<?xml version='1.0' encoding='UTF-8'?><rss xmlns:atom="http://www.w3.org/2005/Atom" xmlns:openSearch="http://a9.com/-/spec/opensearchrss/1.0/" xmlns:blogger="http://schemas.google.com/blogger/2008" xmlns:georss="http://www.georss.org/georss" xmlns:gd="http://schemas.google.com/g/2005" xmlns:thr="http://purl.org/syndication/thread/1.0" version="2.0"><channel><atom:id>tag:blogger.com,1999:blog-8712687967317529203</atom:id><lastBuildDate>Fri, 01 Nov 2024 07:14:18 +0000</lastBuildDate><category>hgh</category><category>IGF</category><category>Guide</category><category>176-191</category><category>insulin</category><category>Human Growth Hormone</category><category>CJC-1295</category><category>GHRH</category><category>IGF-1</category><category>Fragment 176-191</category><category>PEG-MGF</category><category>growth hormone</category><category>GHRP</category><category>HGH fragment 176-191</category><category>Melanotan</category><category>PT-141</category><category>guides</category><category>peptide</category><category>GHRP-6</category><category>fat loss</category><category>growth hormone releasing hormone</category><category>insulin like growth factor</category><category>Beginner’s Guide To IGF1-lr3</category><category>Bremelanotide</category><category>DAC CJC 1295</category><category>GHRP-2</category><category>HGH DOSING</category><category>HGH Frag 176-191</category><category>Hexarelin</category><category>Humalog</category><category>IGF-1 Long R3</category><category>IGF1</category><category>Insulin-Like Growth Factor Recombinant 3</category><category>Ipamorelin</category><category>Peptide Combinations Guide</category><category>Synthetic Growth Hormone</category><category>TB-500</category><category>bacteriostatic water</category><category>bodybuilders</category><category>bodybuilding</category><category>dosing</category><category>injection</category><category>insulin-like growth factor</category><category>long r3 igf-1</category><category>mixing IGF</category><category>peptide 176-191</category><category>protocol</category><category>storage</category><category>191AA Growth Hormone</category><category>A New Peptide Treatment For Healing Acne Scars</category><category>ACE-031</category><category>AICAR</category><category>About CJC-1295</category><category>Actions of Insulin</category><category>Basic peptide guide</category><category>Beginner’s Guide To IGF1-lr3 Reconstituting IGF-1lr3</category><category>Benefits of IGF 1</category><category>Blast Protocol</category><category>Blast Protocol: HGH Igf-1 and insulin</category><category>Bodybuilding Peptides 101</category><category>Bremelanotide (PT-141)</category><category>Bremelanotide PT-141 Instruction</category><category>CJC 1295</category><category>CJC 1295 info for the beginner</category><category>CJC-1293 DAC</category><category>CJC-1293 DAC dosing</category><category>CJC-1295 DAC</category><category>CJC-1295 DAC Dosage</category><category>CJC-1295 Facts</category><category>CJC-1295 Growth Hormone Releasing Hormone</category><category>CJC-1295 dosing</category><category>CJC-1295 with DAC</category><category>Carb-Loading &amp; 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Understanding Peptide Reconstitution&lt;/h2&gt;
&lt;br /&gt;It seems to be increasingly common that users are introducing themselves to the idea of pinning through the use of peptides (although, arguably, hcg usage is also increasing in usage for those running non-injectable cycles). While I personally find these to be a great way to get yourself comfortable with the idea of injecting, it seems many become confused nearly immediately with how to at the first step, reconstitution. So I decided to just create a quick reference for those of you out there, and show you how the simple math required is not intimidating in the least. This guide will be a bit long, as I am hoping to avoid the common questions, but I think it will be a very good guide for some, and maybe too &quot;simple&quot; for others.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;A short disclaimer:&lt;br /&gt;&amp;nbsp;This guide is purely hypothetical, and I do not encourage the use of any PED without the close guidance of a physician. This guide takes no consideration to the laws of your country. I do not condone any illegal activity. It is merely designed to be an educational resource. &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;Alright, so this guide will follow under the assumption that you have aquired your peptide of choice (or hCG), and are ready to reconstitute it.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;You will need the following items:&lt;br /&gt;•Your Peptide Vial&lt;br /&gt;•Bacteriostatic Water&lt;br /&gt;•Alcohol Wipes (available at your local pharmacy, usually near diabetic supplies)&lt;br /&gt;•Insulin Syringe (more on this in a moment)&lt;br /&gt;
&lt;br /&gt;&amp;nbsp;&lt;strong&gt;&lt;em&gt;A quick discussion on syringes&lt;/em&gt;&lt;/strong&gt;:&lt;br /&gt;
&lt;br /&gt;&amp;nbsp;Syringe availability will vary largely depending on the laws of your state/country. In many states, such as mine, low quantity purchases of insulin syringes are available at the pharmacy without the need for a prescription. Laws such as these are in place as a counter measure to help avoid the increase of HIV transmission through unsafe needle usage, by allowing addicts to purchase clean syringes. &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;Size will depend on your source. An insulin syringe will typically range from 29g to 31g. For those unaware, the smaller the gauge (the &quot;g&quot;), the larger the number. So a 31g will be smaller needle width than a 29g. Generally, smaller gauge needles can provide less soreness through injection, but they are also much more fragile. Having used a 31g, I do prefer them for the ease of injection (minimal &quot;pinch&quot; feel), but they do become increasingly fragile, so proper care is required.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;Now that you have your supplies gathered, it is time to reconstitute your peptides. Please make sure that you do this in a clean environment to reduce the risk of contamination. &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;For this example, I will be using a typical 5mg product, as is typical of the GHRPs provided by many companies. Although your particular product may not contain 5mg, the same idea will hold through to other products, just with a different amount of actives. I will also be under the assumption that you will want 100mcg doses (although again, this will vary by product/your required dosing).&lt;br /&gt;
&lt;br /&gt;
&lt;strong&gt;Before you begin, you must do the math to understand how much bacteriostatic water you will need for your reconstitution&lt;/strong&gt;. &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;If you are looking for the said 100mcg doses, from a 5mg vial, then you will have 50 doses from this vial. 100mcg x 50 = 5,000mcg, or 5mg. You can apply this to any amount of product. For example, Ipamorelin is usually available in 2mg vials. In that case, you would have 2,000mcg of Ipamorelin, which divided by 100mcg would give you 20 doses. The amount of dosages is important here, as it will dictate how to utilize your reconstituted product. &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;So back to the original 5mg product, we know we are going to have 50 doses. The idea here then, is to add enough bac water to the peptide in order to allow you to dose those individual dosage. Personally, I like to use as little Bac water as needed, but also attempt to keep it easy enough to dose. The key point here is to know that no matter how much bac water you add to your vial, 1/50 of that will always be 100mcg.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;With that said, if you add 1ml of bac water to the vial, your 100mcg dosage will be 2iu on the syringe. &lt;br /&gt;&amp;nbsp;(1ml = 1cc on your syringe = 100iu, so 100iu/50 doses = 2iu).&lt;br /&gt;
&amp;nbsp;If you add 2ml of bac water to the vial, your 100mcg dosage will be 4iu (200iu/50 doses = 4iu).&lt;br /&gt;
&amp;nbsp;If you add 3ml of bac water to the vial, your 100mcg dosage will be 6iu (300iu/50 doses =6iu).&lt;br /&gt;
&amp;nbsp;It is up to you how much bac water you will like to use, and utilizing the option of keeping this guide non-opinionated, I won&#39;t give a recommendation on this, however, it will be dictated by how large your vial is and how accurate your pins are (a 50iu *sold as 1/2 cc* syring will make it easier to measure smaller amounts, where a 1cc *100iu* syringe will make it more difficult to measure smaller amounts). &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;Once you have an amount chosen, we can move on the the actual reconstitution. In this example, I will reconstitute with 2ml of bac water.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;1. Snap of off the plastic cover of your peptide vial and your bac water. &lt;br /&gt;
&lt;br /&gt;
2. Take an alcohol wipe, and wipe down the rubber top of both the peptide vial and your bac water, and then discard the wipe and allow vials to dry for a second or two.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;3. Take a syringe and remove the safety cap (most will have one cap over the needle, and one over the plunger). Set these caps aside, while taking precaution not to expose your needle to any other object (it is sterile!). Pull the plunger on your syringe to the maximum reading (will usually be either 1/2cc or 1cc) to allow the syringe to fill with air. (It is also common practice to draw this air from the peptide vial. You can do this by inserting the needle into the peptide vial, keeping it right side up, and drawing the air that way. Then pull the syringe from the bottle, and on to step 4). &lt;br /&gt;
&lt;br /&gt;
4. Insert the needle into the rubber portion of your bacteriostatic water. With the syringe inserted, turn the vial of bacteriostatic water upside down, and push the plunger into the syringe (this will cause the air to enter the vial). Then, slowly, draw back on the syringe back to that maximum reading, as it will allow the syringe to fill with bac water. &lt;br /&gt;
&amp;nbsp;Quick Note: The reason you fill your syringe with air, and then insert the air into the vial, is to keep the pressure within the vial, which will allow you to draw with much greater ease. &lt;br /&gt;
&lt;br /&gt;
5. You may now turn the vial of back water back to right side up, and remove your syringe, again taking caution to avoid the needle from coming into contact with anything else.&lt;br /&gt;
&lt;br /&gt;
6. We are now ready to insert the bac water into the peptide vial. I recommend reconstituting slowly, and avoiding adding the bac water directly onto the peptide, and rather down the sides of the vial. Take your peptide vial, and insert the syringe through the rubber stopper on an angle, enough so that once the needle penetrates the rubber, it is angled towards the side of the vial. &lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&amp;nbsp;7. Slowly push down on the plunger allowing the bac water to enter down the sides of the vial. Take your time doing this, as there is no rush.&lt;br /&gt;
&lt;br /&gt;
8. Once all of the bac water is into the vial, remove the syringe and gently (GENTLY!) swirl the vial allowing the peptide to dissolve into the bac water.&lt;br /&gt;
&lt;br /&gt;
9. Depending on the target amount of bac water to be added, and the size of your pin, you must now repeat steps 3-8 until you have added the correct amount of bacteriostatic water. If you are aiming for 2ml of bacteriostatic water, and are using a 1/2cc syringe, this process must be done a total of 4 times, and if using a 1cc syringe, this process must be done a total of twice.&lt;br /&gt;
&lt;br /&gt;
10. Once the proper amount is added, place the caps back on both ends of your syringe and properly discard of it. Do not reuse this syringe for injection.&lt;br /&gt;
&amp;nbsp;Depending on your product, refridgeration might be necessary. If so, store reconstituted product in fridge.&lt;br /&gt;
&lt;br /&gt;
That should be it. Happy research. If you have any questions, feel free to ask, but only do so after having completely read through this guide.&lt;br /&gt;
&amp;nbsp;If you guys like this guide, I might do some later on some common peptides, when I can get to it.&lt;br /&gt;
&amp;nbsp;-h2s &lt;br /&gt;
&lt;br /&gt;</description><link>http://fitness-peptides.blogspot.com/2016/03/understanding-peptide-reconstitution.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-6066683839960534994</guid><pubDate>Tue, 12 Jan 2016 10:40:00 +0000</pubDate><atom:updated>2016-01-12T05:40:55.059-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">IGF-1</category><category domain="http://www.blogger.com/atom/ns#">peptide</category><title>IGF-1 Reverses Aging and Heals damaged brain cells </title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;
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&lt;br /&gt;
&lt;strong&gt;Growth Hormone Production and IGF-1&lt;/strong&gt;The production of growth hormone 
is at its peak during the adolescence period. Most of the HGH is secreted into 
the bloodstream in brief-bursts manner. It also occurs during the early hours of 
deep sleep or REM. Once HGH is in the bloodstream, it stays there for a short 
period, perhaps in a few minutes or longer enough in stimulating its uptake into 
the liver, wherein conversion to growth factors happen. The Insulin Growth 
Factors (IGF-1) are the most important of all these growth factors, also called 
the Somatomedin C. &lt;br /&gt;&lt;br /&gt;Furthermore, the growth hormone acts either indirectly or 
directly through the intermediary insulin growth factors to each organ system in 
the body. Hence, almost nothing is able to escape from its magic touch. Growth 
hormone is also capable of increasing the size of several organs and tissues, 
including the brain. Based on recent studies, involving animals as test 
subjects, HG has manifested the regeneration of damaged brain 
tissue.&lt;br /&gt;&lt;b&gt;&lt;br /&gt;IGF-1&lt;/b&gt;Rather than the growth hormone itself, it is the 
IGF-1 that varies widely throughout the day and is used in measuring how much GH 
has been secreted by the body. Thus, the IGF-1 is responsible for the actions 
and benefits associated with HGH and is 10 times more potent than HGH. To date, 
HG is under investigation as a separate medication for its many indications 
similar to HGH. Phil Micans from the London-based International Aging Systems, 
believes that the IGF-1 will become the top choice among the hormones in just a 
few years. &lt;br /&gt;&lt;b&gt;&lt;br /&gt;HGH and IGF-1 for Anti-aging &lt;/b&gt;Doctor Vincent 
Giampapa, the Clinical Research director of the Longevity Institute 
International, based in Montclair, New Jersey, said that the blueprint of aging 
is under the DNA’s hood of telomere, and considered as the “clock” at the end of 
each chromosome, which is shortened with every cell division.&lt;br /&gt;&lt;br /&gt;Hence, 
reversing the aging at the cellular level is possible through a substance, which 
will restore the length of telomere. However, that substance is still 
unavailable. Giampapa strongly believes that the substance will be available in 
not more than a decade though. Until then, the growth hormone, along with its 
IGF-1 attendant hormone is able to perform the next best thing, assisting in 
keeping the cell as healthy as possible. &lt;br /&gt;&lt;br /&gt;Overall, the ability and function 
of the cell largely depend on the DNA, the genetic material in the nucleus that 
codes for all the enzymes, proteins, and hormones that make it run. Thus, DNA is 
similar to an army under a consistent attack from ultraviolet light, body heat, 
oxygen free-radicals, and many other damaging factors. While the DNA has the 
ability in repairing itself, it still falls short with age, which is the same 
aging process that largely affects the cell. Simultaneously, damage accumulates 
in the cell’s mitochondria, the energy center, which has its separate DNA. Among 
the things to limit the DNA damage is the intake of antioxidant supplements like 
vitamins E and C in bolstering the body’s defenses.&lt;br /&gt;According to Giampapa and 
a hormone replacement therapy specialist Thierry Hertoghe, the latest research 
in Europe indicates that human growth hormone and the IGF-1 could go farther 
than antioxidants, going beyond what antioxidants can do. All the more, HGH and 
IGF-1 can transport raw materials to the cells for repair and 
renovation.&lt;br /&gt;IGF-1 can instigate the delivery of RNA, DNA and nucleic acids 
directly into the cell nucleus. Meanwhile nucleic acids are helpful in repairing 
the damage in the DNA, while stimulating cell division. Growth hormone, on the 
other hand, launches the transport of nucleic acids and amino acids into the 
cell’s cytoplasm, just outside the nucleus. In this process, the HGH and IGF-1 
are not only able to minimize the DNA and cell stellar damage, but also treating 
the DNA and the cell. In all, both hormones can treat the blueprints of the 
aging process.&lt;br /&gt;&lt;br /&gt;Primarily, the IGF-1 is the GH chain’s other end, the 
downstream player, which actually exerts the effects associated with the HGH. It 
is able to cause a great deal of excitement in two groups, including the 
researchers and the group of bodybuilders, who are both using the substance for 
individual purposes. &lt;br /&gt;Meanwhile, the IGF-1 is said to be more potent than the 
HGH, as it latter exerts its effects through the former substance. Without a 
surprise, IGF-1 injections can do what HGH does, plus other effects in 
accordance with its proponents. IGF-1 can increase the lean body mass, while 
reducing fats, building bone, nerves, and muscle all at the same time. Through a 
direct intake, the pituitary gland is avoided, which could be burnt out 
throughout the aging process. &lt;br /&gt;&lt;b&gt;&lt;br /&gt;Anti-Aging Action&lt;/b&gt; – When it comes 
to the anti-aging efforts, the iGF-1 is said to be more potent than the HGH. 
Doctor Keith Kelly conducted a research work, indicating that growth hormone was 
able to reverse the shrinking of the thymus. According to Kelly, only the IGF-1 
worked, and not the GH that worked in his experiment on cells in culture. 
However, both GH and the IGF-1 worked on living animals, saying that both 
substances are significantly elevated in the older test subjects as they were 
treated with growth hormone. He predicted that IGF-1 would be the main player 
though.&lt;br /&gt;&lt;b&gt;&lt;br /&gt;Disease and Brain Aging Prevention&lt;/b&gt; – Among the other 
spectacular uses of GH and IGF-1 is their ability to prevent the effects of 
brain aging, not to mention their capacity to treat such condition. Based on an 
experiment, the substances manifested momentous implications for stroke, brain 
injury, neurodegenerative disease, and aging. A team of scientist based in New 
Zealand said that IGF-1 can halt the death of cells in the brain. &lt;br /&gt;Peter 
Gluckman, Barabara Johnston, along with their colleagues at the University of 
Auckland discovered that IGF-1 injections administered in two hours, following 
brain injury in baby lambs were able to rescue the damaged neurons, salvaging 
cells that would have died during apoptosis, the programmed cell death. 
Apoptosis is the brain cell loss that occurs for up to three days upon the 
initial injury. &lt;br /&gt;In all, the treatment was very effective in stopping the 
death of brain cells in areas such as the cortex, hippocampus, and other areas 
linked with the memory and thinking. Results also manifested in the striatum, 
the brain area that is associated with the Parkinson’s disease in human. Hence, 
IGF-1 replacement reduced seizures in animals suffering from brain 
damage.&lt;br /&gt;The researchers further suggest that IGF-1 could be used in 
preventing the effects of neonatal hypoxia lack of oxygen in the brain that 
occurs during birth. This condition could leave a baby suffering from permanent 
brain damage. This ability of the IGF-1 only opens doors for more possibilities, 
such as the reversal of the programmed cardiac cell death, following a heart 
attack, which can cause a victim with a heart full of dead tissues. &lt;br /&gt;Keep in 
mind that the stroke can destroy the brain tissue, and as the cells die, the 
victim of a stroke is left unable to talk, walk, or think clearly. This also 
plays a significant role in many other neurodegenerative diseases like muscular 
dystrophy, Alzheimer’s disease, and multiple sclerosis (MS). For the very first 
time, there is a considered weapon or treatment against death at the cellular 
level.&lt;br /&gt;&lt;b&gt;&lt;br /&gt;Improvement of Glucose Metabolism&lt;/b&gt; – Similar to insulin, the 
IGF-1 has the same properties with the former as it can also improve the blood 
sugar profiles of patients with Type 2 diabetes. An increase in insulin 
resistance is manifested through high doses of GH, but the administration of 
IGF-1 can actually regulate the insulin resistance.&lt;br /&gt;Researchers Bernard 
Beaufrere and Nelly Mauras from Jacksonville, Florida’s Nemours Children&#39;s 
Clinic studied several things, including the effect of IGF-1 on protein 
metabolism as the substance has the ability to halt protein-wasting brought 
about by glucocorticosteroid drugs such as prednisone, as well as its effects on 
glucose and insulin metabolism. The researchers divided the group of volunteers 
into three: IGF-1 alone, Prednisone alone, and IGF-1 plus prednisone. &lt;br /&gt;The 
study discovered that 100 micrograms of IGF-1 per kilogram of body weight that 
was administered twice a day, was able to enhance the protein metabolism of the 
body, in the same manner as growth hormone. IGF-1 decreased the protein 
breakdown among the subjects who took prednisone, whereas, GH in an earlier 
research resulted in insulin resistance and carbohydrate intolerance when 
administered with prednisone did not cause diabetes-like effects. Rather, the 
volunteers who received IGF-1 with prednisone had a regular glucose metabolism. 
