inhibitory effects on 5-reductase (50.48% at 20mg)[157] although a study in human prostate tissue in vitro noted that low concentrations (300nM) increased activity of this enzyme while higher concentrations (3mM) were potently inhibitory.[158]

When looking at the subdivisions of 5-reductase, the type I variant is effectively inhibited in skin cells with an IC50 of 2M while it is fairly ineffective on type II[159] and in these tissues it is still synergistic with B6.[156]

In infertile men, regardless of whether circulating testosterone was above or below the predetermined threshold (4.8ng/mL) supplemental zinc was able to increase circulating concentrations of DHT.[152]

A zinc deficiency in rats is associated with an increased expression of estrogen receptors (57%)[146]

IGF-1[160][117] and IGFBP3[160] are reduced in persons experiencing a dietary zinc deficiency, which is normalized upon supplementation.

An increase in IGF-1 has been noted in elderly persons given 30mg zinc supplementation daily for four weeks, where the 22.4+/-4.7% increase seen with a whey protein supplement was boosted to 48.2+/-14%.[161]

Leptin is known to interact with zinc at the level of the pineal gland[53] and may mediate its actions.[162] A zinc deficiency is known to reduce leptin production and secretion from adipocytes[163] which has been detected in rats[164] and humans.[120]

Leptin secretion can be positively influenced by insulin[165] although as zinc repletion does not influence insulin[120] this is not thought to be a mechanism of action. TNF- and interleukin-2 (IL-2) have both been found to be increased when a zinc deficient person has their zinc status restored[120] and these factors are known to induce leptin expression.[166] IL-2 itself is zinc dependent,[167] and it is thought that the influence on leptin couldl also be indirect via these two molecules.

In men with marginal zinc deficiency (restricted to about 5mg daily for 4+/-2 months), supplementation of 30-60mg elemental zinc (as acetate) daily for 6-12 weeks is associated with a 64% increase in leptin relative to the deficient state.[120]

Reductions in taste acuity are among the first noticeable signs of zinc deficiency, usually alongside anorexia (loss of appetite) and impairment in cognition.[168] This is likely because of a zinc-dependent enzyme, gustin, being reduced in activity when salivary zinc is low[169] and this condition is easily treated with supplemental zinc.[170]

Adolescents given zinc supplements over the course of ten weeks have been noted to experience increases in taste acuity as assessed by recognition thresholds for salt was improved;[171] these subjects (adolescent girls in India) usually have zinc deficiency rates around 58.3-65%[172][173] and thus the observed effects could be from normalizing a deficiency.

Loss of taste associated with chemotherapy does not appear to be rehabilitated with supplementation of 220mg zinc sulfate (50mg elemental zinc) twice daily.[174]

In low socioeconomic children at risk for zinc deficiency, 15mg elemental zinc daily for ten weeks is associated with reduced plaque formation on teeth.[175]

Zinc chloride appears to be capable of preventing secretagogue-induced acid secretion in rat and human stomach tissue,[176] which although therapeutic for the stomach may limit its own subsequent absorption.[177]

Trace minerals appear to be altered in their concentrations in the cirrhotic liver and serum, with a known decrease in zinc[178][179] and increase in copper[179][180] relative to healthy controls; the deficiency in zinc appears to positively correlate with disease progression.[181]

In persons with liver cirrhosis, supplementation of 50mg elemental zinc (as sulfate) daily for 90 days is associated with improvements in cirrhotic state as assessed by Child-Pugh score (6.56 down to 5.72; 13% improvement) which was associated with less bodily copper levels.[182]

Very high levels of zinc intake (330mg daily) has been implicated in alleviating leaky gut syndrome in those with Crohn’s Disease.[183] It can also prevent or alleviate damage to the intestinal mucosa and some to the liver done by alcohol[184][185][186] and due to alcohol causing zinc depletion, can also provide therapeutic-like benefit in treating alcohol-induced damage to the gut and liver.[187][188] Many of these effects were noted as dose dependent, but were seen at 3-5mg/kg bodyweight (an incredibly high dose).

Zinc deficiency is associated with impaired hearing in mice and rats, which is normalized upon consuming enough dietary levels of zinc.[189][190] This may be related to relatively high concentrations of zinc in some ear structures (cochlea and vestibule) where it exerts protective effects from stessors[191] possibly related to its role as a neuromodulator or as a component of Cu/Zn superoxide dismutase;[192] the latter of which is known to be protective of hearing.[193]

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Zinc – Scientific Review on Usage, Dosage, Side Effects …



High and Low Testosterone Levels in Men

Nov 14th, 2018
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What is testosterone?

Testosterone is considered to be the “male hormone” that’s produced in men by the testes. Although women’s ovaries produce some testosterone, the hormone is produced in much higher concentrations in men and it is responsible for many of the secondary sex characteristics seen in men such as a deeper voice and hair on the chest, in addition to contributing to a healthy libido, building muscle mass, and maintaining energy levels.

The problems associated with high testosterone levels are infrequent and rare in middle-aged and elderly men who are not receiving testosterone or other steroid treatments. When the testosterone level becomes out of balance, it usually becomes too low rather than too elevated.

