• Due to excessive bot signups along with nefarious actors we are limiting forum registration. Keep checking back for the register link to appear. Please do not send emails or have someone post to the forum asking for a signup link. Until the current climate changes we do not see a change of this policy. To join the forum you must have a compelling reason. Letting us know what skills/knowledge you will bring to the community along with the intent of your stay here will help in getting you approved.

Achilles heel of cancer discovered - its lack of CO2

haidut

Member
Joined
Mar 18, 2013
Messages
18,409
Location
USA / Europe
Several years ago I posted about a study demonstrating that an Achilles heel of cancer had been found - i.e. its addiction to fat (not glucose, as doctors and media continue to mindlessly parrot).

As my readers know from my other posts and various podcasts, excessive fatty acid oxidation (FAO) translates into lower CO2 levels due to the fact that FAO produces less CO2 per unit of substrate (fat or glucose) oxidized, while also producing a lot more reactive oxygen species (ROS). The lower production of CO2 results in relative hypoxia inside the tumor compared to the rest of the organism and that further accelerates tumor growth. Since CO2 and lactic acid are inversely correlated, lower CO2 means higher lactate levels inside the tumor and that means more angiogenesis (lactate is the most potent endogenous stimulator of VEGF) and more tumor growth. A new study below now demonstrates that the low CO2 levels are not just a minor side effect of tumor metabolism (i.e. excessive FAO) but in fact another crucial "defense" mechanism that tumor cells use to grow and metastasize. Namely, the study found that tumors overexpress the enzyme carbonic anhydrase (specifically isoenzyme CAIX), and that inhibiting CAIX fully stopped cancer growth. In fact, the results from the animal experiments were so promising that there is an ongoing Phase I human trial for patients with pancreatic cancer using the same patented CAIX inhibitor (SLC-0111) the study below discusses. So, it does look like combining FAO inhibitors and CA inhibitors may be viable interventions for cancer that may have truly curative effects. Interestingly enough, the study also found that increased expression of CAIX prevented a type of apoptosis process in cancer cells known as ferroptosis. This is an apoptosis is driven by iron accumulation inside the cells, and it may explain the presence of so-called "anemia of chronic disease" (actually a condition of intracellular iron overload) in most cancer patients. It looks like the high ferritin levels (and thus high intracellular levels of iron) seen in this condition are an adaptive response by weakened/sick cells through which they attempt to commit apoptosis and prevent further damage to the organism. However, the lack of CO2 through the overexpression of CAIX prevents that process from achieving its goal, which not only allows the tumor to survive but also further weakens and sickens the patient due to the chronically elevated intracellular levels of iron.

A quick note on the specific drug used in the study. It is a new, patented chemical targeting specifically the CAIX isoenzyme. As such, its long term safety is unknown and the cost of using it will probably be prohibitive for most people unless it is prescribed by a doctor. In addition, there is plenty of evidence that tumors overexpress multiple CA isoenzymes, which means using a drug selective for just isoenzyme IX is likely to be less therapeutic compared to a drug that targets most/all of them. One such broad-spectrum CA inhibitor is acetazolamide, and it is a drug with decades of usage behind its back, lacking major side effects. So, the available evidence suggests that using acetazolamide would be preferable to the new, patented drug used in the study below. Moreover, recent studies have discovered that vitamin B1 (thiamine) is also a powerful CA inhibitor, on multiple CA isoenzymes, with overall effects and potency very similar to acetazolamide.

Thus, using thiamine in comparable daily doses (1,000mg-1,500mg) to acetazolamide should be able to achieve the same effects with even less risk of side effects. Since thiamine also activaves PDH while also inhibiting PDK, further cements its potential as a therapy for cancer. As far as the FAO aspect of cancer metabolism, niacinamide and aspirin are perhaps the best-known and least risky options to limit both availability (through lipolysis) and oxidation of lipids by the "cancer" cells. Multiple animal studies have demonstrated robust anti-cancer effects of niacinamide in HED of 3,000mg-5,000mg daily and aspirin in the same dose range. Since vitamin B1 (thiamine) and niacinamide have synergistic effects, it seems reasonable to propose vitamin B1+B3 combination (in the dose ranges discussed above) as a generic/systemic intervention for cancer regardless of its type/location, and adding aspirin to that combination (even at lower doses than discussed above) would likely potentiate the anti-cancer effects of the vitamin combination even more.

