OLYMPIC

Welcome bro,good seeing the meso fam coming here.

very minimal but hey you look good. quality > quantity ?

welcome to the board bro

https://northernlifters.com/forum/32-womens-health-fitness/ theres the section,made it for women. we can create sub topics in there. Would be an honor if ya ran it ?

Welcome sir

Welcome to the board. Your reviews section is up aswell ?

Welcome to the board bro.

Here is a study: An Esp Pediatr. 1978 Oct;11(10):675-82., Modifications of insulin and growth hormone after medium chain triglycerides ingestion (author's translation) [Article in Spanish] Valls E, Herrera E, Díaz M, Barreiro P, Valls A. Authors determined the variation of glucose, ketone bodies (KB), free fatty acids (FFA), insulin and growth hormone (HGH) in blood produced by the ingestion of 1.5 g./kg. of medium chain triglycerides (MCT) in 10 healthy children between 5 and 11 years. Blood values were determined starting 30 minutes before the MCT ingestion and at 30 minutes intervals until 120 minutes post ingestion and a final determination at 180 minutes. The glucose did not change. The KB were increased (p less than 0.01) from 30 to 120 minutes and the FFA from 90 (p less than 0.01) to 120 minutes (p less than 0.001) after ingestion. Insulin secretion was elevated between 30--90 minutes with a peak value at 60 minutes (p less than 0.001). HGH began to increase at 60 minutes, remaining elevated at the last determination at 180 minutes. The HGH basal value was 0.5 +/- 0.2 ng./ml.; began to increase at 60 minutes and reached the value of 3.9 +/- 1.06 ng./ml. and 4.8 +/- 2.04 ng./ml. at 90 and 120 minutes respectively (p less than 0.001). We do not know the origin of the HGH increase. The changes may explain FFA elevation and other metabolic actions of MCT. The glucose-insulin ratio showed that the hyperinsulinemia was not caused by an increased glucose level. Note GH rose during the time FFA were found in circulation. MCT oil will not interfere w/ GH release. Just the opposite. ...almost the opposite by a factor of 10. Shhhhhhh.... be very quiet....

