Saturday, December 28, 2013
Thursday, December 19, 2013
Another promising paradigm for cancer treatment would be to focus on the manipulation of metabolic pathways of cancer cells. Scientists are discovering that cancer cell metabolic pathways may be unique or at least more limited than normal cells. And it is these metabolic limitations that could be exploited. First off, we know that all cells in the body can generate energy using several anaerobic and aerobic mechanisms. These metabolic pathways include: anaerobic glycolysis, aerobic respiration (TCA cycle), oxidative phosphorylation, lipolysis (ketogenic), and gluconeogenesis,
One of the first identified biochemical hallmarks of tumor cells was a shift in glucose metabolism from aerobic oxidative phosphorylation to anaerobic glycolysis (the "Warburg effect" or "Warburg hypothesis"). Now, scientists have revealed that cancer cellular functions and growth are primarily dependent upon the anaerobic metabolism of glucose, fructose and lipid (lypolysis). Aerobic respiration via the TCA-cycle and Oxidative phosphorylation is very complex and requires intact mitochondria. Because of that complexity, mutated cancer cells can rarely depend on aerobic metabolism for energy. Instead, they rely primarily on the much simpler anaerobic glycolysis; using glucose and fructose as fuel. Otto Warburg, 1931 Nobel Laureate, was first to measure and explain the mechanisms behind the large amounts of lactic acid produced by cancer cells.
However, when glucose levels are low, cancer cells are in a pinch. They can't do aerobic respiration, so lacking glucose, they instead turn to ketogenic lipolysis for energy. But cancer cells have the complex machinery needed to transport lipids into the cell. Instead, in a low glucose environment, they use their damaged oxidative phosphorylation pathway and other pathways to generate high levels of reactive oxygen species (ROS). These ROS are then secreted into the cells microenvironment where they damage nearby cells. In this way, cancer cells begin to parasitize nearby cells and literally eat their host alive.
New studies suggest that cancer cells may not generate ROS themselves, but instead, reprogram neighboring stromal fibroblast cells to generate high amounts of ROS for them. The ROS then damage neighboring cells resulting in lipid peroxidation, and the production of lactate, and ketones which the cancer cells can use for energy. Through this mechanism, tumors do not need much of a blood supply. Understanding how cancer cells metabolize energy, we can now develop new strategies to kill them.
Together, the medicines, herbs, and vitamins listed above should do two things. First, a low-fructose diet together with Metformin and DCA will serve to inhibit both gluconeogenesis and anerobic glycolysis and force cancer cells into lipolysis. While we want the force the cancer into a ketogenic state, a ketogenic diet and dehydration are discouraged because scientists believe that cancer cells may thrive on lactic acid and ketones. That said, this first strategy should force the cancer cells to depend primarily on lipolysis for energy.
Next, iron chelation is added to inhibit ROS formation. Antioxidants like Vitamin C, E, Co-enzyme Q10, and Cumin are added to prevent remaining ROS oxidative damage to surrounding tissues. Also, anti-inflammatory and immune modulating agents such as aspirin, cimetidine could be added to reduce inflammation and boost cellular and humeral immunity. All together, cancer cells should not be left with any alternative energy alternatives. Then, at that point, cancer cells would turn cannibalistic and should undergo autophagy.
The hope is that a paradigm focused on metabolic manipulation, will be not only more effective at curing cancer, but will avoid the terrible side effects of traditional cytotoxic chemotherapy. However, until this new paradigm is proven, it will most likely be necessary to test this new paradigm in between rounds of traditional cytotoxic chemotherapy.
Metabolic Manipulation: A New Cancer Treatment Paradigm
Mebendazole: tubulin disrupting agent induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells. Healthy melanocytes were unaffected.
Cimetidine: prevents histamine binding and indirectly enhances local anti-tumor response via IL-18 signaling to the immune system's natural killer and T cells.
Dichloracetate (DCA): DCA inhibits pyruvate dehydrogenase kinase (PDK), an inhibitor of pyruvate dehydrogenase, a key enzyme in glucose metabolism. DCA blocks anerobic glucose metabolism in cancer cells from glycolysis inducing apoptosis. [orphan drug used to treat lactic acidosis].