What are the signs and symptoms of low testosterone levels in men?

The most common “out of balance” testosterone levels are found to be on the low side of normal; this occurs because a male’s highest testosterone level usually peaks at about age 20, and then it decreases slowly with age. It has been suggested that a 1% decrease in testosterone level per year is not unusual for middle-aged (30 to 50 years old) and older males. While this decrease may not be noticeable in some men, others may experience significant changes starting in their middle-aged years or more commonly at age 60 and above. This drop in testosterone levels is sometimes termed hypogonadism, “male menopause” or andropause.

Low testosterone levels may result in a decline in:

Additional symptoms of in low-T in men may include:

What are normal or average testosterone levels in men?

In general, the normal range in males is about 270 to 1070 ng/dL with an average level of 679 ng/dL. A normal male testosterone level peaks at about age 20, and then it slowly declines. Testosterone levels above or below the normal range are considered by many to be out of balance. Moreover, some researchers suggest that the healthiest men have testosterone levels between 400 – 600 ng/dL.

What are the benefits of higher than normal testosterone levels?

Examples of benefits, which are modest, of men having higher than average testosterone levels include:

What are the disadvantages of having higher than average testosterone levels?

Examples of drawbacks or disadvantages of men having higher than average testosterone levels include:

What are anabolic steroids, and what their side effects?

Both men and women that utilize anabolic steroids to gain an athletic “edge” (for example, some professional athletes) or to increase muscle mass (for example, some bodybuilders) may experience high levels of testosterone and develop complications, and side effects, for example:

What is the treatment for low-T in men?

There is treatment available low testosterone levels. Doctors may prescribe medications that contain testosterone such as:

What men should not use testosterone therapy?

Not all men may be candidates for this type of treatment.

How often should a man have his testosterone levels checked?

So, how does one ensure that testosterone levels remain in balance? Some doctors suggest that monitoring testosterone levels every five years, starting at age 35, is a reasonable strategy to follow. If the testosterone level falls too low or if the individual has the signs and symptoms of low testosterone levels described above, testosterone therapy can be considered. However, once testosterone therapy is initiated, testosterone levels should be closely monitored to make sure that the testosterone level does not become too high, as this may cause stress on the individual, and high testosterone levels may result in some of the negative problems (described previously) seen.

Finding the appropriate balance of testosterone is possible through discussions with your doctor, and it requires your willingness to have testosterone levels checked before the initiation of therapy and then checked routinely in the future.

Medically reviewed by Michael Wolff, MD; American Board of Urology


FDA evaluating risk of stroke, heart attack and death with FDA-approved testosterone products.

Harvard Health Publications, Harvard Medical School. Is testosterone replacement therapy safe? Take a look at the latest evidence in the February 2014 Harvard Men’s Health Watch.

National Institute on Drug Abuse. DrugFacts: Anabolic Steroids.

St. Louis Post-Dispatch. New medical review refutes link between testosterone replacement therapy and heart disease; low t institute weighs in.

Southeastern Medical Oncology Center. Polycythemia is a Common Blood Problem. Low Testosterone (Hypogonadism).

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High and Low Testosterone Levels in Men



Sermorelin Acetate Cost, Review of Benefits and Comparison …

Nov 12th, 2018
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hGH Replacement Therapy has been a popular Anti-Aging and performance enhancing treatment since as early as 1990, but unfortunately, use of hGH does not come without risks.

Sermorelin acetate has become a popular alternative as it enables you to obtain the benefits of hGH Therapy, without the associated risks.

This article looks more closely at the benefits of Sermorelin injections as a hGH alternative and the cost associated with it.

To begin with, it is a good idea to have an understanding of what sermorelin acetate is and what role it plays when administered via injection.

Scientifically sermorelin acetate is referred to as growth hormone releasing factor 129 NH2-acetate, this is because it is a peptide which contains the first 29 amino acids that make up growth hormone produced in our bodies.

This contributes to sermorelins function as a growth hormone secretagogue (a substance which causes another substance to be secreted Wikipedia) in this case, the substance whose secretion is promoted is growth hormone.

For this reason, sermorelin is often also referred to as an hGH stimulator and is considered an excellent alternative to hGH.

One important thing to understand about Sermorelin is that it promotes healthy function of the pituitary (the gland responsible for our bodys production of hGH) during the aging process.

This is a far cry from aggressive administration of hGH which can, in fact, negatively impact normal pituitary function.

Another distinct advantage of using sermorelin instead of hGH is the cost involved.

hGH typically costs $1000+ per month of treatment, sermorelin is a much more affordable option with 3 months treatment of sermorelin costing significantly less than just one month on hGH.

In fact, sermorelin is available at as low as $290 per month for a 9mg vial.


Anti-Aging Peptides

Sermorelin 9mg



From $292 per month

Performance Peptides

Sermorelin 9mg

GHRP-2 9mg

GHRP-6 9mg

From $317 per month

Besides the obvious advantages of sermorelin injections detailed above, you may want to know how you can benefit from using this therapy.

Perhaps the easiest way to understand the potential benefits of hGh replacement therapy is to look at the symptoms of hGH decline and the effect hGH replacement has on those symptoms.

