Take Your Fat Loss To A Whole New Level In 2017
By Kevin DiDonato MS, CSCS, CES
So here’s the story.
The other day we explained sick fat cells and how they can kill you slowly. Well, today, we are going to explain how fat stored in your cells is made into usable energy through a process called lipolysis.
You body needs fuel. Luckily for us, our muscles and liver provide a quick energy source in the form of stored sugar. However, in the absence of food or nutrients, our body uses our stored sugar. Luckily we have another storage system which has plenty of stored energy.
You see, your very own fat cells are full of stored energy! When your body needs energy, it will start a complicated process (called lipolysis) that breaks down your stored fat in order to utilize the stored energy. Here’s exactly how it works:
When we eat, food is used or stored as energy for future use. When we eat any type of fat or excess calories, research suggests, these nutrients are processed and stored in adipocytes. Adipocytes are pockets in adipose tissue where fatty acids are stored for later. In order for us to utilize the stored energy, certain hormones have to be released. These hormones begin the process of splitting and releasing the stored energy.
However, not having enough foods could stress out your body. Research suggests that this stress could increase the production and release of Epinephrine and Norepinephrine. These two crucial hormones (which are produced in the adrenal glands), may stimulate fatty acids to mobilize and get them ready to be processed and used for energy.
Epinephrine binds to the surface of the cell, stimulating the production and release of adenylate cyclase. This increases the level of cAMP in the cell. The increased level of cAMP activates another hormone, PKA, stimulating the release of hormone-sensitive lipase (HSL).
Next, the fat that is stored in the cell mobilizes and moves towards the surface of the cell. Once it reaches the surface, another hormone called Hormone Sensitive Lipase (HSL), splits the mobilized fat at a certain point in the fatty acid chain. The specific point? It just so happens that they triacylglycerol (stored fat) is broken off at the chemical backbone of the molecule. Now, once it is split, the fatty acid then moves into the bloodstream, where it will eventually travel to your muscles or other cells for use. Once it reaches the cell, the fatty acid is then transported from the cell surface to the mitochondria, where the fat is finally burned and used for energy.
Two potent nutrients have been shown in research to aid in this process. We all know Capsaicin is hot! Capsimax® is an encapsulated bead(s) of Capsaicin, which could allow the beadlets to enter the gut and move it into the intestines, with little breakdown. Capsimax® is most effective in the intestines. Once the beadlets enters the intestines, research shows, there is a slow release of Capsaicin into the bloodstream. This allows Capsaicin to work effectively without the immense burn you would get from eating Capsaicin.
Capsaicin gives peppers their heat. Capsaicin, some studies show, can dramatically increase Epinephrine released by your body, which could stimulate fatty acid breakdown. Result: more fat cells shredded and used for energy!
The other potent nutrient, Raz K®, works to help this process. Raz K® could help to mobilize stored fat and move it to the surface of the cell shows some clinical research. Once there, the fat cell is broken down, sending it on its way to other areas of the body.
Raspberry ketones are found naturally occurring in red raspberries. This molecule has been shown in research to increase the rate of lipolysis (which again is the breakdown of triacylglycerides into a more usable form). So, this should come as no surprise that Raz K® (concentrated ketones found in red raspberries), may also release Adiponectin, aid in the oxidation of fatty acids, and of course, may increase the rate of lipolysis (according to current studies).
Research done by Park, determined rats who consumed a high-fat diet in combination with raspberry ketones, stunningly showed no additional increase in body weight or body fat. They also showed an increase in lipolysis, or the breakdown of fatty acids in the cell, shipping it to other areas for energy.
In a similar study, Morimoto et al. discovered rats fed a high-fat diet showed a build up of triglycerides in the liver. Those same rats were fed the same fat-enriched diet, this time with the addition of raspberry ketones.
The rats supplemented with raspberry ketones and fed the same high fat diet, surprisingly, did not gain weight. They also did not show any increase in liver weight. However, here’s was the surprise: They did DECREASE their weight and the amount of fat in their livers also decreased! Their final conclusion: raspberry ketones may be able to PREVENT or improve obesity levels and fatty livers.
The main reason why Prograde Metabo 223 X is so effective is the combination of Capsimax® and Raz K® together. Capsimax® could lead to the increase in the secretion of Epinephrine and Norepinephrine, while Raz K® may have the ability to liberate fat from adipocytes, allowing them to be mobilized and burned. This powerful combination, research suggests, could increase fatty acid metabolism and provide more fuel for your fat burning machine to use for energy!
Bloomer, R. Canale, R. Shastri, S. Suvarnapathki, S. Effect of oral intake of caspaicinoid beadlets on catecholamine secretion and blood markers of lipolysis in healthy adult: a randomized, placebo, controlled, double-blind, cross-over study. Lipids In Health And Disease. 2010. Vol. 9(72).
Snitker, S. Fujishima, Y. Shen, H. Ou, S. Pi-Sunyer, X. Furuhata, Y. Sato, H. Takahashi, M. Effects of novel capsinoid treatment on fatness and energy metabolism in humans: possible pharmacogenetic implications. Am J Clin Nutr. 2009. Vol. 89; pp. 45-50.
Morimoto, C. Satoh, Y. Hara, M. Inoue, S. Tsujita, T. Okuda, H. Anti-obese actions of raspberry ketones. Life Sci. 2005. Vol. 77(2); pp. 194-204.
Park, KS. Raspberry ketones increases both lipolysis and fatty acid oxidation in 3T3-L1 adipocytes. Planta Med. 2010. Vol. 76(15);pp. 1654-1648.