&lt;br /&gt;The researchers said the discovery was remarkable in line with the 
glucocorticoids as they are known to curb insulin circulation and decrease 
insulin sensitivity as well. Due to this discovery and other researches, the 
experts now believe that IGF-1 promises treatment for protein catabolic states, 
such as in patients who need IV feedings after a surgery.&lt;br /&gt;&lt;b&gt;&lt;br /&gt;Helping 
Diabetic Patients&lt;/b&gt; – Two double-blinded clinical researches in 1997 also 
showed that recombinant IGF-1 injections could reduce the need for insulin 
remarkably, up to 45% in people suffering from diabetes mellitus, and who are 
insulin-dependent. One particular study involved eight adults aged 24 to 49, the 
other group was 43 children and adolescents aged 8 to 17. IGF-1 resulted in an 
overall lower cholesterol and triglyceride levels in the adult trial, after four 
days of IGF-1 treatment.&lt;br /&gt;The clinical trials were only short-term, which 
lasted for 19 days and four weeks respectively. The insulin requirement that 
dropped remarkably, without serious side effects indicated that IGF-1 is a 
promising drug for diabetes treatment. Although it does not do away with insulin 
requirement, IGF-1 improved the blood sugar control, preventing further 
complications brought about by the disease, like blindness, peripheral nerve 
damage, and heart disease.&lt;br /&gt;&lt;b&gt;&lt;br /&gt;Nerve Regeneration&lt;/b&gt; – Furthermore, 
IGF-1’s potentials also include its ability in repairing the peripheral nerve 
tissue, which have been damaged by illness or injury. A torn nerve means that a 
connection to the muscle is damaged, resulting in loss of movement, along with 
muscle deterioration. To some extent, peripheral nerves could regenerate, but 
severe tears of over a few millimeters can lead to permanent injury. IGF-1, 
however, can repair and reconnect severely injured nerves up to six millimeters, 
a truly remarkable ability.&lt;br /&gt;Hans-Arne Hansson, a Swedish scientist and works 
at the Institute of Neurobiology at the University of Goteborg, discovered that 
IGF-1 combined with other growth factors can stimulate a more drastic 
regeneration. Hansson added that IGF-1 itself, and when combined with further 
growth factors is likely to promote further repair and healing process.&lt;br /&gt;In 
addition, IGF-1 has also shown significant effects on the spinal cord motor 
neurons, involving studies of cells in animals and culture. The motor neuron 
activity in the spinal cord cultures had increased by 150% up to 270%. The 
programmed death of cells in developing chick embryos also decreased in a 
relative manner. The substance also enhanced the emergence of axons of the 
spinal cord motor neurons in animal studies, while increasing intramuscular 
nerve sprouting in normal adult rats. A team of researchers at the Cephalon, 
Inc., West Chester, Pennsylvania said IGF-1 could be the “long-sought endogenous 
motor neuron sprouting factor.&quot;&lt;br /&gt;In all, the implications of IGF-1 are not 
mind-boggling at all as it is highly capable of regenerating the spinal cord 
motor neurons, which is helpful in the treatment of amyotrophic lateral 
sclerosis (ALS), a health condition that results in the loss of cortical motor 
neurons and spinal cord neurons that lead to paralysis, and even death. It could 
likewise help in treating Charcot-Marie-Tooth syndrome, among the peripheral 
neuropathies conditions.&lt;br /&gt;Apparently, Doctor John Wittig of the UCLA has been 
using the substance in preventing AIDS wasting among HIV-infected patients. The 
substance allows more aggressive chemotherapy in certain patients because drugs 
like Crisplatin and Vincristine at higher doses could lead to peripheral 
neuropathies.&lt;br /&gt;&lt;br /&gt;&lt;b&gt;Network of Growth Factors&lt;/b&gt;&lt;br /&gt;Among the body’s 
growth factor army, the IGF-1 is now identified, isolated, and cloned through a 
genetic engineering technology for drug use. Doctor Eric Dupont, a growth factor 
researcher said, GH is equivalent to the general, while the growth factors are 
the foot soldiers in the army. Growth factors act as hormones, hooking onto the 
cell receptors, while sending biochemical signal throughout the cell’s interior. 
On the other hand, hormones generally send a long distance message. Most of the 
growth factors make the local calls.&lt;br /&gt;&lt;br /&gt;&lt;b&gt;IGF-1 as Every Bodybuilder&#39;s 
Dream &lt;/b&gt;&lt;br /&gt;To date, many world-class bodybuilders are making use of 
IGF-1. They have reported massive muscle magnification, up by 20 pounds. Muscle 
Mass 2000 is an article, trumpeting IGF-1 as the most possible and most potent 
bodybuilding drug ever. T.C. Luoma, the author of the article said that IGF-1 is 
widely available in America at the moment, while sold in Venice out of the 
trunks of cars. In Southern California gyms alone, IGF-1 is discreetly sold in 
brown paper bags. There are still no supporting evidences of the bodybuilders’ 
claims, but the anecdotal evidence is certainly building up. &lt;br /&gt;Luoma added 
that bodybuilders have been testifying their IGF-1 experiences, indicating 5% 
drop in their body fat, in only a month. The users also testified that their 
lean body mass increased, and their strength became more incredible. In a 
particular statement, it indicated that the IGF-1 is the most wonderful thing in 
the world. On the contrary, there are skeptics like Doctor Mauro Di Pasquale, a 
performance-enhancing compound expert, although there is a basis for the belief 
on the capacity of IGF-1 taken with HGH. &lt;br /&gt;Over and above, there is a feedback 
mechanism between the HGH in the pituitary gland and the IGF-1 in the liver. HGH 
stimulates the IGF-1 release; however, there could be a rise of IGF-1 levels at 
a certain period in the circulation. This signals the shutdown of GH. Thus, 
there is a lag time throughout this process, and indication that growth hormone 
levels rise at night time, while IGF-1 levels rise in the daytime. Now, 
bodybuilders are hoping that through growth hormone and IGF-1, the effect on 
protein synthesis may be doubled as well. &lt;br /&gt;&lt;br /&gt;&lt;b&gt;Bottom 
Line&lt;/b&gt;&lt;br /&gt;Growth hormone, most especially its army of growth factors such 
as the IGF-1 is widely used by bodybuilders, optimizing its bodybuilding 
effects, including the remarkable anti-aging reversal ability of the substance. 
Clinical trials have also shown IGF-1’s capability in treating various ailments 
like cancer and diabetes.&lt;br /&gt;
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&lt;br /&gt;</description><link>http://fitness-peptides.blogspot.com/2016/01/igf-1-reverses-aging-and-heals-damaged.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-5042608124416536336</guid><pubDate>Mon, 30 Nov 2015 15:02:00 +0000</pubDate><atom:updated>2015-11-30T10:02:00.513-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">TB-500</category><title>Healing Peptide Thymosin Beta 4 – TB500</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;
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&lt;br /&gt;
&lt;h2&gt;
Explanation and common uses of TB-500:&lt;/h2&gt;
Thymosin Beta 4 is the thymosin peptide shown to promote protection, growth, repair, remodeling and healing. Studies have shown that it can promote migration of cells, formation of blood vessels, maturation of stem cells, activation of progenitor cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. Thymosin Beta 4 is the form that is naturally produced within the human body and obviously cant be bought.&amp;nbsp;The synthetic form of Thymosin Beta 4 that is synthesized and manufactured is called TB-500 ie this is what can be bought, injected etc. There is no difference in efficacy between the two&lt;br /&gt;
&lt;div class=&quot;wp-caption alignleft&quot; id=&quot;attachment_627&quot; style=&quot;width: 169px;&quot;&gt;
&lt;div class=&quot;wp-caption-text&quot;&gt;
Buy your tb-500 here&lt;/div&gt;
&lt;/div&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;h3&gt;
Thymosin Beta 4 Dose:&lt;/h3&gt;
Dosage depends on the purpose and severity of the injury / damage you are treating. People generally use between 4 to 8 mg of TB500 per week during the initial (loading) period of 4 to 6 weeks. Afterwards some opt to maintain the effects with a low 2 to 6 mg dose once every 2 weeks. The effects of TB-500 wear off within 2 – 3 weeks of injection.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;h3&gt;
How to take Thymosin Beta 4:&lt;/h3&gt;
1. Get the tops of your vial and bacteriostatic/sterile water vial off.&lt;br /&gt;
2. Using an alcohol pad, clean the top of both vials (tb-500 and water)&lt;br /&gt;
3. Using a new sterile insulin syringe, draw syringe full of air(1ml) and inject it into the bacteriostatic vial then withdraw 1ml of bacteriostatic water.&lt;br /&gt;
4. Inject this 1ml of bacteriostatic water into the side of the tb-500 vial. Don’t force it and don’t spray it onto the lyophilized powder but rather into side of the vial so that the powder merely dissolves into it.&lt;br /&gt;
5. You can repeat step 3 and 4 if you are going to dilute the powder using more than 1ml eg 2ml&lt;br /&gt;
6. Check to see that all powder has dissolved and gently roll vial to ensure it has all dissolved well. DO NOT SHAKE.&lt;br /&gt;
7. If you want to equalize the pressure inside the vial you can pierce it with your insulin syringe but with no plunger in it&lt;br /&gt;
8. Withdraw appropriate amount of the now dissolved tb-500 into your syringe, try and avoid any major bubbles by tapping side of syringe and adjusting plunger. Ready for injection. (You can use a brand new syringe if you want the needle to be sharp and use the one that you pierced the rubber tops of your vials with to simply fill/load the new syringe with)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;strong&gt;Duration:&lt;/strong&gt;&lt;br /&gt;
1.&lt;strong&gt; Thymosin Beta 4&amp;nbsp;loading phase:&lt;/strong&gt;&lt;br /&gt;
&lt;ul&gt;&lt;/ul&gt;
&lt;ul&gt;&lt;/ul&gt;
&lt;ul&gt;
&lt;li&gt;duration: between 4 – 6 weeks&lt;/li&gt;
&lt;li&gt;dosage: between 4 – 8 mg of TB-500 per week&lt;/li&gt;
&lt;li&gt;frequency of injection:2 mg per injection, between 2 – 4 times per week (depending on the total weekly dosage)&lt;/li&gt;
&lt;/ul&gt;
&lt;strong&gt;TB-500 maintainance phase:&lt;/strong&gt;&lt;br /&gt;
&lt;ul&gt;&lt;/ul&gt;
&lt;ul&gt;
&lt;li&gt;duration: as long as needed&lt;/li&gt;
&lt;li&gt;dosage: between 2 – 6 mg of TB-500 per 2 weeks&lt;/li&gt;
&lt;li&gt;frequency of injection:2 mg per injection, between 2 – 3 times per 2 weeks (depending on the total bi-weekly dosage)&lt;/li&gt;
&lt;/ul&gt;
&lt;strong&gt;Dilution:&lt;/strong&gt;&lt;br /&gt;
BA water&lt;br /&gt;
&lt;h3&gt;
Side effects of Thymosin Beta 4 :&lt;/h3&gt;
There have been no reported side effects during the past few years since TB-500 became popular by athletes. For some reason people expect the TB-500 to produce flu-like symptoms. After thorough research through every Thymosin beta-4 related usage log on bodybuilding forums, there are simply no reports to confirm any side effects.&lt;br /&gt;
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&lt;br /&gt;</description><link>http://fitness-peptides.blogspot.com/2015/11/healing-peptide-thymosin-beta-4-tb500.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-1686017164096182312</guid><pubDate>Sat, 14 Nov 2015 14:45:00 +0000</pubDate><atom:updated>2015-11-14T09:45:36.981-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">TB-500</category><title>HOW TO USE TB-500 Thymosin beta 4 for healing benefits</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;
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&lt;br /&gt;
&lt;strong&gt;&lt;br /&gt;&lt;/strong&gt;&lt;br /&gt;
&lt;strong&gt;&lt;/strong&gt;&lt;strong&gt;&lt;/strong&gt;Research has shown that the best results are achieved when using sterile saline solution (Sodium Chloride Injection BP 0.9%) to mix TB-500 (thymosin beta4).&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;strong&gt;Important:&lt;/strong&gt;&lt;br /&gt; Only prepare the vials that will be used immediately. If using doses that are lower than the recommended dose, prepared vials must be stored in the fridge and be used within 8 days.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;strong&gt;TB-500&lt;/strong&gt;&lt;strong&gt; preparation:&lt;/strong&gt;&lt;br /&gt; Remove the plastic protective cap of the sealed vial containing the powder of peptides.&lt;br /&gt;
Insert the filled syringe of 2ml of sodium chloride solution into the rubber top of the vial and release the 2ml of sodium chloride into the vial.&lt;br /&gt;
Remove the syringe and gently rotate the vial until the powder is completely dissolved.&lt;br /&gt;
Ensure that the solution is well mixed with all powder thoroughly dissolved for maximum safety and effectiveness.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;strong&gt;TB-500&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;&lt;strong&gt;Administration:&lt;/strong&gt;&lt;br /&gt; A Subcutaneous (S/C) inj.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;strong&gt;TB-500&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;&lt;strong&gt;Frequency:&lt;/strong&gt;&lt;br /&gt; Research studies have further shown that one (2ml. vial) Sub-Q Inj. each week for six consecutive weeks provides the best results.&amp;nbsp; There after, use only one (2ml. vial) per month.&amp;nbsp; It’s best to give the Sub-Q Inj. 6 days before intense work outs. Therefore for best results, one vial per Sub-Q injection per week for 6 consecutive weeks, then 1 vial per month (the glass vial is 2ml, with 10mg TB-500 per vial), so it is 10mg/2ml).&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;strong&gt;Contraindications:&lt;/strong&gt;&lt;br /&gt; No known contraindication with tb4 peptide products, however tb500 has not been thoroughly tested to know its full effects.&lt;br /&gt; The product should not be used if the subject is pregnant or breast feeding.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
&lt;strong&gt;TB500 Storage:&lt;/strong&gt;&lt;br /&gt; Store the product at room temperature in a non humid environment. An opened vile can be kept for up to 8 days in refrigerated storage.&lt;br /&gt;
&lt;br /&gt;
&lt;strong&gt;What is TB-500?&lt;/strong&gt;TB-500 is a synthetic version of the naturally occurring peptide present in virtually all human and animal cells, Thymosin Beta 4 (TB-500). It is a first-in-class drug candidate that promotes the following*:&lt;br /&gt;
•&amp;nbsp; Endothelial (blood vessels) cell differentiation&lt;br /&gt;•&amp;nbsp; Angiogenesis (growth of new blood cells from pre-existing vessels) in dermal tissues&lt;br /&gt;•&amp;nbsp; Keratinocyte migration&lt;br /&gt;•&amp;nbsp; Collagen deposition; and&lt;br /&gt;•&amp;nbsp; Decreases inflammation.&lt;br /&gt; One of TB500 key mechanisms of action is its ability to regulate the cell-building protein, Actin, a vital component of cell structure and movement. Of the thousands of proteins present in cells, actin represents up to 10% of the total proteins which therefore plays a major role in the genetic makeup of the cell.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
This potent peptide is a member of a ubiquitous family of 16 related molecules with a high conservation of sequence and localization in most tissues and circulating cells in the body. Thymosin beta-4 not only binds to actin, but also blocks actin polymerization and is the actin-sequestering molecule.&lt;br /&gt;
&lt;br /&gt;&lt;br /&gt;
Tß4 was identified as a gene that was up-regulated four-to-six fold during early blood vessel formation and found to promote the growth of new blood cells from the existing vessels. This peptide is present in wound fluid and when administered subcutaneously, it promotes wound healing, muscle building and speeds up recovery time of muscles fibres and their cells.&lt;br /&gt;
An additional key factor of &lt;em&gt;&lt;strong&gt;TB500&lt;/strong&gt;&lt;/em&gt; is that it promotes cell migration through a specific interaction with actin in the cell cytoskeleton. It has been demonstrated that a central small amino acid long-actin binding domain has both blood cell reproduction and wound healing characteristics. These characteristics are uncovered by accelerating the migration of endothelial cells and keratinocytes. It also increases the production of extracellular matrix-degrading enzymes.&lt;br /&gt;
Research confirms that TB500 is a potent, naturally occurring wound repair factor with anti-inflammatory properties. TB-500 is different from other repair factors, such as growth factors, in that it promotes endothelial and keratinocyte migration. It also does not bind to the extracellular matrix and has a very low molecular weight meaning it can travel relatively long distances through tissues.</description><link>http://fitness-peptides.blogspot.com/2015/11/how-to-use-tb-500-thymosin-beta-4-for.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-4369976099694065627</guid><pubDate>Tue, 13 Jan 2015 10:36:00 +0000</pubDate><atom:updated>2015-01-13T05:36:19.447-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">DAC CJC 1295</category><title>DAC CJC 1295</title><description>&lt;h2&gt;DAC CJC 1295&lt;/h2&gt;&lt;br /&gt;
&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;a href=&quot;http://www.superiorpeptide.com/104.html&quot;&gt;&lt;img src=&quot;http://www.basskilleronline.com/sponsors/bassbogo.jpg&quot; /&gt;&lt;/a&gt; &lt;/div&gt;&lt;br /&gt;
DAC conjugated CJC 1295 (Receptor Grade) is an hGH secretogue that is unique by way of an additional lysine molecule that is added to facilitate the DAC complex. This conjugation makes for a much longer half-life.  DAC CJC 1295 tends to have a very limited availability everywhere due to expense and difficulty to manufacture.  CJC 1295 DAC is a exceptionally designed peptide and is known for being the finest of the hGH secretogues. Receptor grade: 98%+ pure 2000mcg / 2ml glass vial. THIS PRODUCT IS INTENDED FOR RESEARCH PURPOSES ONLY. CAN BE HARMFUL IF USED INAPPROPRIATELY.&lt;br /&gt;
&lt;br /&gt;
In the healthy human body, large amounts of growth hormone are stored in the pituitary.  The cells within the pituitary release growth hormone in response to signaling by GHRH (Growth Hormone Releasing Hormone), Ghrelin (of which GHRPs - Growth Hormone Releasing Peptides - are mimetics), and are inhibited from releasing these stores by Somatostatin.  GHRH and Ghrelin act on different populations of somatotropes (GH releasing cells).  GHRP/Ghrelin increases the number of somatotropes releasing GH but not the amount released by each cell;&lt;br /&gt;
GHRH affects both the number of secreting cells and - moreso - the amount they each secrete. [1] GHRH and Ghrelin are released in specific patterns that vary depending on event and environment: post-exercise, in response to slow wave sleep, in certain stages of life and physical development, and so on.&lt;br /&gt;
&lt;br /&gt;
Most people (even the diseased) continue to possess the ability to make GH in the pituitary. The problem is in the signaling of the pituitary to release it (and make more). So yes CJC is meant to replace the external administration of GH in some (but not all) cases. Even most people with diseases that affect growth hormone secretion retain the ability to continue to make GH in their pituitaries.  The disease states and symptoms result, most typically, in altered (dysfunctional) GH release signaling and this also affects the ability of the pituitary to continue to make more GH. [2]&lt;br /&gt;
&lt;br /&gt;
GHRH, which has a forty-four amino acid long chain (and a specific shape - thus making it a peptide as well as a hormone), has been marketed for the longest as Sermorelin.  However, Sermorelin has been demonstrated to be degraded rapidly in the body and is cost-inefficient.  But because most patients in need of GH therapy doretain the ability to produce and secrete their own GH, treatment with a GHRH-type analog remained hypothetically preferable to exogenous  GH treatment.  GH itself when administered exogenously results not only in &quot;unnatural&quot; release patterns, it results universally in down regulation of endogenous GH production - as do many hormones when applied exogenously.  [2]&lt;br /&gt;
&lt;br /&gt;
Sermorelin&#39;s limitations naturally resulted in a variety of formulations of GHRH analogs for therapeutic.  The most effective (in terms of minimal degradation in the body - which is different from half-life)  analogs with the longest half-lives were those created with an attached 3-maleimidopropionic acid (MPA) unit, which results in binding to albumin after exogenous injection into blood plasma.&lt;br /&gt;
The research chemicals CJC-1293 and CJC-1295 are GHRH (the 44-amino acid long version) with 15 aminos removed, thus a total of 29 amino acids, and bound to MPA. [2]  MPA is also called Drug Affinity Complex, and CJC-1295 is often referred to as GHRH with Drug Affinity Complex (DAC).&lt;br /&gt;
&lt;br /&gt;
Based on measured GH release in rats over a two hour period, CJC-1295 released twice as much GH as CJC-1293, thus rendering it preferable based on immediate effectiveness; however, CJC-1293 has a 9% edge in stability (meaning less degradation) with in vitro stability tests.&lt;br /&gt;
CJC-1293, over a two-hour period, results in a rise-fall-rise-fall type pattern whereas CJC-1295 results in more of an inverted-U shape with a more gentle and longer peak. [2]&lt;br /&gt;
&lt;br /&gt;
In a CJC-1295 pulsatility study performed on normal non-GH deficient people reported plasma levels were between 1 and 2 ng/ml or 1000-2000ng/L one week after injection of between 60 or 90 mcg/kg of CJC-1295. In a 100kg man that is a 6mg or 9mg per week dose.&lt;br /&gt;
&lt;br /&gt;
&quot;Knockout rats&quot; are mice with genetically removed M3 muscarinic acetylcholine receptors. The scientists conducting the study [4] inhibited these genes and the mice became dwarves.. Those mice, labeled Br-M3-KO mice experienced short stature and a shrunken pituitary.  Scientists treated Br-M3-KO mice and normal control mice with CJC-1295 for eight weeks, resulting in complete growth restoration in the knockout mice as well as - notably - a restored pituitary size.  More specific data regarding CJC-1295 can be extrapolated by examining some of the control mice, which were not &quot;knockout rats&quot; but still received CJC-1295. The controls, male and female, experienced both accelerated &amp;amp; increased overall growth over the non-CJC-1295-dosed controls. Referring back to the notable finding that pituitary size was restored in knockout specimens dosed with CJC-1295, it is equally notable that the controls who did receive CJC-1295 did not have any pituitary hyperplasia or growth of the pituitary whatsoever.  This supports the conclusion that CJC-1295 is a substantially less risky treatment for non-diseased subjects, and a substantially more beneficial therapy for subjects with pituitary disease, than conventional (synthetic) GH treatment.  [4]&lt;br /&gt;
&lt;br /&gt;
