Phentermine – before you buy Phentermine online without prescription, you need to understand that Phentermine is not sold legally on the web. The most popular brand of Phentermine in North America is Adipex P by Teva Pharmaceuticals. Before you buy Phentermine, you need to visit your primary care physician and ask for prescription. Any type of sale of Adipex with Phentermine online without prescription is illegal. Adipex P usually comes with 37.5mg of Phentermine HCL in capsule or tablet form.
Phentermine – before you buy Phentermine online without prescription, you need to understand that Phentermine is not sold legally on the web. The most popular brand of Phentermine in North America is Adipex P by Teva Pharmaceuticals. Before you buy Phentermine, you need to visit your primary care physician and ask for prescription. Any type of sale of Adipex with Phentermine online without prescription is illegal. Adipex P usually comes with 37.5mg of Phentermine HCL in capsule or tablet form.
Phentermine Classification Phentermine is closely related to psychostimulant drugs such as amphetamine which was also named bases on a contraction of the formal chemical name of the compound, alpha methyl phenyl amine. Phentermine has effects similar to amphetamine on the central nervous system and must be employed with caution as the side effects of phentermine can mimic those of amphetamine.
Phentermine Chemical Structure The chemical structure of phentermine and related chemicals are shown below. The chemical structure is quite similar to both amphetamine and to a variety of naturally occurring neurotransmitters used within the brain for communication between nerve cells such as phenethylamine.
Phentermine / Adipex Mechanism of Action The sympathetic nervous system is designed to prime the body for stress and rapid action, the so called “fight or flight” response. These chemicals signal smooth muscle within the walls of large and medium sized arteries to contract, reducing the volume available to the fluid and cell mass that comprise the blood, raising blood pressure. They act as dromotropes, chronotropes and innotropes on the heart. When influenced by such naturally occurring chemicals or by administered sympathomimetic drugs, the heart will contract more often in a given period of time, the organ will pump a larger volume of blood with each contraction and the internal nerves of the heart, the purkinje fibers and the bundles of His, will conduct impulses more rapidly. In addition, sympathomimetic substances reduce blood flow to the gastrointestinal system and signal fat cells to work in concert with the liver to increase the rate of gluconeogenesis. This relatively inefficient biochemical process is used to increase the concentration of glucose in the blood to serve as an immediately usable fuel for muscles and the brain in a crisis.
Phentermine shares the same mechanism of action as that exerted by amphetamine and other psychostimulant drugs with a similar structure. Phentermine activates the TAAR1 receptor. TAAR1 stands for trace amine associated receptor. The human TAAR family of receptors consists of six distinct proteins. TAAR1 receptors are located within cells found in the stomach, small intestine and astrocytes that act as support cells for neurons within the central nervous system. This receptor is also seen within mono-amine expressing neurons located inside the central nervous system. In these cells, TAAR1 is bound to the internal surface of the pre-synaptic membrane. TAAR receptors have very little surface membrane expression so the ligand that activates them must either be able to diffuse across the cell membrane or be transported through the cell membrane by a separate membrane transport protein. Once inside the cell, the ligand binds to the TAAR1 receptor that then interacts with potassium channels in the cell membrane, reducing the rate of firing of the mono-amine expressing neuron. In addition, the activated TAAR1 receptor activates both intracellular protein kinase A and intracellular protein kinase C. These kinase enzymes then modify mono-amine transport proteins located in the neuron cell membrane tasked with removing mono-amine neurotransmitters from the vicinity of the synapse by phosphorulating a tyrosine residue in each protein. The dopamine transport proteins then cease activity and move out of then cell membrane and into the cell. Further, a certain fraction of mono-amine transporting proteins will rejoin the cell membrane, reverse their function and engage in the release rather than the uptake of mono-amine neurotransmitter. In addition, the drug can serve as a competitive uptake inhibitor of neurotransmitter. These three effects result in higher concentration of mono-amine neurotransmitter within the synaptic cleft. The higher concentration of mono-amine neurotransmitter within the synaptic cleft leads to an increased firing rate of the post-synaptic neuron and the perception of a stimulating effect by the patient.
Phentermine acts on a variety of cells in the central nervous system that generate mono-amine neurotransmitters. The drug exerts its most potent effect on neurons producing norepinephrine. In addition, phentermine increases the concentration of dopamine and serotonin within the synapse between sells that use these mono-amines for communication. The net effect is the reduction of hunger, a cognitive process that is mediated by several nuclei within the section of the brain known as the hypothalmus. The principal structures that are thought to govern the perception of hunger are the ventromedial nucleus, the arcuate nucleus and the lateral hypothalamic nucleus.
Phentermine is also believed to facilitate weight loss via a mechanism operative outside the central nervous system. Phentermine causes the release of norepinephrine and epinephrine into the general circulation. These materials act as hormones, signaling fat cells to mobilize stored material. Fat cells break lipids into two carbon units and ready it for processing via the Kreb’s cycle operative in every cell and by the liver as a raw material for gluconeogenesis.
Application of Phentermine Phentermine is intended for short term use. It is recommended that phentermine be prescribed for obese patients for no longer than 12 weeks and that the medication be used as part of a weight loss program that includes exercise and reduced caloric intake. Phentermine has a lasting effect on appetite that appears to extend beyond the period when the patient takes the medication. Patients prescribed phentermine for 12 weeks who were followed for24 weeks continued to lose weight in the 12 week period when they were not taking the drug. It is uncertain if the continued weight loss is caused by a lingering effect of the drug or by modification of the patient’s eating habits that carried over into the 12 week period when they were no longer taking phentermine.
Since Phentermine is similar in its effects to amphetamine, it is regulated as a controlled substance in most nations. The most comprehensive agreement regarding the regulation of controlled substances is known as the Convention on psychotropic substances. Phentermine is regulated as a schedule IV material, the same level of control applies to low activity narcotics without a strong euphoric effect such as hydrocodone.
The usual adult dose for phentermine is 15 mg to 30 mg. This should be taken by the patient approximately 2 hours after breakfast and one dose should serve to control appetite for 12 to 14 hours. Patients should be cautioned against taking phentermine in the evening as it has the potential to cause insomnia.
Weight Loss Drug Combinations Using Phentermine Although phentermine is intended as monotherapy for obesity control, it has been combined with other agents in single dosage form. The combination of phentermine with either fenfluramine or dexfenfluramine was heavily marketed in the 1990s. In 1996, papers began to appear in the medical literature warning about the enhanced incidence of primary pulmonary hypertension and regurgitant heart valve disease in the population treated with combination anorexic drug therapy. When this population was examined using echocardiography, it was found that 30% of the patients who had been treated with combination anorexic drug therapy for up to 24 months had significant heart valve abnormalities. For patients treated for up to 3 months, the incidence of heart valve abnormalities was less than 3%, a statistic still very much higher than expected in the general population. This approach to obesity management had to be abandoned.