What is Phen-Pro?
"Phen-Pro" is the combination of phentermine and a low dose of one of the following: Prozac, Zoloft, Celexa, Luvox , trazadone or Effexor. The second medicine is necessary because phentermine used alone stops working after a few weeks. The second medicine makes phentermine work longer and better. Although these second medicines are also antidepressants, their use in the phen-pro combination has absolutely nothing to do with depression. Phentermine is not addictive. Phentermine is not "speed". Phentermine does not raise blood pressure.
The reason why some medicine is necessary for very overweight people is that obesity is mainly a consequence of a chemical defect in the brain making the sufferer too hungry. Voluntary diet and exercise nearly always fail because no one is willing to go hungry day after day. Appetite-control is essential for longterm success.
Obesity is a serious disease, more threatening than high blood pressure or high cholesterol. One third of the US population is obese. More than half is overweight. Obesity is the fourth most common cause of death in the US responsible for 300,000 deaths per year. No physician or patient can ignore it.
The reason why some medicine is necessary for very overweight people is that obesity is mainly a consequence of a chemical defect in the brain making the sufferer too hungry. Voluntary diet and exercise nearly always fail because no one is willing to go hungry day after day. Appetite-control is essential for longterm success.
Obesity is a serious disease, more threatening than high blood pressure or high cholesterol. One third of the US population is obese. More than half is overweight. Obesity is the fourth most common cause of death in the US responsible for 300,000 deaths per year. No physician or patient can ignore it.
Why Does Phen-Pro Work?
After reviewing recent published information on serotonin (5HT) receptors and their interaction with the norepinephrine (NE) system in the hypothalamus, I find it impossible as yet to provide a reliable, detailed understanding of how Prozac extends the action of phentermine. There is a lot of information on differential drug binding to receptor proteins but not enough on where the receptors are located and what they do. One thing is clear: the control of appetite and feeding is considerably more complex and spread out through the brain than the simple hypothalamic "appestat" model. Here is what little I think I know . . .
Phentermine increases the release of NE from NE-carrying neurons in the brain. Prozac acts on serotonergic neurons to increase the effective release of 5HT by inhibiting its reuptake.
In the medial hypothalamus, NE acts on alpha-2 receptors to increase hunger. 5HT inhibits this response, through HT1B receptors, by activating G-dependent adenylate cyclase which in turn activates cAMP-dependent protein kinase which (A) inhibits tyrosine hydroxylase (TH), the rate-limiting step in NE synthesis, and (B) phosphorylates calcium channels reducing their permeability and the slow phase of membrane depolarization. Got it?
In the lateral hypothalamus, NE acts in an opposite manner, through alpha-1 receptors, to reduce hunger. Here 5HT works in parallel with NE, through HT2C receptors, to reduce hunger. So it seems 5HT acts in a "push-pull" manner on the two sides of the hypothalamus. Indeed, drugs which activate only the HT2C receptor but not the HT1B receptor do not induce satiety. Only drugs that activate both receptors are fully effective in reducing hunger [Kitchener & Dourish. Psychopharmacology (Berlin) 1994; 113: 369-377] .
Phentermine increases the release of NE from NE-carrying neurons in the brain. Prozac acts on serotonergic neurons to increase the effective release of 5HT by inhibiting its reuptake.
In the medial hypothalamus, NE acts on alpha-2 receptors to increase hunger. 5HT inhibits this response, through HT1B receptors, by activating G-dependent adenylate cyclase which in turn activates cAMP-dependent protein kinase which (A) inhibits tyrosine hydroxylase (TH), the rate-limiting step in NE synthesis, and (B) phosphorylates calcium channels reducing their permeability and the slow phase of membrane depolarization. Got it?
In the lateral hypothalamus, NE acts in an opposite manner, through alpha-1 receptors, to reduce hunger. Here 5HT works in parallel with NE, through HT2C receptors, to reduce hunger. So it seems 5HT acts in a "push-pull" manner on the two sides of the hypothalamus. Indeed, drugs which activate only the HT2C receptor but not the HT1B receptor do not induce satiety. Only drugs that activate both receptors are fully effective in reducing hunger [Kitchener & Dourish. Psychopharmacology (Berlin) 1994; 113: 369-377] .