For you scientists out there, anyone have an opinion about Thomas Seyfried? Lots of posts of what appear to be scientific research on mitochondria's role in the cancer game. His answer seems to be the Keto diet will destroy cancer cells. True or bullshit?
Cancer as a metabolic Disease - Advanced Prostate...
Cancer as a metabolic Disease
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tayninhtom
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Sounds like another bullshit "cure" did absolutely nothing for me
thanks bro
There's probably something going on with cancer and metabolism. The problem stated by Seyfried is that there are two sources of energy for cancer, (1) glucose and (2) amino acids glutamine and glutamate. Keto gets you number one. It's almost impossible to do number two. So the whole thing doesn't really work in the real world. Except maybe it does but we don't know. There is research looking at drugs to suppress the second. If you listen to the good doctor after a while one realizes one is listening to a rhetorical performance and there isn't much new. Behind the whole thing of course is the Warburg effect and the interesting discovery many years ago that cancer cells have a different energy source than normal cells. But so far there isn't a safe recipe you can implement at home that will definitively make a difference. Would be nice if there was. And it's not impossible to imagine that this path of research will lead somewhere very good.
I'll share this with my primary, who's curious. Much Thanks.
All us 'scientists'? Made me smile. 😀
There's a lot of opinions about this guy. Some go as far to say he's a charlatan - not that I agree with that in any way. I genuinely think he has good intentions in trying to help.
I actually think that cancer is a metabolic disease. I also think that what he says is true, but IMO not a realistic treatment. Not that you should rely on my opinion mind you.
The issue, as I remember it, is that cancer can also feed on glutamine. BUT this is one of the most abundant amino acids in your body. He has a therapy that supresses the glutamine side of it whilst you attack the cancer with the diet.
So, even if a diet like keto/vegan/carivore/fruitarian/paleo... or any other diet available under the sun was able to assist in the killing of cancer cells, how do you really surpress the most abundant amino acid in your body? Also, if you think about it, effectiveness aside, is it really a wise thing to do? Maybe - maybe not. I'm certainly not qualified to answer that.
To me, it just looks more like a theoretical solution than a practical one.
What you can do though, as I have done in the past, is email him directly. He does reply to emails.
Maybe he can answer your questions directly.
Hope that helps.
a very complete and detailed explanation, thanks so much.
I vote that it's bullshit.
Thanks TA. I appreciate looking at it.
In fact, prostate cancer is known to feed on fats and proteins, so the keto diet is giving the cancer exactly what it wants. Not that you can starve those cells by switching to a high carb diet either -- cancer cells grow rapidly, so are voracious feeders -- you deny it one food, it will switch to another and cannibalize healthy cells.
Hi, I am wondering if the source (vegetal or animal) makes a difference for cancer metabolism?
Animal protein provide nine types of amino acids while vegetal ones have six. I know that some studies say that meat is bad for you but they roll in bacon and cold cuts which are not good. Look for grass fed beef
As long as you get all 20 amino acids, lipids and carbs it doesn't matter what the source was.
Good stuff.
Just learned a new term because of the discussion here - "metabolic flexibility" - in other words as you say cancer cells can obtain energy from a variety of sources and pursuing keto (sadly) probably doesn't do anything. And might even be a bad idea.
There's another term I learned, which is "metabolic heterogeneity". It means that even within one's own population of cancer cells, or even within a tumor itself, you may have cells that obtain their energy in different ways from each other.
Which kind of implies that cancer is even more evil than one could imagine. Evil in the genius sort of way. It's evil even indirectly in that one may be enticed to waste a lot of time reading about cancer and cancer therapy. Time one could have spent with one's family or on other important things 😂
Good thoughts, let’s not fall into that trap
Count me in the bullshit camp as well. I would say that a diet that reduces inflammation would help to prevent cancer. But once the genetic damage is done, the cancer is not particularly sensitive to subtle diet changes.
TA,Ditto
Concur
Never heard of him but I shall look him up.
I believe Cancer as a metabolic problem is correct, but with a different underlying cause. Initially, there is persisting inflammation problem (cancer is the result of the pan-ultimate state of inflammation) innate immune response is producing lots of free radical (ROS & RNS) to get rid of the inflammation (be it infection, chemical intoxication or trauma). However, under certain condition, the bodily system fails to stop this inflammation. So there is a lot of NO presence in the vicinity of mitochondria. NO has higher affinity to bind with Cytochrome c Oxidase at complex IV of the ETC preventing the electron transfer with Oxygen Oxygen. This creates the direct inhibition of ETC forcing the cells to activate alternative pathway, through aerobic Glycolysis. This would elevate the lactic acid production, which can be transported back to the liver to produce more glucose endogenously through gluconeogenesis process. This would suffice the hungry cells for the moment. As the inflammation persists, then there will come a stage where NO production is extremely high, then this would create a situation for the dissapearance of NO due to the formation of ONOO-, or lack of sufficient substrate (L-Arginine) or Co-Factor (BH4) or to much ADMA while the transcription of iNOS is ever increasing. This would then lead to the uncoupling of iNOS and eNOS to form SOA, elevating for more ONOO- and ROS. With no more NO in the vicinity, ETC can resume, but this time it is not only through glucose but also FAO due to the high demand for energy from teh cancerous cells. All the while Arginase as the builder's army will be activated due to the dissaperance of NO would leave more L-Arginine available for Arginase. This would bring in building material such as Polyamines (for cell proliferation) and Prolines (collagen deposition), but since the fire of inlammation is still raging hard, then this material would not turn to renewed tissue but rather fibrosis. This would set the stage for more tissue damage (due to high inflammation) and at the same time plenty of ATPs .
