Leviathan or Recreate while on CKD

[donny79]

I am currently on a ckd diet for 6 weeks and am looking to add a fat burning supplement. I am considering either leviathan reloaded + dcp or recreate and possibly dcp. Is either better while on a ckd or gonna effect ketosis??

 

[Irish Cannon]

I had great results on Leviathan Reloaded + Ephedrine. LR/E/DCP sounds extremely solid. I haven't tried Recreate so I can't comment on that.

 

[striking]

I used ReCreate and had very nice results the smooth added energy was nice since even though your body will adjust to CKD it can still make you feel slugish at times.

To be honest I wish you luck with your diet I did 8 weeks and had amazing results in fat loss! Be mindfull of muscle wasting and keep the calories up.
It is my belief that with this type of diet you can lose fat reguardless of what your taking it really just came down to what made me feel best.

 

[tribaltek]

I had similar results with both products. They are both solid. Recreate helped more with hunger. LR helped more with energy. Both gave the same benefit in the end.

 

[borobulker]

Here is a pretty cool explanation of ReCreate by Mulletsoldier

ReCreate does not produce appetite suppression through stimulants - rather, through modulating the body's actual satiation pathways. This, as you have found out, needs to work through the acclimation process. ReCreate is significantly lower cortisol, thereby improving insulin sensitivity and improving the efficiency of carbohydrate metabolism; liberating lipid stores, and increasing the oxidation of these fatty acids once in the bloodstream; it is also closely mimicking epinephrine, one of the body's major metabolic hormones. All these things are increasing energy expenditure in the body, and as a result will increase the body's necessity for food. Once your body normalizes, you will experience satiation.

I can totally attest to both products a fat burning 'champions' however that have different demographics. I personally had to lay off of heavy stims (eph, yohim. even heavy caffeine) and that is what lead me to ReCreate and an eventual rep spot with USPlabs. The ReCreate/Anabolic-Pump stack helped me cut from the 276 class in March to compete at 242 in July. I was not on a CKD but i was heavily manipulating CHO intake.

If you have any additional questions regarding ReCreate, let me know.

Also, are you planning to run Anabolic-Pump with your CKD?

 

[donny79]

I wasnt considring it but should I? My goal is to lose body fat but equally or slightly more important to gain lean muscle mass. Thanks everyone.

 

[borobulker]

It would allow you to add limited amount of CHO while staying in ketosis. You will have a lesser insulin response as well. You will also be in an increased lipolytic state.

I am going to quote Mulletsoldier again but it is completely necessary to.

In terms of R-ALA vs. AP on a keto diet...

...While R-ALA's exclusive method of action is Insulin-dependent glucose metabolism, AP also significantly contributes to the processes of Ketosis. Ketosis is the hydrolyzation of stored triglycerides into Fatty Acids, via the process of lipolysis; in fact, Anabolic Pump directly regulates lipogenic processes via AMPk induction, and would significantly contribute to plasma FA levels - thereby used for fuel in the absence of glucose; the inhibition of cholesterol and triglyceride biosynthesis - beneficial because Ketosis is attempting to complete the exact opposite; preventing the redepositing and accumulation of lipids - via exerting transcriptional control over lipid binding genes such as PPAR-y through co-activator inhibition (and its target enzymes); as well as ensuring increased mitochondrial FA oxidation - through inhibiting ACC (acetyl-CoA-carboxylase which inhibits the morphing of acetyl-CoA to malonyl-CoA), as well as directly increasing malonyl-CoA-decarboxylase, and ultimately raising levels of CPT-1; the rate limiting enzyme for mitochondrial FA oxidation.

In all respects, AP contributes to the processes of Ketosis significantly, whereas R-ALA would necessarily be counterintuitive to a Keto-based diet...

