Blocking Vascular Endothelial Growth Factor (VEGF)

Iggy Dalrymple

New member
Joined
Apr 9, 2006
I understand that Xania successfully underwent Avastin eye injections to control her macular degeneration.

AvastinTM was not initially developed to treat your eye condition. Based upon the results of clinical trials that demonstrated its safety and effectiveness, AvastinTM was approved by the Food and Drug Administration (FDA) for the treatment of metastatic colorectal cancer. As a condition of approval, the manufacturer produced a “label” explaining the indications, risks, and benefits. The label explains that AvastinTM works by blocking a substance known as vascular endothelial growth factor or VEGF. Blocking or inhibiting VEGF helps prevent further growth of the blood vessels that the cancer needs to continue growing.http://www.maculacenter.com/Procedures/Avastin.htm
Adenosine Promotes Cancer Cell Growth. Caffeine Inhibits this Promotion

Adenosine is a metabolite of ATP, the energy molecule for all cells. Under normal circumstances adenosine and ATP are not released from cells. However, under conditions of hypoxia, low oxygen tension, adenosine is released. The free adenosine is now able to bind adenosine receptors on the membranes of oxygen stressed cells. The activation of adenosine receptors results in the synthesis of HIF-1 and VEGF, proteins critically important for the growth and stability of cancer cells. Caffeine inhibits the activity of all four adenosine receptors.

VEGF, as we know, stimulates the growth of blood vessels into tissues. Increased vascularization brings more oxygen and nutrients into oxygen stressed tissues. HIF-1 activates VEGF synthesis in addition to stimulating the synthesis of glycolytic enzymes that consume glucose and produce ATP in the absence of oxygen. The internal mass of a tumor is oxygen deprived. This results in the release of adenosine into the tissue spaces and the activation of HIF-1 and VEGF genes. Oxygen deprived cells are completely resistant to chemotherapy drugs and radiation. Tumors literally live in a "soup" of adenosine, which promotes both angiogenesis and the inhibition of a cell mediated immune response against the tumors.

Without question, adenosine is a MAJOR promotor of angiogenesis and cancer cell survival. Although hypoxia stimulates the synthesis and release of VEGF, adenosine stimulates the synthesis and release of BOTH VEGF and IL-8, another powerful angiogenesis factor. The $80,000 a year drug Avastin can form an inhibitory complex with free VEGF, but it cannot inhibit its synthesis. It also has no affect on the synthesis and release of IL-8. Caffeine, as cited in the previous blog essay, inhibits the activity of all four adenosine receptors, thereby blocking the synthesis and release of both VEGF and IL-8.

When adenosine is infused into human volunteers, the blood levels of VEGF increase.

Clearly, adenosine is fundamentally important in promoting angiogenesis and, subsequently, cancer cell growth and development. Simple caffeine is MORE effective than an $80,000 drug in blocking cancer related angiogenesis.

Adenosine is also extremely immunosuppressive. We will discuss this topic in the next essay.


Stay tuned...


Grouppe Kurosawa, Medicine in the Public Interest
Xania, I'm not suggesting that you have caffeine injected into your eyes but do you think caffeine should be investigated as an alternative to Avastin?
 

Xania

New member
Joined
Apr 4, 2006
Location
UK
Now, have I understood this correctly? The consumption of caffeine will inhibit the action of VEGF.
If so, that should help control wet AMD.
 

Xania

New member
Joined
Apr 4, 2006
Location
UK
Iggy, you will have seen that I am enjoying coffee rather more frequently, recently?
I don't know if caffeine would replace Avastin. Maybe the combination of the two would be beneficial. I will ask the eye doc at the next visit - he is surprisingly receptive to new, or even alternative ideas. He has had acupuncture treatment for himself. Being a marathon runner, he suffers musculo-skeletal pains sometimes.
 

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