A Case For High ROS, Antioxidants Are Useless And Potentially Harmful!

[Obi-wan]

Obi-wan, do you take niacinamide, methylene blue, aspirin, magnesium, thiamine, antibiotics, thyroid etc.? Which supplements do you take, if at all?

Are you not worried about the possibility of permanent damage to your testicles happening with the mixture of the treatments for cancer, high ROS, and the antioxidant restriction?

Aitken RJ, Roman SD. Antioxidant Systems and Oxidative Stress in the Testes. In: Madame Curie Bioscience Database [Internet]. Austin (TX): Landes Bioscience; 2000-2013.
PubReader version: Aitken, R. J., & Roman, S. D. (2008). Antioxidant systems and oxidative stress in the testes. Oxidative medicine and cellular longevity, 1(1), 15-24.

Asadi, N., Bahmani, M., Kheradmand, A., & Rafieian-Kopaei, M. (2017). The Impact of Oxidative Stress on Testicular Function and the Role of Antioxidants in Improving it: A Review. Journal of clinical and diagnostic research : JCDR, 11(5), IE01-IE05.

Turner, T. T., & Lysiak, J. J. (2008). Oxidative Stress: A Common Factor in Testicular Dysfunction. Journal of Andrology, 29(5), 488–498. doi:10.2164/jandrol.108.005132


"In conclusion, the present study demonstrates that severe pathologic changes in the testicular tissue are associated with a high level of lipid peroxidation. These findings suggest that overproduction of ROS may play a role in the mechanism of testicular degeneration associated with infertility."
(Source)

I take aspirin, transdermal magnesium, and transdermal K2. Lots of Pau D'Arco and Pyrucet. The question is can one have high ROS without oxidative stress? Looks like a lot of environmental factors involved in oxidative stress of the testes. PUFA peroxidation seems to be a big stressor. At this point my highest priority is to kill the prostate cancer cells that have advanced into my bones.

 

[Logan-]

I am not knowledgeable in this area, but I think, in moderate to long term, your high ROS and antioxidant restriction plan might lower the energy metabolism and injure the mitochondria which would result in a cancerous environment with inefficient energy metabolism and damage from oxidative stress to your body.

From what I have read about this topic, I have gotten the impression that it is the balance between antioxidants and the oxidation in our bodies that is healthy, regardless of having cancer or not.

I think increasing energy metabolism through supplemental thyroid, MB, niacinamide, high sugar and coconut oil intake, daily carrot salad/well cooked mushrooms, cascara sagrada, progesterone etc. while also not restricting the antioxidants could be helpful.

In 1927, Bernstein and Elias found that rats eating a fat free diet had almost no spontaneous cancer, and many studies since then in animals and people have shown a

close association between polyunsaturated fatty acids and cancer. The polyunsaturated

fatty acids in themselves, and their breakdown products, are excitatory and destabilizing

to normal cells, but by modifying the sensitivity and energy production of cells, they limit

cells' ability to respond to stimulation and destabilizing influences. Although they aren't

essential for wound healing (Porras-Reyes, et al., 1992), they and their metabolites, the

prostaglandins, are very conspicuous in wounds and tumors, and their proportion

generally increases with aging. The prostaglandins are involved in several vicious

cycles, including that with HIF mentioned above. This makes the PUFA and

prostaglandins important to consider in relation to optimizing wound healing, and

decreasing cancerization. Aspirin's protective and therapeutic effects in cancer are

starting to be recognized, but there are several other things that can synergize with

aspirin to reduce the circulation of free fatty acids and their conversion to

prostaglandins. Niacinamide, progesterone, sugar, carbon dioxide, and red light protect

against both free fatty acids and prostaglandins.

Since excitation leads to intracellular alkalinity and swelling, reducing the excitation

seems reasonable, and many things which protect cells against excitation also have

demonstrated anticancer effects. Local anesthetics, antihistamines, and antiinflammatory

substances and some anesthetics such as xenon (Weigt, et al., 2009) are safe. Inhibitory substances related to GABA are being investigated for their ability to stop tumor growth. Simply stopping excessive excitation tends to restore the dominance of oxidative respiration over glycolysis.

To restore the supply of oxygen, sugar, and nutrients, swelling must be stopped.