A Phase 1 Study of SLC-0111, a Novel Inhibitor of Carbonic Anhydrase IX, in Patients With Advanced Solid Tumors
http://cancerimmunolres.aacrjournal...019/05/14/2326-6066.CIR-18-0657.full-text.pdf
A Study of SLC-0111 and Gemcitabine for Metastatic Pancreatic Ductal Cancer in Subjects Positive for CAIX - Full Text View - ClinicalTrials.gov
Abstract 2015: Interplay of the pH regulator, carbonic anhydrase IX and the glutamine transporter, ASCT2 in hypoxic tumor microenvironment
Cancer treatment breakthrough: Scientists discover disease's 'Achilles' Heel'

"...Cancer's 'Achilles' Heel' has been identified by scientists. The protein fuels tumours when oxygen levels are low, say scientists. It enables them to adapt and survive - and become more aggressive. The enzyme called CAIX (Carbonic Anhydrase IX) helps diseased cells spread to other organs. It could hold the key to new treatments for the deadliest forms including breast, pancreatic, lungs, bowel and prostate cancers. Study senior author Professor Shoukat Dedhar, of the University of British Columbia in Canada, said: "Cancer cells depend on the CAIX enzyme to survive, which ultimately makes it their 'Achilles' heel.' "By inhibiting its activity, we can effectively stop the cells from growing."

"...As the tumours advance, the blood vessels are unable to provide enough to every part. Over time, the low-oxygen environment leads to a buildup of acid inside the cells. They overcome the stress by unleashing proteins, or enzymes, that neutralise the acidic conditions. The process is behind spread, or metastasis, to other organs - which is what kills patients. Finding a way to prevent it is the 'Holy Grail' of cancer research - turning it into a chronic, rather than fatal, illness. One of the enzymes is CAIX. The Canadian team previously identified a unique compound known as SLC-0111 as a powerful inhibitor. It is currently being tested in clinical trials. Experiments in mice with breast, pancreatic and brain cancers showed its effectiveness. It suppressed tumour growth and spread although there were side effects, with other cellular properties diminished. Now the researchers have demonstrated other weaknesses in CAIX using a technique called genome-wide synthetic lethal screening. The powerful tool systematically deletes one gene at a time to determine if a cancer cell can be killed by eliminating the enzyme. Surprisingly, results pointed to an unexpected role of proteins and processes that control a form of cell death called ferroptosis. It happens when iron builds up and weakens a tumour's metabolism and cell membranes. Dr Dedhar added: "We now know the CAIX enzyme blocks cancer cells from dying as a result of ferroptosis. "Combining inhibitors of CAIX, including SLC-0111, with compounds known to bring about ferroptosis results in catastrophic cell death and debilitates tumour growth.” A large international effort is currently underway to identify drugs that induce ferroptosis. The study is a major step forward in this quest."
 

Sitaruîm

Member
Joined
Jun 14, 2020
Messages
200
Recently moved 900 metres above sea level, I believe all aspects of my health improved, but there are other factors that changed other than the altitude
 

Mauritio

Member
Joined
Feb 26, 2018
Messages
3,820
Great! pyrucet + acetozolamide to fight the cancer .
Speaking of pyrucet, have you heard of that Bulgarian lady that cured her cancer with pyrucet ? Is she still in remission ?
 

Mr.Bollox

Member
Joined
Mar 16, 2021
Messages
3,368
Several years ago I posted about a study demonstrating that an Achilles heel of cancer had been found - i.e. its addiction to fat (not glucose, as doctors and media continue to mindlessly parrot).