I get interested in so many things that I can't keep track. Here were my thoughts at the time and perhaps it is directly relevant to you.Brown Adipose Tissue -From Wikipedia: ...more recently it has become clear that brown fat is not closely related to white fat, but to skeletal muscle, instead. Further, recent studies[3] using Positron Emission Tomography scanning of adult humans have shown that it is still present in adults in the upper chest and neck. The remaining deposits become more visible (increasing tracer uptake) with cold exposure, and less visible if an adrenergic beta blocker is given before the scan. The recent study could lead to a new method of weight loss, since brown fat takes calories from normal fat and burns it. Scientists were able to stimulate brown fat growth in mice, but human trials have not yet begun. Here is a little background science from Effects Of The Melanocortin Agonist Melanotan Ii, Central Pro-Opiomelanocortin And Interleukin-6 Gene Therapies On The Regulation Of Body Weight And Energy Homeostasis, Gang Li, A Dissertation Presented To The Graduate School Of The University Of Florida In Partial Fulfillment Of The Requirements For The Degree Of Doctor Of Philosophy University Of Florida 2003 Brown Adipose Tissue and Energy Expenditure BAT is a specialized fat tissue in mammals heavily innervated by sympathetic nerves. The brown adipocytes contain abundant mitochondria with closely packed cristae that confer the characteristic brown color to this tissue. Thermogenesis in BAT is mainly mediated by norepinephrine activation of sympathetically innervated ß3 adrenoreceptors (Nedergaard et al., 2001). Energy expenditure through brown adipose tissue thermogenesis contributes either to maintenance of body temperature in a cold environment or to consumption of food energy, i.e. cold-induced or diet-induced thermogenesis. Both mechanisms involve a specific and unique protein: the uncoupling protein-1 (UCP1). UCP1, a 32-kDa protein, is exclusively expressed in mitochondria of brown adipocytes where it uncouples respiration from ATP synthesis and dissipates the proton gradient as heat (Nedergaard et al., 2001). Skeletal Muscle and Energy Expenditure Over much of the past century, the skeletal muscle, by virtue of its large size contributing 30–40% of body mass, has been considered the major tissue that enables mammals to adapt to changes in food availability. For example, the rate of heat production during periods of food scarcity is turned down in the skeletal muscle to conserve energy while it is geared up during food abundance to burn excess energy. However, the mechanisms by which skeletal muscle could allow such adaptations remain elusive. UCP3, a UCP1 homologue in muscle, has been proposed to participate in the regulation of thermogenesis and lipid metabolism (Wang et al., 2003). However, several recent studies cast doubt on its physiological relevance to muscle mitochondrial uncoupling (Hesselink et al., 2003; Cadenas et al., 1999; Iossa et al., 2001). Leptin has also been indicated to have direct thermogenic effects in skeletal muscle. Presumably, these effects require both the long form of leptin receptors and PI3K signaling (Dulloo et al., 2002). Muscle-type Carnitine palmitoyltransferase I (M-CPT I) is an important enzyme for energy homeostasis and fat metabolism by modulation of long-chain fatty acid (LCFA) entry into mitochondria, where the LCFAs undergo beta-oxidation (Jeukendrup, 2002). M-CPT I is located in the outer mitochondrial membrane and sensitive to inhibition by malonyl-CoA, which makes it an important site for metabolic regulation. Malony-CoA is the product of a reaction catalyzed by Acetyl-CoA carboxylase (ACC), the first step in fatty acid biogenesis from acetyl-CoA and preserved in nonlipogenic tissues such as skeletal muscles and heart muscle (Jeukendrup, 2002). The formation of malonyl-CoA may therefore offer a main control point of fatty acid catabolism through inhibition of CPT I in muscle. So is it Brown Fat that is a problem for you? I kinda doubt it. I believe the more brown fat you have in the chest area the easier it will be to lose fat there. When you diet down perhaps you are reducing brown fat and making it more difficult to reduce white fat. Perhaps tissue specific resistance to leptin is to blame for white fat accumulation... the tissue may have other signaling defectsHere is how administering MT-II worked in one study: In lean rats, MTII prevented the decrease in brown adipose tissue UCP1, UCP2, and UCP3 expression and muscle UCP3 occurring during food restriction. In obese animals, MTII markedly increased brown adipose tissue (7-fold) and muscle (2.5-fold) UCP3 expression. The decrease in liver carnitine palmitoyltransferase-1 elicited by food restriction in lean and obese rats was prevented by MTII administration. In summary, the effects of MTII resemble those of leptin and are more marked in obese than in lean animals, in keeping with their reported reduced endogenous melanocortin tone. Melanocortin agonists may be useful in the treatment of obesity associated with impaired leptin signaling. - The Leptin-Like Effects Of 3-D Peripheral Administration Of A Melanocortin Agonist Are More Marked In Genetically Obese Zucker (Fa/Fa) Than In Lean Rats, Philippe Cettour-Rose And Franc¸ Oise Rohner-Jeanrenaud, Endocrinology 143: 2277–2283, 2002 Lots of things going on and I don't have a clear idea, just that MT-II may be effective at spot reduction in some spots for some people w/ certain specific characteristics/defects in signaling.