Hyperosmotic fluids act directly on swollen cells, removing water. Stopping excitation

allows a return to efficient metabolism and reduces the injury potential, allowing the pH

to decrease; with lower pH, the cell releases some of its water.

Increasing carbon dioxide lowers the intracellular pH, as well as inhibiting lactic acid

formation, and restoring the oxidation of glucose increases CO2. Inhibiting carbonic

anhydrase, to allow more CO2 to stay in the cell, contributes to intracellular acidification,

and by systemically increasing carbon dioxide this inhibition has a broad range of

protective anti-excitatory effects. The drug industry is now looking for chemicals that will

specifically inhibit the carbonic anhydrase enzymes that are active in tumors. Existing

carbonic anhydrase inhibitors, such as acetazolamide, will inhibit those enzymes,

without harming other tissues. Aspirin has some effect as an inhibitor of carbonic

anhydrase (Bayram, et al., 2008). Since histamine, serotonin (Vullo, et al., 2007), and

estrogen (Barnett, et al., 2008; Garg, 1975) are carbonic anhydrase activators, their

antagonists would help to acidify the hypoxic cells. Testosterone (Suzuki, et al., 1996)

and progesterone are estrogen antagonists that inhibit carbonic anhydrase.

With aging, cells have less ability to produce energy, and are often more easily

stimulated. The accumulation of polyunsaturated fats is one of the factors that reduce

the ability of mitochondria to produce energy (Zhang, et al., 2006, 2009; Yazbeck, et al.,

1989). Increased estrogen exposure, decreased thyroid hormone, an increased ratio of

iron to copper, and lack of light, are other factors that impair the cytochrome oxidase

enzyme.

The increased intracellular alkalinity and intracellular calcium that result from the

combination of those factors increase the tendency of cells to be overstimulated,

leading to aerobic glycolysis, the cancer metabolism. Improving any part of the system

tends to increase carbon dioxide and decrease lactate, permitting differentiated

functioning.

There are many people currently recommending fish oil (or other highly unsaturated

oils) for preventing or treating cancer, and it has become almost as common to

recommend a sugar free diet, "because sugar feeds cancer." This is often, incorrectly,

said to be the meaning of Warburg's demonstration that cancer cells have a respiratory

defect that causes them to produce lactic acid from glucose even in the presence of

oxygen. Cancer cells use glucose and the amino acid glutamine primarily for synthetic

purposes, and use fats as their energy source;the growth stimulating effect of the

"essential fatty acids" (Sueyoshi and Nagao, 1962a; Holley, et al., 1974) shows that

depriving a tumor of those fats retards its growth. The great energetic inefficiency of the

cancer metabolism, which causes it to produce a large amount of heat and to cause

systemic stress, failure of immunity, and weight loss, is because it synthesizes fat from

glucose and amino acids, and then oxidizes the fat as if it were diabetic.

Estrogen, which is responsible for the fact that women burn fatty acids more easily than

men, is centrally involved in this metabolic inefficiency. When a tissue is exposed to

estrogen, within minutes it takes up water, and begins to synthesize fat, with a tendency

to produce lactic acid at the same time. The alkalizing effect of lactic acid production is

apparently what accounts for the uptake of water. Since it takes longer, at least 30

minutes, to produce a significant amount of new enzymes, these early changes are

explained by the activation of existing enzymes by estrogen.

The transhydrogenases, or the transhydrogenase function of the steroid

dehydrogenases, which shift metabolic energy between glycolytic and oxidative

systems, have been shown to explain these effects of estrogen, but the

transhydrogenases can be activated by many stressors. The biological function of the

transhydrogenases seems to be to allow cells to continue growth and repair processes

in a hypoxic environment. Estrogen can start the process by creating new pathways for

electrons, and will promote processes that are started by something else, and

progesterone is estrogen's natural antagonist, terminating the process.

Recently, a group at Johns Hopkins University (Le, et al., 2012) has been working out

the implications of this ability to change the metabolism under hypoxia: Using an

isotope-labeled amino acid, ". . . glutamine import and metabolism through the TCA

cycle persisted under hypoxia, and glutamine contributed significantly to citrate

carbons. Under glucose deprivation, glutamine-derived fumarate, malate, and

citrate were significantly increased." The implication of this is that if the tumor isn't

supplied with sugar, it will increase the rate at which it consumes the host's proteins.