These are detailed below:

Changes in body composition due to decreasing levels of hGH are reflected by a decrease in lean body mass (muscle) and an increase in fat mass.

Correcting hGH levels has been shown to reverse this state by improving muscle mass and reducing fat.

Research indicates that hGH deficiency in adults contributes to a reduction in bone density and therefore increased risk of osteoporosis.

It has also been shown that hGH replacement therapy for greater than 12 months results in improved bone mineral density and hence, lower risk of osteoporosis.

Due to changes in body composition detailed above, muscle strength is understandably compromised. As hGH therapy corrects body composition and improves muscle mass, muscle strength also improves.

The best results are gained after 12 months of hGH therapy.

By improving bone mineral density and increasing muscle mass and strength, hGH therapy can help to prevent joint deterioration that is a feature of arthritis.

Optimal growth hormone levels are also essential for health of connective tissue such as the synovium found in joints.

Exercise performance is reduced in individuals with growth hormone deficiency. This appears to be partially due to reductions in bone density and muscle mass but also in part due to a reduction in oxygen uptake.

hGH therapy for 6 months has been shown to improve exercise performance by improving muscle mass and also oxygen uptake

There is evidence of a greater risk of heart disease in individuals with growth hormone deficiency and it has been hypothesized that this is due to a greater propensity to develop premature atherosclerosis (a build-up of plaque inside the arteries which increases risk of heart attack and stroke).

Growth hormone deficiency also results in changes in heart size and function. These changes have been demonstrated to be reversed after 6 months hGH therapy.

Growth hormone deficiency results in a reduced resting metabolism and replacement therapy reverses this decrease. hGH therapy has also been shown to increase protein synthesis, increase fat oxidation, normalize carbohydrate metabolism and reduce LDL (bad) cholesterol.

These favorable effects on metabolism may in part explain some of the other benefits of hGH including improved hearth health and body composition.

A reduction in skin thickness and all-important skin collagen is another result of growth hormone deficiency. Both conditions are improved by hGH therapy.

Although adults with growth hormone deficiency are not normally considered to have a compromised immune system, there is some evidence to suggest that hGH therapy can help regulate immune function.

It has been demonstrated that people with growth hormone deficiency have more difficulty with sexual relationships and reportedly, lower energy levels.

Many individuals have found an improvement in energy, libido and sexual performance following hGH therapy, some men even claiming an improvement in problems with premature ejaculation.

Reduced psychological well-being has been reported in individuals with growth hormone deficiency and hGH replacement has resulted in improvements in mood, energy and general feelings of well-being.

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Sermorelin Acetate Cost, Review of Benefits and Comparison …



The Healthy Mummy – Weight Loss

Nov 12th, 2018
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Inspiring Weight Loss Stories from Real Mums

Read inspiring stories from our Healthy Mummy community members whove followed our weight loss meal plans designed for busy mums like you. Here youll find healthy weight loss tips, real results, encouraging advice, and Healthy Mummy motivation!

Sometimes, thats all you need to start transforming your mindset, your body, and your life. Inspiration, motivation, and practical tips you can turn into action right away.

Ready to take the first step? Start your weight loss journey join our community and sign up for our next 28 Day Weight Loss Challenge.

Youre in the right place. Here are 5 of our favourite tips for planning healthy meals when youre a busy mum on a budget.

Your body, lifestyle, and situation are unique to you. So, adapt your diet to match! This is especially important for mums who are pregnant or if youre breastfeeding your baby. After all, you need to sustain two people with your diet! So, make sure you get a customisable meal plan suitable for pregnant women or a program that can adapt to your needs as a breastfeeding mum.

Ever come home from work, a shopping trip, or a day out with the kids and just grabbed takeaway because you had no time or energy to cook? Yep, weve all been there. Its not the best option for our health OR our bank accounts. Thats why the best way to stay on track with your weight loss meal plan is to plan ahead and meal prep so youve always got something in the fridge or freezer thats ready to go.

Its always easier to achieve a goal (like sticking to your healthy meal plan!) when youve got someone doing it with you. Surround yourself with a tribe of other mums who want to make positive, healthy changes in their lives too. Youll always have a safe place to share your wins (and struggles) and get a boost when you need it. Plus, youll be able to see whats possible for you and your family because others have done it too.

Do you ever get bored with cooking the same old meals? Its easy to get stuck in a rut with recipes and ingredients same old, same old. Sometimes, finding new recipes can inspire you to make healthier choices and cook meals that are good for you and that your whole family is happy to eat. Check out our weight loss recipes to find some new go-to meals and healthy ingredient options.

These days, there are plenty of tools you can use to make it easier than ever to follow a weight loss meal plan. The Healthy Mummy app, for example, helps you manage your recipes, meal plan, and shopping lists on-the-go (so you never end up at the shops without a list again). Embrace the tech to make planning meals quick and easy.

Feeling inspired? You can check out our free weight loss recipes, create your own weight loss meal plan, and start your journey right away.