This reply was generated via Claude ( I find that it helps to simplify highly technical jargon) Sonnet 3.5...... Cheers
This is an interesting hypothesis about cancer's metabolic and inflammatory origins. Let me analyze the key elements of your proposal:
The Inflammation-NO-Mitochondria Connection
Your core premise about persistent inflammation leading to elevated NO (nitric oxide) production is well-grounded. The interaction between NO and Complex IV (cytochrome c oxidase) of the electron transport chain is indeed documented, and NO can competitively inhibit oxygen binding.
Metabolic Shift
Your description of the metabolic shift to aerobic glycolysis aligns with the Warburg effect. The glucose-lactate-gluconeogenesis cycle you described (Cori cycle) is a known feature of cancer metabolism.
The NO-ONOO- Dynamic
The transition you describe from high NO to its depletion through peroxynitrite (ONOO-) formation is interesting. This could explain the biphasic nature of cancer progression some researchers have observed.
However, I have some questions about your model:
What triggers the initial persistent inflammation that fails to resolve? This seems like a crucial point that would need to be explained.
How does this model account for oncogenic mutations? While metabolic changes are clearly important in cancer, how do they relate to genetic alterations?
Regarding the Arginase pathway: Do you see the polyamine production as a primary driver of proliferation, or more as a supporting factor?
Would you like to elaborate on any of these aspects? I'm particularly interested in your thoughts on how this model might translate to therapeutic approaches.
Persistent inflammation is naturally driven by persistent perturbance. Prolonged infection, be it due to lack of or inadequate intervention or antimicrobial resistance may provoke NF-kB to keep transcribing iNOS and ADMA setting the stage for ever increasing inflammation. iNOS as the producer of NO has certain requirements in order to produce NO, ie. Among others, L-Arginine and BH-4. If anyone of this is not available, then iNOS would be uncoupled and produce Superoxide Anion (radical oxygen). On the other hand, ADMA, which seems to be intended to act as a brake for iNOS activity competes with L-arginine to bind with iNOS catalytic site. Once this happens, then the enzyme would also be uncoupled pushing the elevation of SOA.
Prolonged exposure to carcinogenic molecules may also replicate the same responses as outlined above.
When exposed to prolonged infection or carcinogen, the bodily systems may escalate the counter attack in order to extinguish the perturbance. This is in the form of Peroxynitrate (ONOO-) which is a much stronger oxidator that may cause lipid peroxidation. With more ROS being produced from over active glycolysis, the produced NO will react much faster with ROS rather than performing its physiological duties. Once this happens, then NF-kB will get even more activated transcribing more iNOS setting up for the vicious cycle.
This will ultimately lead to the disappearance of NO and bio-available L-arginine would be available for more active Arginase metabolism, with the downstream effects of more material for cell proliferation, collagen deposition, and also M2 polarization along with angiogenesis. In a normal setting, no vicious cycle, with the elimination perturbances above, NF-kB will be downregulated, and iNOS transcription will be slowed, and Arginase activation would lead to tissue repair and complete cellular modification. In an abnormal setting like in chronic inflammation, we have both pro- and anti-inflammatory processes working simultaneously leading towards to maladaptive tissue repair.
Addressing chronic inflammation problem might require applying the right strategy. Efforts at modifying the midstream or downstream pathway without any attempts at modifying the upstream initiator may only provide relief of symptoms (pain, etc.) but not resolution of the inflammation itself, be it infection or autoimmunity as the underlying driver. For example the use of mAb to inhibit IL-6 expression only leads to reduction of pain but fails to provide cure to RA, as the main driver of inflammation, ie. The vicious cycle of NO will remain active. In addition, as it turns out, IL-6 is actually not the main culprit, due to it is also important for activating the anti-inflammatory downstream pathway (classical vs trans-signalling).
Immune response is so complex that perhaps pushing the wrong button may inadvertently exacerbate the condition. This is the case with the use of NSAID, which mostly aim to inhibit COX activity. Again relief of symptoms might be achieved, but resolution to inflammation is not possible. In addition, this may also create complication due to inhibition of COX may leave available AA for LOX metabolism. This may push towards a different inflammatory problem. One aspect of Steroid work mechanism is the suppression of BH4, through the inhibition of GTPCH I. Initially, depending on the stages of existing inflammation, steroid use may help relieve symptoms, as it my suppress the production of NO. But then again, long term use may exacerbate the situation due to BH4 suppression may lead to NOS uncoupling and elevate ROS expression in the end leading towards complication as discussed above.
