Chinese Growth Hormone + Melanotan II update

Ive been running some chinese growth hormone ( as opposed to pharma grade GH ) for the last 3 weeks. Chinese GH is suppose to be of dubious quality and/or under-dosed but I have to say, ive been VERY impressed with what I have been running. This shit is expensive as hell, each injection costs me £5, ( doing 3iu per day ). At 1 injection per day thats £150 per month.

Initially I became interested in GH because of the various reports that it can improve sleep, but there is way more to it than that it seems. The first thing I noticed is it seems to leave you with an amazing feeling of rejuvenation, like youve had a good restful nights sleep. If I take a shot in the morning when I get home from the nightshift I notice I feel much more refreshed when I wake up in the afternoon even after sleeping only 4 hours. Obviously my cognition is feeling shitty from the lack of sleep, but the rest of my feels pretty damn good to go.

This has lead me wonder if the major link between lack/loss of sleep and poor health is mostly attributable to low GH.

Also GH quite clearly made me drop some fat, without any change in my diet. Infact, I noticed I could eat quite a bit more junk and still stay not gain an inch around my waist, which for me is amazing since my waist is the first thing to expand when I gain fat. ( Gerry mentions the fat loss properties also here ). I dont care what people say, GH definitely pushes you towards leanness, and youll notice this affect literally within the first few shots.

Curious I ran a search on pubmed for growth hormone adipocyte and this study came up. CIDEA is the protein I briefly mentioned in a old post when I was looking at if maybe fasting could kill adipocytes. As spoke of previously, the bottom line is low CIDEA = you get fat

CIDE-A expression is significantly reduced in GHR -/- subcutaneous fat compared to wild-type but is not altered in retroperitoneal or epididymal fat. Likewise, adipocytes are significantly enlarged in GHR -/- subcutaneous adipose tissue relative wild-type mice.nd there may even be undesreibly high residues in edible tissues.

So here they are saying a lack of GH allows subcutaneous fat to go on a hypertrophy rampage.

Anyway, GH is addictive, I can tell this right now. It does make you feel REAL good. Unfortunately I have developed a bit of a problem with mine, recently when I inject, the injection site subsequently turns bright red, swells, turns into a hard lump and gets fucking itchy as hell. I know its histamine causing the itchiness, so it looks like my immune system has developed something of an immune reaction to the GH. I did some searching around and this phenomenon is somewhat common and is suppose to go away with repeated use, but this has me worried. The big itchy red lumps are very ugly.

Melanotan II

OK so ive also been on this for awhile now, the tanning has been very very mild so far, but I also haven't been getting sun. Melanotan II requires you to get at least SOME sun exposure for it to work. Fair Enough. But I have also developed some new freckles, and some existing freckles turned real dark brown. I have also experienced the other side affects, slight drop in appetite and increase libido. The inhibition of appetite is REALLY strong if you take your shot first thing in the morning.

New model for carbohydrate sensitive obesity

The carbohydrate sensitive rat as a model of obesity.    ( link here aswell )

To sum up, these guys have been working on a new model of obesity that can be induced by high-carbohyrate diets, as opposed to be bog standard high-fat diets researchers use to induce obesity in rodents. The important point here is its a model. This is EXACTLY what science is. Scientists create models in an attempt to imitate and predict the real world.

The study is already short and direct to the point so its not worth me paraphrasing it ( its free full text at moment so read it you lazy bums! ) however still I want to highlight a few key points.

The first point is that, not all rats exhibit the same propensity to develop obesity on either the high-fat or the high-carb diet. I.E. some rats just DONT get fat. This is good news for the model because this is what we have observed in humans. Some humans are clearly obesity resistant. While others are quite clearly highly prone to obesity.

BMR and TEF values did not correlate to adiposity gain during either HCD or HFD. Otherwise stated, rats with a low BMR and/or a low TEF did not exhibit any greater propensity to become obese than rats with a high BMR or TEF.

Having a higher energy expenditure does not mean you are less likely to become obese. sucks for CICO. Everytime you here someone say "he/she doesnt gain weight because they have a high metabolism", just think to yourself, thats rubbish!

Considering RQ, no relationship was observed between adiposity gain and Activity-RQ, indicating no link between substrate utilization by muscles and propensity to adiposity.