In conclusion, CJC-1295 is an exciting treatment from the standpoint of cost efficiency, safety, and ease of administration when compared with regular GHRH or synthetic Growth Hormone treatment.  It has been demonstrated to be as effective as GH for most uses, and vastly preferable for safety reasons where feasible.  GH will not be fully supplanted by GHRH analogs such as CJC-1295 for  reasons alluded to above, but the vast majority of treatments in the types of applications mentioned in this article will probably begin to use CJC-1295 for safety, cost-efficiency, and the need to administer only one or two times per week instead of multiple times per day&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2015/01/dac-cjc-1295.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-456200513954520075</guid><pubDate>Tue, 13 Jan 2015 10:36:00 +0000</pubDate><atom:updated>2015-01-13T05:36:08.371-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Raloxifen</category><title>Raloxifen</title><description>&lt;h2&gt;Raloxifen&lt;/h2&gt;&lt;br /&gt;
&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;a href=&quot;http://www.superiorpeptide.com/104.html&quot;&gt;&lt;img src=&quot;http://www.basskilleronline.com/sponsors/bassbogo.jpg&quot; /&gt;&lt;/a&gt; &lt;/div&gt;Raloxifen belongs to the class of compounds known as SERMs or selective estrogen receptor modulators.  SERMs decrease activity of estrogen and are therefore considered an “anti-estrogen” treatment.  However, SERMs do not act by decreasing serum estrogen or aromatase-mediated conversion, but rather through a blocking activity at the estrogen receptor on a cellular level.  In other words, raloxifen and its metabolites are active at the estrogen receptor but not as an estrogen-like stimulus (agonist).  Instead, they prevent estrogen from exerting its effects at the cellular level.  This (as well as other means of blocking estrogenic activity or reducing estrogen levels) creates a rise in testosterone in men because testosterone production is modulated partially via serum estrogen levels.&lt;br /&gt;
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Raloxifen and its sister drug tamoxifen are typically used in treating estrogen-receptor dependent breast cancer in women[1].  Raloxifen may prove to have more diverse uses than tamoxifen for several reasons:&lt;br /&gt;
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Selective estrogen receptor modulators (SERMs) or estrogen agonists/antagonists have shown promise in osteoporosis in that they have the potential to reduce the risk of fracture, and also reduce the risk of breast cancer. SERMs maybe classified according to their core structure, which is typically a variation of the 17 beta-estradiol template and sub-classified according to the side chain at the helix 12 affector region. The best known are the triphenylethylenes such as tamoxifen, used in the management of breast cancer. However, the clinical application of this class of SERMs has been limited due to endometrial stimulation. A second class is the benzothiophenes such as raloxifene and arzoxifene, which have skeletal benefit with little, if any, uterine stimulation.[1]&lt;br /&gt;
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In a study conducted by  Christodoulakis et al, “raloxifene users did not exhibit any difference with respect to sex steroids and HOMA-IR levels.”[2]&lt;br /&gt;
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Raloxifen increased serum testosterone but reduced serum IGF-1 in a study performed by Duschek et al:&lt;br /&gt;
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In aging men serum levels of testosterone and insulin-like growth factor-1 (IGF-1) decline, potential factors in the reduced muscle strength, abdominal obesity, sexual dysfunction and impaired general well being of aging. The partial estrogen agonist and antagonist raloxifene increase serum testosterone levels in aging men, but the effect of raloxifene on serum IGF-1 levels in men is unknown. In this study the effects of raloxifene on IGF-1 levels and the associated increase in serum testosterone were compared to the effects of oral testosterone supplementation…. RESULTS: Compared to placebo raloxifene increased serum testosterone by 20% but it decreased serum IGF-1 levels by 24.5% (95% confidence interval (CI): -13.0 to -36.1%). No significant change in serum IGFBP-3 levels was found. The effect of raloxifene on serum IGF-1 has been observed with other oral estrogens, and, therefore, is likely to be ascribed to the partial estrogen agonist activity of raloxifene.[3]&lt;br /&gt;
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According to Nordt et al, raloxifen may hold potential as an intervention in adolescent gynecomastia: “Newer treatment strategies, such as the antiestrogen raloxifene, have shown promising results; however, further studies are needed to determine long-term efficacy. As a result of the limited pharmaceutical treatment options, many more adolescents are seeking surgical intervention.[4]”&lt;br /&gt;
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As the title of the study suggests, raloxifen is also a promising treatment for male osteoporosis:&lt;br /&gt;
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Raloxifene has been shown to increase bone mineral density of the hip in men receiving androgen deprivation therapy for prostate cancer. Moreover, experimental data demonstrated dramatic increase in cell death in human prostate cancer cell lines after the treatment with raloxifene. All these observations suggest that SERMs may be useful for the prevention and treatment of osteoporosis not only in postmenopausal women but also in elderly men. However, our hypothesis should be tested in a proper designed clinical trial.[5]&lt;br /&gt;
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Kastelan goes on to write that there are still issues of dose and duration to be assessed by further clinical study, as well as more markers of health and physical balance to be weighed against the benefits of raloxifen treatment.&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2015/01/raloxifen.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-3682864752599120091</guid><pubDate>Fri, 26 Dec 2014 11:48:00 +0000</pubDate><atom:updated>2014-12-26T06:48:39.106-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Clomiphene</category><title>Clomiphene</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Clomiphene citrate (USA trade name Clomid) is a selective estrogen receptor modulator (SERM) that increases production of the body&#39;s gonadotropins via disruption of the natural negative feedback system in the hypothalamus.  Clomiphene consists of two bioactive isomers, zuclomifene and enclomiphene.  Zuclomifene is responsible for the primary effects of clomiphene, which consists of binding to estrogen receptors for long periods of time.  Because the receptors cease recycling (and cannot be reused) for the duration, the hypothalamic estrogen number decreases, meaning the body&#39;s feedback system tells it that there is low estrogen.  Estrogen modulation is the body&#39;s primary method of initiating and controlling negative hypothalamic feedback; with perceived low estrogen, GnRH pulsatility is increased and the pituitary releases more luteinizing hormone (LH) and follicle stimulating hormone (FSH).[1]&lt;br /&gt;
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Clomiphene is primarily used to treat female fertility issues via its ability to increase the body&#39;s gonadotropin release.[1]  It is also useful for reasons related to the same mechanisms, as well as novel and newly discovered mechanisms, in treating various forms of male infertility.[1]&lt;br /&gt;
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Schellen writes and highlights well the diverse uses and progressive versatility shown with clomiphene as a potential treatment for an array of issues:&lt;br /&gt;
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After the discovery that Clomiphene-citrate (Clomid) increased the secretion of gonadotropins, it was first used to induce ovulation and later on it was also used in males in certain cases of infertility. The effects of Clomid on the hypothalamic-pituitary level made it also possible to use it for a dynamic evaluation of the hypothalamic-pituitary gonadal axis in both females and males. [2]&lt;br /&gt;
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Clomiphene is often used by bodybuilders who self-administer anabolic-androgenic steroids (AAS) to control undesirable estrogenic side-effects such as gynecomastia, acne, and mood-swings, similar to the way drug tamoxifen and the aromatase inhibitors letrozole, exemestane, and anastrozole are used.   Users of AAS also frequently use clomid to exploit its gonadotropin-stimulating effect, in order to increase testosterone levels from a suppressed baseline after a &quot;cycle&quot; of steroids via release of gonadotropin releasing-hormone, follicle stimulating hormone, and luteinizing hormone.&lt;br /&gt;
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In some cases clomiphene may be preferable over other options such as testosterone therapy for hypogonadism because, as the researches quoted below note, testosterone administration actually causes infertility in many cases; further, as many cases of hypogonadism may be steroid-abuse-induced, testosterone would be ruled out in those cases:&lt;br /&gt;
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Hypogonadism has a number of important clinical consequences related to androgen deficiency and impaired spermatogenesis. The cause of this condition is multifactorial and can result from hypothalamic, pituitary or gonadal dysfunction as well as factors that affect hormonal signaling along the hypothalamic-pituitary-gonadal axis. While testosterone replacement is the most common treatment, it can paradoxically lead to infertility, and may be a less physiologic therapy for patients with secondary hypogonadism due to pituitary dysfunction. Clomiphene citrate, and its derivatives, may allow for restoration of gonadal function by restoring physiologic pituitary function in a subset of patients with hypogonadism.[3]&lt;br /&gt;
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Tan and Vasudevan document a case study in which clomiphene successfully treated (by standards of testosterone levels, LH pulsatility, and restoration of pituitary-gonadal axis and feedback system) premature andropause induced by long-term steroid abuse:&lt;br /&gt;
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Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.[4]&lt;br /&gt;
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Taylor and Levine find clomiphene citrate suitable for long-term use in place of testosterone gel replacement therapy for treating sexual dysfunction and the set of symptoms generally associated with hypogonadism or andropause:&lt;br /&gt;
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CC represents a treatment option for men with hypogonadism, demonstrating biochemical and clinical efficacy with few side effects and lower cost as compared with TGRT.[5]&lt;br /&gt;
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Kanayama et al recommend clomiphene as part of a comprehensive treatment program for AAS abusers:&lt;br /&gt;
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...AAS suppress the male hypothalamic-pituitary-gonadal axis via their androgenic effects, potentially causing hypogonadism during AAS withdrawal. Men experiencing prolonged dysphoric effects or frank major depression from hypogonadism may desire to resume AAS, thus contributing to AAS dependence.  AAS-induced hypogonadism may require treatment with human chorionic gonadotropin or clomiphene to reactivate neuroendocrine function, and may necessitate antidepressant treatments in cases of depression inadequately responsive to endocrine therapies alone.[6]&lt;br /&gt;
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Citations:&lt;br /&gt;
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[1]Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006.&lt;br /&gt;
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[2]Schellen TM. Clomiphene treatment in male infertility. Int J Fertil. 1982;27(3):136-45.&lt;br /&gt;
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[3]Kaminetsky J, Hemani ML.  Clomiphene citrate and enclomiphene for the treatment of hypogonadal androgen deficiency.  Expert Opin Investig Drugs. 2009 Dec;18(12):1947-55.&lt;br /&gt;
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[4]Tan RS, Vasudevan D. Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse. Fertil Steril. 2003 Jan;79(1):203-5.&lt;br /&gt;
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[5]Taylor F, Levine L. Clomiphene citrate and testosterone gel replacement therapy for male hypogonadism: efficacy and treatment cost. J Sex Med. 2010 Jan;7(1 Pt 1):269-76.&lt;br /&gt;
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[6]Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG Jr. Treatment of  anabolic-androgenic steroid dependence: Emerging evidence and its implications.  Drug Alcohol Depend. 2010 Jun 1;109(1-3):6-13.&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/12/clomiphene.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-737789098626078484</guid><pubDate>Fri, 26 Dec 2014 06:37:00 +0000</pubDate><atom:updated>2014-12-26T01:37:22.613-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">CJC-1293 DAC</category><category domain="http://www.blogger.com/atom/ns#">CJC-1293 DAC dosing</category><title>CJC-1295 DAC 5mg</title><description>&lt;h2&gt;&lt;em&gt;CJC-1295 DAC 5mg&lt;/em&gt;&lt;/h2&gt;&lt;br /&gt;
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CJC-1295 DAC has shown some amazing results as a growth hormone releasing hormone (GHRH) analog. Not only has CJC-1295 shown the ability to increase growth hormone and IGF-I secretion and its benefits, but it has been able to do so in very large amounts. Recent research studies have shown that CJC - 1295 stimulates GH and IGF-1 Secretion, and will keep a steady increase of HGH and IGF-1 with no increase in prolactin, leading to intense fat loss, and increases protein synthesis.&lt;br /&gt;
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is a long acting Growth Hormone Releasing Hormone, which causes the anterior pituitary  to release more growth hormone. GHRH is released in pulses in the body, which alternate with corresponding pulses of somatostatin (growth-hormone inhibiting-hormone). Clinical Research was first conducted for &lt;a href=&quot;http://www.peptideuse.com/category/cjc-1295/&quot; target=&quot;_blank&quot;&gt;&lt;b&gt;CJC-1295&lt;/b&gt;&lt;/a&gt; during the mid-2000s. The objective of the peptide was to treat visceral fat deposits in obese AIDS patients, as increased levels of exogenous hgH are presumed to increase lipolysis (fat loss). The clinical research was ultimately successful for most research subjects. Ghrelin, released from the gut, which circulates and acts as a hunger hormone, has synergistic activity in the body with GHRH and also suppresses somatostatin to make way for the GHRH pulse. Studies shows that combining a GHRP-6 with CJC 1295 DAC, significantly increase the release of GH and IGF-1 production without an increase in prolactin. An example of a GHRP (GH Releasing Peptide) is Hexarelin or GHRP-2. CJC 1295 DAC is a exceptionally designed peptide and is known for being the finest of the hGH secretogues. The DAC (Drug Affinity Complex) portion increases the half-life by binding with serum albumin and protects the CJC-1295 DAC peptide from degradation. This was formed when a lysine link was bounded to DACs to a reactive chemical called maleimidoproprionic acid (MPA).&lt;br /&gt;
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&lt;h2 style=&quot;color: #f15616;&quot;&gt;CJC-1295 DAC vs. CJC-1295 No DAC&lt;/h2&gt;&lt;div align=&quot;justify&quot;&gt;CJC-1295 DAC and CJC-1295 (also known as &lt;strong&gt;Modified GRF 1-29&lt;/strong&gt;) are both Growth Hormone Releasing Hormones (GHRH). Their action in the human body is identical but the difference between the two peptides are the span of the half-life. Modified GRF 1-29 and Sermorelin have a very short acting half-life of about 30 minutes, while CJC-1295 DAC has a half-life that can last up to approximately 8 days. Many a scientist have reported that the short half-life of &lt;a href=&quot;http://www.peptideuse.com/&quot; title=&quot;Sermorelin&quot;&gt;&lt;strong&gt;Sermorelin&lt;/strong&gt;&lt;/a&gt; and Modified GRF 1-29 is considered to be much more natural as they produce a short pulse of Human Growth Hormone.&lt;/div&gt;&lt;h2 style=&quot;color: #f15616;&quot;&gt;ConjuChem and The Development of CJC-1295 DAC&lt;/h2&gt;&lt;div align=&quot;justify&quot;&gt;&lt;b&gt;&lt;i&gt;CJC-1295 DAC&lt;/i&gt;&lt;/b&gt; is a tetrasubstituted peptide analogue of Growth Hormone Releasing Hormones with D-Ala, Gln, Ala, and Leu substitutions at positions 2, 8, 15, and 27 respectively. A Canadian biotechnology company called ConjuChem had invented CJC-1295. Clinical Research on CJC-1295 first began during the mid-2000s. The goal of the peptide, acting to raise hgh like Ipamorelin, was to treat visceral fat deposits in obese AIDS patients because it is presumed that increased levels of exogenous hgH increase fat loss, or lipolysis. In one study, results showed that the measured GH release in rats over a two hour period showed that CJC-1295 released twice as much GH as CJC-1293 DAC. This result makes it preferable for immediate effectiveness as a result of the longer peak. With the use of a Growth Hormone Releasing Peptide (GHRP), such as Growth Hormone Releasing Hexapeptide (GHRP-6) in conjuction with CJC-1295 DAC, a study has shown that the GHRP’s create a Growth Hormone pulse which helps the CJC-1295 work effectively. Clinical research&#39;s involving CJC-1295 have shown that it had been successful for most research subjects..&lt;/div&gt;&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/12/cjc-1295-dac-5mg.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-1163550315116517522</guid><pubDate>Tue, 23 Dec 2014 21:00:00 +0000</pubDate><atom:updated>2014-12-23T16:00:07.882-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">S4</category><category domain="http://www.blogger.com/atom/ns#">SARMs</category><category domain="http://www.blogger.com/atom/ns#">Selective Androgen Receptor Modulators</category><title>SARMs S4</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;
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SARMs, Selective Androgen Receptor Modulators, are a relatively new class of research chemicals that have selective androgenic activity in a given area of the body.[1] &amp;nbsp;The specific activity is determined by which androgen receptors are activated and in what tissue.[1] &amp;nbsp;The clinical capability of SARMs is expected to be more broad and diverse than anabolic/androgenic steroids like testosterone, which are almost never a first choice for treatment.[1] &amp;nbsp;Testosterone and its ilk are considered unsuitable because their androgenic activity is systemic, meaning that undesirable side effects such as virilization in women, left ventricular hypertrophy in patients receiving doses exceeding a certain level, and various other effects that are difficult to prevent are commonplace&lt;br /&gt;
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In addition to the specific targeted nature of the first-generation SARMs, they offer a major advantage in practical applied treatment over the androgens: they can be dosed orally without liver toxicity, which means that applied treatments require less training of subjects and in the future, use of the research chemicals may be possible for a larger group where injection or oral toxicity of anabolic steroids previously prevented indication by practitioners.[1]&lt;br /&gt;
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Ke and Wang speculate that in elderly men with osteoporosis, or at risk of osteoporosis, could benefit from SARM therapy that (unlike testosterone and its derivatives) does not have any activity on the testes or prostate.[2]&lt;br /&gt;
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While future SARMs may be developed with zero androgenic effect in target tissue at all, which would provide benefits such as (for example) anabolism of bone or muscle tissue with zero side effects, current SARMs all have some degree of androgenic effect in tissue, though still less than testosterone. &amp;nbsp;The anabolic/androgenic ratio of SARMs currently available is between 3:1 and 10:1, whereas testosterone is 1:1.[3]&lt;br /&gt;
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S-4 is an experimental or investigation-stage proprietary SARM research chemical developed by GTx Inc for treatment of benign prostatic hypertrophy, muscle wasting, and osteoporosis.[4] &amp;nbsp;S-4 is considered a partial agonist of the androgen receptors in target tissue.[3] S-4 has less pronounced &amp;nbsp;anabolic and androgenic compared to other SARMs. In trials treating BPH induced in animal models, S-4 reduced prostate weight as effectively as finasteride and without producing any reduction in muscle mass or other side effects common with androgen receptor binding compounds.[5] Gao et al suggest that by binding to androgen receptors, S-4 prevents DHT from binding and activating, but bypasses the expected anti-androgenic effects that would occur from occupying androgen receptors due to the fact that S-4 itself is a partial agonist of androgen receptors.[6] &amp;nbsp;S-4 has also been shown to prevent bone loss, reduce body fat, and improve muscle strength and body composition in orchidectomized and ovariectomized rats.[7,8]&lt;br /&gt;
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1] Mohler ML, Bohl CE, Jones A, Coss CC, Narayanan R, He Y, Hwang DJ, Dalton JT, Miller DD. &amp;nbsp;Nonsteroidal selective androgen receptor modulators (SARMs): dissociating the anabolic and androgenic activities of the androgen receptor for therapeutic benefit. Journal of Medicinal Chemistry 52 (12): 3597–617. 2009.&lt;br /&gt;
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[2] Ke HZ, Wang XN, O&#39;Malley J, Lefker B, Thompson DD. Selective androgen receptor modulators--prospects for emerging therapy in osteoporosis? J Musculoskelet Neuronal Interact 5 (4): 355. 2005.&lt;/div&gt;
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[3]Yin D, Gao W, Kearbey JD, Xu H, Chung K, He Y, Marhefka CA, Veverka KA, Miller DD, Dalton JT. Pharmacodynamics of selective androgen receptor modulators. Journal of Pharmacology and Experimental Therapeutics. 2003 Mar;304(3):1334-40.&lt;/div&gt;
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[4]Hanada K, Furuya K, Yamamoto N, Nejishima H, Ichikawa K, Nakamura T, Miyakawa M, Amano S, Sumita Y, Oguro N. Bone anabolic effects of S-40503, a novel nonsteroidal selective androgen receptor modulator (SARM), in rat models of osteoporosis. Biol. Pharm. Bull. 26 (11): 1563–9. 2003.&lt;/div&gt;
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[5] Gao W, Kearbey JD, Nair VA, Chung K, Parlow AF, Miller DD, Dalton JT. Comparison of the pharmacological effects of a novel selective androgen receptor modulator, the 5alpha-reductase inhibitor finasteride, and the antiandrogen hydroxyflutamide in intact rats: new approach for benign prostate hyperplasia. Endocrinology. 2004 Dec;145(12):5420-8.&lt;/div&gt;
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[6] Gao W, Kim J, Dalton JT. Pharmacokinetics and pharmacodynamics of nonsteroidal androgen receptor ligands. Pharmaceutical Research. 2006 Aug;23(8):1641-58.&lt;/div&gt;
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[7] Kearbey JD, Gao W, Narayanan R, Fisher SJ, Wu D, Miller DD, Dalton JT. Selective Androgen Receptor Modulator (SARM) treatment prevents bone loss and reduces body fat in ovariectomized rats. Pharm Res. 2007 Feb;24(2):328-35.&lt;/div&gt;