As my readers know from my other posts and various podcasts, excessive fatty acid oxidation (FAO) translates into lower CO2 levels due to the fact that FAO produces less CO2 per unit of substrate (fat or glucose) oxidized, while also producing a lot more reactive oxygen species (ROS). The lower production of CO2 results in relative hypoxia inside the tumor compared to the rest of the organism and that further accelerates tumor growth. Since CO2 and lactic acid are inversely correlated, lower CO2 means higher lactate levels inside the tumor and that means more angiogenesis (lactate is the most potent endogenous stimulator of VEGF) and more tumor growth. A new study below now demonstrates that the low CO2 levels are not just a minor side effect of tumor metabolism (i.e. excessive FAO) but in fact another crucial "defense" mechanism that tumor cells use to grow and metastasize. Namely, the study found that tumors overexpress the enzyme carbonic anhydrase (specifically isoenzyme CAIX), and that inhibiting CAIX fully stopped cancer growth. In fact, the results from the animal experiments were so promising that there is an ongoing Phase I human trial for patients with pancreatic cancer using the same patented CAIX inhibitor (SLC-0111) the study below discusses. So, it does look like combining FAO inhibitors and CA inhibitors may be viable interventions for cancer that may have truly curative effects. Interestingly enough, the study also found that increased expression of CAIX prevented a type of apoptosis process in cancer cells known as ferroptosis. This is an apoptosis is driven by iron accumulation inside the cells, and it may explain the presence of so-called "anemia of chronic disease" (actually a condition of intracellular iron overload) in most cancer patients. It looks like the high ferritin levels (and thus high intracellular levels of iron) seen in this condition are an adaptive response by weakened/sick cells through which they attempt to commit apoptosis and prevent further damage to the organism. However, the lack of CO2 through the overexpression of CAIX prevents that process from achieving its goal, which not only allows the tumor to survive but also further weakens and sickens the patient due to the chronically elevated intracellular levels of iron.

A quick note on the specific drug used in the study. It is a new, patented chemical targeting specifically the CAIX isoenzyme. As such, its long term safety is unknown and the cost of using it will probably be prohibitive for most people unless it is prescribed by a doctor. In addition, there is plenty of evidence that tumors overexpress multiple CA isoenzymes, which means using a drug selective for just isoenzyme IX is likely to be less therapeutic compared to a drug that targets most/all of them. One such broad-spectrum CA inhibitor is acetazolamide, and it is a drug with decades of usage behind its back, lacking major side effects. So, the available evidence suggests that using acetazolamide would be preferable to the new, patented drug used in the study below. Moreover, recent studies have discovered that vitamin B1 (thiamine) is also a powerful CA inhibitor, on multiple CA isoenzymes, with overall effects and potency very similar to acetazolamide.

Thus, using thiamine in comparable daily doses (1,000mg-1,500mg) to acetazolamide should be able to achieve the same effects with even less risk of side effects. Since thiamine also activaves PDH while also inhibiting PDK, further cements its potential as a therapy for cancer. As far as the FAO aspect of cancer metabolism, niacinamide and aspirin are perhaps the best-known and least risky options to limit both availability (through lipolysis) and oxidation of lipids by the "cancer" cells. Multiple animal studies have demonstrated robust anti-cancer effects of niacinamide in HED of 3,000mg-5,000mg daily and aspirin in the same dose range. Since vitamin B1 (thiamine) and niacinamide have synergistic effects, it seems reasonable to propose vitamin B1+B3 combination (in the dose ranges discussed above) as a generic/systemic intervention for cancer regardless of its type/location, and adding aspirin to that combination (even at lower doses than discussed above) would likely potentiate the anti-cancer effects of the vitamin combination even more.