Forty years ago the work of Shapot and Blinov was showing the same effect, except

that they demonstrated the involvement of the whole organism, especially the liver, in

interaction with the tumor (Blinov and Shapot, 1975).

The alkaline cancer cell surrounds itself by the acid that it emits, and this extracellular

acidity increases the ability of fatty acids to enter the cell (Spector, 1969); cancer cells,

although they are synthesizing fat, also avidly take it up from their environment

(Sueyoshi and Nagao, 1962b). This fat avidity is so extreme that cancer cells in vitro will

eat enough polyunsaturated fat to kill themselves. This has been offered as proof that

fish oil kills cancer. Saturated fats, however, have a calming effect on cancer cells,

inhibiting their aerobic glycolysis (Marchut, et al., 1986) while permitting them to resume

the respiratory production of energy.

The foods that nourish the patient well enough to support healing while permitting

energy reserves to be built up are also the foods that don't interfere with the hormones,

that don't cause spurious excitation of the tissues. The polyunsaturated fats directly

stimulate the stress hormones, activate the excitatory amino acid signals, and directly

excite cells, while the saturated fats have opposite effects, and are anti-inflammatory,

and also don't interfere with mitochondrial function. When we eat more carbohydrate

than can be oxidized, some of it will be turned into saturated fats and omega-9 fats, and

these will support mitochondrial energy production. Carbohydrates in the diet also help

to decrease the mobilization of fatty acids from storage; niacinamide and aspirin support

that effect. Sugars are probably more favorable than starches for the immune system

(Harris, et al., 1999), and failure of the immune system is a common feature of cancer.

Polyunsaturated fats are generally known to suppress the immune system. Foods that

provide generous amounts of sodium, calcium, magnesium, and potassium, help to

minimize stress. Trace minerals and vitamins are important, but can be harmful if used

excessively--iron excess is important to avoid.

Emodin, an anti-inflammatory substance found in cascara sagrada bark and other

plants, is similar to other molecules that have been used for treating cancer, and one of

its effects is to lower HIF: "Consistently, emodin attenuated the expression of

cyclooxygenase 2 (COX-2), VEGF, hypoxia inducible factor 1 alpha (HIF-1!), MMP-1

and MMP-13 at mRNA level in IL-1" and LPS-treated synoviocytes under hypoxia" (Ha,

et al., 2011). MMP-1 and MMP-13 are collagenase enzymes involved in metastasis.

When cells are fully nourished, supplied with protective hormones, and properly

illuminated, their ability to communicate should be able to govern their movements,

preventing--and possibly reversing--metastatic migration.

(Ray Peat, Cancer - Disorder and Energy)

 

[Obi-wan]

I am not knowledgeable in this area, but I think, in moderate to long term, your high ROS and antioxidant restriction plan might lower the energy metabolism and injure the mitochondria which would result in a cancerous environment with inefficient energy metabolism and damage from oxidative stress to your body.

From what I have read about this topic, I have gotten the impression that it is the balance between antioxidants and the oxidation in our bodies that is healthy, regardless of having cancer or not.

I think increasing energy metabolism through supplemental thyroid, MB, niacinamide, high sugar and coconut oil intake, daily carrot salad/well cooked mushrooms, cascara sagrada, progesterone etc. while also not restricting the antioxidants could be helpful.



(Ray Peat, Cancer - Disorder and Energy)

Actually an oxidative state increase energy metabolism. A reductive state decreases energy metabolism. Redox balance is great if you do not have disease or stress. Cancer protects itself from death via antioxidants. Cancer is smart. The mitochondria in cancer is defective and must be eliminated. I have been dealing with it for 2 years+. If you do not eliminate it, it will eliminate you. You would think differently if you had the Grim Reaper following you around...If you read the entire thread you will see that a cell is constantly going back and forth from an oxidative state to a reduction state trying to achieve redox balance. Slight ROS creates signaling and causes differentiation in a normal cell but proliferation in a cancer cell. High ROS will kill a cancer cell but not a normal cell. That's why the chart below makes so much sense

 

[Obi-wan]

Sorry for repeating but keep this in mind



You can easily dampen the acute response with external antioxidants and keep the steady state response high.