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The Healthy Mummy – Weight Loss



Healthy Meal Plan For Weight Loss | 5-Day Free Menu

Nov 12th, 2018
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This 5-day sample meal plan for weight loss is all about eating more, not less.

You learn about lots of healthy, filling meals and snacks that can help you not only weigh less but also feel your very best.

This healthy meal plan for weight loss includes all kinds of satisfying, hunger-curbing foods like mustard-coated salmon, sweet potatoes, and hearty Italian-style soups.

By switching from a bowl of cold, dried cereal to one of hot whole-grain cereal and fruit, youd take in approximately 100 fewer calories each day. That one simple change to your daily diet could help you drop about 10 pounds in one year. Plus, hot cereal has more staying power. It tends to fill you up better and longer than dried cereal.

If desired, add a little nonfat milk or soymilk and a packet of sugar substitute (a good choice is Splenda).

1 steamed 6-inch corn tortilla with fresh or grilled vegetables (such as onions, green bell peppers, and tomatoes) and no-added-salt salsa.

Warm the tortilla between slightly moistened paper towels in the microwave for about 1 minute, then top with veggies and salsa; fold

For your salads, break out of the lettuce-and-tomato box. All kinds of veggies and fruit can go into your salad. Try diced sweet potatoes, yellow squash, red bell peppers, cucumbers, red cabbage, red onions, and more.

And always keep in mind that no oil, even so-called good ones, should be considered a weight-loss food. Coating your salad with oil can tally up as many calories as a scoop of premium ice cream.

Make your own. Its easy! From one 14-ounce can of no-salt-added cannelini beans, spoon out 2 tablespoons of beans. Puree the rest. In a medium nonstick pot, saut 5 cloves of chopped garlic until translucent. Add 2 cups low-sodium chicken broth and 1 head of escarole, chopped, or a package of frozen chopped spinach. Simmer for about 15 minutes. Add pureed beans, red pepper flakes and black pepper, to taste, and cook 1 minute longer. Garnish with the beans you spooned out plus, if you desire, a little chopped red bell pepper. Refrigerate or freeze what you dont eat for easy soup prep for a future lunch or dinner.

Especially popular among our guests at the Pritikin Longevity Center are Greek-style yogurts such as Oikos and Fage. So rich and creamy tasting! If you need a little sweetness to cut the tart flavor, simply add diced banana, or stir in 1 packet of Splenda

A gigantic Farmers Market-style salad with a variety of fresh seasonal produce and fresh herbs, such as fresh baby arugula and radicchio, and red wine vinegar sassed up with a little horseradish. Enjoy visiting your local Farmers Market every week and asking the vendors, Whats new and tasty this week? What would make great ingredients for my salad?

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When dining out and ordering fish, request that your fish not be salted or basted in calorie-dense ingredients like olive oil and butter. Healthier cooking options include steaming, broiling, or grilling.

Contrary to popular belief, potatoes are a great food for helping you lose weight. Its what we put on top of our potatoes butter, cheese, and bacon bits that turn them into waistline-busting foods.

Egg white omelet stuffed with 1 cup of assorted grilled vegetables, such as onions, bell peppers, mushrooms, and broccoli, and a dollop of nonfat ricotta cheese.

In a nonstick skillet misted with a little cooking oil spray, stir fry until brown diced baked potatoes with sliced onions, sliced green bell pepper, freshly ground black pepper, and paprika.

Yes! Cocoa can be part of a healthy meal plan for weight loss! For cocoa: Mix nonfat milk or soymilk, 1 tablespoon cocoa powder, and 1 packet of sugar substitute, such as Splenda (if desired).

Like vegetables, fruits are fabulous weight-loss foods because theyre big foods, that is, foods that are bulked up by lots of fiber and water. With big foods, youll be eating a lot of food (which will satisfy your hunger) but not a lot of calories.

Heres a great example: For the same number of calories that are in a handful of peanuts (about two ounces), you can eat 2 pounds of strawberries (about five of those green boxes that strawberries come in.) Eating big foods like strawberries, salads, and other fruits and vegetables can prevent hunger from taking over and taking you places you dont want to go

Big salad of baby greens with Pritikin-Style Thousand Island Dressing, which has less than one-quarter the calories and sodium of regular Thousand Island Dressing. What a gift for your heart and waistline! To make dressing, combine thoroughly the following: cup plain fat-free Greek yogurt, cup fat-free sour cream, cup unsweetened, low-sodium ketchup (good brand is Westbrae), teaspoon oregano, and teaspoon granulated garlic.

Sandwich of fresh roasted turkey breast (3 to 4 ounces) with 2 slices of low-sodium, whole-grain bread with assorted veggies, like baby greens and sliced tomatoes. Smear the bread with 1 tablespoon of low-sodium stone-ground mustard.

Did you know that bread and rolls are the No. 1 source of salt in the American diet, accounting for more than twice as much sodium as salty junk food like potato chips? Thats why its so important to look for low-sodium varieties of bread (a good brand is Food for Life).

