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Thread: fina burns fat?

  1. #1
    remz's Avatar
    remz is offline New Member
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    Oct 2002

    fina burns fat?

    ive read on some sites that fina helps burns fat, but then again i hear that fina doesnt really burnfat, no steroid really does.. so whats the truth here?

  2. #2
    gundam675's Avatar
    gundam675 is offline Senior Member
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    Apr 2003
    well fina speeds up ur metabolism, but if u want to burn fat i would go with something like winny/clen /fina or winny/clen/t3 u can even add fina in there !

  3. #3
    Sigmund Froid is offline Associate Member
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    Oct 2002
    "It's the strongest androgen receptor binder on the planet. It has ferocious anti-glucclocorticoid actions and I have a theory that it is a potent activator of endogenous Prostaglandins (particularly F2a) which gives it some terrific lipid burning potential."



  4. #4
    BDTR's Avatar
    BDTR is offline Retired
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    Jul 2003
    Yup, I ALWAYS lose fat from fina.

  5. #5
    Pheedno is offline Respected Member
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    Apr 2002
    Miller's Crossing
    To help explain some of what Sig put up, heres an article detailing Prostaglandins taken from

    Prostaglandins are derivatives of fatty acids that are produced in most tissues of the body and have varying physiologic actions. Prostaglandins, thromboxanes and leukotrienes are all classified as members of the prostaglandin or eicosanoid class. The first prostaglandins were so named after their initial isolation from semen in the 1930's because they presumably were added by the prostate. Since then they have been found in most every tissue in the body.

    Prostaglandins are often second messengers within cells acted upon by other hormones. There are many classes of prostaglandins with the differences being conferred by substitutions to the pentane ring of the basic 20 carbon molecular skeleton. Prostaglandins are synthesized from arachidonate in the cell membrane by the action of phospholipase A2. From here two synthetic pathways, the cyclooxygenase and lipoxygenase pathways, compete with one another to form prostaglandins and thromboxane or leukotriene, respectively. Because they are lipid soluble they can pass easily out through cell membranes.

    In the cyclooxygenase pathway, the prostaglandins D, E and F plus thromboxane and prostacyclin are made. Thromboxanes are made in platelets and cause constriction of vascular smooth muscle and platelet aggregation. Prostacyclins, produced by blood vessel walls, are antagonistic to thromboxanes as they inhibit platelet aggregation.

    Prostaglandins have diverse actions dependent on cell type but are known to generally cause smooth muscle contraction. They are very potent but are inactivated rapidly in the systemic circulation and the inactive metabolites are excreted primarily in urine. Non-steroidal anti-inflammatories, such as aspirin, indomethacin and ibuprofen, inhibit the enzyme cyclooxygenase and therefore decrease prostaglandin synthesis. The anti-inflammatory corticosteroids inhibit the activation of phospholipase A2 by causing the synthesis of an inhibitory protein called lipocortin. It is lipocortin that inhibits the activity of phospholipases and therefore limits prostaglandin production.

    Leukotrienes are made in leukocytes and macrophages via the lipoxygenase pathway. They are potent constrictors of the bronchial airways. They are also important in inflammation and hypersensitivity reactions as they increase vascular permeability and attract leukocytes. Indeed, the slow-reacting substance of anaphylaxis is actually a mixture of leukotrienes.

    Clinical Implications
    The vasoconstrictive and muscle constricting activities of prostaglandins contribute to the normal sloughing of the endometrial lining during menstruation. However, excessive production of prostaglandins in the uterine endometrium is involved in the pain, cramping, vomiting, and diarrhea of dysmenorrhea.

    Prostaglandins are also involved in maintaining the patency of the ductus arteriosus in the fetal heart. The ductus arteriosus is a channel from the pulmonary artery to the aorta that closes shortly after birth. Blocking prostaglandin synthesis leads to ductal closure, a fact that has been employed in premature infants. In such cases, the administration of indomethacin can close the ductus and prevent the need for surgery. Conversely, in neonates with ductus-dependent heart deformities, prostaglandins can maintain the ductus prior to surgical correction of the deformity.

    Prostaglandins have been investigated as bronchodilators but the side effects of inhalation have made this undesirable. Investigations into altering the chemical structure to avoid such adverse side effects are underway. Prostaglandins are also being studied for their effects on the cardiovascular and gastrointestinal systems.

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