A Phase 1 Study of SLC-0111, a Novel Inhibitor of Carbonic Anhydrase IX, in Patients With Advanced Solid Tumors
http://cancerimmunolres.aacrjournal...019/05/14/2326-6066.CIR-18-0657.full-text.pdf
A Study of SLC-0111 and Gemcitabine for Metastatic Pancreatic Ductal Cancer in Subjects Positive for CAIX - Full Text View - ClinicalTrials.gov
Abstract 2015: Interplay of the pH regulator, carbonic anhydrase IX and the glutamine transporter, ASCT2 in hypoxic tumor microenvironment
Cancer treatment breakthrough: Scientists discover disease's 'Achilles' Heel'

"...Cancer's 'Achilles' Heel' has been identified by scientists. The protein fuels tumours when oxygen levels are low, say scientists. It enables them to adapt and survive - and become more aggressive. The enzyme called CAIX (Carbonic Anhydrase IX) helps diseased cells spread to other organs. It could hold the key to new treatments for the deadliest forms including breast, pancreatic, lungs, bowel and prostate cancers. Study senior author Professor Shoukat Dedhar, of the University of British Columbia in Canada, said: "Cancer cells depend on the CAIX enzyme to survive, which ultimately makes it their 'Achilles' heel.' "By inhibiting its activity, we can effectively stop the cells from growing."

"...As the tumours advance, the blood vessels are unable to provide enough to every part. Over time, the low-oxygen environment leads to a buildup of acid inside the cells. They overcome the stress by unleashing proteins, or enzymes, that neutralise the acidic conditions. The process is behind spread, or metastasis, to other organs - which is what kills patients. Finding a way to prevent it is the 'Holy Grail' of cancer research - turning it into a chronic, rather than fatal, illness. One of the enzymes is CAIX. The Canadian team previously identified a unique compound known as SLC-0111 as a powerful inhibitor. It is currently being tested in clinical trials. Experiments in mice with breast, pancreatic and brain cancers showed its effectiveness. It suppressed tumour growth and spread although there were side effects, with other cellular properties diminished. Now the researchers have demonstrated other weaknesses in CAIX using a technique called genome-wide synthetic lethal screening. The powerful tool systematically deletes one gene at a time to determine if a cancer cell can be killed by eliminating the enzyme. Surprisingly, results pointed to an unexpected role of proteins and processes that control a form of cell death called ferroptosis. It happens when iron builds up and weakens a tumour's metabolism and cell membranes. Dr Dedhar added: "We now know the CAIX enzyme blocks cancer cells from dying as a result of ferroptosis. "Combining inhibitors of CAIX, including SLC-0111, with compounds known to bring about ferroptosis results in catastrophic cell death and debilitates tumour growth.” A large international effort is currently underway to identify drugs that induce ferroptosis. The study is a major step forward in this quest."

how do you think the carbonic anhydrase inhibiting activity of pomegranate juice or caffeine compares to that of vitamin B1 or acetazolamide?

also, catechins from green tea, as well as something called "rosmarinic acid" found in a few spices and maybe fruits are also carbonic anhydrase inhibitors. I dont have the sources on hand but life extension said those are both carbonic anhydrase inhibitors. im not sure how powerful they are compared to vitamin B1 or acetazolamide. I think green tea extract has other issues like potential liver issues from higher doses, and I think it is a 5 AR inhibitor as well.



wikipedia lists steven johnsons syndrome as a potential side effect of acetazolamide. do you think it is risky using acetazolamide, or high doses of vitamin b1 on a consistent basis? My concern with the b1 is the risk of the megadoses potentially inhibiting other nutrients or amino acids or minerals? would you have to megadose every b vitamin if megadosing b1, or can you megadose b1 in hundreds of milligrams whilst using small doses of the other b vitamins? im thinking of taking in several hundred milligrams b1 every other day regularly.