Metformin: suppresses the AMPK/mTOR/S6K1 axis and several protein kinases. Metformin may also specifically target the cancer-initiating stem cells, thereby preventing cancer relapse when used in combination with cytotoxic chemotherapy (dandelion root hypothesis). [Beware Cimetidine and Metformin are secreted by the same cation pump in renal tubules]
Low Fructose Diet: Pancreatic cancers use the sugar fructose to activate a key cellular pathway that drives cell division
Black Cumin Seed: Nigella sativa oil containing thymoquinone has been demonstrated to reduce the growth and size of tumors in rats.
Co-Enzyme Q10: (Ubiquinone) lipid soluble antioxidant that stimulates the immune system leading to higher antibody levels, greater numbers and/or activities of macrophages and T cells and increased resistance to infection.
Vitamin C and NAC: both human lymphoma or human liver cancer cells which produce high levels of free radicals were suppressed with these antioxidants in a DNA damage independent mechanism. Researchers believe that the antioxidants destabilizing a tumor's ability to grow under oxygen-starved conditions.
Desferrioxamine: iron chelator that binds iron and limits a key limiting metabolite needed for tumor growth. High iron levels also inhibit the immune system.
Tuesday, December 17, 2013
Wednesday, December 11, 2013
Tuesday, December 03, 2013
Monday, November 25, 2013
In 1997, President Bill Clinton issued Presidential decision directive (PDD) 60. This directive radically changed US stratigic nuclear policy from "launch on warning" to "retaliate after absorbing a first strike". President Clinton's justification for this change was based on the false premise that in the so-called "Post-Cold War Era", Russia and China are no longer nuclear threats.
Robert Bell, senior director for defense policy and arms control at the National Security Council, verified information about PDD 60 in an interview on December 23, 1997. Bell pointed out that while the United States has always had the "technical capability" to implement a policy of launch on warning, it has chosen not to do so. "Our policy is to confirm that we are under nuclear attack with actual detonations before retaliating".
Hello? Are you serious? The whole strategy that makes nuclear weapons a deterrent is that under a "launch on warning" policy, whichever nation launches first looses and whichever nation launches second wins. If you take US nuclear missiles off "launch on warning" and switch to a policy of "retaliation after absorbing a nuclear first-strike", there won't be anything left over to retaliate with. You loose. Especially since 1. most all US nukes are sitting in vulnerable fixed silos, and 2. the US has been unilaterally downsizing our nuclear arsenal.
"Launch on Warning" means the US would launch its nuclear missiles after it has been varified that a country like Russia and China have premptively launched on the US but before enemy warheads have arrived. Under "Launch on Warning" the US would retaliate while the enemy ICBMs are still in the air, and before they have detonated in the US.
The reason "Launch on Warning" assures that whomever launches first looses and whomever launches second wins is that a country would likely only launch 50% of its nukes during a first-strike. Most of the incoming nukes will be targeting our nukes here in the US to prevent a retaliatory counter-attack. However, how "Launch on Warning" works is the launch-second country can simply track the incoming ICBMs and predict which silos are being targeted. The US would then launch the nukes only in those targeted silos. The "launch on warning" ICBMs would then target the remaining unlaunched ICBMs back in the attacking nation. When Russia's ICBMs arrive, those nukes strike empty silos. When the US nukes arrive on the other end, they target and destroy remaining ICBMs in Russia.
If the US only uses 50% of its nukes to target the remaining Russian nukes, then the US is left with 50% remaining ICBMs and Russia is left with 0% ICBMs. This is how the "Launch on Warning" strategy assures that whomever initiates a nuclear firstrike looses and why the "Launch on Warning" policy is the only real and effective nuclear deterrence policy.
The new and current nuclear policy to "Retaliate after Absorbing a First-strike" is an unwinnable policy that does more to invite attack than deter it.
Unfortunately the only thing the public thinks it knows about nuclear stragedy is from the movie "War Games" which equates Global Thermonuclear War with a game of tick-tack-toe.
Saturday, November 23, 2013
Thursday, November 21, 2013
Tuesday, November 12, 2013
Monday, November 04, 2013
Saturday, November 02, 2013
Monday, October 28, 2013
Saturday, October 26, 2013
Wednesday, October 23, 2013
Wednesday, October 16, 2013
Tuesday, October 15, 2013
Sunday, October 13, 2013
Wednesday, October 09, 2013
So, do you think there is a warning there about the Order 66 and the Jedi Purge? Who will be the "force sensate" who will possibly be targeted and purged?
Maybe the NWO will collect "meta-data", profile and make kill lists of conspiracy theorists and constitutionalists. The NWO has aleady used the power of the IRS, HHS, EPA etc to target certain groups. Whose to say they won't one day target these groups with drones?