The way you construct things is very particular to the individual. For instance when my blood glucose rises to 145 and takes a while to come down post-meal I will end up storing some of my nutrient intake in adipose tissue. However for other people, this ill defined "spill threshold" may be 185. So you need to know your body.Timing is important. After you exercise (weights, cardio, etc.) your body is more likely to store nutrients in the liver, muscle and non-adipose tissue. Thats why doing a couple sessions of activity a day (run, hike, swim, lift, cardio, yoga...) immediately followed by a meal is more beneficial....because you have a couple of windows where nutrient uptake is skewed favorably.In fact post-exercise your body secretes a different blend of growth hormone.It releases more of the 20kDa variety then it normally does probably in an attempt to avoid hyperglycemia.If you are using various compounds and attempting to build muscle you can eat higher GI carbs as well as protein. But if you are attempting to stay lean, if you are recomping or dieting, if you are completely natural and don't want to gain fat then even though the post-exercise window is permissive you still need to watch the amount & Glycemic load of the carbs you ingest.I gave up whey protein shakes years ago and when I am staying lean my post workout carb source is usually oatmeal and a piece of fruit. The protein source is easy to digest whole foods such as fish followed by a red meat meal.Razor Ripped preached several great carb sources that have minimal impact on blood sugar. He preached Ezekiel Bread (not the one with raisins), barley, lentils, berries. In the U.S. Ezekiel makes a pasta & a cereal that are identical to the low GI bread. If you are not in the U.S. then look for breads made up of sprouted grains. You can make low G.I. foods yourself with grainy items such as barley, flax-seed, wheat bran, oat bran, wholemeal flour, etc.Here is a low GI muffin recipe I found on the web last year which I make frequently. Two of them raise my blood glucose level only 8-9 points. 1 cup wheat bran 1/2 cup oat bran 1 cup whole wheat flour 1/2 cup skim milk 2 each large eggs 1 tablespoon vanilla extract 1/2 teaspoon ground cinnamon 1/8 teaspoon ground nutmeg 1 tablespoon baking powder 1/2 cup Splenda 14 ounces canned pumpkin Preheat oven to 350f. Spray a muffin tin with cooking spray to prevent sticking. Do not use papers. Beat eggs and add the milk, vanilla, cinnamon, nutmeg and sweetener. Mix the oat and wheat bran and add the wet ingredients. Set aside for 5 minutes to soften. Once softened, add the remaining ingredients and stir just to blend. Spoon into the muffin tin and bake approx 25-30 minutes or until the muffins pull away from the sides of the pan. They are very moist and may not 'test' done. Let cool for 10 minutes before removing from pan. Let cool completely and refrigerate any leftovers. Serving Size : 12 muffins Per Serving: 101 Calories; 2g Fat (12.7% calories from fat); 5g Protein; 21g Carbohydrate; 5g Dietary Fiber; 36mg Cholesterol; 156mg Sodium. In my opinion people waste money on whey protein & WMS, etc.Instead they should just use whole food.I don't have a set amount of carbs. If I am seriously dieting then I switch off of carbs as I approach bed. I want the blood glucose to come down. At bed time I take a little bit of Vanadyl Sulfate so that my blood sugar is gone while I sleep. While I sleep I burn a little fat... when I wake up I drink a little black coffee and do some empty stomach cardio. That cardio session will burn fat immediately and so the entire session is a fat burning session. Then I eat breakfast.I do something like an intense one hour hike on a mountain trail as a separate session to really get the metabolism going for the day. Afterwards I eat.There's not a lot of tricks to it. You just reorganize the way you eat. Space out the meals so there is 3 hours between them. Construct meals with a low Glycemic Load. Increase the activity to burn off the mobilized fat.Don't drastically drop calories!!!