Ketosis is simply the process of your body hydrolyzing (chemical breakdown via the interjection of a water molecule to form two end products, or the reaction of a substrate with water) stored triglycerides (fatty acid chains combined with a glycerol, and the body's primary source of stored adipose) to be used as fuel; Ketosis is the recognition by your body of chronic starvation. It therefore causes lipolysis (breakdown of stored triglycerides into respective fatty acids and glycerol molecules) in order to provide fuel in the absence of glucose (your body uses these as fuel via B-Oxidation). AP is beneficial, because it will expedite (speed up) this process due to its direct interconnectivity with many of the above mentioned processes.

a) It increases levels of CPT-1. CPT-1 is the rate-limiting (controls the rate at which a process can occur) enzyme of B-Oxidation (the oxidizing of fatty acids to be used as fuel), and increasing it increases the amount of lipids your mitochondria will use as fuel. This is important, because even during Ketosis where lipolysis (break up of TG into FAs) is occurring, if you do not oxidize (burn) the FAs, they will simply redeposit.

b) On the note of redepositing, AMPk inhibits the accumulation and synthesis of TGs and cholesterol. Why is this beneficial, and tied into the above point? Because if the redepositing of lipids is inhibited, they will be forced to circulate the bloodstream continually; with the increasing of CPT-1, the possibility is increased they will subsequently be oxidized.

Now, as I said, R-ALA is not an anti-lipogenic (compound which inhibits the accumulation, differentiation, or biosynthesis of lipids) and would not assist as greatly as AP would on a "carb-up" during Ketosis. The primary goal of Ketosis is releasing stored triglycerides into the bloodstream to be oxidized: AP accomplishes this. The fundamental step to remaining in Ketosis is low blood sugar levels: AP accomplishes this.

So everybody is on the same page, I'll review some of the relevant terms here.

PPAR-y (gamma) stands for Peroxisome Proliferated Activated Receptor, and is a subclass in a family of receptor proteins that exert transcriptional control over lipid binding genes and enzymes. This essentially means that it controls the differentiation (unspecialized cells developing into specialized functions; such as preadipocytes differentiating into adipocytes), proliferation (rapid growth and multiplication) and accumulation (plasma triglycerides and FAs bonding to stored adipose) of lipids by regulating the mRNA expression of genes responsible for carrying out these effects.

ACC stands for acetyl-CoA-carboxylase, and is responsible for the carboxylation of Acetyl-CoA into Malonyl-CoA. This process highly regulates the storage of plasma triglycerides, and inhibits the B-Oxidation of FAs by cell mitochondria, as Malonyl-CoA directly inhibits CPT-1: The rate-limiting step for mitochondrial B-Oxidation.

Malonyl-CoA-decarboxylase performs the exact opposite function of ACC, and catalyzes the conversion of Malonyl-CoA back into Acetyl-CoA and a carbon dioxide emission. It therefore directly increases levels of CPT-1, and subsequently the B-Oxidation of FAs.

Now, all this is important for one, primary factor: AMPk (adenosine monophosphate kinase) exerts transcriptional (limits the mRNA expression of) control of PPAR-y, while also exerting post-translational control over its co-activation factors, as well as directly regulating levels of ACC, Malonyl-CoA-decarboxylase, and therefore levels of Malonyl-CoA and CPT-1. Now, why is that important? Because all of the aforementioned compounds directly regulate the storage of circulating triglycerides and fatty acid chains, and therefore regulate the differentiation and proliferation (growth) of lipids (fat). This is the exact opposite effect one desires when attempting to enter ketosis (Acetyl-CoA directly induces ketone body production by the liver as well) - one desires the inhibited synthesis of triglycerides and cholesterol, the increased B-Oxidation of fatty acids, and the decreased redepositing and accumulation of lipids. By raising AMPk (and research has directly shown ACC and MCD inhibition as well, while Corsolic Acid potently regulates PPAR-y mRNA expression in adipose) AP contributes significantly to effects which are beneficial to Ketosis.

Here is a shorthand legend:

PPAR-y: Peroxisome Proliferated Activated Receptor

Function: Diverse, but in an adipose tissue, lipid-specific respect, it exerts gene expression of lipogenic storage factors (genes which regulate the storage of lipids). Also keep in mind there are three subclasses of PPAR-y: PPAR-y1, PPAR-y2, PPAR-y3. It is Gamma 2 which is dominantly expressed in adipose tissue, and responsible for lipid storage.

ACC: Acetyl-CoA-Carboxylase

Function: Carboxylates Acetyl-CoA into Malonyl-CoA, which subsequently lowers levels of CPT-1, and therein the oxidation of Fatty Acids by mitochondria.

Malonyl-CoA-Decarboxylase

Function: Decarboxylates Malonyl-CoA into Acetyl-CoA and Carbon Dioxide, thereby raising levels of CPT-1 and increasing mitochondrial oxidation.