Keep stocked in your refrigerator or freezer a box of veggie burgers (look for low-sodium varieties). Veggie burgers are a much better choice for your waistline and heart than ground meat. Veggie patties have only about half the calories of regular red meat patties, and zero heart-hurting saturated fat. Plus, theyre so easy to cook just one or two minutes in the microwave. While toasting your whole-wheat bun, take from your pantry a jar of roasted red bell peppers and top your veggie patty with a couple of luscious slices. Smear your bun with a little low-sodium Dijon mustard.

1 or more cups (its hard to go overboard on fresh veggies!) of steamed fresh vegetables, such as asparagus, broccoli, and/or cauliflower, with lemon juice and sauted garlic.

Hot whole-grain cereal, such as oatmeal, cracked wheat, barley or polenta, made with 1 cup nonfat milk or soymilk and 1 cup fresh or frozen blueberries.

There are many great choices of whole-grain hot cereals; just make sure you buy one with no added sugar or salt.

If desired, add a little nonfat milk or soymilk and 1 packet of sugar substitute (a good choice is Splenda).

Look for fat-free low-sodium varieties, or make your own.

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Did you know that four ears of corn has the same number of calories as one medium serving of French fries? (The corn tastes better, too.)

cup 1% no-salt-added cottage cheese with cup to 1 cup fresh diced fruit, or use pop-top canned fruits packed in juice or water, no sugar added.

A big salad of baby spinach and other fresh veggies, such as sliced carrots and tomatoes, topped with your favorite canned no-salt-added beans. Toss salad with about teaspoon of wasabi (to taste) and 3 to 4 tablespoons of rice vinegar.

Look for no-salt-added varieties of canned beans since rinsing the beans through a colander removes only 30% of the added sodium.

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Give your brown rice a nice savory spin by adding freshly minced garlic. At the last minute, add in fresh herbs like thyme and Italian parsley and just about any vegetable you have on hand, like chopped cucumbers, celery, onions, and tomatoes.

If you’ve enjoyed this Healthy Meal Plan for Weight Loss, you’ll love the Weight Loss Spa Menu

Red Bean and Leftover Veggie Soup

While there are probably plenty of pre-made bean and veggie soup options that just need a few minutes to heat through on the stovetop, making your own soup is really easyand a great idea for your health. Homemade soups are much lower in sodium about 100 milligrams or less per 2-cup serving. By contrast, 2 cups of many canned soups contain a blood-pressure-busting 1,200 milligrams or more, a worrisome amount considering that health experts recommend consuming no more than 1,500 milligrams of sodium for the entire day. This is also a great way to use up all those leftover vegetables in your crisperpretty much anything works in this soup.

Directions:Put into a soup pot 1 can of no-salt-added red beans (drained), 4 cups low-sodium vegetable juice like Knudsens Very Veggie Low-Sodium Juice, 2 to 3 teaspoons oregano or Italian-style seasoning, and 2 cups of any veggies you already have sitting in the refrigerator bin, such as carrots, celery, and onions. Rough-chop the vegetables into bite-size pieces and bring to a boil, simmering until vegetables are crisp-tender, about 10 to 15 minutes. If desired, top with a tablespoon of fat-free sour cream.

Put together a sandwich of tuna (canned preferably low-sodium, light, and packed in water) with 1 tablespoon nonfat mayo or nonfat plain yogurt, chopped celery, and onions, topped with baby spinach or peppery arugula, on 100% whole-wheat bread (low-sodium)

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Enjoy the rich flavor of sweet potatoes? While home on Sundays, cook up a batch. Wrap each one in foil and bake for about an hour at 425 degrees F, or until their luscious, sweet juices start to ooze out into the foil. At work the following week, just pop one in the microwave for a quick warm-up. Theyre loaded with taste, so they dont need any extra toppings. If you want a little zest, swirl in a teaspoon or two of no-salt-added Dijon mustard or a quarter cup of plain nonfat Greek yogurt.

A big salad with a variety of lettuces, plus tomatoes, cucumber, and any other veggies you have in the fridge, including varieties youve never thought of adding to salads but actually taste delicious, like sliced fennel.

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Ah, quinoa. This healthy, rich-tasting whole grain/seed has so many nutritional riches that it puts refined grains like white rice to shame. Tofu is the perfect sidekick because its both waistline-friendly (per bite, tofu tends to have about one-third the calories of meat and poultry) and heart-friendly (tofu has no artery-damaging saturated fat or cholesterol).

Directions: Rinse 1 cup of quinoa in cold water. In a medium saucepan, combine quinoa with 1 tablespoon curry powder and 1 teaspoon turmeric. Add 2 cups low-sodium chicken broth and bring to a boil. Cover and simmer until the water is absorbedabout 15 minutes. Stir in 1 cup shredded carrots and 1 cup cubed firm tofu. Makes about 4 one-cup servings. Refrigerate remaining servings for an easy, healthy snack or meal later in the week.

Blend together until smooth and creamy your favorite fresh berries, silken tofu, Splenda (if needed), and a little vanilla extract.

Think oatmeal is boring? You havent tried Chef Anthonys sweet/ tangy Oatmeal Supreme, always a favorite among guests at Pritikin. Its a great meal for losing weight, and starting your day.

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If desired, add a little nonfat milk or soymilk and 1 packet of sugar substitute (a good choice is Splenda).