SO in this model, the fuel you burn during exercise doesnt seem to predict your obesity prone-ness

Now heres the punchline, the strongest predictor of being sensitive to carbohydrate induced obesity the researchers found was your respiratory quotient in the postprandial state.

 In general, the Rest-RQ response increased above High-Carb-Diet food quotient (FQ; 0.955) only in Carb-sensitive rats (Figure S5) which means that during this period, the proportion of fat used to fuel energy metabolism was less than the proportion of fat in the meal and was significantly higher than in CR rats between 120 and 180 minutes after ingestion of the meal.

Calculation of resting glucose and lipid oxidation (Rest-Gox and Rest-Lox) from Rest-RQ and REE showed that ingestion of the HC test-meal increased Rest-Gox and decreased Rest-Lox significantly more in CS rats

So, in this model of obesity, ( which may or may not accurately reflect human obesity ), it is the postprandial handling of the nutrients that determines if you become fat or not. ( on high-carb diet only ) If you are carbohydrate-obesity-sensitive, then what happens is when you eat carbohydrate, fat oxidation is overly suppressed. Wonder why that is? Insulin hyper-secretion?

 in Carb-Sensitive rats, already under High-Carb diet since weaning (though chow rather than the high quality synthetic HCD used during this experiment), a defective post-prandial substrate partitioning characterized by a larger post-meal increase in Rest-Glucose-oxidation and a larger post-meal inhibition of Rest-Lipid-oxidation can be considered as potentially responsible for the larger adiposity gain.

Since this observation was made early in the life of the rats, this metabolic difference can be considered as a cause rather than a consequence of sensitivity to adiposity gain under HCD 

Whoa, it almost looks like the researchers are saying that ( in this model ), your propensity to become obese on a high-carb diet is determined from birth, possibly through genetic/epigenetic factors I might guess?

This rings so painfully true for me because I was fat right from a very young age and I was raised on a high-carbohydrate diet. Lowcarb will unfortunately probably have to be a lifelong thing for me if I want to keep my weight down.

its all about the insulin!

In response to my comment on Wooo's blog about ric drasin coming out and saying that carbs determine body fatness, another bodybuilder has recently come out proclaiming the same thing, carbs/insulin play a HUGE role in body fatness.

In the video he touch's on stuff I have mentioned here previously, that the more easily and fast digesting the carb, the more fattening it is. AKA processed carbs.

Elevated fasting insulin is the cause of the obesity epidemic. I feel quite confident about this.  The postprandial insulin spikes play a role in body fatness, but I think it is the elevated fasting insulin causing the rampaging fat tsunami;s. It is the failure to expose yourself to low insulin levels, especially during the overnight fast, that results in never-ending fat accumulation.  Your suppose to properly oscillate in and out of the anabolic/catabolic states between eating and fasting.  But you never quite properly enter the catabolic state with the high fasting insulin. When you get your fasting insulin low enough, then sex steroids will determine fat deposition in the body. I also have a feeling that it is elevated fasting insulin activating aromatase constantly as to why we have so many men with gyno + low T.

So what determines fasting insulin?

No-one knows! other than the obvious fact of the recent days carbohydrate intake influencing it, the others factors involved seem to be obscure. If you search on pubmed for fasting insulin, theres very little research in this area. However we do know the GI tract plays a huge role in insulin secretion, both fasting and postprandial.

An interesting study recently came out detailing how the GI tract is reprogrammed after gastric surgery. The surgery changes the GI tract so that it itself becomes a major source for glucose disposal. More glucose disposed of in the GI tract means less hitting the bloodstream and less needing to be disposed of in adipose tissue. Will that cause weight loss?  The reprogramming of the GI tract to act as a glucose sink was initiated by exposing it to undigested nutrients.

Still further, another new study looked at lipolysis in overweight vs lean subjects. They found that overweight subjects had reduced catecholamine stimulated lipolysis. In the study they say this....

The factors regulating the expansion of human adipose are less well known.

Funny, I thought it was all about calories?

Whats the cause of this catecholamine resistance in fat people? *I think its the elevated fasting insulin*

How to reduce fasting insulin?

Well other than avoiding carbohydrate, there is one food I think actively reduces fasting insulin, sauerkraut, the combination of vinegar and fibre seems to be very potent at reducing insulin. I even think that the more sauerkraut you eat, the more weight it will force you to lose, provided you keep carbs in check.