Axokine Diet Pill Review
Here’s what you need to know about Axokine…
With an increase incidence of abnormal weight gain and associated metabolic disorders (i.e., type II diabetes and cardiovascular diseases), the need for newer therapeutic strategies to stem this epidemic continues to grow.
The most common drugs used in the management of obesity are appetite suppressants (eg, Phentermine). These drugs are only effective for short term weight loss, and have plenty of side effects to go along with them.
Thus, a long standing wish of obesity drug researchers has been the quest for an effective, natural substance with fewer sideeffects.
Researchers though they’d found the holy grail with leptin, an adipocyte-derived hormone. However, despite initial successes with leptin on both patients and animals, further studies failed to confirm its effectiveness — largely due to the patents’ development of resistance to its action.
This observation was further confounded by the high levels of natural leptin documented in overweight individuals. This ineffectiveness of endogenous leptin was due to the development of leptin resistance, and leptin even at very high concentrations is ineffective in reducing the body weight of clinically obese patients.
And so the quest continued.
As with so many things, it was blind luck that lead researchers to the next “holy grail”. During experiments on animals with motor neuron disease, a chemical called ciliary neurotrophic factor (AXOKINE), was found to cause profound weight loss.
Axokine was found to act on the feeding center in the hypothalamic area of the brain — as did leptin. Further research in this field has shown that Axokine induced weight loss was via mechanism similar to that of leptin. Both have been found to activate similar molecular pathways resulting in weight loss. This explains why the weight-reducing effects of Axokine are free of side effects. Axokine differs from leptin in that it does not appear to normally play a physiologic role in weight control.
Axokine diet pills have been found to be effective in leptin resistant, diet induced obesity — similar to that of human obesity. Axokine has been found to suppress food intake without triggering hunger or associated stress responses associated with food deprivation. Thus, unlike forced dieting or other treatments for obesity, Aoxkine treatment lowers the weight set point of the body in the hypothalamic area of the brain. Best of all, Cessation of Axokine administration does not result in a spree of overeating and immediate rebound weight gain.
At 0.1 mg/kg/day Axokine produced a marked reduction in food intake and bodyweight. Improvement in insulin levels and fat metabolism was also seen in the animal models. There was no increase in circulating levels of certain steroids on therapy with Axokine, indicating that the therapy was not stressful.
Compare this to the steroid response to forced dieting. Forced dieting increases circulating steroids resulting in muscle wasting, weak bones and other unwanted effects. Therefore Axokine is unique in its ability to produce weight loss at physiological levels through a leptin-like mechanism, in situations were leptin itself is not effective and axokine diet pills do this without inducing a stressful response.
However, in the same animal models, at supra-physiological doses AXOKINE was associated with a significant elevation in steroid levels and a decrease in spontaneous motor activity. The weight loss was very rapid and severe (33% of body weight within 7 days) resulting in significant loss of lean body mass.
Even at such high doses, the muscle wasting seen with Axokine was much lower than would have been seen following equivalent levels of food deprivation. Research has demonstrated that enforced food-restriction activates hunger signals that make compliance with any diet difficult. Treatment with Axokine produces the same degree of weight loss without activating the hunger center and the person doesn’t even realize that he is dieting.
It should be noted that though Axokine diet pills are free of adverse effects at physiological levels, severe muscle wasting may be produced at higher doses. Recent reviews on Axokine has suggested that it ran into some problems during phase III clinical trials.
The patients developed antibodies to Axokine, which resulted in drug resistance and decreased effectiveness. Further reports are awaited. Even though research involving Axokine in the management of obesity is still in its infancy, it gives all of us a hope for a novel and side effect free treatment for obesity.