Open up a big bag of baby carrots and dip them into your freshly made no-oil-added, no-salt-added hummus. Simply whip up in your food processor a can of no-salt-added chickpeas/garbanzo beans, fresh tomatoes, lemon juice, garlic, a jalapeno pepper (if you like your hummus hot and spicy), and fresh herbs like cilantro and dill. Add a little water, if necessary, until the desired consistency is achieved.

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Butter beans are as delicious as they sound: big, meaty and filling, with a mild flavor that works well with bright, assertive flavors like lemon and scallions.

1 can no-salt-added butter beans cup chopped scallions (also known as green onions)Juice from half a lemonRed chili pepper flakes, to taste2 to 3 cups chopped fresh Romaine lettuce and/or baby arugula

In a medium mixing bowl, combine butter beans, scallions, lemon juice, and pepper flakes. Spoon over lettuce greens.

Sear, skin side up, a 4-ounce cut of salmon in a hot nonstick skillet and cook until well browned on the bottom, 3 to 5 minutes. Turn and cook till slightly translucent in center, 1 to 3 minutes. Transfer salmon to serving dish. To skillet add teaspoon grated orange peel, 3 ounces orange juice, and cup white wine. Boil until reduced by half, about 3 minutes. Stir in 1 teaspoon fresh thyme leaves. Spoon sauce over salmon.

Cooking up soba (the Japanese word for buckwheat) noodles instead of white-flour noodles is a great way to cut calories. A cup of soba has just 113 calories; a cup of white pasta, about 200. Plus, soba noodles are full of fiber, protein, and B vitamins.

Combine in large bowl:2 large cucumbers, peeled, seeds removed, and sliced tablespoon paprikaPinch cayenne pepperPinch black peppercorns, freshly ground cup fresh lemon juiceLet cucumber mixture sit for a few minutes while you cook 8 ounces of soba noodles according to package directions. After cooking and draining sobas, toss in bowl with cucumber mixture and gently blend.

Pour a 6-ounce bag of pre-washed baby spinach in a hot wok sizzling with a small amount of water or white wine, 1 tablespoon of lemon juice, and minced garlic. Stir spinach till wilted.

Smoothie made in blender with 1 cup nonfat plain yogurt, cup crushed ice, banana, and fresh or frozen berries.

Tags: meal plansweight loss

Eugenia Killoran has been the food and fitness journalist for the Pritikin Program since 1992. She has published more than 3,000 articles, lectures, and book chapters on a wide variety of healthy living and weight-loss topics.

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Healthy Meal Plan For Weight Loss | 5-Day Free Menu



Best Weight Loss Pills 2018 | Top Diet Pills That Work Fast

Nov 12th, 2018
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1. PhenQ review

Editor Rating: (4.8stars)

Editor Rating:(4.6stars)

Editor Rating: (4.8stars)

Where to buy: The Official Phen375 Website

Editor Rating:(4.9stars)

Where to buy: The Official Phen24 Website

5. PhenBlue review(4.5stars)PhenBlue another trustworthy product from Intechra Health gives you the best weight loss pills which not only help you get back your lean and healthy body but also improve your overall health. Make of 100% clinically-researched ingredients, PhenBlue is recommended for everyone.Does PhenBlue need a prescription? NO! PhenBlue is 100% natural.How does PhenBlue work? PhenBlue drives your healthy living results through the roof with the ability to:

6. APEX-TX5 reviewAPEX-TX5has spread its reputation through the world because of top-quality pharmacologically ingredients that are manufactured in the US and contain great benefits. You, as a customer, can completely put your faith upon APEX-TX5 an optimal selection for both adults, size or body shape.Does APEX-TX5 need a prescription? NO! APEX-TX5 does not require any prescription or doctor approval because its 100% natural and herbal.How does APEX-TX5 work?

7. Adiphene reviewWhat Adiphene gives you is a powerful thermogenic and energy booster which will help to speed up your metabolism and burn out every single fat cell. Like most best weight loss pills, this one is again all-natural together with no dangerous side effects.Does Adiphene need a prescription? NO! Its 100% natural and herbal.How does Adiphene work?

Editor Rating:(4.8stars)

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Best Weight Loss Pills 2018 | Top Diet Pills That Work Fast



Image Weight Loss Centers | Houston Weight Loss Clinics

Nov 12th, 2018
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Our methods build self confidence and make you stronger. We do this one person at a time. Gain a stronger character, stronger body and a stronger sense of self esteem. We help you set and achieve your goals. Although it requires effort, you can also have fun while you do it. Above all else, we have complete confidence in you!

The hardest step to making changes is always the first one. Its never easy to commit to creating a new and healthier you. It is, however, well worth the effort!

What we provide is a way for you to get rid of your doubts and fears and transform them into courage and a willingness to take action. The challenge is to overcome the tendency to be a couch potato and rise above the habit of being lazy and lethargic.

Image Weight Loss Centers is committed to helping you achieve your true potential and bringing out a younger, healthier and more vibrant you.

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Weight loss | All tech news

Nov 12th, 2018
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Weight loss refers to a reduction ofbody mass due to a loss of body fat and lean mass. It is acontext of medicine, health andphysical fitness.

