This food that causes cancer to grow

This food that causes cancer to grow

[cmamad id=”7178″ align=”center” tabid=”display-desktop” mobid=”display-desktop” stg=””]Before cancer starts, there is tissue that is not getting enough oxygen.

Tissue that doesn’t get much oxygen is what I call zombie tissue.

Zombie tissue starts spewing out all kinds of “crying for help” signals –like a crime victim screaming for help.

And like a crime victim, the zombie tissue is hoping help arrives, but it doesn’t always come.

Scientists call these “crying for help” signals cytokines.

From there, blood vessels begin to grow like crazy on that zombie tissue, and it becomes cancerous.

One of the keys to cancer is the rapid, almost runaway growth of blood vessels.

It’s something called angiogenesis.

You want blood vessels growing in a systemized way, so angiogenesis isn’t a good thing.

[cmamad id=”7179″ align=”center” tabid=”display-desktop” mobid=”display-desktop” stg=””]

Because if they’re out of control, they start feeding too much blood and nutrients to small amounts of tissue.

And like life, one section using too many resources deprives another section.

So this process happens at the expense of the rest of the body.

Scientists at the University of California at Davis looked into this situation.

They recently discovered the role of omega-6 PUFA fats in stimulating this cancerous growth of blood vessels.

The study itself is a very technical mouthful, and I’ll try to make it very simple.

It starts with omega-6 fatty acids.

These are the fats found in vegetable, peanut, soy, and corn oil — nearly all of today’s cooking oils.

Nearly all — with the exception of coconut oil.

And all of these oils, except for coconut, are cancer causing foods.

These fatty acids feed into what is called the COX pathway.

Maybe you’ve heard of Cox-2 inhibitors which are pain relievers, including aspirin.

Cox inhibitors interfere with the COX process — which is a very inflammatory pain producing process.

It turns out that this process also is very powerful in creating too much blood vessel growth too quickly — or cancer-inducing angiogenesis.

“Many diseases result in unregulated angiogenesis, including cancer,” said Rand, one of the scientists who did this study.

“There’s uncertainty regarding the link between unsaturated fats and cancer…”

This study is a very good basic research study.

But I’ll note that one of the big Pharma companies reviewed the study.

The peer review process is supposed to be done by objective scientists, but that’s not entirely the case today.

But large pharmaceutical corporations can be part of the review process.

So much for objectivity… anyway.

Despite that, I think it’s an important study because it points to the role of PUFA fats in increasing or even causing cancer.

Inhibiting COX led to a dramatic decrease in tumor growth, suggesting that the contribution of EETs to angiogenesis and subsequent tumor growth may be attributed to downstream metabolites formed by COX.

This is yet another reason to avoid PUFAs at all costs.

 

 


Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.
Tumor angiogenesis image 
http://img.medscapestatic.com/slide/migrated/editorial/cmecircle/2003/2629/images/hurwitz/slide03b.gif 

Study Reveals How Dietary Fats May Contribute To Tumor Growth 
http://blogs.ucdavis.edu/egghead/2017/04/26/study-reveals-dietary-fats-may-contribute-tumor-growth/ 

Cyclooxygenase-derived proangiogenic metabolites of epoxyeicosatrienoic acids
http://www.pnas.org/content/114/17/4370.abstract 

Be the first to comment

Leave a Reply

Your email address will not be published.