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[8] Gao W, Reiser PJ, Coss CC, Phelps MA, Kearbey JD, Miller DD, Dalton JT. Selective androgen receptor modulator treatment improves muscle strength and body composition and prevents bone loss in orchidectomized rats. &amp;nbsp;Endocrinology. 2005 Nov;146(11):4887-97.&lt;/div&gt;
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&lt;br /&gt;</description><link>http://fitness-peptides.blogspot.com/2014/12/sarms-s4.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-5997520124315040820</guid><pubDate>Sat, 25 Oct 2014 16:30:00 +0000</pubDate><atom:updated>2014-10-25T12:30:11.505-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Ostarine / MK-2866</category><title>Ostarine / MK-2866</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;
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&lt;span style=&quot;font-size-adjust: none; font-stretch: normal; font: 14px/normal Helvetica;&quot;&gt;&lt;strong&gt;Ostarine / MK-2866&lt;/strong&gt;&lt;/span&gt;&lt;br /&gt; Ostarine or MK-2866 (CAS# 1235370-13-4) is a research chemical developed originally by Merck Inc. and now owned by GTx Inc.&amp;nbsp; It is undergoing trials for Phase II (human) research.&amp;nbsp; MK-2688 belongs to a class of chemicals known as SARMs or selective androgen receptor modulators.&amp;nbsp; SARMs create selective anabolic activity at certain androgen receptors and not others, hence their name.&amp;nbsp; Compared to testosterone, the sex hormone, the advantage of SARMs such as MK-2688 is that they do not have androgenic activity in non-skeletal-muscle tissues.&amp;nbsp; MK-2866 is undergoing clinical trials for and may eventually be medically indicated and approved for prevention of cachexia, atrophy, and sarcopenia primarily in the elderly and sick population.&lt;br /&gt;&lt;br /&gt; Testosterone and other androgenic anabolic steroids (AAS) are very effective at preventing muscle-wasting as well as increasing appetite and physical strength in humans and animal test subjects.&amp;nbsp; However, AAS have a specific set of side-effects related to their non-specific androgen receptor activity that makes them contraindicated in many cases where they would otherwise be useful.&amp;nbsp; Additionally, testosterone is subject to enzymatic conversion to a number of other bioactive hormones such as estrogen via the aromatase enzyme and DHT via the 5-alpha-reductase enzyme.&amp;nbsp; While additional drugs may be prescribed to lower aromatase and 5-AR, or to minimize the side effects of AAS in some other fashion, testosterone is primarily only indicated for male hormone replacement therapy due to the fact that it is a problematic and complicated compound to use for its androgenic properties and the side-effects can vary greatly from individual to individual.&amp;nbsp; Even primarily-anabolic AAS such as oxandrolone (Anavar), which are often used in terminally ill patients, do not entirely circumvent androgenic and other problematic side-effects.&lt;br /&gt;&lt;br /&gt; Ostarine exerts its anabolic effects on skeletal muscle tissue almost exclusively, and therefore represents a new potential treatment option for a wide spectrum of conditions from age-related muscular atrophy (sarcopenia), AIDS or cancer-related wasting/cachexia, and even an agent to minimize atrophy during recovery periods from serious surgery or similar situations.&amp;nbsp; It is effective in not only maintaining lean body mass (LBM) but actually increases it:&lt;br /&gt; In the study, Ostarine met the primary endpoint of LBM, measured by a dual energy X-ray absorptiometry (DEXA) scan, by demonstrating statistically significant increases in LBM compared to baseline in both the Ostarine 1 mg and 3 mg treatment cohorts. Specifically, the change from baseline in LBM for the placebo, 1 mg and 3 mg treatment groups was 0.1 kg (p=0.874 compared to baseline), 1.5 kg (p=0.001) and 1.3 kg (p=0.045), respectively, at the end of the 16-week trial.[1]&lt;br /&gt;&lt;br /&gt; Dr. Adrian Dobs, MD, MHS, an investigator in the Phase II trial for treatment of cancer cachexia, had the following to say about MK-2688:&lt;br /&gt; Approximately half of all cancer patients suffer from the devastating effects of cancer induced muscle loss. Increasing lean body mass may improve patients&#39; quality of life and even their response to cancer treatment. These Phase II results demonstrate the potential of a SARM to fill an important unmet need as there are currently no FDA-approved therapies available for cancer cachexia.[1]&lt;br /&gt;&lt;br /&gt; As mentioned above as well as by Dobs, there exist few treatments for cachexia, no FDA-approved indicated treatments, and certainly no ideal treatments; the same is true of the majority of muscle-wasting conditions.&amp;nbsp; Muscle-wasting related to cancer is the cause of a full 20% of cancer-related deaths, and it is likely that in related and similar conditions the instance of morbidity is equally high.[1]&lt;br /&gt;&lt;br /&gt; As mentioned by Furuya, the effects of MK-2688 translate to anabolism in bone as well as skeletal muscle tissue, which means it could be indicated in an extremely wide variety of uses such as osteoporosis and as a concurrent treatment with drugs that reduce bone density, such as the class of cancer-treatment drugs known as selective estrogen receptor modulators:&lt;br /&gt; Many efforts to produce novel drug materials maintaining a desired biological activity with an adequate tissue selectivity, which is so-called selective androgen receptor modulators (SARMs) , are being performed. As one of such efforts, studies on SARMs against bone tissues which possess a significant potential to stimulate a bone formation with reducing undesirable androgenic virilizing activities are in progress all over the world.[2]&lt;br /&gt;&lt;br /&gt; Maddedu and Mantovani suggest in a review of candidate-drugs for cachexia that a tailored combination regimen may be more effective than any one currently-researched drug:&lt;br /&gt; There are no published conclusive phase III controlled clinical trials nor general consensus about treatment approaches despite several years of coordinated efforts in basic and clinical research. Consequently, practice guidelines for the prevention and treatment of cancer-related muscle wasting are lacking. The purpose of this review is to supply an update on the promising agents and/or combined approaches for the treatment of cancer cachexia. RECENT FINDINGS: The choice for cancer cachexia treatment in clinical practice is very limited: the only approved drugs in Europe are progestagens. Several drugs with a strong rationale have failed or have not shown univocal results in clinical trials: they include eicosapentaenoic acid, cannabinoids, bortezomib and anti-tumor necrosis factor (TNF)-alpha monoclonal antibody. Several emerging drugs have shown promising results but are still under clinical investigation [thalidomide, selective cyclooxygenase (COX)-2 inhibitors, ghrelin mimetics, oxandrolone, olanzapine]. Moreover, increasing knowledge of cachexia pathophysiology and preliminary clinical findings seem to suggest that a combined treatment approach may be the most effective option. SUMMARY: A number of promising new agents are currently being developed but are not as yet regarded as standard of care. They include: selective COX-2 inhibitors, ghrelin mimetics, oxandrolone, selective androgen receptor modulators (ostarine), olanzapine, anti-IL-6 antibody and an innovative approach of multitargeted combined treatment. The data reported seem to suggest that the most effective treatment for cancer cachexia may be a combination regimen rather than single-agent treatments. This is in keeping with the general consensus that cancer cachexia is a multifactorial process and, hence, a potentially effective approach should be multimodal.[3]&lt;br /&gt;&lt;br /&gt; Cititations:&lt;br /&gt; [1] “GTx Presents Phase II Ostarine (MK-2866) Cancer Cachexia Clinical Trial Results At Endocrine Society Annual Meeting.” Medical News TODAY. 6-14-2009. http://www.medicalnewstoday.com/articles/153779.php; Accessed 9-21-2010.&lt;br /&gt; [2] Furuya K. [Translated title from Japanese: Bone and Men&#39;s Health. Bone selective androgen receptor modulators]. Clin Calcium. 2010 Feb;20(2):225-33.&lt;br /&gt; [3] Madeddu C, Mantovani G. An update on promising agents for the treatment of cancer cachexia.&amp;nbsp; Curr Opin Support Palliat Care. 2009 Dec;3(4):258-62.&lt;/div&gt;
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*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.&lt;/div&gt;
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&lt;br /&gt;</description><link>http://fitness-peptides.blogspot.com/2014/10/ostarine-mk-2866.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-2231346756798219612</guid><pubDate>Sat, 25 Oct 2014 16:16:00 +0000</pubDate><atom:updated>2014-10-25T12:16:34.083-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">DAC CJC 1295</category><title>DAC CJC 1295</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;
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&lt;span style=&quot;font-family: Helvetica; font-size: 14px;&quot;&gt;&lt;strong&gt;DAC CJC 1295&lt;/strong&gt;&lt;/span&gt;&lt;br /&gt;
&lt;div style=&quot;font-size-adjust: none; font-stretch: normal; font: 11px/normal Helvetica; margin: 0px 0px 10px;&quot;&gt;
DAC conjugated CJC 1295 (Receptor Grade) is an hGH secretogue that is unique by way of an additional lysine molecule that is added to facilitate the DAC complex. This conjugation makes for a much longer half-life. &amp;nbsp;DAC CJC 1295 tends to have a very limited availability everywhere due to expense and difficulty to manufacture. &amp;nbsp;CJC 1295 DAC is a exceptionally designed peptide and is known for being the finest of the hGH secretogues. Receptor grade: 98%+ pure 2000mcg / 2ml glass vial. THIS PRODUCT IS INTENDED FOR RESEARCH PURPOSES ONLY. CAN BE HARMFUL IF USED INAPPROPRIATELY.&lt;/div&gt;
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In the healthy human body, large amounts of growth hormone are stored in the pituitary. &amp;nbsp;The cells within the pituitary release growth hormone in response to signalling by GHRH (Growth Hormone Releasing Hormone), Ghrelin (of which GHRPs - Growth Hormone Releasing Peptides - are mimetics), and are inhibited from releasing these stores by Somatostatin. &amp;nbsp;GHRH and Ghrelin act on different populations of somatotropes (GH releasing cells). &amp;nbsp;GHRP/Ghrelin increases the number of somatotropes releasing GH but not the amount released by each cell;&lt;br /&gt; GHRH affects both the number of secreting cells and - moreso - the amount they each secrete. [1] GHRH and Ghrelin are released in specific patterns that vary depending on event and environment: post-exercise, in response to slow wave sleep, in certain stages of life and physical development, and so on.&lt;br /&gt;&lt;br /&gt; Most people (even the diseased) continue to possess the ability to make GH in the pituitary. The problem is in the signalling of the pituitary to release it (and make more). So yes CJC is meant to replace the external administration of GH in some (but not all) cases.Even most people with diseases that affect growth hormone secretion retain the ability to continue to make GH in their pituitaries. &amp;nbsp;The disease states and symptoms result, most typically, in altered (dysfunctional) GH release signalling and this also affects the ability of the pituitary to continue to make more GH. [2]&lt;br /&gt;&lt;br /&gt; GHRH, which has a forty-four amino acid long chain (and a specific shape - thus making it a peptide as well as a hormone), has been marketed for the longest as Sermorelin. &amp;nbsp;However, Sermorelin has been demonstrated to be degraded rapidly in the body and is cost-inefficient. &amp;nbsp;But because most patients in need of GH therapy doretain the ability to produce and secrete their own GH, treatment with a GHRH-type analog remained hypothetically preferable to exogenous &amp;nbsp;GH treatment. &amp;nbsp;GH itself when administered exogenously results not only in &quot;unnatural&quot; release patterns, it results universally in downregulation of endogenous GH production - as do many hormones when applied exogenously. &amp;nbsp;[2]&lt;br /&gt;&lt;br /&gt; Sermorelin&#39;s limitations naturally resulted in a variety of formulations of GHRH analogs for therapeutic. &amp;nbsp;The most effective (in terms of minimal degradation in the body - which is different from half-life) &amp;nbsp;analogs with the longest half-lives were those created with an attached 3-maleimidopropionic acid (MPA) unit, which results in binding to albumin after exogenous injection into blood plasma.&lt;br /&gt; The research chemicals CJC-1293 and CJC-1295 are GHRH (the 44-amino acid long version) with 15 aminos removed, thus a total of 29 amino acids, and bound to MPA. [2] &amp;nbsp;MPA is also called Drug Affinity Complex, and CJC-1295 is often referred to as GHRH with Drug Affinity Complex (DAC).&lt;br /&gt;&lt;br /&gt; Based on measured GH release in rats over a two hour period, CJC-1295 released twice as much GH as CJC-1293, thus rendering it preferable based on immediate effectiveness; however, CJC-1293 has a 9% edge in stability (meaning less degradation) with in vitro stability tests.&lt;br /&gt; CJC-1293, over a two-hour period, results in a rise-fall-rise-fall type pattern whereas CJC-1295 results in more of an inverted-U shape with a more gentle and longer peak. [2]&lt;br /&gt;&lt;br /&gt; In a CJC-1295 pulsatility study performed on normal non-GH deficient people reported plasma levels were between 1 and 2 ng/ml or 1000-2000ng/L one week after injection of between 60 or 90 mcg/kg of CJC-1295. In a 100kg man that is a 6mg or 9mg per week dose.&lt;br /&gt;&lt;br /&gt; &quot;Knockout rats&quot; are mice with genetically removed M3 muscarinic acetylcholine receptors. The scientists conducting the study [4] inhibited these genes and the mice became dwarves.. Those mice, labeled Br-M3-KO mice experienced short stature and a shrunken pituitary. &amp;nbsp;Scientists treated Br-M3-KO mice and normal control mice with CJC-1295 for eight weeks, resulting in complete growth restoration in the knockout mice as well as - notably - a restored pituitary size. &amp;nbsp;More specific data regarding CJC-1295 can be extrapolated by examining some of the control mice, which were not &quot;knockout rats&quot; but still received CJC-1295. The controls, male and female, experienced both accelerated &amp;amp; increased overall growth over the non-CJC-1295-dosed controls. Referring back to the notable finding that pituitary size was restored in knockout specimens dosed with CJC-1295, it is equally notable that the controls who did receive CJC-1295 did not have any pituitary hyperplasia or growth of the pituitary whatsoever. &amp;nbsp;This supports the conclusion that CJC-1295 is a substantially less risky treatment for non-diseased subjects, and a substantially more beneficial therapy for subjects with pituitary disease, than conventional (synthetic) GH treatment. &amp;nbsp;[4]&lt;br /&gt;&lt;br /&gt; In conclusion, CJC-1295 is an exciting treatment from the standpoint of cost efficiency, safety, and ease of administration when compared with regular GHRH or synthetic Growth Hormone treatment. &amp;nbsp;It has been demonstrated to be as effective as GH for most uses, and vastly preferable for safety reasons where feasible. &amp;nbsp;GH will not be fully supplanted by GHRH analogs such as CJC-1295 for &amp;nbsp;reasons alluded to above, but the vast majority of treatments in the types of applications mentioned in this article will probably begin to use CJC-1295 for safety, cost-efficiency, and the need to administer only one or two times per week instead of multiple times per day. [3]&lt;br /&gt;&lt;br /&gt;&lt;span style=&quot;font-size-adjust: none; font-stretch: normal; font: 10px/normal Helvetica;&quot;&gt;&lt;strong&gt;Citations&lt;/strong&gt;: &lt;br /&gt; [1] Lewis UJ. Growth hormone: what is it and what does it do? Trends Endocrinol Metab 1992;3:117-121&lt;br /&gt; [2] Synthesis and Biological Evaluation of Superactive Agonists of Growth Hormone-Releasing Hormone, J Izdebski, J Pinski, JE Horvath, G Halmos, K Groot and AV Schally, Proceedings of the National Academy of Sciences, Vol 92, 4872-4876&lt;br /&gt; [3] Pulsatile Secretion of Growth Hormone (GH) Persists during Continuous Stimulation by CJC-1295, a Long- Acting GH-Releasing Hormone Analog, Madalina Ionescu and Lawrence A. Frohman, The Journal of Clinical Endocrinology &amp;amp; Metabolism 2006 91(12):4792-4797&lt;br /&gt; [4] Neuronal M3 muscarinic acetylcholine receptors are essential for somatotroph proliferation and normal somatic growth, Dinesh Gautam, PNAS April 14, 2009 vol. 106 no. 15&lt;/span&gt;&lt;/div&gt;
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*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.&lt;/div&gt;
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Research shows it can prevent cancer causing skin damage by increasing the natural UV sun protective pigment melanin.  Melanin can be found in the skin cells in varying quantities naturally based on ethnicity: African, Hispanic, Middle East, Indian, Asian, and European etc.  Researchers know that melanin is produced in the skin to protect from sun exposure, but until now personal genetics limited melanin production, especially for the fairest skin types such as redheads, blondes, and those with blue eyes.  MT2 gradually increases the amount of melanin your skin can produce, and with minimal sun exposure even the palest individuals can develop an attractive and beneficial tan. Many researchers also noticed reduced wrinkles and improved skin texture, possibly also related to the skins protective response to the sun.  MT2 is the second generation of melanotan, and has reduced side effects compared to MT1.  Additionally, redheads naturally produce a different shade of melanin, and will benefit from the improved melanotan 2 formula to create a darker and more even tan&lt;/div&gt;
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&lt;h1 style=&quot;font-size: 12pt;&quot;&gt;
&lt;span style=&quot;font-size: 12pt;&quot;&gt;&lt;span style=&quot;font-family: Georgia;&quot;&gt;IGF 1 Supplements &lt;/span&gt;&lt;/span&gt; &lt;/h1&gt;
&lt;h1&gt;
&lt;span style=&quot;font-weight: normal;&quot;&gt;&lt;span style=&quot;font-family: Georgia; font-size: 12pt;&quot;&gt;The growth hormone IGF 1 or insulin-like growth factor is similar to insulin in its molecular structure. It is made up of 70 single-chained amino acids with three intramolecular disulfide bridges. This hormone plays a major part in every person’s bodily functions and growth.&lt;/span&gt;&lt;/span&gt;&lt;/h1&gt;
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&lt;span style=&quot;font-size: 12pt; font-weight: bold;&quot;&gt;&lt;span style=&quot;font-family: Georgia;&quot;&gt;&lt;/span&gt;&lt;/span&gt;&amp;nbsp;&lt;/h1&gt;
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&lt;span style=&quot;font-size: 12pt; font-weight: bold;&quot;&gt;&lt;span style=&quot;font-family: Georgia;&quot;&gt;Mechanism of Action&lt;/span&gt;&lt;/span&gt;&lt;span style=&quot;font-size: 12pt;&quot;&gt;&lt;/span&gt; &lt;/h1&gt;
&lt;h1&gt;
&lt;span style=&quot;font-family: Georgia; font-size: 12pt; font-weight: normal;&quot;&gt;Insulin-like growth factor 1 receptor binds to particular receptors to activate cell proliferation and growth. Once the anterior pituitary gland produces the growth hormone, it is released in the blood stream. This growth hormone then signals the liver to produce insulin-like growth hormones. The body’s growth and development relies on the process involved with these hormones. The hormone also has effects on the body’s cellular DNA synthesis.&lt;/span&gt;&lt;/h1&gt;
&lt;h1&gt;
&lt;span style=&quot;font-size: 12pt; font-weight: bold;&quot;&gt;&lt;span style=&quot;font-family: Georgia;&quot;&gt;Benefits&lt;/span&gt;&lt;span style=&quot;font-family: Georgia;&quot;&gt; of IGF 1&lt;/span&gt;&lt;/span&gt;&lt;span style=&quot;font-size: 12pt;&quot;&gt;&lt;/span&gt; &lt;/h1&gt;
&lt;h1&gt;
&lt;span style=&quot;font-family: Georgia; font-size: 12pt; font-weight: normal;&quot;&gt;The IGF hormone plays an active role in adult body anabolism and in children’s body development and growth. It is one of the hormones responsible for cell growth and repair that is vital to body tissues such as the muscles, liver, bones, kidneys, nerves, lungs and skin. Studies have also shown that the insulin-like growth hormone’s positively affects athletes’ or bodybuilders’ tissue repair and regeneration.&lt;/span&gt;&lt;/h1&gt;
&lt;h1&gt;
&lt;span style=&quot;font-family: Georgia; font-size: 12pt; font-weight: normal;&quot;&gt;Insufficiency in the insulin-like growth hormone leads to growth defects such as stunted growth. People with an IGF deficiency often experience dwarfism and increased body aging. IGF 1 supplements can be taken along with Ipamorelin to increase growth. These supplements result in rapid cell growth and repair.&lt;/span&gt;&lt;/h1&gt;
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&lt;h1&gt;
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&lt;br /&gt;</description><link>http://fitness-peptides.blogspot.com/2014/10/benefits-of-igf-1.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-5248764435069798289</guid><pubDate>Sat, 25 Oct 2014 16:13:00 +0000</pubDate><atom:updated>2014-10-25T12:13:40.270-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">CJC-1295 with DAC</category><title>CJC-1295 with DAC </title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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&lt;h1&gt;&lt;span style=&quot;color: #666666; font-family: &amp;quot;Garamond&amp;quot;,&amp;quot;serif&amp;quot;; font-size: 14pt;&quot;&gt;&lt;inline style=&quot;color: black; font-family: Georgia;&quot;&gt;CJC-1295 with DAC is a long acting version of GHRH (Growth Hormone releasing hormone)  modified form (GRF 1-29) with drug affinity complex)&lt;/inline&gt;&lt;/span&gt;&lt;/h1&gt;&lt;h1&gt;&lt;span style=&quot;color: #666666; font-family: &amp;quot;Garamond&amp;quot;,&amp;quot;serif&amp;quot;; font-size: 14pt;&quot;&gt;&lt;inline style=&quot;color: black;&quot;&gt;&lt;/inline&gt;&lt;/span&gt; &lt;/h1&gt;&lt;inline style=&quot;font-family: Georgia;&quot;&gt;&lt;span style=&quot;color: #666666; font-family: &amp;quot;Garamond&amp;quot;,&amp;quot;serif&amp;quot;; font-size: 14pt;&quot;&gt;&lt;inline style=&quot;color: black;&quot;&gt;CJC-1295 w/o DAC Mod 1-29&lt;/inline&gt;&lt;/span&gt;&lt;br /&gt;
&lt;span style=&quot;color: #333333; font-family: &amp;quot;Garamond&amp;quot;,&amp;quot;serif&amp;quot;; font-size: 10.5pt;&quot;&gt;&lt;inline style=&quot;color: black;&quot;&gt;CJC-1295 is a tetrasubstituted peptide of 29 amino acid length, primarily functioning as a growth hormone releasing hormone (GHRH) analog. CJC 1295 without dac (synonym CJC 1295 w/o dac-complex, modified form GRF 1-29 without DAC-complex) belongs to peptides hormones and contains 29 amino acids; as well it is quite stable analog of growth hormone releasing hormone with D-Ala, Gln, Ala and Leu substitutions in certain positions – 2,8,18, 27, and in a such way it is enhance this protein’s biological activity. Its molecular formula is C152H252N44O42 and its molecular mass is 3367.97.&lt;/inline&gt; &lt;/span&gt;&lt;/inline&gt;&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/10/cjc-1295-with-dac.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-2803778443229414586</guid><pubDate>Thu, 07 Aug 2014 11:07:00 +0000</pubDate><atom:updated>2014-08-07T07:07:00.883-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">AICAR</category><category domain="http://www.blogger.com/atom/ns#">an amide-conjugated nucleoside</category><title>AICAR, an amide-conjugated nucleoside</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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&lt;/script&gt;&lt;/div&gt;&lt;b&gt;&lt;i&gt;&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;AICAR&lt;/a&gt;&lt;/i&gt;&lt;/b&gt;&lt;br /&gt;