It occur unintentionally due to malnourishment to improve an actual obesestate.

In above the paragraph names and information of actors and actress is given who lose their weight:

Melissa Ann McCarthy was born on 26 August 1970 and She is an American actress, comedian, writer, producer and fashion designer.

She received twoPrimetime Emmy Award, oneGolden Globe Award and twoScreen Actors Guild Awards. She also received nominations foraBAFTA Award andAcademy Award for Best Supporting Actress.

Recently, she lost a whopping 75 pounds and now she is looking very beautiful. She made the globe come to a stop when she appeared in her new avatar.

she is not a size 4and she has put in hard work to gain the unachievable. In an interview with TMZ, she opened up about her weight loss.

Rebel Melanie Elizabeth Wilson was born on 2nd March in the year 1980. She is an Australian actress, writer and producer.

After graduating from theAustralian Theatre for Young People she began her career. In 2003, she appeared as a Toula on theSpecial Broadcasting Service.

Special broadcasting service is a comedy series ofPizzaand thesketch comedyseries. She got many accolades such as a Tropfest award, Detroit Film Critics Society award for Breakthrough Performance.

Recently, she did to lose 35 pounds and she is looking slim and hot. She stopped counting calories and she started counting the amount of dietary fiber that she was consuming per day.

She start eating her stress and she take it seriously and make an effort to get rid of this habit.

Susan Magdalane Boylewas born on 1 April 1961 and her estimated net worth is about $35 million.She is an Scottish singer and she becomes popular when she appeared in TV programme.

In 2 April 2009, She appeared in TV programme as a contestant inBritains Got Talentand sing a song. The song which she sing in a TV programme is I Dreamed a Dream fromLes Miserables.

In 2013, she received twoGrammy Awardsnominations. She achieved 3 World Music Awards, a peoples choice award, a Japan Gold Disc Award andARIA Music Awards.

Recently, She has lost a whopping 50 pounds and she looks slimmer and healthier.In 2012, she diagnosed with type 2 diabetes than she decided to start living a healthy life.

She was born on 10 August 1979 in McIntyre, Georgia, United States. She has three ChildrenAlana Thompson, Anna Shannon and more.

shedropped 300 lbs after seven months and her trim figure look amazing.

Adele Laurie Blue Adkinswas born on 5th May in the year 1988.She is an English singer and songwriter.

In 2006, she graduated fromBRIT Schoolfrom Arts and Technology. Later, her friend posted her demo onMySpace and She got a recording contract byXL Recordings.

In 2009,She received the awards forBest New ArtistandBest Female Pop Vocal Performance at the51st Annual Grammy Awards.

In 2007, she received theBrit Awardsand won theBBCSound of 2008poll. She also achieved six Grammy Awards forAlbum of the Year and twoBrit Awards forBritish Album of the Year.

Recently, she lose 30 lbs every day by eating several nutritional food like green vegetables and fruits.

She was born on 6 May, 1983 and sheis an American actress. In 2009, she appeared in filmPrecious and got her first role.

Due to precious movie she earned theIndependent Spirit Award for Best Female Leadand also got aGolden Globe awardandAcademy Award for Best Actress.

Recently, she lose her weight and now she is looking slim and beautiful. When she and her older brother diagnosed with Type 2 diabetes then shemade the decision to get the surgery.

Christopher Michael Prattwas born on 21st June in the year 1979. He is an American actor and after casting movie guardian of galaxy, He becomes popular.

In 2013, He nominated for the Critics Choice Television Award for Best Supporting Actor in a Comedy Series.

He ditched 60 pounds in six months.In 1 of August, he was lose 300 pounds when he auditioned for the Marvel movie scheduled to release.

Precious is a 2009 Americandrama film and this film directed and co-produced byLee Daniels. In this movie Sidibe plays a role of portrays young woman struggling against poverty and abuse.

After trying lots of hard work and eating lots of nutritional food to lose fat naturally. ThePrecious star turned to do laparoscopic bariatric surgery.

She was born on 30 October, 1987 and sheis an American model. She has appeared in the front and cover of fashion magazines. Fashionmagazinessuch asVogue,Harpers Bazaar, Glamour andElle.

She has appeared onThe Tonight Show with Jay Leno,Entertainment Tonight andCBS News.She was also interviewed byNPRaboutplus size modeling.

Recently she lose her weight and look like a beauty women. She used nutritional food such as green leafy vegetable and fruits to decrease her fat. She also used some diet to decrease her fat.

William Leonard Roberts II was born on 28th January in the year 1976. He is known professionally by hisstage nameRick Ross. He is an American rapperand entrepreneur.

Rick Ross has awarded four Grammy Awards by theNational Academy of Recording Arts and Sciencesof the United States.

In 2017, he showed off his slimmed down physique on theGrammy Awards red carpet. His weighed was 350 lbs but now He lost 75 lbs.

John Stephen Goodmanwas born on 20 June, 1952 and he is an American actor.

He became popular because of playing Dan Connerin theABCTV series Roseanne. He loses more than100 lbs.

