PeatThemAll
Member
- Joined
- Oct 3, 2015
- Messages
- 280
Follow along with the video below to see how to install our site as a web app on your home screen.
Note: This feature may not be available in some browsers.
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
Wow, so much disinformation from actual doctors!
OK, first and foremost, the statement about cancer cells being somehow hooked on sugar is wrong. Cancer cells actually love fat more than anything else:
Cancer cells use fat oxidation for survival | Ray Peat Forum
All you need to read is the first paragraph. Niacinamide/Aspirin to the rescue of every cancer patient! Well, it is probably not enough but you get the point.
Couple of other points. Despite what "cancer gurus" like Amanda Mary say you cannot simply deprive cancer cells of glucose. The cancer will get its glucose either from diet or by eating your muscles at an amazing speed. And if it breaks down muscle tissue it will not only kill the person much faster through cachexia but the breakdown of muscle tissue will also generate glutamine, which cancer cells also love and thrive on; arginine, which will increase NO production; and cysetine, which will help the cancer increase its reductive potential, provide even more sulfhydryl groups for cancer growth, and serve as a powerful anti-oxidant for the tumor to resist destruction from chemotherapy, radiation, and even internal ROS.
There is a reliable way to starve cancer cells of glucose and that is by feeding the organism the so-called 2-deoxy-d-glucose (2-DG).
2-Deoxy-D-glucose - Wikipedia, the free encyclopedia
Given the pervasiveness of this flawed thinking, 2-DG is of course being tried to starve tumors of sugar. It failed, even though initially it seems to restrain tumor growth. Dietary restriction of sugar seems to have the same effects and then the tumor rebounds because it starts to break down muscle tissue for sugar. And of course, like anything that inhibits glucose oxidation, 2-DG has serious cardiac side effects.
"...2-DG is uptaken by the glucose transporters of the cell. Therefore, cells with higher glucose uptake, for example tumor cells, have also a higher uptake of 2-DG. Since 2-DG hampers cell growth, its use as a tumor therapeutic has been suggested, and in fact, 2-DG is in clinical trials [3] A recent clinical trial showed 2-DG can be tolerated at a dose of 63 mg/kg/day, however the observed cardiac side-effects (prolongation of the Q-T interval) at this dose and the fact that a majority of patients' (66%) cancer progressed casts doubt on the feasibility of this reagent for further clinical use.[4] However, it is not completely clear how 2-DG inhibits cell growth. The fact that glycolysis is inhibited by 2-DG, seems not to be sufficient to explain why 2-DG treated cells stop growing."
Now, a much saner approach would be not to somehow deprive the tumor of sugar but consider cancer cells as cells that cannot fully metabolize sugar. It is well-known and undisputed that cancer cells have dramatically downregulated activity and levels of PDH. That is the main reason they overproduce lactate. When glucose is metabolized it produces pyruvate and NADH. If PDH is working, pyruvate is converted into Acyl-Co-A and feeds into the Krebs cycle. If PDH is not working, both pyruvate and NADH build up. The cell depends on NAD for survival and will do anything to get it back. Typically, if metabolilsm is working well, NADH will be oxidized back into NAD in the electron transport chain. However, in hypoxic conditions or malfunctioning metabolism there is no way to oxidize NADH back to NAD. So, the cell used the only material available to it for oxidation and that is the excess pyruvate that builds up during glycolysis. The enzyme lactate dehydrogenase (LDH) is what takes pyruvate and NADH and used pyruvate to oxidize NADH back to NAD and that process converts pyruvate to lactate. However, even that process is not sufficient to meet the NAD needs to of the cells quickly enough so they die. That is why people with cancer have abnormally high LDH levels - first because it is elevated to convert pyruvate to lactate and NADH to NAD, and second because when even that process is not fast enough the cell dies spilling its LDH into the bloodstream.
So, what does one do in situations like that?