The role of Mutation
In the perspective of inflammation as the original driver of oncogenesis, mutation serves as a result rather than a cause. If we take the above outline of the chaotic situation in TME, with high level of Oxidative stress, it is only natural to deduce that this may cause some damage. ROS and RNS may cause direct oxidative and nitrosative damage to DNA, proteins and lipids. This may drive genomic instability and epigenetic alterations (eg. DNA methylation, histone modification). ONOO- may induce nitration of tyrosine residues in proteins, altering their function. Nitrative stress may lead to inactivation of DNA repair enzymes (eg. PARP, OGG1) heading towards the accumulation of mutations. High inflammation comes along with inflammatory cytokines like IL-6, TNF-a and IFN-g along with ROS. This may activate the PI3K/AKT and NF-kB pathways, which upregulate mTOR and downregulate AMPK. mTOR hyperactivation may lead to the suppression of autophagy. ROS and ONOO- may trigger lipid peroxidation producing reactive aldehydes like 4-HNE and MDA that form adducts with DNA and proteins. This will induce the mutations in lipid metabolism genes (like FAT2, ACACA, SCD1) to enhance membrane repair and resistance to peroxidation. So the final deduction is mutation is a result rather than cause, which is in a way actually a survival mode of the cells against the unforgiving TME.
Since you can't starve the body from an abundant amino acid glutamine that is when the Press pulse therapy comes into play.
Every one has the answer but we still can't cure it ....
My two cents worth is that starving cancer cells does not necessarily kill them. In fact, the main problem with cancer cells is that they do not die. Therefore, the way to cure cancer is by killing the cancer cells.The body has killer t-cells, which do just that.Heat also kills cancer cells. All cancer cells die at 106 degrees F.
If it's too good to be true it probably isn't. No harm in trying but IMHO relying only on diet is delusional.
I watched several of his videos along with PCa client like Guy Tettenbaum . All good stuff. only drawback is He has a therapy that supresses the glutamine side of it that we can not get. But there are supps that help. Keto and fasting all help but it doesn't end there. Most important one needs to be disciplined with these protocols. How many could water fast for 10, 20 or 40 days . mimic fast maybe. My thoughts for Me is keto, Ivermectin Fenbendazole or Mebendazole. and Nitazoxinide and a half dozen select supps might be a better option along with SOC. For me this is easy and obtainable. Again I will say more info on this subject; Rumble- Sunfruit Dan channel and research all med studies on these drugs and cancer. Joe Rogan had Mel Gibson on where he briefly talked about his friends with stage 4 and use of ....
Because joe Rogan and Mel Gibson are experts on cancer.
Hey 85745 not to work up the crowd just curious on your experience with Nitazoxinide. That an over, fenb. You can PM not to start a debate. I’m considering all those after my last doxecetal infusion.
Thanks
I just started (about 2weeks ) now Nitazoxinide 500mg in morning and 500mg evening. No SE's to note. All I have to go on is what the studies suggest: Nitazoxanide (NTZ) is a drug that may help treat prostate cancer and bone metastasis:
Anti-cancer properties
NTZ is an antiparasitic and anti-viral drug that can stop prostate and colon cancer cells from growing. It works by breaking down beta-catenin, a protein that helps cancer cells survive and multiply. NTZ also blocks the Wnt/β-catenin pathway.
Bone metastasis
NTZ may be a potential treatment for bone metastasis in prostate cancer. It can inhibit acetylated KLF5-induced bone metastasis by modulating KLF5 function.
Repurposed drug
NTZ is a repurposed drug that was originally used to treat parasites like tapeworms. Researchers are hopeful that NTZ may lead to new treatments for prostate and colon cancer There are many articles written on this subject that can be accessed on a simple search as a matter of interest and knowledge. How one interprets these studies is the right of an individauls own choosing.
Danger Will Robinson! The bendazolites are near 😳
You can get DON which blocks the glutamine pathway. It's explained at skool.com/ketoforcancer/about. It's a membership $12.00 a month. There is a free trial. A lot of research and info on finding doctors and nutritionist who specialize in MTOC. Of course I would always encourage to use this along side conventional treatment.
It should be noted that as an asterisk, Dr. Seyfried states that caloric restriction can achieve the same metabolic benefits in his view as ketogenic dieting.
Ketogenic diets can be stressful to the kidneys (due to generally higher protein intake and potassium deficiencies in such diets), and many prostate cancer sufferers already have kidney damage due to chemo and urinary blockages by tumors. If someone with advanced PCa wants to experiment with Dr. Seyfried's ideas, they may prefer to follow a CRON strategy instead using a Mediterranean or pescatarian diet.
total bs for prostate cancer !
True.This is why FDG PET scans detect cancer. The more aggressive the cancer, the more glycolytic.
For me, I read studies and articles and then weigh there validity against existing other acknowledged long term ones. Additionally, thinking of these studies as cures or substantive treatments may be risky.
Many supplements and diets may be able to assist in keeping your body as healthy as possible and reinforcing our immune response but cannot substitute for other forms of treatment yet. There is no body of scientific studies measuring the effects of diet and supplements for treating cancer in general and PCa specifically. There simply is no funding for it.
We each must do what we think is best and keep living our lives to their fullest!
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