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Introduction &lt;br /&gt;
&lt;br /&gt;
AICAR, an amide-conjugated nucleoside, is an analog of adenosine.  The international nonproprietary name (INN) of AICAR is acadesine; the full unabbreviated name is 5-Amino-1-(5-O-phosphono-ß-D-ribofuranosyl)-1H-imidazole-4-carboxamide (Chemspider aicar entry. (n.d.), and it is variously referred to as AICA riboside, AICA ribonucleotide, Z-nucleotide, and ZMP (however, it should be noted that ZMP specifically refers to the phosphorylated form – AICA riboside monophosphate – that is converted within cells after administration of AICAR).  Its actions are primarily mediated by selective AMPK activation as well as conversion into factors that also act on AMPK. &lt;br /&gt;
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 &lt;br /&gt;
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&lt;b&gt;AMPK: The key to understanding AICAR&lt;/b&gt;&lt;br /&gt;
 &lt;br /&gt;
In seeking to understand AICAR, researchers are well-served by first understanding AMPK.  AMPK, long known to play a role in cellular energy-switching from use of ATP to ADP and AMP as an energy-transfer substrate, has recently (within the past decade) been shown to act as a cellular as well as whole-body energy “sensor” that plays an active and intriguing role in many systemic processes, and of which dysregulation contributes to many disease states.  &lt;br /&gt;
Because AICAR induces AMPK signaling through a relatively direct pathway, is used in many studies to study and better understand AMPK itself.  At the time of writing (2012), however, there are vastly more published inquiries into AMPK than of AICAR specifically; since AICAR’s effects are similar (or identical to) AMPK, it is possible to better AICAR by closely reviewing AMPK studies to infer AICAR’s effects.&lt;br /&gt;
 &lt;br /&gt;
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&lt;b&gt;AICAR therapeutic uses&lt;/b&gt;&lt;br /&gt;
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The actions of AICAR vary greatly by method of administration, duration of application, and dosage.  Administration of exogenous AICAR orally or by injection shows promise for a plethora of medical problems and disease states: ischemia, hypertension, diabetes, obesity, cancer, Alzheimer’s disease, and even aging may be addressed to varying degrees by use of AICAR as a drug (Salminen et al). &lt;br /&gt;
&lt;br /&gt;
Lifestyle factors such as overeating or under-exercising appear to initiate a cascade of pathological events that are mediated by altered AMPK signaling; AMPK expression is associated with exercise and periods of not eating.  Other genetic factors also predispose individuals to AMPK dysregulation.  Eventual effects of AMPK dysregulation – such as obesity, diabetes, even Alzheimer’s disease – can be treated or even partially reversed by AICAR-induced AMPK expression, whereas diet or exercise may not exert a major effect past an early or undetectable point in the pathology.&lt;br /&gt;
Currently, AICAR (under the INN acadesine) is in use as a myoprotective agent: when applied, it protects the heart against myocardial reperfusion (re-introduction of blood-flow) after ischemia (restriction of blood-flow, either acutely or chronically.  It is also being researched for treatment of lymphoma.&lt;br /&gt;
AMPK acts in nearly all tissues of the body, both as a local cellular energy balance signal and sensor – controlling energy-in versus energy-out pathways in response to changes in other cellular factors and available energy – and as a systemic controller of metabolic state and other non-metabolic processes.  AMPK also acts as an important bridge between cellular and peripheral tissue energy regulation and systemic energy regulation.  AMPK acts within the master control switch of the body, the hypothalamus, as well as in nearly all types of cells.&lt;br /&gt;
 &lt;br /&gt;
&lt;br /&gt;
&lt;b&gt;&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;Research uses of AICAR peptides&lt;/a&gt;&lt;/b&gt;&lt;br /&gt;
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AICAR is useful in researching the purine synthesis pathways and their downstream effects to better interpret biomarkers for different disease states. Most cancer cells rely on the de novo purine synthesis pathway, while normal cells prefer the salvage pathway; many chemotherapeutic drugs inhibit purine synthesis.  A better understanding of these differences between cancer cells and normal cells should lead to more-selective less-toxic chemotherapy drugs, as well as better ability to tailor therapies to individuals via improved understanding of biomarkers related to purine synthesis inhibition in various cell types (Boccalatte et al, 2009).&lt;br /&gt;
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&lt;b&gt;AICAR, AMPK, and purine synthesis pathways&lt;/b&gt;&lt;br /&gt;
 &lt;br /&gt;
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Endogenous AICAR also exists in cells; it is an intermediate in the de novo purine nucleotide synthesis pathway, specifically in the generation of inosine monophosphate (IMP), from which adenosine monophosphate and adenosine triphosphate are generated (Berg et al, 2002). However, as an exogenous AMPK-activator, AICAR does not disrupt AMP-to-ATP ratios within cells. A few of the effects of AICAR administration such as induction of apoptosis in cultured immortalized T-cell lymphocytes, do not involve activation of AMPK (López et al, 2003).&lt;br /&gt;
ATP (adenosine triphosphate) acts within the human body as an energy transfer molecule within cells.  It is an unstable molecule with high-energy phosphate bonds; when the bonds are “broken” via hydrolysis, the released energy is utilized within cells to do work.  ATP breaks down into ADP (adenosine diphosphate) and phosphate.  ADP can be further hydrolyzed into AMP (adenosine monophosphate) to release more energy.  Shifts in the ratio of ATP to AMP correlate with energy balance; a lower ratio means that less energy is available and/or ATP demand is high due to exercise demand.  AMPK inhibits energy- consuming pathways such as protein synthesis and fatty acid synthesis, and upregulates energy-generating pathways such as fatty acid oxidation and glucose transport.&lt;br /&gt;
AMPK expression changes according to ATP-to-AMP (and ADP) ratios, which fluctuate according to energy availability.  AMPK expression or absence then exerts an appropriate effect according to energy availability: energy storage in times of surplus, energy usage in times of scarcity.&lt;br /&gt;
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&lt;b&gt;&lt;br /&gt;
Roles of AMPK signaling in various physiological systems and states&lt;br /&gt;
&lt;/b&gt; &lt;br /&gt;
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In 2008 AICAR research at the Salk institute in San Diego, California generated headlines like the LA Times article “’Exercise Pill could take the work out of workouts.” The portrayal as a pill can mimic exercise has intrigued the public, despite some factual errors (Bamford et al write “AICAR treatment did not alter the MHC-based fibre type composition in fast- or slow-twitch muscles” (2003) and the 2008 article merely discussed specific gene-expression related to the structural adaptation found in endurance athletes (Narkar et al, 2008)):&lt;br /&gt;
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 &quot;Doping,” the use of pharmacological agents to improve athletic performance for competition, is controversial and intrigues the public mind.  AICAR improved treadmill performance in untrained mice by 45% (Narkar et al, 2008), leading to speculation that it may work as a performance-enhancing drug (PED) in humans.  Tests have been developed for AICAR use in professional athletes, but since the 2008 articles the medical community has focused on AICAR as a way to better understand the profound role of AMPK in health and disease states and on AICAR as a treatment for a variety of pathologies.&quot;&lt;br /&gt;
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&lt;b&gt;AMPK and mTOR in resistance and endurance exercise&lt;/b&gt;&lt;br /&gt;
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In humans, AMPK is increased in response to both endurance and resistance training, but mTOR response is thought to be specific to resistance training (Vissing et al, 2007).  Basal concentrations of mTOR and AMPK were not permanently affected in a study of three groups (control, endurance, resistance training) undertaking ten weeks of training (Vissing et all, 2007).  Although Nader speculates (2006) that concurrent endurance and strength training may be counterproductive due to the potential of AMPK (expressed with endurance training)  to limit mTOR’s effect, Medeiros et al found that in the rat swimming increases transduction activity of proteins involved in insulin-dependent protein synthesis and the mTOR pathway (2011). &lt;br /&gt;
The likely explanation is that presence or absence of factors such as insulin and amino acids is as important an influence on the ultimate physiological outcome of exercise as the nature of the exercise; AMPK expression occurs in a fasted state regardless of nature of exercise, as well as in response to any exercise; mTOR proteins are expressed primarily in a fed state, and in response to resistance exercise – but are unlikely to be expressed in significant quantities if the exercise is performed fasted.&lt;br /&gt;
The increased potential for mTOR protein transduction after endurance exercise may be explained by the cross-talk between AMPK and mTOR; AMPK acts as an mTOR control and regulates plasticity of muscle tissue (Lantier et al, 2010).  As a therapeutic agent, this suggests that ongoing AICAR use should not significantly disrupt signaling cascades relevant to anabolism provided that insulin and amino acids are present during and after resistance exercise.&lt;br /&gt;
In an animal model of obesity, Williamson and Drake (2011) found that two weeks of AICAR administration paradoxically promoted muscle-growth.  The authors of the study hypothesize that lower fasting AMPK levels, which relate to insulin-resistance found in obese, aging, or otherwise insulin-resistant muscle tissue, results in an overall lower metabolic capacity of the tissues and therefore a reduction in mTOR effect; normalizing AMPK levels results in a net reduction of mTOR with a surprising effect:&lt;br /&gt;
&lt;br /&gt;
Our recent data show that short-term (2-week), daily treatment of obese (ob/ob) mice with AICAR normalized their hyperactive, fasted-state mTOR signaling. Along with the expected reductions in circulating blood glucose and insulin concentrations, and muscle lipid and glycogen content after AICAR treatment, translational capacity and mass (including muscle fiber areas) of the plantar flexor muscle complex were significantly increased in the obese treated mice. It is our view that the oxidative metabolism/capacity of the muscle and the regulatory processes of muscle growth (i.e. mTOR and translational control) need to be normalized to elicit growth in insulin resistant (e.g. obese, aged) muscle.&lt;br /&gt;
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Paradoxically, mTOR reduction in certain physiological states by AMPK/AICAR can result in improved protein synthesis and muscle-cross section.&lt;br /&gt;
Lantier et al, 2010). AMPK directly inhibits mTORC1, the mTOR complex involved in overloading-induced hypertrophy of muscle cells (Lantier et al, 2010).&lt;br /&gt;
Lantier et al tested the effect of total AMPK inhibition in myotubes and found that it resulted in myotubes 1.5 times bigger than AMPK-expressing myotubes.  However, the AMPK-deficient myotubes failed to respond to mTOR pathway activation: while they started with an initial greater size, they did not increase in size whatsoever when stimulated with mTOR pathway effectors (Lantier et al, 2010). &lt;br /&gt;
One possible explanation is that protein synthesis could not be increased any further and so the mTOR effector had no effect, but another – echoing Drake and Williamson’s 2011 paper – is that AMPK deletion limits muscle growth due to limiting energy-generating capabilities necessary for muscle growth (Lantier et al, 2010). &lt;br /&gt;
AMPK also limits cardiac hypertrophy, and AMPK deletion results in cardiac hypertrophy (Lantier et al, 2010), a state probably caused in part by mTOR overexpression. &lt;br /&gt;
Fatty acid synthesis and oxidation&lt;br /&gt;
AMPK is a master lipid metabolism regulator (Lim et al, 2009): high levels of AMPK inhibit cholesterol and fatty acid synthesis.  AMPK also acts as a cellular signal to increase fatty acid oxidation by indirectly increasing levels of carnitine palmitoyltransferase-1 (CPT-1), which is the rate-limiting factor in mitochondrial uptake of free fatty acids (FFAs). In other words,  AICAR and AMPK increase the upper limit of the body’s ability to burn stored fat for energy.&lt;br /&gt;
Yin finds that AMPK is upregulated in fat cells during beta-adrenergic agonist-induced lipolysis due to intracellular fat level via cAMP increases and greater phosphorylation of AMPK, and AMPK is necessary for optimal beta-induced lipolysis (2005).&lt;br /&gt;
AMPK dysregulation is implicated in obesity: lipolysis is inhibited and constant low-grade fatty acid synthesis may take place.  A steady caloric surplus (energy surplus) suppresses AMPK, resulting in reduced release of fat for fuel usage, and instead resulting in constant low-grade fat storage.&lt;br /&gt;
Direct application of AICAR is likely to result in improved lipolysis and fat oxidation, as well as decreased levels of fatty acid synthesis.  This is a revelation for development of future obesity treatment strategies.&lt;br /&gt;
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Conclusion&lt;br /&gt;
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&lt;b&gt;&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;AICAR&lt;/a&gt; &lt;/b&gt;has yet to be realized as a mainstream treatment, likely because wide-range systemically acting drugs with profound cellular and systemic effects are difficult to press into medical use under current the regulatory climate in the United States, Canada, and EU countries; the wide range of effects raises hard-to-answer questions about the safety and appropriateness of AICAR for any given disease, particularly “lifestyle” conditions such as obesity and insulin resistance, which have accepted “lifestyle” remedies of diet and exercise and accepted medical remedies as they reach a certain point in pathology.&lt;br /&gt;
In the case of Type 2 diabetes, further animal and human safety and efficacy studies could prove AICAR to be a viable candidate, but the current drug metformin is a viable AMPK-targeting agent; AICAR could also be a financially risky choice for investors with a viable (if perhaps less-effective) similar drug on the market.  In the case of Alzheimer’s disease, AICAR may also prove to be a next-generation treatment; a better understanding is needed, though, as AMPK appears to play a role in advancing late-stage Alzheimer’s.&lt;br /&gt;
For now, AICAR will continue to be used by researchers to better understand the effects of AMPK (and as a treatment for lymphoma and after cardiac ischemia); doubtless, medical advances will continue to be made due to AICAR’s usefulness as a research aid, regardless of when AICAR itself is brought in as a therapeutic agent for the conditions discussed herein.&lt;br /&gt;
Note:  Researchers who inquire about personal aicar peptide use including, but not limited to bodybuilding, dosing, injections or cycling will be added to our DO NOT SELL LIST. &lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/08/aicar-amide-conjugated-nucleoside.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-5103080681250946505</guid><pubDate>Tue, 05 Aug 2014 11:05:00 +0000</pubDate><atom:updated>2014-08-07T04:39:09.369-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Melatonin + GH Peptides for Double Results!</category><title>Melatonin + GH Peptides for Double Results!</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Melatonin + GH Peptides for Double Results! &lt;br /&gt;
&lt;br /&gt;
Perhaps a better/more appropriate title for this article would be:&lt;br /&gt;
&lt;br /&gt;
&lt;b&gt;&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;Melatonin + GH peptides for possibly improved GH release!&lt;/a&gt;&lt;/b&gt;&lt;br /&gt;
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That title sounds a little silly. But, I feel a little silly having not researched this matter more fully before drawing conclusions. While I still believe there is something to this protocol- as I experienced results with it that caught my attention before even finding any research on it- there is much more to the matter than what I have posted simply within the article. If I get a bit more info in the future I&#39;ll update with whatever I can! &lt;br /&gt;
&lt;br /&gt;
There has been a bit of debate over whether this info is valid when using a GHRP in addition to a GHRH. I want anyone reading this to take a look at this thread on needtobuildmuscle.com&lt;br /&gt;
&lt;br /&gt;
In it, member JKlooking talks about why he disagrees with my findings on this. Basically, the original study I quoted from, posted here, used melatonin + GHRH to induce a much greater GH pulse release. JK&#39;s contention is that when you add in a GHRP to the equation you are basically making the melatonin redundant. He gives some good background for why he thinks this and that&#39;s why I want you to take a look at his info and draw your own conclusions.&lt;br /&gt;
&lt;br /&gt;
I still believe that the melatonin has an effect by inhibiting somatostatin, or possibly through some other mechanism, and adds efficiency to the overall equation even in the presence of GHRP. Though a case could be made against this, I still haven&#39;t seen anything that directly refutes my theory (or definitively proves it either in all fairness!). Plus, my original enthusiasm for this topic was sparked by results I was getting from this method before I even looked into the &quot;science&quot; of the matter. I had tried other gh peptide protocols and used varying amount of GH previously, but when I dosed it in this way (naturally using the melatonin as I was doing the protocol before bed!) I got light euphoric feelings at first. And, I experienced increased effects and side-effects that I&#39;d never experienced before!&lt;br /&gt;
&lt;br /&gt;
Although that is totally subjective, it still bears weight for me personally. I&#39;d urge anyone already using GH peptides to give this protocol a try for 3 weeks and see what it does for you. You may or may not experience the slight euphoria that I did. Maybe I&#39;m just sensitive to it in that way, not everyone likely will be. But, I&#39;d be surprised if you didn&#39;t see some increased efficiency (better fat burning, better sleep etc) from it!&lt;br /&gt;
&lt;br /&gt;
I guess I&#39;m a stick in the mud when I find something I feel works. But, I really urge you to both read the counterpoints to this argument and to give the protocol a chance in the real world. At worst you&#39;ll get a good night&#39;s sleep from the melatonin and you can always go back to your old protocol at a later time. For me, it gave me better results than using gh peptides 3 x day on their own or even 5-6 iu of GH every day. My guess is that you&#39;d see something similar doing it my way or using 2 doses of GH peptides with an iu of GH 15 min. afterwards without the melatonin. In other words, if you are already using GH with your peptides in multiple doses per day, this 1 dose per night won&#39;t give you better results. It&#39;s not a miracle. I do believe it is better with the melatonin than without. That is all.&lt;br /&gt;
&lt;br /&gt;
Perhaps the effects of melatonin in this case have more to do with its actions on GHBPs (growth hormone binding proteins) and higher resulting free GH. I don&#39;t know. A study found here talks about using 5 mg of oral melatonin increasing serum GH levels 157% over baseline and noting the differences when measuring free GH vs. other methods. Have a read through if you are interested. There may be more here than previously thought.&lt;br /&gt;
&lt;br /&gt;
For example, consider the way the standard &quot;peptide + GH&quot; dose is done- you take the GH peptides &quot;kicking off&quot; a strong GH pulse and then add in an iu of GH to give it a boost that the body recognizes as a natural part of the original pulse. Perhaps the relatively (when compared to GH peptides) small increase in serum GH seen with oral melatonin increases the total GH output from the full protocol (melatonin, wait 1 hr then gh peptides, 15 min later GH) in a somewhat similar fashion- perhaps adjusting the new baseline or perhaps adding to the amount of free GH by somehow inhibiting the GHBPs.&lt;br /&gt;
&lt;br /&gt;
Again, obviously I&#39;m not a bio-chemist! lol. I&#39;m just a curious gym rat. Like I say, give my methods a try, read all the literature you can on the topic if you wish and then draw your own conclusions! :)&lt;br /&gt;
&lt;br /&gt;
Enjoy the article below!&lt;br /&gt;
&lt;br /&gt;
I stumbled on this by accident. I always take &lt;b&gt;melatonin &lt;/b&gt;before bed and one night I took my melatonin an hour before my ipamorelin (similar to ghrp-6) and cjc-1295 (mod grf 1-29) and noticed what seemed to be a greater feeling of GH release. Euphoria, sleepiness etc. that was more profound than with just one substance or the other. When I added in an iu of GH 15 min later it was even greater. Now I&#39;ve stopped my other peptide shots and just do this one protocol per night. The side effects (stiff fingers/hands) got to be too great with multiple shots per day. These are side effects generally seen with very high doses of GH alone.&lt;br /&gt;
&lt;br /&gt;
I knew about 1-2 iu of GH promoting a much bigger &quot;pulse&quot; when combined with peptides (Thanks to Datbetrue on professionalmuscle.com). But, I wondered what part melatonin could possibly play in it. But, I had always heard that it created a slight GH release on its own.&lt;br /&gt;
&lt;br /&gt;
Here&#39;s what I found-&lt;br /&gt;
&lt;br /&gt;
Clin Endocrinol (Oxf). 1993 Aug;39(2):193-9.&lt;br /&gt;
Melatonin stimulates growth hormone secretion through pathways other than the growth hormone-releasing hormone.&lt;br /&gt;
&lt;br /&gt;
Valcavi R, Zini M, Maestroni GJ, Conti A, Portioli I.&lt;br /&gt;
2a Divisione di Medicina Interna, Arcispedale S. Maria Nuova, Reggio Emilia, Italy.&lt;br /&gt;
Abstract&lt;br /&gt;
&lt;br /&gt;
OBJECTIVE: There is evidence that melatonin plays a role in the regulation of GH secretion. The aim of this study was to investigate the neuroendocrine mechanisms by which melatonin modulates GH secretion. Thus we assessed the effect of oral melatonin on the GH responses to GHRH administration and compared the effects of melatonin with those of pyridostigmine, a cholinergic agonist drug which is likely to suppress hypothalamic somatostatin release.&lt;br /&gt;