1. Boost PDH by any and all means possible. The chemical dicholoroacetate (DCA), that pretty much everybody has heard of as possible cancer treatment, boosts PDH activity. Unfortunately, it is also toxic to the glycolysis enzymes and eventually becomes a carcinogen itself. However, thiamine, which is a cofactor of PDH does not have these side effects and at least one study found it comparable to DCA for cancer treatment.
Thiamine acts similarly to DCA and may be helpful in cancer | Ray Peat Forum
Thiamine is also carbonic anhydrase inhibitor and will raise CO2 levels, which will also oppose lactate buildup.
Thiamine is a carbonic anhydrase inhibitor as effective as acetazolamide | Ray Peat Forum
And thiamine also lowers ammonia, which is likely to be high in people with cancer as they break down muscle tissue under the "wise" advice of their doctor to lower glucose intake.
Thiamine reduces both lactate and ammonia | Ray Peat Forum
In addition, to PDH, there is also PDC. That enzyme is a biotin-dependent enzyme and is an alternative "consumer" of pyruvate and converts it into oxaloacetate to also feed into the Krebs cycle. I don't know the exact dose for biotin but given the recent clinical trial with MS, starting with 300mg seems like a good bet since that dose raised ATP production and increased CO2.
2. Provide alternative oxidizing agents if oxygen is not available or unable (as in cancer) to oxidize NADH. Methylene blue is prime example of a substance that can completely replace oxygen in the metabolic pathways. It also stimulates the activities of electron transport chain comp[lexes II, III, and IV and also boosts levels of cytochrome C oxidase. Vitamin K can also serve as alternative electron carrier if CoQ10 is unavailable or very low (as in cancer).
3. Provide substances that oppose the Warburg phenotype systemically. Thyroid hormone, quinones, methylene blue, tetracyclines, dopamineric agents, anti-estrogens, anti-serotonin agents, anti-glucocorticoid agents, anti-aldosterone agents, etc can all contribute to that effect but thyroid hormone is the master regulator.
I can list at least 20 other steps that are key in inhibiting cancer growth and restoring normal cell function, but those are already posted on the forum. What gives me anxiety is that if these simple biochemical processes are not something that the doctor is likely to know and apply, then your doctor is much more likely to kill you than help you since these same biochemical principles apply to all therapies and all drugs for any condition. ANYTHING that inhibits respiration, be it in the step of glycolysis, Krebs cycle, or electron transport chain, WILL cause a disease of some kind and eventually cancer if the patient lives long enough and does not die from earlier complications.
I suppose creating a Wiki page that summarizes this well would greatly help in dispelling some of the myths being propagated by medical professionals that are so focused on their specific (and usually genetically-driven) field that none of them even tries to look at the big picture. You want to try for yourself? Next time you see your primary care doctor ask him/her what happens in the body when somebody restricts sugar intake. Jut ask for simple explanation of the processes that kick in and how the body adapts. I have tried it with 7 of my friends so far who are all M.D. and got either a blank stare or an insulted response "I don't work in metabolics/diabetes".
Been reading much discussion here about lactate (bad guy) and CO2 (good guy). As a new comer I am not permitted to post links yet, so I will recommend Googling: Johannes Kuhl Waltraut Fryda L+ Lactic acid.
These European doctors treated many people with a dextrorotatory Lactic acid to undo the effects of levorotatory lactic acid which they saw as one of the principal culprits in cancer proliferation. According to them, the differences between these two forms of lactic acid is profound. Hopefully, I'll soon be able to provide links to the sites that cover their protocols in some detail.
Been reading much discussion here about lactate (bad guy) and CO2 (good guy). As a new comer I am not permitted to post links yet, so I will recommend Googling: Johannes Kuhl Waltraut Fryda L+ Lactic acid.
These European doctors treated many people with a dextrorotatory Lactic acid to undo the effects of levorotatory lactic acid which they saw as one of the principal culprits in cancer proliferation. According to them, the differences between these two forms of lactic acid is profound. Hopefully, I'll soon be able to provide links to the sites that cover their protocols in some detail.
Isn't that the isomer from bacteria?