I actually think niacinamide is good but it will dampen high ROS which I do not want in my case

 

[Inaut]

@Obi-wan i’m glad to have found your posts on this forum. We need brave people like you who are taking their health in their own hands. I will pray for you and know you will succeed in overcoming this :)

 

[Mito]

Cancer is smart. The mitochondria in cancer is defective and must be eliminated.

That’s right according to Dr. Seyfried, cancer cell generate most of the energy they need to grow from the mitochondria and it comes mostly from the Krebs Cycle. Only about 5% of ATP for cancer cell energy comes from the electron transport chain so the mitochondria is defective.

Dr. Thomas Seyfried proposes that OxPhos is not working well in the mitochondria of cancer cells. He claims that most of the ATP production comes from substrate level phosphorylation (TCA cycle) and the ETC is producing a very small percentage of the total ATP produced in the mitochondria of cancer cells.
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[Inaut]

d-Limonene sensitizes docetaxel-induced cytotoxicity in human prostate cancer cells: Generation of reactive oxygen species and induction of apoptosis

Thoughts ?

 

[Obi-wan]

That’s right according to Dr. Seyfried, cancer cell generate most of the energy they need to grow from the mitochondria and it comes mostly from the Krebs Cycle. Only about 5% of ATP for cancer cell energy comes from the electron transport chain so the mitochondria is defective.

It looks like Succinic acid is producing most of the ATP along with Lactic Acid producing ATP in the Cytosol. If the ETC is not working properly (Complex 1, 2,3, or 4) then more ROS should be generated but the cancer cell protects itself with GSH. Chemo will produce even more ROS. Pyrucet should lower the GSH/GSSG ratio. Pau D 'Arco should help with apoptosis. The question I have would using MB (methyl blue) to help generate more ATP from the ETC be beneficial? Through prior experimentation with Succinic acid and Malic acid supplementation I did not feel I got a good result...

 

[magnesiumania]

How can I consume more ROS? :)

Whole food vitamin C. The ascorbic acid part is responsible for oxidation. Its a pro-oxidant. Tyrosinase, P, K and J factors are the antioxidant part of vitamin C.

 

[Obi-wan]

d-Limonene sensitizes docetaxel-induced cytotoxicity in human prostate cancer cells: Generation of reactive oxygen species and induction of apoptosis

Thoughts ?

First of all THANK YOU @Inaut for your kind thoughts and prayers. It means a lot to me! Second this study is a great find!

Docetaxel (Taxotere) is the chemo that I am currently on.

"Docetaxel, which belongs to the class of chemotherapeutics known as taxanes, is a semisynthetic analog of paclitaxel. Docetaxel's main therapeutic mode of action is the suppression of microtubule dynamic assembly and disassembly, rather than microtubule bundling, leading to apoptosis, and the blocking of Bcl-2 expression.[26,27] "

"Cells have an elaborate defense system for protection against free radical-induced damage that involves generation of GSH, cysteine and antioxidant enzymes, including GSH peroxidase, superoxide dismutase and catalase.[32] Further analysis demonstrated H2O2 as a major cytotoxic molecule of ROS in docetaxel-induced cell death. H2O2 is known as a cell-death mediator in diverse kinds of cell death including that induced by tumor necrosis factor-α, UV irradiation, and other anticancer drugs.[33–35] Docetaxel alone induced certain amounts of ROS with cell death, whereas addition of d-limonene generated a greater amount of ROS, followed by more cell death. At both treated and nontreated phases, the intracellular ROS levels correlated well with the sensitivity to the treatment with docetaxel plus d-limonene. The exposure of docetaxel with d-limonene makes H2O2-scavenging systems break down more rapidly, which is typically observed as the decrease of GSH amount. The differential effects of combined treatment on the prostate cancer cells and on normal prostate epithelial cells may be due to the expression of more effective endogenous antioxidant mechanisms in the normal cells than in the malignant ones. (this suggests that normal cells have a higher antioxidant mechanism than malignant ones) It has been reported that docetaxel down regulates several genes for cell proliferation, mitotic spindle formation, transcription factors, and oncogenesis, and up regulates several other genes related to induction of apoptosis and cell cycle arrest in prostate cancer cells, suggesting pleiotropic effects of docetaxel on prostate cancer cells.[36–38]"

