Cancer ages us

Dr. Weeks’ Comment: Cancer, which happens exclusively in a suboptimal oxygen depleted environments, is driven by inflammation and that is why cancer ages us because aging itself (referred to by gerontologists as “inflamaging”) is excessive inflammation. 

The SIRT1 gene controls aging and  the drink made from 3 organic non-GMO anti-inflammatory seeds called SOUL has been demonstrated by 3rdparty independent Brunswick Lab to slow down the aging process by 62%.  (Yes, You read that accurately).


Cellular Anti-aging Assay (SIRT1) measures the anti-aging ability of a material using SIRT1 production in human cells as a biomarker for anti-aging. SIRT1 is a protein that is believed to play important roles in longevity and reduction of age-related diseases. Previous studies have shown that when mammals age, SIRT1 expression decreases, where induction and activation of SIRT1 has been associated with extended lifespan. These studies have triggered the search for SIRT1 activators that may be used as dietary supplements to promote health and longevity. 

Cellular Anti-aging Assay (SIRT1 assay) determines the ability of a test material to stimulate SIRT1 protein expression in human cells, which translates to the material’s anti-aging potential. SIRT1 expression level of human cells treated with and without test materials are compared, and maximum percentage of the SIRT1 expression change is reported. The concentration used that induced maximum percentage of the SIRT1 expression change is noted. 

• Bioavailability of anti-aging compounds
• 62% increase in the stimulation of the anti-aging enzyme, SIRT1

• No cellular toxicity at concentrations tested 

So eat the seeds to reduce inflammation, cancer and aging. Simple.

Cell Cycle. 2011 Jul 1;10(13):2059-63.


Accelerated aging in the tumor microenvironment: connecting aging, inflammation and cancer metabolism with personalized medicine.

Lisanti MP1 et al


Cancer is thought to be a disease associated with aging. Interestingly, normal aging is driven by the production of ROS and mitochondrial oxidative stress, resulting in the cumulative accumulation of DNA damage. Here, we discuss how ROS signaling, NFκB- and HIF1-activation in the tumor microenvironment induces a form of “accelerated aging,” which leads to stromal inflammation and changes in cancer cell metabolism. Thus, we present a unified model where aging (ROS), inflammation (NFκB) and cancer metabolism (HIF1), act as co-conspirators to drive autophagy (“self-eating”) in the tumor stroma. Then, autophagy in the tumor stroma provides high-energy “fuel” and the necessary chemical building blocks, for accelerated tumor growth and metastasis. Stromal ROS production acts as a “mutagenic motor” and allows cancer cells to buffer-at a distance-exactly how much of a mutagenic stimulus they receive, further driving tumor cell selection and evolution. Surviving cancer cells would be selected for the ability to induce ROS more effectively in stromal fibroblasts, so they could extract more nutrients from the stroma via autophagy. If lethal cancer is a disease of “accelerated host aging” in the tumor stroma, then cancer patients may benefit from therapy with powerful antioxidants. Antioxidant therapy should block the resulting DNA damage, and halt autophagy in the tumor stroma, effectively “cutting off the fuel supply” for cancer cells. These findings have important new implications for personalized cancer medicine, as they link aging, inflammation and cancer metabolism with novel strategies for more effective cancer diagnostics and therapeutics.

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