"SJS may be caused by the medications rivaroxaban,[17] vancomycin, allopurinol, valproate, levofloxacin, diclofenac, etravirine, isotretinoin, fluconazole,[18] valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil,[19] lamotrigine, nevirapine,[8] pyrimethamine, ibuprofen,[20] ethosuximide, carbamazepine, bupropion, telaprevir,[21][22] and nystatin.[23][24]

Medications that have traditionally been known to lead to SJS, erythema multiforme, and toxic epidermal necrolysis include sulfonamide antibiotics,[8] penicillin antibiotics, cefixime (antibiotic), barbiturates (sedatives), lamotrigine, phenytoin (e.g., Dilantin) (anticonvulsants) and trimethoprim. Combining lamotrigine with sodium valproate increases the risk of SJS"
 

Lejeboca

Member
Joined
Jun 19, 2017
Messages
882
This is an apoptosis is driven by iron accumulation inside the cells, and it may explain the presence of so-called "anemia of chronic disease" (actually a condition of intracellular iron overload) in most cancer patients. It looks like the high ferritin levels (and thus high intracellular levels of iron) seen in this condition are an adaptive response by weakened/sick cells

Per Ray's explanation, since lactic acid prevails over CO2 in cancerous cells, they become more alkaline than normal cells and 'open the gate' to metal entry, such as calcium and iron.
Ceruloplasmin, which is elevated in cancers (see, e.g., Serum ceruloplasmin as a diagnostic marker of cancer) , is apparently not only a "cancer marker" but also a defensive mechanism, converting iron to a state for a tight binding to trasferrin. So along with CO2, maintaining good copper levels is important. Ceruloplasmin also directly inhibits lipid auto-oxidation: Ray Peat Interview - KMUD August 20, 2021
. Since vitamin B1 (thiamine) and niacinamide have synergistic effects, it seems reasonable to propose vitamin B1+B3 combination (in the dose ranges discussed above)

A quick note: From this thread/post All We Needed Was B-Complex? and my own experience, coffee depletes vitamin B1.
 
Last edited:

Mr.Bollox

Member
Joined
Mar 16, 2021
Messages
3,368
Per Ray's explanation, since lactic acid prevails over CO2 in cancerous cells, they become more alkaline than normal cells and 'open the gate' to metal entry, such as calcium and iron.
Ceruloplasmin, which is elevated in cancers (see, e.g., Serum ceruloplasmin as a diagnostic marker of cancer) , is apparently not only a "cancer marker" but also a defensive mechanism, converting iron to a state for a tight binding to trasferrin. So along with CO2, maintaining good copper levels is important. Ceruloplasmin also directly inhibits lipid autoperoxidation: Ray Peat Interview - KMUD August 20, 2021


A quick note: From this thread/post All We Needed Was B-Complex? and my own experience, coffee depletes vitamin B1.
doesnt copper increase ceruloplasmin, vitamin C decreases it, and vitamin A iirc also increases it?

how does coffee deplete b1?
does it have thiaminases?

ive been curious, what sort of b vitamins need to be supplemented with people who consume milk, orange juice, coconut water, small amounts of liver, and a burger and white bread once a week or so? I imagine b1 is one important one since its lacking in foods... what else... does b1 necessitate also supplementing other b vitamins...
 

Lejeboca

Member
Joined
Jun 19, 2017
Messages
882
doesnt copper increase ceruloplasmin, vitamin C decreases it, and vitamin A iirc also increases it?

You don't want ceruloplasmin to be low. As long as you have enough Vit. D and no Vit. A overload, I don't think, it will skyrocket.
 

