Targeting Alpha 2 for maximum fat loss

Phosphate Bond · 2021-11-01T08:59:04Z

I figured it would be interesting to get peoples opinions on this. It appears to me that the alpha 2 is at the crux of the problem involving the adipocyte. Typically it is upregulated in adipocytes resistant to lipolysis and having it downregulated is advantageous for being able to generate a cAMP respone (cAMP initiates lipolysis)One ligand for the alpha 2 is ATP (intracellular) which results in both opening the k+ channel and pumping intracellular calcium extracellularly. Now this good for three reasons- 1) lowering intracellular calcium reduces actions of phosphodiesterase and obese people are known to have high levels of calcium in their adipocytes 2.) opening the potassium channel resets the gradient for the Beta 2 (beta 2 is diametrically opposed to alpha 2 at potassium channels) 3.) ATP iteslf is a substrate for adenylate cyclase to act (ATP--> cAMP)There are several ways to increase intracellular ATP. Training that improves blood flow and thus the delivery of oxygen via hemoglobin . Thyroid hormone improves the rate of ATP synthesis. Perhaps certain nutrients like r-alpha lipoic acid help re-direct energy metabolism through the quicker and more efficient complex 1 rather than complex II. EPA is known to promote ATP formation several ways and seems to act via alpha 2 mechanisms.So the question in my mind is where do you go from here? I've used products like fish oil and R-ala in the past and feel they have a place in supplementation but there use must carefully being integrated into the plan. Actually excessive fish oil supplementation produces an interesting effect: It basically increases ATP too much along a beta 2 blockade produced by arachidonic acid depletion. What happens is the potassium channel opens, however since there is beta 2 blockade the cell has no other pathway to control this movement of potassium other than calcium influx to lower the ATP. This will continue over and over again until a state of hypometabolism is reached which probably corresponds with phosphatidylserine replacing phosphatidylinositol (second messanger of alpha 1) Actually that is the difference between EPA and DHA, both increase beta receptor sensitivity but in different ways. EPA helps increase ATP and DHA does this by calcium influx (which you need for visual acuity) which opposes cAMP.Lately I've been trying a blend of arachidonic acid and EPA Which I think may get me the best of both worlds. . The EPA increases ATP and reduces calcium levels while the AA controls the outward movement of potassium but has no effect on extracellular calcium movement inward (at least from the exterior of the cell...it may cause calcium release from the sarcosplasmic reticulum as ATP drops, It may also impair the ability of the cell to pump out calcium already there, but that's why you make sure alpha 2 is fully activated before doing this.). In skeletal muscle the intracellular movement of potassium is an anabolic effect from AA and is probably tied to PPAR beta effects occuring there also (which helps burn the fat released at the same time)Or maybe I should just stick to manipulating energy metabolism independent of omega 3s with stuff like R-ala/thiamine analogs? Or maybe a combination of both?One thing I am fairly confident saying is that calcium influx in a low ATP environemnt (alpha 2 upregulated) would be a disaster. All it would do is increase intracellular calcium with little hope of being able to pump it out. Like I said before obese people have this problem as evidenced by the the high 1,25 OH vitamin D in their fat cells accompanied by the intracellular calcium which blunts ATP accumumulation and cAMP. Unfortunately DHA by itself could do this if used in the wrong situation. The take home message here is you need to fix intracellular calcium problem before attempting to increase cAMP.In a nutshell:EPA: alpha 2 agonistAA: beta 2 agonist (let me say that it at least appears to be necessary and/or possibly enhances beta 2 response)Both alpha 2 and beta 2 fully activated leads to maximal cAMP potential via alpha 1s unobstructed ability to raise cAMP through Beta 1. "Crosstalk" between alpha 1 and beta 1 is clearly documented in the literature and I can explain this to anyone interested. This alpha 1 to beta 1 cAMP response should also be fairly resistant to downregulation in a manner similar to Beta 3 (which I'm not really sure exists per se, "Beta 3" may just be a metabolic state where cooperation between alpha 1 and beta 1 is maximized)

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Phosphate Bond

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Topic starter 01/11/2021 5:33 pm

Interesting discussion that pertains to this so I thought I'd add it in.

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OwnYourInstinct

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01/11/2021 6:01 pm

Xylometazoline, a nasal decongestant is a potent a-2 adrenergic receptor agonist with affinity for a-1 as well..

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