Christine Michelle Metzwas born on 29 September, 1980 and sheis an American actress and singer. She became popular due to playing Kate Pearson in theNBCdrama.

In 2017, she achieved a Primetime Emmy Awards for Best Supporting Actress and aGolden Globe Awards.

She lost 100 pounds in less than five months because of eating a 2,000 calorie diet andwalk daily 20 minutes. Now, she is looking very hot and slim.

Lena Dunham was born on 13 May 1986 and sheis an American actress, writer, producer and director.She became famous due to she is creator, writer and the star of the HBO seriesGirls.

She received manyEmmy Award nominationsand twoGolden Globe Awards.She also directed several episodes ofGirls.

She also became the first woman to win theDirectors Guild of America Award for Outstanding Directing Comedy Series. She has lost 138 pounds.

Jonah Hill Feldsteinwas born on 20th December 1983. He is an American actor, director, producer, screenwriter and comedian.

He is known for his comedic roles in films such as Accepted which was launch on 2006,Grandmas Boywhich was launch on 2006,Superbad which was launch on 2007,Knocked Up which was launch on 2007,Forgetting Sarah Marshallwhich was launch on 2008 and Get Him to the Greekwhich was launch on 2010. Now, He is looking very smart and slim.

are Grapefruit, Cinnamon, Ginger, Lemon, Peppermint, Bergamot and Fennel.

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Weight loss | All tech news



Weight Loss Drugs Prescription and OTC by

Nov 12th, 2018
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What are OTC diet pills?

Only one over-the-counter diet pill is approved for weight loss: a reduced-dose formulation of orlistat known as Alli. It works by preventing absorption of about a third of ingested fat. While side effects from Alli are slightly lower than with its prescription cousin (because of the lower dose): they remain unpleasant: oily stools and discharge and potential bowel accidents if too much fat is eaten at one sitting. Alli’s manufacturer recommends keeping total fat consumption to about 30% of calories a day and spreading it out over three meals. The net weight loss effect with Alli: about 50% greater than diet and exercise alone.

What do I need to know about OTC diet supplements?

Many other over the counter diet supplements are promoted as helping with weight loss, but few have actually been proven to work. Worse, some of the ingredients used in OTC diet supplements may be dangerous. The Food and Drug Administration classifies herbal products as dietary supplements. This means that they are unregulated and can be marketed without the years of testing and regulatory review required for prescription (and nonprescription) drugs. Remember that supplements can have side effects, and you should check with your doctor first before taking any type of supplement, including OTC diet pills.

Here are some common ingredients seen in OTC diet supplements:

Green tea extract: cases of liver problems in people using concentrated green tea extracts have been reported.

Hydroxycitric acid: Derived from the fruit of a tree native to Southeast Asia. It generally appears to be safe, although one maker recalled its products after they were associated with liver damage. Other health problems reported included seizures, cardiovascular disorders, and serious muscle damage. These products contained many other ingredients, and it is unclear which ingredients or doses were associated with the liver problems.

Chromium: A mineral that people can get through diet, particularly meats, whole-grains, and some vegetables and fruits. It has been linked to side effects such as headaches and dizziness as well as more serious health problems at high doses.

Conjugated linoleic acid (CLA): Found naturally in meat and dairy products, it may cause stomach upset.

Hoodia: Derived from an African plant native to the Kalahari Desert. Hoodia products typically contain other additional ingredients. Its safety is not yet known.

Chitosan: Made from the starch found in shellfish.

Pyruvate: Produced by the body as a result of the breakdown of carbohydrate and protein from food and found naturally in foods such as cheese, wine, and red apples.

St. John’s wort: Used mainly as an antidepressant, this herb can interact with numerous other drugs.

Aloe: Sometimes marketed as an “internal” cleanser, aloe causes a strong cathartic effect in the intestines. That can lead to mineral depletion or worse if users have pre-existing intestinal issues, such as ulcerative colitis.

Cascara: An effective laxative but ineffective weight loss agent, cascara interacts with other drugs and can throw off the body’s mineral balance.

Glucomannan: Derived from a plant root, glucomannan has been banned in several countries because when exposed to liquid it swells and can result in a gastrointestinal obstruction.

Guarana: A natural stimulant, guarana can increase blood pressure.

Yerba mate: Often used in a tea, yerba mate ingestion can result in high blood pressure and overstimulation of the central nervous system. It may also be linked to esophageal cancer.

Guar gum: It is used in the food and pharmaceutical industries as a thickening agent, but taken alone, guar gum can swell on contact with liquid, potentially leading to an obstruction.

Ephedra (ma huang): Consumers should not be able to find OTC supplements containing this ingredient, because the FDA banned its sale in dietary supplements in 2004. Use of ephedra can cause high blood pressure and other cardiovascular problems.

SOURCES: (Healthy Weight Forum)Nutr Metab Cardiovasc Dis 2008 Feb; 18(2): 158-68 (website: (Teachers Domain) (Obesity Action Council) (Daily Med) (American Association of Retired Persons)www.pdrhealth.comNIH, Office of Dietary Supplements websiteOver-the-Counter and Herbal Remedies for Weight Loss

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