DESIGN: The study consisted of four protocols carried out during the afternoon hours. Study 1: oral melatonin (10 mg) or placebo were administered 60 minutes prior to GHRH (100 micrograms i.v. bolus). Study 2: GHRH (100 micrograms i.v. bolus) or placebo were administered at 0 minutes; oral melatonin or placebo were given at 60 minutes and were followed by a second GHRH stimulus (100 micrograms i.v. bolus) at 120 minutes. Study 3: placebo; oral melatonin (10 mg); oral pyridostigmine (120 mg); melatonin (10 mg) plus pyridostigmine (120 mg) were administered on separate occasions. Study 4: placebo; oral melatonin (10 mg); oral pyridostigmine (120 mg); melatonin (10 mg) plus pyridostigmine (120 mg) were administered on separate occasions 60 minutes prior to a submaximal dose (3 micrograms i.v. bolus) of GHRH.&lt;br /&gt;
SUBJECTS: Four groups of eight normal male subjects, ages 22-35 years, were randomly assigned to each protocol.&lt;br /&gt;
MEASUREMENTS: Growth hormone was measured by RIA at 15-minute intervals.&lt;br /&gt;
RESULTS: Oral melatonin administration had a weak stimulatory effect on GH basal levels. Prior melatonin administration approximately doubled the GH release induced by supramaximal (100 micrograms) or submaximal (3 micrograms) doses of GHRH. Melatonin administration restored the GH response to a second GHRH challenge, given 120 minutes after a first GHRH i.v. bolus. The GH releasing effects of pyridostigmine, either alone or followed by GHRH, were greater than those of melatonin. However, the simultaneous administration of melatonin and pyridostigmine was not followed by any further enhancement of GH release, either in the absence or in the presence of exogenous GHRH.&lt;br /&gt;
CONCLUSIONS: Our data indicate that oral administration of melatonin to normal human males increases basal GH release and GH responsiveness to GHRH through the same pathways as pyridostigmine. Therefore it is likely that melatonin plays this facilitatory role at the hypothalamic level by inhibiting endogenous somatostatin release, although with a lower potency than pyridostigmine. The physiological role of melatonin in GH neuroregulation remains to be established.&lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/08/melatonin-gh-peptides-for-double-results.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-7823284710244674161</guid><pubDate>Sun, 03 Aug 2014 10:59:00 +0000</pubDate><atom:updated>2014-08-03T06:59:00.024-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Decreased body fat</category><category domain="http://www.blogger.com/atom/ns#">Hexarelin Peptide</category><category domain="http://www.blogger.com/atom/ns#">Improved sleep</category><category domain="http://www.blogger.com/atom/ns#">Increased IGF-1 levels</category><category domain="http://www.blogger.com/atom/ns#">Increased lean mass</category><category domain="http://www.blogger.com/atom/ns#">Increased rate of wound/injury healing</category><title>Hexarelin Peptide Explored </title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Hexarelin Peptide Explored &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;b&gt;&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;Hexarelin&lt;/a&gt;&lt;/b&gt; belongs to the category of drugs known as GHRP’s (growth hormone releasing peptides), which are also sometimes referred to as GH secretagogues. They include GHRP-2, GHRP-6, Ipamorelin, and Hexarelin. Hex’s primary function is to stimulate the pituitary gland to produce more growth hormone. Like the other GHRPs, it has a 2-fold mechanism of action, in that it causes an increase in GH through amplifying the natural growth hormone releasing hormone (GHRH) signal transduction pathway, as well as by suppressing the actions of Somatostatin.&lt;br /&gt;
&lt;br /&gt;
Hexarelin demonstrates several unique characteristics which differentiates it from other GHRP’s. Most notably, Hexarelin has been shown to be the most potent GH releaser on a mcg to mcg basis, outperforming the other drugs in its class. It has also been shown to result in a more rapid rate of desensitization in comparison to the other GHRP’s, although the rate and extent at which desensitization progresses is often a topic of misunderstanding. Common dosing guidelines have frequently advised that researchers discontinue administration after just 2 weeks of use, suggesting that further experimentation would result in an insignificant GH spike, in response to this increased desensitization. This is not the case.&lt;br /&gt;
&lt;br /&gt;
In one particular study, the aim of which was to determine the rate of desensitization with daily use, blood work was performed on test subjects at the end of weeks 1, 2, 4, and 16. After evaluating the results of this blood work, researchers concluded that Hexarelin, when dosed at 1mg/kg and 2mg/kg per day, displays minimal difference in desensitization after 1 week of treatment and 4 weeks of treatment. However, after 16 weeks of treatment, GH release was considerably blunted. We should also note that 4 weeks after Hexarelin was discontinued, researchers administered the peptide a 2nd time in conjunction with additional blood work. The results of this blood work revealed that 4 weeks of discontinuance had completely reversed the desensitizing effects of the drug.&lt;br /&gt;
&lt;br /&gt;
Clearly, the outcome of this study has significant application to our own research efforts. Based on the above, Hexarelin can be researched at 4 week increments, or possibly longer, before a break is required. Since blood work was not done during weeks 5-15 of this study, we cannot say for certain at which point GH release starts to significantly decline, so it is probably better to play it safe rather than sorry in this case and keep personal research to 4 weeks at a time. In terms of off-time, while sensitivity to Hex’s GH releasing effects was completely restored 4 weeks after discontinuance, anecdotal evidence suggest that sensitivity will return within only 1-2 weeks of off-time.&lt;br /&gt;
&lt;br /&gt;
Like most other GHRP’s, Hex also elevates prolactin and cortisol post-administration. Generally, prolactin and cortisol are viewed in a negative light, due to their ability to instigate unwanted side effects, BUT…levels must be elevated considerably outside of the normal range in order for any of these issues to manifest. Time and time again studies have shown that the GHRP’s do not elevate prolactin or cortisol high enough to be problematic.&lt;br /&gt;
&lt;br /&gt;
Another manner in which Hexarelin distinguishes itself from the rest of the pack (aside from Ipamorelin) is in the area of appetite stimulation. As Ghrelin mimetics, many of the GHRP’s elicit an increase in appetite, which can range from mild to extreme in various individuals. Hexarelin is absent of this side effect, allowing those who have difficulty adhering to their diet a way to elevate GH levels without suffering through their self-imposed caloric deprivation. Certainly, this should be a consideration when selecting which GH peptide is right for you.&lt;br /&gt;
&lt;br /&gt;
One possible side effect associated with Hexarelin is the disturbance of natural sleep patterns. These alterations in sleeping patterns may cause some individuals to have difficulty falling and/or staying asleep, but many do not experience this problem. At any rate, by avoiding use late at night, this potential issue is eliminated.&lt;br /&gt;
&lt;br /&gt;
Growth hormone has numerous documented benefits, making it one of the most diverse drugs in our PED arsenal. Some of these benefits include:&lt;br /&gt;
&lt;br /&gt;
* Decreased body fat&lt;br /&gt;
* Increased lean mass&lt;br /&gt;
* Increased collagen production&lt;br /&gt;
* Improved sleep quality&lt;br /&gt;
* Increased cellular repair&lt;br /&gt;
* Increased in IGF-1 levels&lt;br /&gt;
* Increased bone density&lt;br /&gt;
* Increased rate of wound/injury healing&lt;br /&gt;
* Improved immune function&lt;br /&gt;
* Improved overall wellbeing&lt;br /&gt;
* Improved exercise tolerance&lt;br /&gt;
&lt;br /&gt;
Typical dosing guidelines for &lt;b&gt;&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;Hexarelin&lt;/a&gt;&lt;/b&gt; range between 50-200 mcg per inject, with 100 mcg being considered the standard. Most will find a dose of 100 mcg to be more than suitable. According to documented research, a single 100 mcg injection is capable of eliciting a temporary elevation in GH similar to what one would experience when administering 10 IU of GH in a single injection. The differentiating factor in this comparison is the length of time GH levels remain elevated post-injection. With exogenous GH, levels remain elevated for roughly 7-8 hours, while levels will fall to baseline within 90 minutes of administering Hexarelin. This is why most users will choose to administer this GHRP no less than 2-3X per day.&lt;br /&gt;
Hexarelin is the most efficacious GHRP available, allowing for impressive elevations in GH levels with few downsides. For those of you who normally research products such as GHRP-2 or Ipamorelin at traditional dosages, you may want to consider giving this unique GH peptide a shot for your next research project. Don’t let prior misconceptions fool you. Hexarelin is one of the most under-rated GHRP’s on the market and certainly more effective than other drugs in the same class on a mcg to mcg basis. So long as proper procedures are adhered to in terms of ON/OFF time (during which time an alternate GHRP can be researched), Hexarelin can be used as semi-permanent fixture in your GH peptide program. &lt;br /&gt;
by Mike Arnold &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;b&gt;Hexarelin &lt;/b&gt;belongs to the category of drugs known as GHRP’s (growth hormone releasing peptides), which are also sometimes referred to as GH secretagogues. They include GHRP-2, GHRP-6, Ipamorelin, and Hexarelin. Hex’s primary function is to stimulate the pituitary gland to produce more growth hormone. Like the other GHRPs, it has a 2-fold mechanism of action, in that it causes an increase in GH through amplifying the natural growth hormone releasing hormone (GHRH) signal transduction pathway, as well as by suppressing the actions of Somatostatin.&lt;br /&gt;
&lt;br /&gt;
&lt;b&gt;Hexarelin &lt;/b&gt;demonstrates several unique characteristics which differentiates it from other GHRP’s. Most notably, Hexarelin has been shown to be the most potent GH releaser on a mcg to mcg basis, outperforming the other drugs in its class. It has also been shown to result in a more rapid rate of desensitization in comparison to the other GHRP’s, although the rate and extent at which desensitization progresses is often a topic of misunderstanding. Common dosing guidelines have frequently advised that researchers discontinue administration after just 2 weeks of use, suggesting that further experimentation would result in an insignificant GH spike, in response to this increased desensitization. This is not the case.&lt;br /&gt;
&lt;br /&gt;
In one particular study, the aim of which was to determine the rate of desensitization with daily use, blood work was performed on test subjects at the end of weeks 1, 2, 4, and 16. After evaluating the results of this blood work, researchers concluded that Hexarelin, when dosed at 1mg/kg and 2mg/kg per day, displays minimal difference in desensitization after 1 week of treatment and 4 weeks of treatment. However, after 16 weeks of treatment, GH release was considerably blunted. We should also note that 4 weeks after Hexarelin was discontinued, researchers administered the peptide a 2nd time in conjunction with additional blood work. The results of this blood work revealed that 4 weeks of discontinuance had completely reversed the desensitizing effects of the drug.&lt;br /&gt;
&lt;br /&gt;
Clearly, the outcome of this study has significant application to our own research efforts. Based on the above, Hexarelin can be researched at 4 week increments, or possibly longer, before a break is required. Since blood work was not done during weeks 5-15 of this study, we cannot say for certain at which point GH release starts to significantly decline, so it is probably better to play it safe rather than sorry in this case and keep personal research to 4 weeks at a time. In terms of off-time, while sensitivity to Hex’s GH releasing effects was completely restored 4 weeks after discontinuance, anecdotal evidence suggest that sensitivity will return within only 1-2 weeks of off-time.&lt;br /&gt;
&lt;br /&gt;
Like most other GHRP’s, Hex also elevates prolactin and cortisol post-administration. Generally, prolactin and cortisol are viewed in a negative light, due to their ability to instigate unwanted side effects, BUT…levels must be elevated considerably outside of the normal range in order for any of these issues to manifest. Time and time again studies have shown that the GHRP’s do not elevate prolactin or cortisol high enough to be problematic.&lt;br /&gt;
&lt;br /&gt;
Another manner in which Hexarelin distinguishes itself from the rest of the pack (aside from Ipamorelin) is in the area of appetite stimulation. As Ghrelin mimetics, many of the GHRP’s elicit an increase in appetite, which can range from mild to extreme in various individuals. Hexarelin is absent of this side effect, allowing those who have difficulty adhering to their diet a way to elevate GH levels without suffering through their self-imposed caloric deprivation. Certainly, this should be a consideration when selecting which GH peptide is right for you.&lt;br /&gt;
&lt;br /&gt;
One possible side effect associated with Hexarelin is the disturbance of natural sleep patterns. These alterations in sleeping patterns may cause some individuals to have difficulty falling and/or staying asleep, but many do not experience this problem. At any rate, by avoiding use late at night, this potential issue is eliminated.&lt;br /&gt;
&lt;br /&gt;
Growth hormone has numerous documented benefits, making it one of the most diverse drugs in our PED arsenal. Some of these benefits include:&lt;br /&gt;
&lt;br /&gt;
* Decreased body fat&lt;br /&gt;
* Increased lean mass&lt;br /&gt;
* Increased collagen production&lt;br /&gt;
* Improved sleep quality&lt;br /&gt;
* Increased cellular repair&lt;br /&gt;
* Increased in IGF-1 levels&lt;br /&gt;
* Increased bone density&lt;br /&gt;
* Increased rate of wound/injury healing&lt;br /&gt;
* Improved immune function&lt;br /&gt;
* Improved overall wellbeing&lt;br /&gt;
* Improved exercise tolerance&lt;br /&gt;
&lt;br /&gt;
Typical dosing guidelines for Hexarelin range between 50-200 mcg per inject, with 100 mcg being considered the standard. Most will find a dose of 100 mcg to be more than suitable. According to documented research, a single 100 mcg injection is capable of eliciting a temporary elevation in GH similar to what one would experience when administering 10 IU of GH in a single injection. The differentiating factor in this comparison is the length of time GH levels remain elevated post-injection. With exogenous GH, levels remain elevated for roughly 7-8 hours, while levels will fall to baseline within 90 minutes of administering Hexarelin. This is why most users will choose to administer this GHRP no less than 2-3X per day.&lt;br /&gt;
Hexarelin is the most efficacious GHRP available, allowing for impressive elevations in GH levels with few downsides. For those of you who normally research products such as GHRP-2 or Ipamorelin at traditional dosages, you may want to consider giving this unique GH peptide a shot for your next research project. Don’t let prior misconceptions fool you. Hexarelin is one of the most under-rated GHRP’s on the market and certainly more effective than other drugs in the same class on a mcg to mcg basis. So long as proper procedures are adhered to in terms of ON/OFF time (during which time an alternate GHRP can be researched), Hexarelin can be used as semi-permanent fixture in your GH peptide program. &lt;br /&gt;
by Mike Arnold&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/08/hexarelin-peptide-explored.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-4471900785368734884</guid><pubDate>Sat, 02 Aug 2014 10:57:00 +0000</pubDate><atom:updated>2014-08-02T06:57:00.482-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Sermorelin</category><title>Sermorelin: a review </title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency.&lt;br /&gt;
&lt;br /&gt;
&lt;a href=&quot;http://www.truepeptide.com/100.html&quot;&gt;&lt;b&gt;Sermorelin&lt;/b&gt;&lt;/a&gt;, a 29 amino acid analogue of human growth hormone-releasing hormone (GHRH), is the shortest synthetic peptide with full biological activity of GHRH. Intravenous and subcutaneous sermorelin specifically stimulate growth hormone secretion from the anterior pituitary. Hormone responses to intravenous sermorelin 1 microg/kg bodyweight appear to be a rapid and relatively specific test for the diagnosis of growth hormone deficiency. False positive growth hormone responses are observed in fewer children without growth hormone deficiency after sermorelin than after other provocative tests.&lt;br /&gt;
&lt;br /&gt;
Adult data indicate that the combination of intravenous sermorelin and arginine is a more specific test and this merits evaluation in children with growth hormone deficiency. However, normal growth hormone responses to intravenous sermorelin cannot exclude growth hormone deficiency due to a hypothalamic deficit: subnormal growth hormone response to other provocative tests is needed to confirm the presence of disease in these patients. Limited data indicate that once daily subcutaneous sermorelin 30 microg/kg bodyweight given at bedtime is effective in treating some prepubertal children with idiopathic growth hormone deficiency. &lt;br /&gt;
&lt;br /&gt;
Significant increases in height velocity were sustained during 12 months&#39; treatment with sermorelin and data in a few children suggest the effect is maintained for 36 months of continued treatment. Sermorelin induced catch-up growth in the majority of growth hormone-deficient children. Slow growing, shorter children with delayed bone and height age appear to have a good response to treatment with sermorelin. The effect of long term treatment with once daily subcutaneous sermorelin 30 microg/kg bodyweight on final adult height is yet to be determined. &lt;br /&gt;
&lt;br /&gt;
The effects of the recommended dosage of sermorelin have not been directly compared with those of somatropin. However, increases in height velocity from baseline values with subcutaneous sermorelin 30 microg/kg bodyweight per day, given as continuous infusion or as 3 divided doses, were less than those in children receiving once daily subcutaneous somatropin 30 microg/kg bodyweight. Intravenous single dose and repeated once daily subcutaneous doses of sermorelin are well tolerated. Transient facial flushing and pain at injection site were the most commonly reported adverse events.&lt;br /&gt;
&lt;br /&gt;
CONCLUSIONS: &lt;br /&gt;
&lt;br /&gt;
Sermorelin is a well tolerated analogue of GHRH which is suitable for use as a provocative test of growth hormone deficiency when given as a single intravenous 1 microg/kg bodyweight dose in conjunction with conventional tests. Limited data suggest that once daily subcutaneous sermorelin 30 microg/kg bodyweight is effective in promoting growth in some prepubertal children with idiopathic growth hormone deficiency.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/08/sermorelin-review.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-6165709432229695029</guid><pubDate>Fri, 01 Aug 2014 10:54:00 +0000</pubDate><atom:updated>2014-08-01T06:54:58.178-04:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Liothyronine sodium)</category><category domain="http://www.blogger.com/atom/ns#">T3 (Cytomel</category><title>T3 (Cytomel, Liothyronine sodium) </title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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T3 (Cytomel, Liothyronine sodium)&lt;/a&gt; &lt;br /&gt;
Cytomel is the most common synthetic version of the T3 or triiodothyronine. T3 is not produced directly by the thyroid gland but by the thyroid-stimulating hormone or THS. THS is also responsible for the production of T4 or thyroxine. Cytomel (T3) does speed fat loss. As a guideline, for most 12.5 mcg/day is a conservative “supplement” sort of dosing that seems to have no detectable adverse effect on thyroid function at all. 25 mcg/day is a “supplement” sort of dosing that does have some inhibitory effect. 50 mcg/day is a reasonably conservative bb’ing sort of dose that, of course, is more inhibitory. 75 mcg/day is getting into more of a problem area, 100 mcg/day in many cases leads to loss of muscle size and strength. These doses are in reference to legit T3 provided in tablets such as Cytomel. Liquid formulations are usually unstable and as a result, the above numbers in many cases won’t match up to experiences with liquid products, or for that matter, experience with a liquid product at one time may not match up with experience at a different time, due to the stability problem.&lt;br /&gt;
&lt;br /&gt;
Drugs with thyroid hormone activity, such as Cytomel, are used for the treatment of obesity since they are effective fat-burning agents.&lt;br /&gt;
Cytomel exerts its fat-burning ability via the following metabolic pathways and processes.&lt;br /&gt;
&lt;br /&gt;
Cytomel up-regulates the beta-2 adrenergic receptors in fat tissues. In lipolysis, or the breakdown of fat in fat tissues, the enzyme HSL (hormone sensitive lipase) plays a significant part. HSL controls the rate of lipolysis. For HSL to be activated, epinephrine and nonepinephrine (catecholomines) are necessary. These catecholomines bind to the beta-2 receptors, and thus when Cytomel up-regulates the beta-receptors, there is a corresponding increase in the ability of catecholomines to activate HSL, resulting to increased lipolysis.&lt;br /&gt;
&lt;br /&gt;
This drug is likewise known to increase the UCP-3 or uncoupling protein-3. This process significantly increases lipolysis. Further, Cytomel also stimulates growth hormone (GH) production, as substantiated by several studies. And since GH is a thermogenic, it contributes to this drug’s fat-burning action. This is why when athletes are using Cytomel they find no need to use HGH&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/08/t3-cytomel-liothyronine-sodium.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-2650059369851298360</guid><pubDate>Wed, 12 Feb 2014 00:35:00 +0000</pubDate><atom:updated>2014-02-11T19:35:00.065-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Blast Protocol: HGH Igf-1 and insulin</category><category domain="http://www.blogger.com/atom/ns#">growth hormone</category><category domain="http://www.blogger.com/atom/ns#">hgh</category><category domain="http://www.blogger.com/atom/ns#">IGF-1</category><category domain="http://www.blogger.com/atom/ns#">post workout protocol</category><title>Blast Protocol: HGH Igf-1 and insulin</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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I highly recommend using a minimal schedule for all short chain sequence peptides, which include igf, insulin and even gh. I recommend using no more than 3 days per week, 2 days is fine, but no more than 3. The reason for this is that we are trying to prevent cell over-saturation and closure. All three products should be used in a similar manner.&lt;br /&gt;
&lt;br /&gt;