Glucose is an indispensable metabolic fuel for the brain. For the reason that the brain is unable to synthesize glucose or store more than a few minutes supply as glycogen, it is critically dependent on a continuous supply of glucose from the circulation. "At normal (or elevated) arterial glucose concentrations, the rate of blood-to-brain glucose transport exceeds the rate of brain glucose metabolism. However, as arterial glucose levels fall below the physiological range, blood-to-brain glucose transport becomes limiting to brain glucose metabolism, and ultimately survival." - Hypoglycemia in Diabetes, Philip E. Cryer, Diabetes Care 26:1902-1912, 2003So what happens at various blood glucose levels?For practical purposes we can say that the body desires to maintain a stable glucose level in blood plasma of around 90 ng/dL. Blood glucose levels above that threshold are viewed as excess energy and this engenders a storage response via the pancreatic secretion of insulin. The hormone insulin removes glucose from blood plasma until levels return to 90ng/dL at which point insulin ceases to be active. Below that insulin triggering blood glucose threshold of 90ng/dL, down to about 70ng/dL, there is insufficient circulating energy and therefore the hormone glucagon is released to catabolize stored energy and make it available to the brain and body. Physical activity or energy demanding activity without the presence of circulating glucose or concurrent intake of food requires stored energy. Activity is the catalyst that drives the blood glucose level below 90ng/dL. Below 70ng/dL of glucose in blood plasma the body becomes concerned and because the brain is a critical organ and needs glucose, this threshold is considered critical. The hormone epinephrine (adrenaline) is released at this stage in order to trigger a quick release of stored energy to get blood glucose levels back to normal.The body when it is in this emergency state will burn anything for fuel and muscle can be catabolized. It is best to avoid this state.When you diet you can not lose fat in the presence of the hormone insulin. You want to have the hormone glucagon active and this requires that your blood glucose levels be between 70ng/dL and 90ng/dL. Glucagon acts to free up stored energy by signaling the adipocytes to activate Hormone-sensitive lipase which converts triglycerides into free fatty acids. Hormone-sensitive lipase is a vital component of fat mobilization and is a positively active force in the presence of glucagon and inhibited in the presence of insulin.Fatty acids have very low solubility in the blood however serum albumin, binds free fatty acids, and thereby increases their effective solubility by a factor of about 1000. Serum albumin transports fatty acids to organs such as muscle and liver for oxidation and this happens when blood sugar is low.So what is the minimal amount of glucose needed to trigger insulin & why again is insulin bad?From the textbook Biochemical and Physiological Aspects of Human Nutrition, Stipanuk et al. ed. 2000 Insulin ...is secreted in response to changes in circulating glucose; a change of as little as 2mg/100ml of plasma can be detected by the pancreas. Insulin release can also be stimulated in response to certain amino acids in the circulation. Other important signals for insulin secretion include gut hormones and nervous stimulation. - p395 In adipose tissue insulin increases fatty acid uptake and triacylglycerol storage via increases in lipoprotein lipase activity, and at the same time decreases lipolysis by decreasing hormone-sensitive lipase activity. The latter may be one of insulin's strongest actions because it occurs at very low insulin levels and effectively lowers the levels of free fatty acids in the circulation thereby decreasing there utilization as fuel. - p396 Is there way to minimize glucose's influence?Again from the textbook Biochemical and Physiological Aspects of Human Nutrition, Stipanuk et al. ed. 2000 Soluable viscous polysaccharides [certain fibers] can delay and even interfere with the absorption of nutrients... Positive benefits of delayed nutrient absorption include an improvement of glucose tolerance and a lowering of serum cholesterol levels. Delayed absorption of carbohydrates results in a lower postprandial (following a meal) glucose level. In general the more viscous the fiber the greater the effect on blood glucose. This is similar to the effect seen with eating several small meals rather than one large meal. When glucose is absorbed in small amounts over an extended period, such as seen with viscous fibers, the insulin response is attenuated (Pick, et al. (1996) Oat bran concentrate bread products improve long term control of diabetes: A pilot study J. Am Diet Assoc 96:1254-1261) ... Viscosity of the polysaccharides and their ability to form gels in the stomach appear to slow gastric emptying. This in turn results in a more uniform presentation of the meal to the small intestine for absorption. [Poorly soluble fibers that do not form gels such as wheat and cellulose have little effect...unlike those that do which include guar gum, pectin, psyllium, oat bran.] - p146. 147 A Practical ExperimentFor two days I used my glucose monitor to check my blood glucose after ingestion of coffee. Black coffee w/ no additives = zero rise in glucose Black coffee w/ Stevia = a 2 point rise in glucose Black coffee w/ Splenda = a 5 - 8 point rise in glucose. Coffee w/ Splenda & generic Coffee Mate creamer = 15+ point rise in glucose Coffee w/ Splenda & 2% Lactose free Milk = 17+ point rise in glucose So for me the caffeine in a cup of coffee does not effect blood glucose BUT the additives sure as heck do!How do you reduce the rise in blood glucose w/ these additives (besides the obvious)? ....add FIBER.So ingesting 2 grams of Psyllium Husk powder just prior to drinking Coffee w/ Splenda & Coffee Mate creamer resulted in only a 4 point rise in blood glucose. WOW!So how does Growth Hormone fit in to all of this?First recognize that there will be periods of time post meal where blood glucose and thus insulin will be elevated. There is no fat loss during this time and Growth Hormone will not be effective during these periods.With this recognition it makes sense to reduce the amplitude and area under the curve (in graph-type language) of insulin spikes. Meals should be constructed with both the glycemic index of foods in mind and the total glycemic load of the meal. Fiber should be used to reduce blood glucose levels.With this recognition it makes sense to maximize the time period when glucagon is active. That requires insulin to return to baseline quickly after a meal and a sufficient period of time between meals to allow glucagon to have an effective impact. Activity between meals as well as the presence of GH will have positive impacts on fat loss.The reason it is necessary to write about everything in this post is so that you understand how easy it is to waste Growth Hormones fat loss potential and what one must do to maximize GH's fat loss power.Too often someone will use GH and admit that their diet wasn't very good. That negates much of GH's positive impact on fat loss.I also wanted to put GH into a proper context which sadly is often lacking in people who hope for better body attainment. The things I have barely touched on are of utmost importance and make up the backbone of a sound fat loss protocol.GH can be a very useful adjunct to a properly constructed protocol which focuses on food intake with proper hormonal impact and sustained activity level.Use of GHFrom other posts we understand that GH has a dual role to play in a diet. It can increase the rate of fat loss and it can help inhibit the breakdown of muscle. So you want to administer GH in smaller amounts, you want to have off periods (i.e. time when GH is not active) so that the intracellular pathways can reset and you want to maximize the frequency of administration.So we need to understand the impact of GH dose on levels of GH in plasma to set a schedule. We can extrapolate from the chart from the GH study posted above. Assuming a linear relationship (since 7.5ius were active for 12 hours & 15ius for 24 hours) we can assume that a dose of 2ius of synthetic GH administration will elevate GH in plasma for 3.2 hours. If we need about 4 hours off (we can probably round down to 3.8 hours) we can dose 2ius of GH every 7 hours. For ease of fitting a dosing schedule into our lives we can round up to 8 hours and say that we can dose 2ius three times a day spaced out by 7-8 hours.Since GH isn't effective for fat loss in the presence of insulin we probably want the meals that have the biggest impact on blood glucose and thus insulin to be ingested during the time GH is not active. After that meal is digested and insulin rises and then falls back to 90ng/dL we can administer GH and be confident it will have a positive impact on our overall fat loss protocol.