"We speculated that docetaxel together with d-limonene might cause GSH depletion to exacerbate oxidative stress. We therefore determined the effect of a combination treatment on intracellular levels of GSH, and the results are shown in Figure 2D. Treatment of DU-145 cells with docetaxel together with d-limonene for 6, 12 and 24 h caused a rapid decline in the level of GSH by about 67.3, 77.3 and 86.4%, respectively, compared with control at zero-time. Docetaxel treatment alone caused a decrease in the level of GSH by about 54.5, 72.7 and 76.4% for the same time-points. These observations led us to conclude that ROS generation probably involves both a non-mitochondrial mechanism and a mitochondria-mediated phenomenon."

"In this study, we determined that non-toxic low doses of d-limonene in the combination treatments with docetaxel have shown a significantly enhanced apoptotic effect on hormone-refractory DU-145 prostate cancer cells. This study showed that combination treatment of prostate cancer cells with docetaxel and d-limonene can overcome the resistance of prostate cancer cells to apoptosis and that the generation of ROS, activation of caspase-9 and caspase-3 may play a role in enhanced cytotoxicity.

Looks like D-limonene is a great find!

 

[Obi-wan]

d-Limonene sensitizes docetaxel-induced cytotoxicity in human prostate cancer cells: Generation of reactive oxygen species and induction of apoptosis

Thoughts ?

See https://www.amazon.com/Wellness-Res...&s=gateway&sr=8-1-spons&psc=1#customerReviews

 

[Inaut]

See https://www.amazon.com/Wellness-Res...&s=gateway&sr=8-1-spons&psc=1#customerReviews

Pretty good price. I’m taking Jarrow Formulas D Limonen from iHerb. Only 500mgs though per cap....

When I’m done with my stock I’m going to buy the 32 oz bottle off eBay from Blubonic Labs.

I really like this supplement as I have had liver/gallbladder problems for quite some time and it’s quite effective for detoxification—-including estrogen (not to mention effects on gaba)

Hoping it helps in your arsenal Obi

 

[Mito]

If the ETC is not working properly (Complex 1, 2,3, or 4) then more ROS should be generated but the cancer cell protects itself with GSH. Chemo will produce even more ROS.

Dr. Seyfried tells us that only 5% of the ATP generated by cancer cells come from the electron transport chain (75% from TCA cycle & 20% outside of the mitochondria via glycolysis). It appears that the ATP from the ETC comes mostly from Complex I (maybe this means it’s only complexes II, III, and IV that are defective).

“Recent evidence highlights that the cancer cell energy requirements vary greatly from normal cells and that cancer cells exhibit different metabolic phenotypes with variable participation of both glycolysis and oxidative phosphorylation. NADH–ubiquinone oxidoreductase (Complex I) is the largest complex of the mitochondrial electron transport chain and contributes about 40% of the proton motive force required for mitochondrial ATP synthesis. In addition, Complex I plays an essential role in biosynthesis and redox control during proliferation, resistance to cell death, and metastasis of cancer cells. Although knowledge about the structure and assembly of Complex I is increasing, information about the role of Complex I subunits in tumorigenesis is scarce and contradictory. Several small molecule inhibitors of Complex I have been described as selective anticancer agents; however, pharmacologic and genetic interventions on Complex I have also shown pro-tumorigenic actions, involving different cellular signaling. Here, we discuss the role of Complex I in tumorigenesis, focusing on the specific participation of Complex I subunits in proliferation and metastasis of cancer cells.“
The Mitochondrial Complex(I)ty of Cancer

 

[Obi-wan]

Dr. Seyfried tells us that only 5% of the ATP generated by cancer cells come from the electron transport chain (75% from TCA cycle & 20% outside of the mitochondria via glycolysis). It appears that the ATP from the ETC comes mostly from Complex I (maybe this means it’s only complexes II, III, and IV that are defective).