Birdie

Member
Joined
Aug 10, 2012
Messages
3,805
Location
USA
doesnt copper increase ceruloplasmin, vitamin C decreases it, and vitamin A iirc also increases it?

how does coffee deplete b1?
does it have thiaminases?

ive been curious, what sort of b vitamins need to be supplemented with people who consume milk, orange juice, coconut water, small amounts of liver, and a burger and white bread once a week or so? I imagine b1 is one important one since its lacking in foods... what else... does b1 necessitate also supplementing other b vitamins...
Re: coffee and thiamine, Dr Costantini says not to drink coffee along with your thiamine dose. He said this is because coffee is acidic.. He also said not to drink oj with thiamine for the same reason. But he said it was fine to have both oj and coffee away from your thiamine dose. Thank goodness.
 

miraddo

Member
Joined
Nov 3, 2020
Messages
61

View: https://www.youtube.com/watch?v=ahDYNNFnFrI


In short, yes coffee does increase the requirements for B1 and may cause a deficiency but that is because it increases the metabolic rate. This same process happens when a hypothyroid person effectively treats their hypothyroidism - they require more nutrients and minerals.

Hypothyroidism and polyunsaturated fats ameliorate dietary nutritional deficiencies because they suppress metabolism and increase reliance on stress hormones like cortisol and estrogen - allowing the organism to "go longer on less."

This may be desirable in short term emergency situations, but is not desirable in the long term as it leads to the "General Adaptation Syndrome" so called by Hans Selye, characterised by accelerated aging and tissue atrophy due to the catabolic effects of these stress hormones.
 

Mr.Bollox

Member
Joined
Mar 16, 2021
Messages
3,368
Re: coffee and thiamine, Dr Costantini says not to drink coffee along with your thiamine dose. He said this is because coffee is acidic.. He also said not to drink oj with thiamine for the same reason. But he said it was fine to have both oj and coffee away from your thiamine dose. Thank goodness.
orange juice contains a lot of thiamine compared to other foods, 0.2mg per cup maybe more.
does the acidity mess with absorption or disintegrate the thiamine?
 

Birdie

Member
Joined
Aug 10, 2012
Messages
3,805
Location
USA
Haidut - Thank you for this writeup. I just copied it for my husband to read. He takes 1000mg thiamin upon awakening. Then, 1000mg again about 1/2 after lunch. He has been doing this a la Dr Costantini for Parkinson's symptoms with great results.

He also takes aspirin and niacin amide, so your article is great reinforcement. He is 86 and people that age are susceptible to... Lots of Stuff. Thanks again.

Oh, things were posted while I wrote. Will take a look.
 

Birdie

Member
Joined
Aug 10, 2012
Messages
3,805
Location
USA
Might be helpful. A lot of questions and answers by Dr Costantini who practiced in Italy but helped Parkinson's Patients worldwide.

HDT Therapy – HIGH-D0SE THIAMINE (HDT) THERAPY for Parkinson's Disease
 

haidut

Member
Thread starter
Joined
Mar 18, 2013
Messages
18,409
Location
USA / Europe
Great! pyrucet + acetozolamide to fight the cancer .
Speaking of pyrucet, have you heard of that Bulgarian lady that cured her cancer with pyrucet ? Is she still in remission ?

Still alive, and no tumor in the lungs, nor any metastases. She was declared terminal in January 2020.
 

haidut

Member
Thread starter
Joined
Mar 18, 2013
Messages
18,409
Location
USA / Europe
Haidut - Thank you for this writeup. I just copied it for my husband to read. He takes 1000mg thiamin upon awakening. Then, 1000mg again about 1/2 after lunch. He has been doing this a la Dr Costantini for Parkinson's symptoms with great results.

He also takes aspirin and niacin amide, so your article is great reinforcement. He is 86 and people that age are susceptible to... Lots of Stuff. Thanks again.

Oh, things were posted while I wrote. Will take a look.

Eating more protein and adding gelatin or BCAA to each meal may help with serotonin depletion and increasing dopamine. The symptoms of Parkinson are mostly due to high serotonin.

If the nutritional measures are not enough then anti-serotonin chemicals like low-dose Benadryl (no more than 50mg daily), 2mg-4mg cypro, or 10mg-20mg famotidine may be able to help.
 

Mauritio

Member
Joined
Feb 26, 2018
Messages
3,820
Still alive, and no tumor in the lungs, nor any metastases. She was declared terminal in January 2020.
Wow . How much did she take again?

