With ProLon® Five Days Is All It Takes | El Paso, TX.

Recent science has unleashed the power of fasting to optimize body aging and dismantle chronic diseases, e.g., obesity, diabetes, cancer, autoimmune disorders, Alzheimer’s and cardiovascular disease. At Chiropractic Scientist, Doctor. Alex Jimenez’s mission is to educate the public about the health benefits of fasting. The idea is to introduce it to them in a safe, effective way through the Fasting Mimicking Diet (FMD).

Pre-clinical and clinical studies have proven that periodic fasting, done for several consecutive days, is a very powerful intervention that our bodies learned to naturally cope with by protecting and rejuvenating itself. These two factors are both anti-aging measures that offer additional health benefits. The 5-Day ProLon Fasting Mimicking Diet has been clinically tested and found to promote beneficial effects in a wide variety of conditions ranging from excess weight and fasting blood glucose, to growth factors associated with DNA damage and aging.

Min Wei; Sebastian Brandhorst et al.
Fasting‐Mimicking Diet and Risk Factors for Aging, Diabetes, Cancer and Cardiovascular Disease.

5-Day Program

The ProLon meal plan is followed 5 days per month. Once an individual has finished the five-day plan, they go back to a normal healthy diet the last twenty-five days. Fasting with the Prolon® plan follows a low carbohydrate/protein meal and contains the good kind of fatty acids. The FMD® recipe keeps your body on a fasting-type mode, that triggers protection measures that the body has developed. This causes the body to optimize its performance, rejuvenate cells, and thrive.

Unboxing the ProLon Fasting Mimicking Diet

Age-related Disease: A Revolution Is Coming

I just finished reading a groundbreaking book called The Longevity Diet: Discover the New Science Behind Stem Cell Activation and Regeneration to Slow Aging, Fight Disease, and Optimize Weight, which was written by Valter Longo, PhD,1 who is director of the Longevity Institute at the University of Southern California and a principal scientist in the development and study of the fasting mimicking diet (FMD). I have followed Dr. Longo’s career for many years with great admiration. He has been published in top-tier journals. In his book, Dr. Longo writes about some exciting findings regarding the FMD research group consisting of 16-month-old mice, which are described as being the equivalent of a 45-year-old human: “A stem cell-dependent process rejuvenated the immune system. Regeneration also occurred in the liver, muscle, and brain. Levels of several types of stem cells increased.”1 He went on to explain: “The fasting itself destroys many damaged cells and damaged components inside the cells but it also activates stem cells.”1

Jeffrey S. Bland, PhD, FACN, FACB, Associate Editor

Fasting-Mimicking Diet Promotes b-Cell Regeneration to Reverse Diabetes

• Fasting mimicking diet induces prenatal-development gene expression in adult pancreas
• FMD promotes Ngn3 expression to generate insulin-producing b cells
• Cycles of FMD reverse b-cell failure and rescue mice fromT1D and T2Dd
• Inhibition of PKA or mTOR promotes Ngn3-driven b-cell regeneration in human T1D islets

Stem-cell-based therapies can potentially reverse organ dysfunction and diseases, but the removal of impaired tissue and activation of a program leading to organ regeneration pose major challenges. In mice, 4-day fasting mimicking diet (FMD) induces a stepwise expression of Sox17 and Pdx-1, followed by Ngn3-driven generation of insulin-producing b cells, resembling that observed during pancreatic development. FMD cycles restore insulin secretion and glucose homeostasis in both type 2 and type 1diabetes mouse models.

In human type 1 diabetes pancreatic islets, fasting conditions reduce PKAand mTOR activity and induce Sox2 and Ngn3expression and insulin production. The effects of the FMD are reversed by IGF-1 treatment and recapitulated by PKA and mTOR inhibition. These results indicate that an FMD promotes the reprogramming of pancreatic cells to restore insulin generation in islets from T1D patients and reverse both T1D andT2D phenotypes in mouse models.

Chia-Wei Cheng,1,6,7Valentina Villani,2,7Roberta Buono,1,5,7Min Wei,1Sanjeev Kumar,4Omer H. Yilmaz,6Pinchas Cohen,1Julie B. Sneddon,3Laura Perin,2and Valter D. Longo1,4,5,8,*