if you are trying to lose bodyfat then you want to take advantage of GH's increase in lipolysis. What is lipolysis? According to Wikipedia it "is the breakdown of fat stored in fat cells. During this process, free fatty acids are released into the bloodstream and circulate throughout the body." According to Dat it "is the breakdown of fat stored in fat cells. During this process, free fatty acids are released into the bloodstream and circulate throughout the body." So circulating free fatty acids are occuring and it is your job to maximize beta oxidation (or the extent to which they will penetrate the cell and be broken down in the mitochondria ...to generate acetyl-coa which enters the Krebs cycle). "Burn off" the fatty acids so to speak.So you do that by being active during this time period & by not eating (or taking huge amounts of caffeine/stimulants/ephedra) which can raise blood glucose and thus insulin. Anything from not just sitting at a desk to actively performing cardio will fulfill your responsibilities.If you have plenty of money you can load up on L-carnitine to help in the transport...But better yet is to maximize FFA mobilization and couple that with cardio.You can maximize FFA mobilization or lipolysis by increasing GH.One thing I am experimenting with is administering GHRH/GHRP to create a GH pulse. Twenty minutes or twenty-five minutes later adding 1iu of synthetic GH. This so far (limited experience so far) seems to greatly amplify that GH pulse...which increase the FFAs in my blood stream......which then makes me go do some steady state cardio for 1 hour or more .....followed by not eating immediately after words during the remaining time that GH is active.The cost of administering just 1iu of synthetic GH once a day on top of the GHRH/GHRP pulse is really low... but I am conjecturing gives you more bang for the buck then trying to find the "metabolic enhancer" which as I pointed out can also interfere with lipolysis.