I recommended pyrucet over at another forum to someone who's husband has been given a few weeks to live ,but I dont know how receptive she was about that idea.
 

akgrrrl

Member
Joined
Apr 28, 2018
Messages
1,047
Location
Alaska
Several years ago I posted about a study demonstrating that an Achilles heel of cancer had been found - i.e. its addiction to fat (not glucose, as doctors and media continue to mindlessly parrot).

As my readers know from my other posts and various podcasts, excessive fatty acid oxidation (FAO) translates into lower CO2 levels due to the fact that FAO produces less CO2 per unit of substrate (fat or glucose) oxidized, while also producing a lot more reactive oxygen species (ROS). The lower production of CO2 results in relative hypoxia inside the tumor compared to the rest of the organism and that further accelerates tumor growth. Since CO2 and lactic acid are inversely correlated, lower CO2 means higher lactate levels inside the tumor and that means more angiogenesis (lactate is the most potent endogenous stimulator of VEGF) and more tumor growth. A new study below now demonstrates that the low CO2 levels are not just a minor side effect of tumor metabolism (i.e. excessive FAO) but in fact another crucial "defense" mechanism that tumor cells use to grow and metastasize. Namely, the study found that tumors overexpress the enzyme carbonic anhydrase (specifically isoenzyme CAIX), and that inhibiting CAIX fully stopped cancer growth. In fact, the results from the animal experiments were so promising that there is an ongoing Phase I human trial for patients with pancreatic cancer using the same patented CAIX inhibitor (SLC-0111) the study below discusses. So, it does look like combining FAO inhibitors and CA inhibitors may be viable interventions for cancer that may have truly curative effects. Interestingly enough, the study also found that increased expression of CAIX prevented a type of apoptosis process in cancer cells known as ferroptosis. This is an apoptosis is driven by iron accumulation inside the cells, and it may explain the presence of so-called "anemia of chronic disease" (actually a condition of intracellular iron overload) in most cancer patients. It looks like the high ferritin levels (and thus high intracellular levels of iron) seen in this condition are an adaptive response by weakened/sick cells through which they attempt to commit apoptosis and prevent further damage to the organism. However, the lack of CO2 through the overexpression of CAIX prevents that process from achieving its goal, which not only allows the tumor to survive but also further weakens and sickens the patient due to the chronically elevated intracellular levels of iron.

A quick note on the specific drug used in the study. It is a new, patented chemical targeting specifically the CAIX isoenzyme. As such, its long term safety is unknown and the cost of using it will probably be prohibitive for most people unless it is prescribed by a doctor. In addition, there is plenty of evidence that tumors overexpress multiple CA isoenzymes, which means using a drug selective for just isoenzyme IX is likely to be less therapeutic compared to a drug that targets most/all of them. One such broad-spectrum CA inhibitor is acetazolamide, and it is a drug with decades of usage behind its back, lacking major side effects. So, the available evidence suggests that using acetazolamide would be preferable to the new, patented drug used in the study below. Moreover, recent studies have discovered that vitamin B1 (thiamine) is also a powerful CA inhibitor, on multiple CA isoenzymes, with overall effects and potency very similar to acetazolamide.

Thus, using thiamine in comparable daily doses (1,000mg-1,500mg) to acetazolamide should be able to achieve the same effects with even less risk of side effects. Since thiamine also activaves PDH while also inhibiting PDK, further cements its potential as a therapy for cancer. As far as the FAO aspect of cancer metabolism, niacinamide and aspirin are perhaps the best-known and least risky options to limit both availability (through lipolysis) and oxidation of lipids by the "cancer" cells. Multiple animal studies have demonstrated robust anti-cancer effects of niacinamide in HED of 3,000mg-5,000mg daily and aspirin in the same dose range. Since vitamin B1 (thiamine) and niacinamide have synergistic effects, it seems reasonable to propose vitamin B1+B3 combination (in the dose ranges discussed above) as a generic/systemic intervention for cancer regardless of its type/location, and adding aspirin to that combination (even at lower doses than discussed above) would likely potentiate the anti-cancer effects of the vitamin combination even more.