The protocol is as follows; inject all products post workout, preferably after training large muscle groups which cause the most glycogen depletion, hence providing faster uptake of peptides. A sample layout is to inject Monday, Wednesday, and Friday.&lt;br /&gt;
&lt;br /&gt;
Immediately post-workout inject 10-15iu of growth hormone IM, using a insulin pin and inject in any small muscle group such as delts, triceps, or biceps. Wait 20 minutes for the half-life clearance and conversion to IGF-1 to begin its sequence from the growth hormone and then inject a small dose of IGF-1 to create a synergistic super charge of the conversion process. I would recommend no more than 30mcg at this time. 10 minutes later you will take Humalog insulin only, and inject 5iu. I recommend starting with 5iu because Humalog has a very rapid onset and is easy to control with sugar. In conjunction with IGF-1, you will be hyper-sensitive to insulin so start small and slowly work your way up to a maximum dose of 12iu post-workout. You will want to have around 80-100 grams of simple sugars such as dextrose and grape juice and an additional 60 grams of whey protein at the same time as your insulin. You will then eat another moderate glycemic index meal one hour after your high glycemic shake.&lt;br /&gt;
&lt;br /&gt;
The reason for the high dose growth hormone is to take what would normally be your one week intake of HGH and spread it out into 3 equal doses, injected post work out. This will create a truly anabolic rich environment and you will also benefit from full uptake due to your post work out depleted state.&lt;br /&gt;
So there is our post-workout regime, 3 days per week. Certainly you should take more than this, shouldn’t you? For most lifters, this protocol will be sufficient for growth. For someone with at least 6 months of gh use, 5 or more cycles of insulin and who no longer responds to typical IGF-1 protocols, the following regime may be followed: In addition to the above outline post-workout method, you may add additional doses of IGF-1 as well as insulin on the same day as your post-workout injection.&lt;br /&gt;
&lt;br /&gt;
I would highly recommend you take 15mcg IGF-1 an additional two times per day. By taking less IGF-1 more often you will prevent cell over-saturation as well as receptor down-regulation. Creating a cell rich environment that saturates the cells infrequently will target massive cell proliferation. In addition you will take insulin 20 minutes after the IGF-1 on those 2 additional injections creating an anabolic rich environment that will last all day, 3 days per week.&lt;br /&gt;
For a sample protocol for someone that works out after work, I would recommend you do the following: Take 15mcg upon rising in the morning, followed by 10iu Humulin R or Humalog 20 minutes later. Immediately eat a carbohydrate rich meal with quality protein and low fat such as bananas, oatmeal and egg whites.&lt;br /&gt;
For lunch, take another 15mcg IGF-1 with 10iu insulin and have another moderate glycemic carbohydrate meal and protein with minimal fats. Follow the above listed post workout protocol to complete your three time injection schedule which will be used three times per week.&lt;br /&gt;
&lt;br /&gt;
If you follow the outline laid out for you above to the letter, you will put on a massive amount of lean mass with a minimal amount of fat. You will need an anabolic and androgen rich environment to complete the schedule such as testosterone and tren in addition to the peptide products. T3 and T4 will not be necessary on this schedule as your thyroid levels will not be affected. &lt;br /&gt;
By: Gavin Kane&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/02/blast-protocol-hgh-igf-1-and-insulin.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-8052825805705384599</guid><pubDate>Tue, 11 Feb 2014 00:30:00 +0000</pubDate><atom:updated>2014-02-10T19:30:01.624-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">hgh</category><category domain="http://www.blogger.com/atom/ns#">IGF-1 Manual</category><category domain="http://www.blogger.com/atom/ns#">long r3 igf-1</category><title>Introduction into IGF-1</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Introduction into IGF-1&lt;br /&gt;
&lt;br /&gt;
IGF-1 isn&#39;t new. All mammals make IGF-1 and would die without it. IGF-1 secretion in the human body can be thought of as belonging to two separate, broad categories: Autocrine and Paracrine. While there are many versions of IGF-1 in the body, these are the broad categories that need to be understood in order to know exactly what you are doing when supplementing IGF-1. This thread focusses on practical application rather than pure science, as most IGF-1 researchers reading this material are bound to have more interest in actual effects of the product than its chemistry or whatnot.&lt;br /&gt;
&lt;br /&gt;
Firstly, definitions&lt;br /&gt;
&lt;br /&gt;
Autocrine: An IGF-1 molecule that is expressed by the cell for use within itself is known as autocrine IGF-1. This IGF is only active within the cell itself and on its surface. AAS increase the expression of IGF-1 by muscle cells. Cancerous tumors, for example, express autocrine IGF-1 much more than normal cells, and that is one factor of their unnaturally accelerated growth, division and multiplication.&lt;br /&gt;
&lt;br /&gt;
Paracrine: Also known as systemic IGF-1, this molecule is synthesized by the liver. Its synthesis is rate-limited by the availability in the liver of both insulin and growth hormone and is the main reason for the widely known synergy between insulin and hGH administration. This IGF-1 acts differently than the autocrine and it effects every organ in the body. It is also the main vector of effects of hGH administration, meaning that most of the effects gained by hGH administration can also be gained by directly administering IGF-1. All IGF-1 administration is of the paracrine type.&lt;br /&gt;
&lt;br /&gt;
IGFBP: This is a binding protein that plays much the same function to IGF-1 as SHBG, or sex hormone binding globulin plays to testosterone and estrogen. A binding protein holds on to its target molecule, temporarily inactivating it. The dynamics of IGFBP are somewhat complex, but let it be known that IGFBP is sort of a nemesis to IGF-1 since it renders it inactive.&lt;br /&gt;
&lt;br /&gt;
Long R3 IGF-1: I will spare you the boring details of why it is called Long R3 and rather go into how it is functionally different from the natural form. The normal IGF-1 molecule has a very short half-life, approximately 20 minutes. It is either taken up by IGF-1 receptors on cells, or inactivated by IGFBPs. This is the reason why people injected huge amounts of many mg every day of IGF-1 15 years ago, whereas today the normal dose in a few dozen micrograms. What happened? Someone modified the natural IGF-1 molecule just enough that it would retain all its good properties and yet would resist being bound by IGFBPs. This is the Long R3 form of IGF-1. This is what you buy, practically no one tries to sell the natural form anymore. This has a half-life of about 12 hours.&lt;br /&gt;
&lt;br /&gt;
Media Grade: This is the more usual grade of Long R3 IGF-1 that you see on the market. It is about 95% pure IGF-1 with some other incomplete peptides in it. And since the dose of IGF-1 is so small, the maximum 5% impurities of media grade represent a truly tiny amount. And the meaning of impurities in this context is simply some amino acids, either loose or in peptide form. In all likelihood that 5% of non-IGF-1 peptides is truly harmless.&lt;br /&gt;
&lt;br /&gt;
Receptor Grade: Receptor-grade IGF-1 is guaranteed to be at least 99% pure Long R3 IGF-1 peptide. This grade is only used in advanced human trials in very specific spots on the planet. It is a truly rare thing and does not offer the bodybuilder any real-life advantage over media grade. It is also unavailable. There has been batches of some substance sold as &quot;Receptor grade IGF-1&quot; over the last year or so and here a very serious warning must be given. There is a peptide which is only the receptor binding portion of the IGF-1 molecule, which is a cellular lab product which contains bovine peptides and prions. This stuff has no other function than to bind to the IGF-1 receptor. It has no beneficial properties but blocks the receptor from being used by actual IGF-1. Some very bad or misinformed people have been selling this to bodybuilders as receptor grade IGF-1. This stuff can be very toxic. Prions cause CNS trouble of which mad cow disease is an example.&lt;br /&gt;
&lt;br /&gt;
AA: Short for Acetic Acid, a commonly-used solvent for diluting the IGF-1 powder. This is said to keep the fragile IGF-1 molecule more stable than other solvents. This point is heavily debated. AA is an acid and it tends to kill whichever tissue you inject it into. It is best to dilute the IGF-1 with as little AA as can be done, and then to dilute this solution again when injecting so as to damage the target tissue as little as possible.&lt;br /&gt;
&lt;br /&gt;
BW: Bacteriostatic water. This is simply purified water mixed with 0.9% Berylic Alcohol. Microorganisms cannot survive in this water. It is a very common solvent for injections and should be easily obtainable even from your local drugstore. BW is not an ideal solvent for long-term IGF-1 solution and storage as it tends to degrade much more quickly in BW than in AA. Again there is much debate as to how quickly IGF-1 does degrade in BW.&lt;br /&gt;
&lt;br /&gt;
Secondly, Effects&lt;br /&gt;
&lt;br /&gt;
Muscle satellite cell prolferation is the single most important effect of IGF-1 to us bodybuilders. In order to perfectly understand what this means, we must examine how muscles grow.&lt;br /&gt;
&lt;br /&gt;
Muscle grows in two ways: the amount of contractile protein inside a fiber increases, which increases muscular strength and the space taken up by that additional strand of protein is added lean body mass. This is a comparatively small amount of size, but a lot of strength. The second way that muscles grow is when satellite cells merge with real muscle cells and donate their nucleus. Satellite cells have only one nucleus. And muscle cells, unlike the other cells in the human body, have at least one nucleus, without a set ceiling to how many there can be.&lt;br /&gt;
&lt;br /&gt;
Myonucleii are the parts of the cell that are responsible for protein synthesis and expression. Whenever you damage a muscle through training, the rebuilding process that ensues is accomplished mostly by the myonucleii, which make new contractile protein which is used to repair and when possible upgrade the muscle cell&#39;s ability to generate and withstand force. Moreover, the size of a muscle cell is directly proportional to its myonuclear number, i.e. the number of nucleii that the cell contains. So the maximum amount of carbohydrate, water, minerals and protein that a muscle cell can absorb and retain are all dependent on ONE thing: the myonuclear number.&lt;br /&gt;
&lt;br /&gt;
Moreover, the ability to recover (and upgrade) from damage is also proportional to the myonuclear number. As such, having high myonuclear numbers should be on top of every bodybuilder&#39;s priority list. Now how do we get the satellite cells to donate their nucleii? Interestingly, it is the autocrine IGF-1 that signals adjacent satellite cells to donate their myonucleii. Autocrine IGF-1 expression happens with exercise and is proportional to many things, including the level of androgen receptor stimulation. Yes this means that one of the ways in which anabolic steroids help growth is through the added expression of autocrine IGF-1 and merging of satellite cells.&lt;br /&gt;
&lt;br /&gt;
One very interesting theory of steroids is that the decreasing results from successive cycles, which have absolutely nothing to do with receptor downregulation, actually has more to do with having merged more and more of the satellite cells into the muscles and having less and less new satellite cells for merging and donation purposes.&lt;br /&gt;
&lt;br /&gt;
As you guessed, exogenous IGF-1 administration fixes this splendidly by its potent stimulation of satellite cell hyperplasia. Hyperplasia pulls a lot of carbohydrate and protein from the bloodstream to make new cells. This also requires a very large amount of energy, which can be obtained from burning fats, since the energy expenditure is not extremely rapid. The low blood glucose that ensutes IGF-1 administration as well as greatly increased triglyceride metatolism on the part of the dividing myoblasts compound to generate a substantial fatloss effect.&lt;br /&gt;
&lt;br /&gt;
When injected, IGF-1 floats around until it finds an IGF-1 receptor or another binding site such as the IGFBP. Of course for the usual Long R3 form that most use, the IGFBP is not a factor and the IGF molecule will just wander until it finds a receptor. Exercise upregulates the trained muscle&#39;s receptor, bringing it to the cell&#39;s surface and &quot;opening&quot; it for business with an IGF-1 molecule. Once IGF-1 binds to that site, it will be absorbed by the cell and metabolized. One IGF-1 molecule can only trigger one receptor. Obviously, we want to target muscle receptors, as all other cell types also have IGF-1 receptors. Skin &amp; hair follicles, sure why not. What you want to avoid growing are bones, internal organs such as intestines, and tumors. Interestingly, the highest concentration of IGF-1 receptors are in the gut.&lt;br /&gt;
&lt;br /&gt;
Thirdly, usage&lt;br /&gt;
&lt;br /&gt;
This is where stuff gets somewhat debatable. Best IGF-1 treatment protocol isn&#39;t a science yet. It is nowhere close to the state of advancement that AAS use has attained, and there will be much argument as to which protocol is best. Still, I will attempt to give an objective, wide-ranging set of available options for the IGF-1 researcher.&lt;br /&gt;
&lt;br /&gt;
For a good while now, it has been found that a dose of 40mcg divided in bilateral administration in the muscles trained gave good results. It has been found that after 30 to 40 days of such a protocol, results diminish and stop. From this fact has stemmed an effective protocol recommending 30-day cycles of 40mcg daily IGF-1 bilateral intramuscular administration, followed by 30 days off. This works, no doubt about it. Most users prefer cycles of 25 days on, 25 days off since the 40mcg dose will use up one miligram in a cycle. IGF-1 receptors seem to downregulate proportionally to the dosage used.&lt;br /&gt;
&lt;br /&gt;
Some people have tried 80mcg with a greater immediate response. I have seen up to 200mcg daily administration and of course short-term effects are proportional to the dosage administered. Some people find that they get a better pump when injecting the IGF-1 preworkout. Others feel that IGF-1 should be something more than a simple pump product and use it postworkout in an attempt to generate as much mitosis of myoblasts as possible.&lt;br /&gt;
&lt;br /&gt;
Based on the science posted above about IGF-1 biochemistry and effects, the following points stand out as a base to fashion a good IGF-1 treatment protocol. Firstly, the most important effect to be sought is myoblast mitosis, as ONLY IGF-1 can achieve this effect, arguably the single most important thing for bodybuilding. Anything else should be seen as a bonus. Secondly, you want to use just enough IGF-1 to initiate mitosis in the target muscle and avoid spillover of the peptide to systemic distribution where probability says it will grow your guts instead of your muscles. This stuff is far from free and &quot;GH guts&quot; are far from aesthetic. Thirdly, you want this quantity of IGF-1 to be in as small a volume of liquid as practical. Fourthly, you want to administer the IGF-1 immediately postworkout when the receptors are maximally stimulated. Any other administration timing is suboptimal.&lt;br /&gt;
&lt;br /&gt;
Now because IGF-1 treated cells leech glucose from the bloodstream like crazy, it is possible to go into hypoglycemia from IGF-1 supplementation. Feed carbs steadily from the time of the injection up until about 6-8 hours afterwards or whenever glycemia stabilizes. This is effect is dose-dependent.&lt;br /&gt;
&lt;br /&gt;
Fourthly, Storage&lt;br /&gt;
&lt;br /&gt;
*Study conducted by Gropep&lt;br /&gt;
&lt;br /&gt;
The stability of a liquid solution of LR3IGF-I was monitored for a period of two years at storage conditions of -20 C, +4 C, +22 C, and +37 C. The final concentration of LR3IGF-I was in acetic acid. At various time points, samples were taken and compared to a lyophilized control (stored at 4 C). Listed below are the stability results for each respective storage condition.&lt;br /&gt;
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&lt;/script&gt;&lt;/div&gt;Storage Condition: -20 C (-4 F)&lt;br /&gt;
Biological Potency No Change up to 2 years&lt;br /&gt;
Immunological Activity No Change up to 2 years&lt;br /&gt;
Mobility of protein No Change up to 2 years&lt;br /&gt;
Elution Profile by reversed phased HPLC No Change up to 2 years&lt;br /&gt;
&lt;br /&gt;
Storage Condition: +4 C (39.2 F)&lt;br /&gt;
Biological Potency No Change up to 2 years&lt;br /&gt;
Immunological Activity No Change up to 2 years&lt;br /&gt;
Mobility of protein No Change up to 2 years&lt;br /&gt;
Elution Profile by reversed phased HPLC No Change up to 2 years&lt;br /&gt;
&lt;br /&gt;
Storage Condition: +22 C (71.6 F)&lt;br /&gt;
Biological Potency No Change up to 2 years&lt;br /&gt;
Immunological Activity No Change up to 2 years&lt;br /&gt;
Mobility of protein No Change up to 2 years&lt;br /&gt;
Elution Profile by reversed phased HPLC No Change up to 2 years&lt;br /&gt;
&lt;br /&gt;
Storage Condition: +37 C (98.6 F)&lt;br /&gt;
Biological Potency No Change up to 1 year&lt;br /&gt;
Immunological Activity No Change up to 1 year&lt;br /&gt;
Mobility of protein No Change up to 1 year&lt;br /&gt;
Elution Profile by reversed phased HPLC No Change up to 1 year&lt;br /&gt;
&lt;br /&gt;
In conclusion, there is no significant difference in the potency of LR3IGF-I associated with the storage of the liquid formulation when stored at this range of temperatures. There is no evidence for loss of biological activity at any of the tested temperatures when stored as a liquid product. As you can see IGF can be quite stable for even a year at room temperature, but if you want to keep it around for a while then stick it into the fridge. So the best way to store LR3 that is suspended in BA (benzoic acid) is in the freezer. The BA won’t allow it to freeze. And if you have it suspended in AA (acetic acid), store it in the fridge.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/02/introduction-into-igf-1.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-2131475395274435307</guid><pubDate>Mon, 10 Feb 2014 00:26:00 +0000</pubDate><atom:updated>2014-02-09T19:26:00.314-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">steroids</category><category domain="http://www.blogger.com/atom/ns#">The truth about Peptides and what to expect</category><title>The truth about Peptides and what to expect</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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For all who have been misinformed or mislead about these cutting edge supplements, or those just getting interested, this is a must read&lt;br /&gt;
&lt;br /&gt;
For all the people out there that looking for instant gratification, these may not be your supplement of choice. But for the guys that are willing to go and bust our butts in the gym day in and day out and we don&#39;t need to see an inch added our arms this week to come back and do it again next week because we know that if you keep coming back that’s where the true rewards begin.&lt;br /&gt;
&lt;br /&gt;
Don&#39;t be fooled by other companies advertising steroid like effects from Peptides like MGF or IGF or any type of GH. It’s a false claim made to make sales. And its place/people like this that are ruining the peptide business. People don&#39;t see anything close to the results they got from their last cycle of AAS and immediately think they got screwed or scammed or that Peptides are junk and a waste of money. This is the fault of the seller for not informing the client.&lt;br /&gt;
&lt;br /&gt;
When you do a cycle of AAS, what’s next?? PCT of course. All AAS users have the same fears at the end of each cycle. They don&#39;t want to lose their hard earned gains. The gains that came so fast and so easy, but can be lost in the blink of an eye without proper PCT. And even with good PCT it’s still hard to keep everything. Then there is the other evil. ESTROGEN!!! You are popping Anti-E&#39;s and AI&#39;s and progestin blockers that cost you a ton extra because you don’t want those bitch tits or that bloat, or the sudden fat gain. AAS = great gains, followed by anxiety. Now I&#39;m not going to knock AAS they are a cornerstone. They give undeniable results. But at the cost of side effects, and PCT anxiety and cost. So they aren’t perfect. You spend your off time trying to maintain, let alone trying to make gains....&lt;br /&gt;
&lt;br /&gt;
Now let’s look at what happens during a cycle of Peptides. Taken right with good diet and exercise just like you would for an AAS, but maybe not quite as many calories as some do on heavy cycles, you will see some small gains, some leaning out, but no where near the 20lbs of beef you put on last test/tren cycle. You might be lucky with 5lbs over the course of 6-8 weeks. But here is where it gets good. All those gains, there yours, not going anywhere, not going to suddenly start to subside, they aren’t going to result in some post cycle bloat, ***** tit formation, or fat gain. In fact your metabolism will be slightly higher from the gains. Anxiety free... no wait!!! It’s better than anxiety free; you should be just as stoked now as when you started the cycle. Because after you do a cycle of Peptides like IGF or MGF especially. The gains are going to come better after the cycle then they did before. Unlike AAS where you try to gain and then maintain.&lt;br /&gt;
&lt;br /&gt;
You see steroids make the adult muscle cells (myotubules) bigger, but the bigger these cells get as we all know the harder and harder it is to make them even bigger. These myotubules are limited in size by the amount of nuclei they contain. The closer they get to being maxed the harder for them to grow and when they are maxed well that’s about it.... gains will be few and far between. Myotubules don&#39;t divide like other cells so you pretty much have as many as you’re going to have for the most part. Hyperplasia does occur but it is a very rare process. This is where some people refer to the genetics. Because your genetics determines largely your # of myotubules you have, and the hormones that regulate them.&lt;br /&gt;
&lt;br /&gt;
This is where Peptides make their mark. Growth factors in short lead to an increase in the potential of the myotubules to grow because they can influence the stem cell pools of the muscle which are their for growth and repair, to fuse with the adult myotubules and increase the # of nuclei. This means they can grow more again, and grow easier. Individual mechanisms for each peptide may very, but this is the overall effect they are all going for. So after taking some Peptides you will experience better gains than before, with relatively non existent side effects, no PTC, no anxiety. These are supplements with an investment in mind, a future goal beyond the current cycle, and realistic view that real gains don&#39;t have to come in 6-12 week segments but can come all year round.&lt;br /&gt;
&lt;br /&gt;
