November 2009

Freely Available journal article at "Open Longevity Science" (2009) "Oxaloacetic Acid Supplementation as a Mimic of Calorie Restriction." In the article, we review not only our previously published work, but also the work of many other researchers that document oxaloacetate supplementation to reduce fasting glucose levels, it's action as a powerful antioxidant, protection of mitochondrial DNA (a big plus), and protection of eye, brain and pancreas tissues. There is also in-vitro evidence that very small amounts of oxaloacetate builds intracellular "junk" within human lung cancer cells which prevents them from reproducing, even after the oxaloacetate is removed from the cells. Normal cells continue to divide normally with oxaloacetate. We further provide a case study of a 73 year old diabetic woman who reduced and stabilized her glucose levels by taking oxaloacetic acid. In 75 days she reduced her fasting glucose levels by 24%, reduced her insulin resistance by 34%, and reduced the amplitude of her glucose "swings" by 55%. Persons with normal glucose functioning will see an increase in glucose uptake by the muscle tissue, and only a small drop in fasting glucose levels (fyi, mine was about 8%). Fasting glucose levels tend to stabilize even in persons with normal glucose functioning. The information all points to the use of oxaloacetic acid as a calorie restriction mimetic.

Download for free: http://www.bentham.org/open/tolsj/openaccess2.htm and click on "Hot Topic: Calorie Restriction Mimetics".  This will bring you to a page where you can download the article for free.

Oxaloacetate shown to increase lifespan through AMPK and FOXO/DAF16

October 2009

The research out of UCSD and UCLA in "Aging Cell" documents that excess oxaloacetate supplemented to C. elegans causes an increase in lifespan of 25%, p<< 0.001.  The article also strongly suggests that the molecular pathways activated by oxaloacetate supplementation are the same pathways as are activated in dietary restriction.  The article suggests that the numerous benefits of dietary restriction may be achievable with oxaloacetic acid supplementation.

See Link for Aging Cell Journal Article

Calorie Restriction Significantly increases the Lifespan and Health-span of Primates

August 2009

As part of Cohort 2 of the Interventions study, the transplant drug Rapamycin increased the lifespan of normally fed mice.  Unlike resveratrol, which did not increase the lifespan of normally fed mice, Rapamycin significantly increased both male and female lifespan.  Rapamycin has been documented to change the expression levels of several genes.  This molecular pathway is called the "Target of Rapamycin" or mTOR pathway.  Reductions in the mTOR pathway have been previously shown to increase lifespan in invertibrates, and now has also been shown to increase lifespan in mice.  Unfortunately, Rapamycin has several side effects, which include systemic reductions in the immune system which your body uses to fight off disease.  Because of these strong side effects, Rapamycin should not be used as an anti-aging drug. 

Rapamycin fed late in life extends lifespan in genetically heterogeneous mice

Note that benaGene is in Cohort 4 of the NIA "Interventions" study.  We look forward to positive results from this study without the side effects of rapamycin.

NIA begins Aging "Intervention" testing with benaGene

September 2007

Large scale testing of benaGene's active ingredient begins this week within the National Institute of Aging (NIA) "Interventions" program.  The NIA tests a few compounds per year in an attempt to extend the lifespan and health span of mammals (mice).  Results of this large study will be published with Terra Biological's personnel.

More on the Intervention Testing Program can be found at the following web site: http://www.nia.nih.gov/ResearchInformation/ScientificResources/InterventionsTestingProgram.htm

Increases in NAD+ Levels Dictate Cell Survival

September 2007

"A major cause of cell death caused by genotoxic stress is thought to be due to the depletion of NAD+ from the nucleus and the cytoplasm."

"It is generally accepted that depletion of NAD+ stimulates a number of proapoptotic pathways, including the relocalization of AIF from the outer mitochondrial membrane to the nucleus."

Recearchers at Harvard, Cornell and the NIA examine mitochondrial levels of NAD+.  It is not certain if the NAD+ in the mitochondria come from genes within the Mitochondria or from import from the cytoplasm.  It may be both.

See: http://www.cell.com/content/article/abstract?uid=PIIS0092867407009737

Note from Terra Biological: benaGene is thought to work by increases in the NAD+ levels.