I thought you might be interested in this because almost no nutritionists or people involved in bodybuilding know this. But in the world of aging and longevity research there is the knowledge that the lipid make up of the cellular membrane influences cellular metabolism. High DHA content in phospholipids of the cellular membrane is associated with high metabolic activity and this leads into the "membrane pacemaker" theory of metabolism.This theory proposes that highly polyunsaturated acyl chains impart physical properties to cellular membrane bilayers that enhance and speed up the molecular activity of membrane proteins and consequently the metabolic activity of cells, tissues and the whole animal.There is a positive correlation in the animal kingdom between body size and cellular metabolism with smaller animals possessing cellular membranes with higher DHA content and thus higher cellular metabolisms. Larger animals, humans for instance have cellular membranes with a lot less DHA and thus slower cellular metabolism.All of this is correlated to lifespan. Highly polyunsaturated acyl chains (primarily DHA) are very susceptible to peroxidative damage. This kind of damage shortens lifespan.The brain however is not correlated to any of this and in humans posses high DHA content in the cellular membrane & thus higher metabolism. It is thought that evolution probably weeded out those sluggish thought creatures that had slower brain cell metabolism.How does it work? Well the physical properties of polyunsaturates primarily DHA are such that these lipid chains are flexible and active compared to unsaturated lipids. Because of the active or rapid movement of DHA lipids they exert lateral pressure on neighboring molecules in the cellular membrane. This creates greater activity in membrane enzymes, Na+/K+-ATPase molecules and thus ion channels become approximtely 25% more active. A large part of cellular energy goes into operating those channels.Similar sorts of activity occur in the mitochondrial membrane proteins.A good & recent review of all of this is The links between membrane composition, metabolic rate and lifespan, A.J. Hulbert, Comparative Biochemistry and Physiology, Part A 150 (2008) 196–203Now we know from source material such as Evolutionary Aspects of Diet, the Omega-6/Omega-3 Ratio, and Gene Expression by Artemis P. Simopoulos found in the book Phytochemicals: Nutrient-Gene Interactions, Mark S. Meskin (Editor), CRC; 1 edition (February 22, Phytochemicals: Nutrient-Gene Interactions, Mark S. Meskin (Editor), CRC; 1 edition (February 22, 2006) that: "... the polyunsaturated fatty acid (PUFA) composition of cell membranes is to a great extent dependent on the dietary intake." So if you ingest a large quantity of Omega 3 fatty acids which contain high DHA content you will alter the makeup of the cellular membrane such that it is composed of more DHA which will increase cellular metabolism. This is great for dieting but increases the potential oxidative damage. Enough to effective lifespan? Probably not. But it should increase energy expenditure and thus be beneficial on a diet.

hmm i dont know,give it a whirl and take pics lol

i got some dnp saved up for my next use,possibly in fall. quite stoked for it. extremely hard to come across but i prefer low dosage of dnp over clen

ive asked admin to create a post and get that sorted. should happen shortly

ive asked rep to join,he will soon

might aswell join the porn industry while youre at it ?

Ill make his intro better,welcome to our new MOD who will be helping members learn about crypto and how to be safe and secure from banks and others ?

hahah love it

serum tests were done,twice. both score 10.0 and 10.2 ,i saved them from northern for that purpose. Janoshik who is quite popular on many boards,you can access the tests there.

if thats the case,id add on stanolone and proviron as they do all that.

he didnt mean product was bullshit,he was referring to one guy promoting it while being biased. Hes right in that manner. The product itself is phenomal.I saved the tests they did wiht janoshik,the sales rep was a moron though

cheers bro,glad to here that and welcome to the new board. New concept and ideas with smart admins(minus me) ?