When you add all that up, the cost of &lt;b&gt;&lt;i&gt;Peptides&lt;/i&gt;&lt;/b&gt; is not as far overhead as you might think. It cost a lot of money to bring this caliber of products to the market. Peptides are complicated structures, not simple molecules like AAS. But if you in this business for the long hall, Peptides have extremely good benefits to offer.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
article  by spywizard &lt;br /&gt;
&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/02/the-truth-about-peptides-and-what-to.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-1287732373510353228</guid><pubDate>Sat, 08 Feb 2014 19:00:00 +0000</pubDate><atom:updated>2014-02-08T14:39:38.380-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Bremelanotide</category><category domain="http://www.blogger.com/atom/ns#">PT-141</category><title>Bremelanotide (PT-141)</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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PT-141 (Bremelanotide) is the first of a new class of drugs called melanocortin agonists being developed to treat sexual dysfunction. The mechanism of action of PT-141 (Bremelanotide) may offer significant safety and efficacy benefits over currently available products because it acts on the pathway that controls sexual function without acting directly on the vascular system. Clinical data indicates that PT-141 (Bremelanotide) may be effective in treating a broad range of patients suffering from ED. The nasal formulation of PT-141 (Bremelanotide) being developed is as convenient as oral treatments, is more patient-friendly than invasive treatments for ED, such as injections and trans-urethral pellets, and appears to result in a rapid onset of action.&lt;br /&gt;
About PT-141&lt;br /&gt;
&lt;br /&gt;
&amp;nbsp;Bremelanotide (PT-141) was developed from Melanotan 2 (MT-II). PT-141 is a metabolite of MT-II that lacks the C-terminal amide function-stripping away tanning properties&lt;br /&gt;
PT-141 is the only synthetic aphrodisiac. Studies have shown Bremelanotide to be effective in treating sexual dysfunction in both men (erectile dysfunction or impotence) and women (sexual arousal disorder). Unlike Viagra and other related medications (PDE5s), PT-141 does not act upon the vascular system, but directly through the nervous system (hypothalamus) to increase desire. Viagra, Cialis and Levitra are not considered aphrodisiacs as they do not have any direct effect on the libido. However, treatment with PDE5 inhibitors and PT-141 are known to have a synergistic effect.&lt;br /&gt;
&amp;nbsp;Bremelanotide is a melanocortin peptide hormone. PT-141 binds to the melanocortin 4 receptor (MC4R) in particular in the brain. Nine out of ten volunteers experienced sexual arousal in trials. The aphrodisiac effects of Bremelanotide are in a class of its own. &lt;br /&gt;
&lt;br /&gt;
&amp;nbsp;Bremelanotide comes in 10mg and 2mg vial sizes. Peptides photographed at right are synthesized by the same laboratory, contain no filler and therefore the difference is visible. Freeze dried Melanotan peptides (PT-141) are very durable and stable. Most PT-141 comes in the industry standard 10mg size. The 2mg PT-141 is used more as a travel peptide or couples dose. As a lifestyle peptide, the 10mg product is a lot to consume and may offer up to 20 doses when dosing light. The PT-141 peptide reconstituted with bacteriostatic water remains potent in the fridge for months. Nasal sprays, pre-mixed PT-141, pills and loose powder are not legitimate. There are successful reports of snorting and nasal spray experiences...however they are few and far between.&lt;br /&gt;
&amp;nbsp;Bremelanotide, injected (subcutaneously), has a unique window of opportunity lasting six to 72 hours. In lab trials female rats exposed to PT-141 began &quot;flirting&quot; with male rats for sex. Postures and movements left no doubt in the male rats minds that they were in the mood. The human PT-141 date is one where the dosage precedes the activity by at least a couple hours. When the stars align, hours after the injection, ...this is your window of opportunity, enjoy.&lt;br /&gt;
&lt;br /&gt;
Example- 1ml(cc) bacteriostatic water per 10mg PT-141 vial equates to a 1mg dose approximately each 10 units on a U100 insulin syringe. &lt;br /&gt;
&amp;nbsp;Example- 1ml(cc) bacteriostatic water per 2mg PT-141 vial equates to a 1mg dose approximately every 50 units on a U100 insulin syringe.&lt;br /&gt;
&lt;br /&gt;
Recommended strategy for mixing and dosing would be to reconstitute with the volume that yields a .1ml injection.&lt;br /&gt;
&amp;nbsp;Example- 1ml(cc) bacteriostatic water per 10mg PT-141 vial equates to a 1mg dose approximately each 10 units on a U100 insulin syringe. &lt;br /&gt;
&amp;nbsp;Example- .2ml(cc) bacteriostatic water per 2mg PT-141 vial equates to a 1mg dose approximately every 10 units on a U100 insulin syringe.&lt;br /&gt;
&lt;br /&gt;
&amp;nbsp;Dosing: Read as much as possible to gain clarity and align expectations. Gradually dosing increases likelihood for success without sides. A test dose of .25-.5mg on the first attempt is recommended. 1mg, give or take a quarter, is the efficacious dose which yields the most positive reports by users.&lt;br /&gt;
&amp;nbsp; &lt;br /&gt;
Nasal spray for women who are sniffy about sex&lt;br /&gt;
&amp;nbsp; &lt;br /&gt;
Robin McKie, science editor&lt;br /&gt;
It is the seducer&#39;s ultimate dream: a potion that will turn a woman&#39;s cold indifference into warm sexual interest. Sound improbable? Not any more. Scientists last week revealed they had successfully tested a nasal spray, PT-141, that sent &#39;healthy, normal women&#39; into states of high sexual arousal.&lt;br /&gt;
&#39;The crucial point about PT-141 is that it directly targets the brain&#39;s arousal centre,&#39; said Dr Carl Spana, president of Palatin Technologies, of New Jersey. Originally uncovered through tests on rats, the drug aroused female rodents &#39;so quickly they started mounting males&#39;, added Spana.&lt;br /&gt;
Now the company hopes to market PT-141 for humans in two or three years though Spana stressed Palatin&#39;s main target was people with sexual problems: men with impotence and women with low arousal.&lt;br /&gt;
&lt;br /&gt;
Given that more than 40 per cent of women suffer from &#39;female sexual dysfunction&#39; - they are interested in sex but cannot reach climax - this still gives PT-141 a massive market while at the same time providing hope for a lot of unsatisfied men.&lt;br /&gt;
The drug could even prove to be more popular than Viagra which works by directly stimulating blood flow in sexual organs. But for many women, it is lack of libido - not physiological difficulties - that causes them problems. By contrast, PT-141 targets the brain&#39;s arousal centre and looks more likely to defrost sexual interest, says Palatin.&lt;br /&gt;
This point was underlined last week when Professor Raymond Rosen of New Jersey&#39;s University of Medicine and Dentistry revealed results of the first human trials of PT-141. Sixteen healthy women were given the drug and 16 were given a placebo. All were shown erotic videos, while detectors measured blood flow in their vaginas.&lt;br /&gt;
The women given placebos hardly reacted while those on PT-141 had pronounced increases in blood flow - results that demonstrate the drug has potential that goes well beyond its use only as a medical aid, though Spana counselled caution. &#39;The drug can only be administered as a nasal spray - which isn&#39;t good for seducers. You can&#39;t put it in a drink and sticking it up a girl&#39;s nose is hard to do surreptitiously, after all.&lt;br /&gt;
&#39;On the other hand, related compounds could easily be made into pills one day, though I still don&#39;t think they will turn on a woman who was previously totally uninterested in a man or in having sex. She has to be halfway there already.&#39;&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/02/bremelanotide-pt-141.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-6240065108122118983</guid><pubDate>Thu, 16 Jan 2014 18:58:00 +0000</pubDate><atom:updated>2014-02-08T14:40:01.884-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">Bremelanotide PT-141 Instruction</category><category domain="http://www.blogger.com/atom/ns#">PT-141</category><title>Bremelanotide PT-141 Instruction</title><description>&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Bremelanotide PT-141 Instruction&lt;br /&gt;
Bremelanotide PT 141 Dosage:&lt;br /&gt;
Light: .5mg&lt;br /&gt;
&amp;nbsp;Common: 1mg&lt;br /&gt;
&amp;nbsp;Large: 2mg&lt;br /&gt;
Trusted Supplier: PT-141 &lt;br /&gt;
Bremelanotide PT-141 was developed from Melanotan 2 (MT-II). PT-141 is a metabolite of melanocyte stimulating hormone that targets desire.&lt;br /&gt;
PT-141 bremelanotide molecule research chemical&lt;br /&gt;
Treatment:&amp;nbsp; PT-141 is the only synthetic aphrodisiac. The aphrodisiac effects of Bremelanotide are in a class of its own. Studies have shown Bremelanotide to be effective in treating sexual dysfunction in both men (erectile dysfunction or impotence) and women (sexual arousal disorder). Nine out of ten volunteers experienced sexual arousal in clinical trials. Unlike Viagra and other related medications (PDE5s - blood pushers), PT-141 acts upon the nervous system. Viagra, Cialis and Levitra are not considered aphrodisiacs as they do not have any direct effect on the libido. However, treatment with PDE5 inhibitors and PT-141 have known synergy.&lt;br /&gt;
&amp;nbsp;Men&#39;s Journal Magazine: ...it took hold. I felt a great surge of affection (greater than any regular level of arousal). My body tingled and I developed an erection that wouldn’t quit. For two hours the drug wouldn’t let me out of its grasp — nor my wife out of mine.&lt;br /&gt;
Men&#39;s Journal PT-141&lt;br /&gt;
Females: Women who took part in trials said that they felt a &quot;tingling and a throbbing&quot; along with &quot;a strong desire to have sex.&quot; An initial flush occurs post injection, followed by nausea which is dose dependent. For most, effects generally do not take place until a couple hours post injection, peaking around the four hour mark. Men said PT-141 made them feel &quot;younger and more energetic&quot; as well as sexually interested and aroused. &quot;You&#39;re ready to take your pants off and go,&quot; said user &quot;a product that makes you not only able to but eager to.&quot; &lt;br /&gt;
&lt;br /&gt;
Window of Opportunity: Bremelanotide, injected (subcutaneously), has a unique window of opportunity lasting six to 72 hours. In lab trials female rats exposed to PT-141 began &quot;flirting&quot; with male rats for sex. Postures and movements left no doubt in the male rats minds that they were in the mood. The human PT-141 date is one where the dosage precedes the activity by at least a couple hours. When the stars align, hours after the injection, ...this is your window of opportunity, enjoy.&amp;nbsp; &lt;br /&gt;
Bremelanotide PT141 Peptide: Bremelanotide sold online comes in 10mg vials. As a lifestyle melanocortin research peptide, the 10mg product is a lot to consume and may offer up to 20+ doses when dosing PT-141 conservatively. Quality PT141 reconstituted with bacteriostatic water remains potent and preserved for months. &lt;br /&gt;
Mixing PT-141: Bacteriostatic water is used for reconstitution.&lt;br /&gt;
Example- 1ml(cc) bacteriostatic water per 10mg PT-141 vial equates to a 1mg dose approximately each 10 units on a U100 insulin syringe. &lt;br /&gt;
&amp;nbsp;Example- 1ml(cc) bacteriostatic water per 2mg PT-141 vial equates to a 1mg dose approximately every 50 units on a U100 insulin syringe.&lt;br /&gt;
Recommended strategy for mixing and dosing would be to reconstitute with the volume that yields a .1ml injection.&lt;br /&gt;
Example- 1ml(cc) bacteriostatic water per 10mg PT-141 vial equates to a 1mg dose approximately each 10 units on a U100 insulin syringe. &lt;br /&gt;
&amp;nbsp;Example- .2ml(cc) bacteriostatic water per 2mg PT-141 vial equates to a 1mg dose approximately every 10 units on a U100 insulin syringe.&lt;br /&gt;
PT141 Dosing: Read as much as possible to gain clarity and align expectations. Gradually dosing melanotan peptides increases likelihood for success without sides (desensitization occurs rapidly). Test PT-141 dosage of .25-.5mg on first attempt is recommended. 1mg, give or take a quarter, is the efficacious dose yielding most positive reports.&lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
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</description><link>http://fitness-peptides.blogspot.com/2014/01/bremelanotide-pt-141-instruction.html</link><author>noreply@blogger.com (Unknown)</author></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-8712687967317529203.post-3280823548807458968</guid><pubDate>Mon, 07 Oct 2013 00:51:00 +0000</pubDate><atom:updated>2014-02-08T14:41:59.797-05:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">fast acting insulin</category><category domain="http://www.blogger.com/atom/ns#">for bodybuilding</category><category domain="http://www.blogger.com/atom/ns#">Humalog</category><category domain="http://www.blogger.com/atom/ns#">insulin</category><title>Humalog - fast acting insulin for bodybuilding</title><description>&lt;h2&gt;Humalog - fast acting insulin for bodybuilding  &lt;/h2&gt;&lt;div style=&quot;float: left; margin-bottom: 10px; margin-right: 10px; margin-top: 10px; text-align: center;&quot;&gt;&lt;script type=&quot;text/javascript&quot;&gt;&lt;!--
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Humalog Insulin (Fast Acting)&lt;br /&gt;
Substance: insulin&lt;br /&gt;
Delivery: 10ml vial (40IU/1ml)&lt;br /&gt;
Average Dose: 1iu per 15 - 20 pounds bodyweight&lt;br /&gt;
Half Life: 1.5 - 3 hours&lt;br /&gt;
Water Retention: Yes&lt;br /&gt;
Aromatization: &lt;br /&gt;
DHT Conversion:&lt;br /&gt;
&lt;br /&gt;
Insulin is a powerful hormone in the human body, responsible for regulating glucose levels in the blood. This is a function that your life constantly depends on. Before going any further I must stress that insulin use by those who do not medically require it can be a very risky endeavor. It is important not only to research and understand the risks involved, but to really give some thought to just how important a little extra boost is to you. Misusing insulin can have tragic results. Immediate death, coma or the possible development of insulin dependent diabetes in a previously healthy athlete are all possible, be extremely careful. &lt;br /&gt;
&lt;br /&gt;
In the human body insulin is secreted by the pancreas. The release of this hormone is most closely tied to glucose, although a number of other factors including pancreatic &amp;amp; gastrointestinal hormones, amino acids, fatty acids and ketone bodies are also involved. Its role in the body is to control the uptake, utilization and storage of amino acids, carbohydrates and fatty acids by various cells of your body. The activity of insulin is both anabolic and anti-catabolic, the hormone stimulating the use and retention cellular nutrients while inhibiting their breakdown. Skeletal muscle cells are among the many targets of this hormone&#39;s action, and the reason pharmaceutical insulin has made its way into the realm of athletics. But this is a little tricky because insulin can also promote nutrient storage in fat cells, obviously an unwanted result. Athletes have found however, that a strict regimen of intense weight training and a diet without excess caloric intake can result in insulin showing a much higher affinity for protein and carbohydrate storage in muscle cells. This could produce rapid and noticeable growth, the muscles beginning to look fuller (and sometimes more defined) almost immediately after starting insulin therapy. &lt;br /&gt;
&lt;br /&gt;
The fact that insulin use cannot be detected by urinalysis has ensured it a place in the drug regimens of many professional bodybuilders. Insulin is often used in combination with other &quot;contest safe&quot; drugs like human growth hormone, thyroid medications and low dose testosterone injections, and together can have a dramatic effect on the users physique without fear of a positive urinalysis result. Those who do not have to worry about drug testing however, find insulin and anabolic/androgenic steroids a very synergistic combination. This is because the two actively support an anabolic state through different mechanisms, insulin enhancing the transport of nutrients into muscle cells and steroids (among other things) increasing the rate of cellular protein synthesis. &lt;br /&gt;
&lt;br /&gt;
The actual medical purpose for insulin is to treat different forms of diabetes. Specifically the human body may not be producing insulin (Type-I diabetes) or may not recognize insulin well at the cell site although some level is present in the blood (Type-Il diabetes). Type-I diabetics are therefore required to inject insulin on a regular basis, as they are left without a sufficient level of this hormone. Along with medication, the individual will need to constantly monitor blood glucose levels and regulate their sugar intake. Together with lifestyle modifications such as regular exercise and developing a balanced diet, insulin dependent individuals can live a healthy and full life. Untreated, diabetes can be a fatal disease.&lt;br /&gt;
&lt;br /&gt;
As we have discussed earlier, regular insulin is the most popular choice and will be the subject of our intake discussion. Before one even considers using insulin, they should become very familiar with using a glucometer. This device gives you a quick number reading of your blood glucose level and can be indispensable in helping you manage your insulin/carbohydrate intake. &lt;br /&gt;
&lt;br /&gt;
Insulin is used in a wide variety of ways. The dosages can vary significantly among athletes, and are often dependent upon factors like insulin sensitivity and the use of other drugs. Most users choose to administer insulin immediately after a workout, which is likely the most &quot;anabolic&quot; time of the day to use this drug. Insulin is always injected subcutaneously, or below the surface of the skin but without entering muscle tissue. This is given by pinching a fold of skin, commonly in the arm or abdominal area. A small &quot;insulin needle&quot; is used, approximately ?â€ long, 27-29 gauge thickness and holding one third to one full cc. These are available over-the-counter in many states. A full cc (or ml) equates to 100 international units (l.U.), a scale that is clearly labeled on an insulin syringe. It is important that the injection site be left alone after insulin has been injected and not rubbed. This is to prevent the drug from releasing into circulation too quickly. It is also a good idea to rotate injection sites regularly; otherwise a localized buildup of subcutaneous fat may develop due to the lipogenic properties of this hormone. &lt;br /&gt;
&lt;br /&gt;
Among bodybuilders, dosages used are usually in the range of 1IU per 15-20 pounds of lean bodyweight. First- time users should at first ignore body weight guidelines however, and instead start at a low dosage with the intention of gradually working up to this point. For example, on the first day of insulin therapy you could begin with a dose as low as only 2 lU. Each consecutive post-workout application this dosage can be increased by 1 IU, until the user determines a comfortable range. This is safer and much more tailored to the individual than simply calculating and injecting a dose, as many find they tolerate much more or less insulin than weight guidelines would dictate. Athletes using growth hormone in particular often have higher insulin requirements, as HGH therapy is shown to both lower secretion of, and induce cellular resistance to, this hormone. &lt;br /&gt;
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One also must remember that it is very important to consume carbohydrates for several hours following insulin use. One will generally follow the rule-of-thumb, of ingesting at least 10 grams of simple carbohydrates per IU of insulin injected (with a minimum immediate intake of 100 grams regardless of dose). This is timed approximately 20 to 30 minutes after the drug has been administered. The use of a carbohydrate replacement drink such as Ultra FueK by Twin Labs would probably be a good idea, as this is a fast and reliable carbohydrate source. It is best to always have something like this on-hand should you begin to notice too low a drop in glucose levels. Many athletes will also take creatine monohydrate with their carbohydrate drink, since the insulin may help force the creatine into the muscles. An hour or so after injecting insulin, one will eat a good meal or consume a protein shake. The carbohydrate drink and meal/protein shake are absolutely necessary. Without them, blood sugar levels can drop dangerously low, and the athlete will most likely enter a state of hypoglycemia. &lt;br /&gt;
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Many taking insulin will also notice a tendency to get sleepy some time after injecting the drug. This is an early symptom of hypoglycemia, and a clear sign the user should be consuming more carbohydrates. One should absolutely avoid the temptation to go to sleep at this point, as the insulin may take its peak effect during rest and blood glucose levels could be left to drop significantly. Unaware of this condition during sleep, the athlete may be at a high risk for going into a state of severe hypoglycemia. We have of course already discussed the serious dangers of such a state, and unfortunately here simply consuming more carbohydrates will not be an option. Those experimenting with insulin would therefore be wise to always stay awake for the duration of the drug&#39;s effect, and also avoid using insulin in the early evening to ensure the drug will not be inadvertently active when retiring for the night. &lt;br /&gt;
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Many athletes prefer to bring their insulin with them to the gym, injecting in the locker room (or car) immediately after a workout. Although insulin should be refrigerated, it is fine to keep it in a gym bag or car so long as it is not left out for too long and it is kept away from heat/direct sunlight. Rather than waiting to the end of a workout, some actually prefer to inject their insulin dosage during training, 30 minutes prior to the end of a session. Immediately following the workout the user will consume a carbohydrate drink in this case. Such timing may make the insulin more efficient at bringing glycogen to the muscles, but also increases the danger of hypoglycemia as carbohydrate consumption may be inadvertently delayed. Some will go so far as to inject a few units before lifting to improve their pump. This practice is risky and best left to those very experienced with insulin. Finally, some bodybuilders opt to inject insulin upon waking in the morning. After the injection they will consume a carbohydrate drink. Later, perhaps one hour after the injection, a full breakfast will be consumed. Some athletes find this application of insulin very beneficial for putting on extra mass while others will tend to store excess fat. If using more than one application of insulin per day it would also be a good idea to restrict the total daily intake to no more than 20-40 IU. &lt;br /&gt;
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Remember to be very careful, one mistake in dosage or diet can be potentially fatal   &lt;br /&gt;
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