A Phase 1 Study of SLC-0111, a Novel Inhibitor of Carbonic Anhydrase IX, in Patients With Advanced Solid Tumors
http://cancerimmunolres.aacrjournal...019/05/14/2326-6066.CIR-18-0657.full-text.pdf
A Study of SLC-0111 and Gemcitabine for Metastatic Pancreatic Ductal Cancer in Subjects Positive for CAIX - Full Text View - ClinicalTrials.gov
Abstract 2015: Interplay of the pH regulator, carbonic anhydrase IX and the glutamine transporter, ASCT2 in hypoxic tumor microenvironment
Cancer treatment breakthrough: Scientists discover disease's 'Achilles' Heel'

"...Cancer's 'Achilles' Heel' has been identified by scientists. The protein fuels tumours when oxygen levels are low, say scientists. It enables them to adapt and survive - and become more aggressive. The enzyme called CAIX (Carbonic Anhydrase IX) helps diseased cells spread to other organs. It could hold the key to new treatments for the deadliest forms including breast, pancreatic, lungs, bowel and prostate cancers. Study senior author Professor Shoukat Dedhar, of the University of British Columbia in Canada, said: "Cancer cells depend on the CAIX enzyme to survive, which ultimately makes it their 'Achilles' heel.' "By inhibiting its activity, we can effectively stop the cells from growing."

"...As the tumours advance, the blood vessels are unable to provide enough to every part. Over time, the low-oxygen environment leads to a buildup of acid inside the cells. They overcome the stress by unleashing proteins, or enzymes, that neutralise the acidic conditions. The process is behind spread, or metastasis, to other organs - which is what kills patients. Finding a way to prevent it is the 'Holy Grail' of cancer research - turning it into a chronic, rather than fatal, illness. One of the enzymes is CAIX. The Canadian team previously identified a unique compound known as SLC-0111 as a powerful inhibitor. It is currently being tested in clinical trials. Experiments in mice with breast, pancreatic and brain cancers showed its effectiveness. It suppressed tumour growth and spread although there were side effects, with other cellular properties diminished. Now the researchers have demonstrated other weaknesses in CAIX using a technique called genome-wide synthetic lethal screening. The powerful tool systematically deletes one gene at a time to determine if a cancer cell can be killed by eliminating the enzyme. Surprisingly, results pointed to an unexpected role of proteins and processes that control a form of cell death called ferroptosis. It happens when iron builds up and weakens a tumour's metabolism and cell membranes. Dr Dedhar added: "We now know the CAIX enzyme blocks cancer cells from dying as a result of ferroptosis. "Combining inhibitors of CAIX, including SLC-0111, with compounds known to bring about ferroptosis results in catastrophic cell death and debilitates tumour growth.” A large international effort is currently underway to identify drugs that induce ferroptosis. The study is a major step forward in this quest."
Outstanding! Yet another life-giving post from one of our best humans. Respect and gratitude.
 

haidut

Member
Thread starter
Joined
Mar 18, 2013
Messages
18,409
Location
USA / Europe
Wow . How much did she take again?

I recommended pyrucet over at another forum to someone who's husband has been given a few weeks to live ,but I dont know how receptive she was about that idea.

I think she was doing the full 24-25 drops daily dose once daily, in the morning. She also started using vitamin K2 (Kuinone) at a dose of 15mg-20mg daily after the tumor disappeared. Not sure why she added vitamin K, I guess hoping to prevent recurrence...
 

Soren

Member
Joined
Apr 5, 2016
Messages
1,398
Would supplementing say a teaspoon of baking soda in orange juice be a reliable way to increase CO2?
 

Similar threads

Top