Disclaimer: This is just a rough (very rough unedited) collection of some of my personal thoughts on possible mechanisms behind cancer. It is definitely not medical advice. My professional education is in robotics (they don’t get cancer) and my highest level of biology education is grade 10 high school… so if you’re taking my medical advice on faith then you’ve got things wrong with you that no one can solve.
Cancer is believed to be caused by genetic mutations that cause cells to go crazy and do things that they wouldn’t generally do (Somatic Mutation Theory):
A great deal of research has been done to find out what these mutations are and document them, however, after much genomic mapping, no single genetic smoking gun has been found.
cancer cells do the following:
• they ferment glucose without oxygen (glycolysis) for energy rather than burn glucose or fat with oxygen (oxidative phosphorylation)
• they don’t die off when they should (failed apoptosis),
• they do not perform oxidation even in the presence of oxygen. (Warburg effect)
• They use up vast amounts of glucose compared to other cells as glycolysis is much less efficient than oxidation. ie: you get fewer ATPs out for each glucose molecule consumed (this is how a PET scan works as it looks for increased glucose usage using ‘radioactive glucose’)
• Some cancers cause the growth of additional blood vessels in an effort to get more energy (glucose) (Angiogenesis)
• eventually some cancers become able to live in the blood or lymph system and travel to new sites (metastatic) and travel from the original site and relocate somewhere else to create another tumor.
The major flaw in cancer research:
The belief that genetic mutation is the start of the process rather than the end. Cancer cells that stick around are ones that are able to survive off of glycolysis alone. This is called survivorship bias. It’s very common in fitness marketing. example: Everyone who does crossfit is lean and fit, just look at them… actuallity: all the people who weren’t fit enough or genetically gifted enough to complete the grueling crossfit methodology dropped out or became injured and aren’t being counted. Crossfit didn’t so much make people fit, it provided unnatural selection pressure to weed out all those that didn’t meet the minimum level to continue. In this analogy, all the fit lean people are metastatic cancers and researchers are wondering what makes them fit and lean, whereas they should be looking at the entire population of people who originally joined Crossfit and wonder what made them join to begin with.
Yet another Analogy: A bus load of tourists crash in the mountains (breakdown of OxPhos). Many die in the initial crash (Apoptosis). Some tourists happened to bring coats with them, and they manage to not freeze to death as soon as some of the others (conversion to running on glycolysis for their energy needs). Eventually the remaining survivors get hungry. Some are hungry enough to start eating some of the dead tour mates (Angiogenesis)…. these are the ones that survive. Eventually they are rescued and return home… now with a taste for human flesh (Zombism.. I mean Metastasis)
Current cancer research is directed at limiting the number of coats allowed on buses rather than making the buses safer, looking for a safer route through the mountain, or providing food supplies for emergencies.
Ketogenic diets keep the tourists alive without feeding the zombies… eventually the zombies die.
Curing Zombies: find research about cancer cells dedifferentiating back to healthy cells when given the right environment.
What causes cells to turn cancerous:
Some cancers are cause by infection by viruses that turn them cells cancerous for their own propagation (I won’t deal with those at this point)
Some people are born with genetic mutations that are cancerous (these people would have issues from birth)
if random genetic mutations or damage are the root cause of cancer then we would expect the rates of cancer to be linear as we age. Ie: you would find the same percentage of kids with cancer as seniors, as cells are constantly multiplying at similar rates as we age.
Since cancers are typically found with higher frequency as we get older, it implies that what is happening is not singular breakdowns of the genetic code, but a buildup of damage over time that eventually overwhelms the body’s ability to circumvent it.
all throughout our lives the cells are mutating at the same rate, but as we get older there are more buses breaking down in the mountains.
what causes the bus to break down? Ie: breakdown of oxphos system: (hint inhibition of Cytochrome C by blue light and cardiolipin by Omega 6 fats)
what causes the breakdown of apoptosis? Ie: why do cells not kill themselves when they are low on energy: (hint Cytochrome C oxydase and cardiolipin are key factors)
how do we prevent zombification of cancer cells? Starve them using ketogenic diets. (not this only deals with existing cancer cells, it doesn’t do anything to change the environment that is causing cells to initially turn cancerous)
can we reverse zombification of cancer cells?
do we need to go to war with cancer? Remember cancer cells are us (they have our DNA), going to war with yourself is quite literally suicide. There is some evidence to suggest that cancerous cells can be converted back to normal healthy cells depending on their environment.
Topics for continued investigation:
The crucial mitochondrial respiratory enzyme, cytochrome c oxidase, declines with aging (Paradies, et al., 1997), as the lipid cardiolipin declines, and the enzyme’s activity can be restored to the level of young animals by adding cardiolipin.
The composition of cardiolipin changes with aging, “specifically an increase in highly unsaturated fatty acids” (Lee, et al., 2006). Other lipids, such as a phosphatidylcholine containing two myristic acid groups, can support the enzyme’s activity (Hoch, 1992). Even supplementing old animals with hydrogenated peanut oil restores mitochondrial respiration to about 80% of normal (Bronnikov, et al., 2010).
look into the key differences between glucose based metabolism vs. fat based impact on NAD vs. NADH and their impact on ROS generation; Which substrate produces fewer ROS? Also Redox state in cancer cells.
T3 works on cytochrome oxydase
Field with 1000 sheep surrounded by 4ft fence. Average sheep can only jump 3 feet. Above average sheep can jump 4 ft. but there are sheep dogs outside to keep this under control. When there’s lots of food to eat, all the sheep stay put. If food becomes scarce some sheep will try to jump the fence to get at the food outside. If the field runs completely out of food, all the sheep will do is keep trying the fence again and again, as they have no option. Eventually enough will get out to overwhelm the dogs. These fence jumping sheep are then free to go to other fields where they start breeding a new line of high jumpers. repeat.
modern approach is geared towards killing the sheep after they’ve started jumping the fence, or burning entire fields that have good jumpers… wouldn’t it be better to just keep them well fed and get more dogs? (not sure how to deal with ketones in this analogy – basically food/breeding program for low jumping sheep only)