“Recent evidence highlights that the cancer cell energy requirements vary greatly from normal cells and that cancer cells exhibit different metabolic phenotypes with variable participation of both glycolysis and oxidative phosphorylation. NADH–ubiquinone oxidoreductase (Complex I) is the largest complex of the mitochondrial electron transport chain and contributes about 40% of the proton motive force required for mitochondrial ATP synthesis. In addition, Complex I plays an essential role in biosynthesis and redox control during proliferation, resistance to cell death, and metastasis of cancer cells. Although knowledge about the structure and assembly of Complex I is increasing, information about the role of Complex I subunits in tumorigenesis is scarce and contradictory. Several small molecule inhibitors of Complex I have been described as selective anticancer agents; however, pharmacologic and genetic interventions on Complex I have also shown pro-tumorigenic actions, involving different cellular signaling. Here, we discuss the role of Complex I in tumorigenesis, focusing on the specific participation of Complex I subunits in proliferation and metastasis of cancer cells.“
The Mitochondrial Complex(I)ty of Cancer

Interesting article that reviews the complexity of Complex 1 and the pros and cons of Complex 1 inhibition which I would disagree with since it also controls redox. In the article I cited earlier it was shown that Docetaxel plus D-limonene shows a greater increase in ROS and greater depletion of GSH resulting in cell death. Maybe Complex 1 is needed to accomplish this. The big question is increasing OXPHOS a good thing or bad thing in killing cancer cells?

 

[Obi-wan]

If Complex 2, 3, 4 are defective how about an alternative mitochondrial electron transfer : Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers: Methylene blue connects the dots. - PubMed - NCBI. Methylene blue connects the dots:

" cancers, including glioblastoma, have increased glucose uptake and rely on aerobic glycolysis for energy metabolism. The switch of high efficient oxidative phosphorylation to low efficient aerobic glycolysis pathway (Warburg effect) provides macromolecule for biosynthesis and proliferation. Current research indicates that methylene blue, a century old drug, can receive electron from NADH in the presence of complex I and donates it to cytochrome c, providing an alternative electron transfer pathway. Methylene blue increases oxygen consumption, decrease glycolysis, and increases glucose uptake in vitro. Methylene blue enhances glucose uptake and regional cerebral blood flow in rats upon acute treatment. In addition, methylene blue provides protective effect in neuron and astrocyte against various insults in vitro and in rodent models of Alzheimer's, Parkinson's, and Huntington's disease. In glioblastoma cells, methylene blue reverses Warburg effect by enhancing mitochondrial oxidative phosphorylation, arrests glioma cell cycle at s-phase, and inhibits glioma cell proliferation. Accordingly, methylene blue activates AMP-activated protein kinase, inhibits downstream acetyl-coA carboxylase and cyclin-dependent kinases. In summary, there is accumulating evidence providing a proof of concept that enhancement of mitochondrial oxidative phosphorylation via alternative mitochondrial electron transfer may offer protective action against neurodegenerative diseases and inhibit cancers proliferation.

 

[Logan-]

More:

L. Tretter, G. Horvath, A. Hölgyesi, F. Essek, V. Adam-Vizi, Enhanced hydrogen peroxide generation accompanies the beneficial bioenergetic effects of methylene blue in isolated brain mitochondria, Free Radical Biology and Medicine, Redirecting

Komlodi,T.,Tretter,L.,Methylene blue stimulates substrate-level phosphorylation catalysed by succinyl-CoA ligase in the citric acid cycle, Neuropharmacology (2017), Redirecting

 

[Obi-wan]

More:

L. Tretter, G. Horvath, A. Hölgyesi, F. Essek, V. Adam-Vizi, Enhanced hydrogen peroxide generation accompanies the beneficial bioenergetic effects of methylene blue in isolated brain mitochondria, Free Radical Biology and Medicine, Redirecting

Komlodi,T.,Tretter,L.,Methylene blue stimulates substrate-level phosphorylation catalysed by succinyl-CoA ligase in the citric acid cycle, Neuropharmacology (2017), Redirecting

Looks like MB generates more H2O2 which is higher ROS

"In summary, our results demonstrate significant bioenergetic improvement by MB in isolated respiration-impaired mitochondria, in particular a modest, but significant increase in ATP synthesis and a restoration of ΔΨm, which could be important in the beneficial in vivo neuroprotective and cognitive-enhancing action of MB. However, the highly elevated H2O2 generation observed in our in vitro study has to be considered in the estimation of the overall oxidative state in vivo in mitochondria under treatment with MB.

 

[Inaut]

why dont we like ozone as an effective oxidant again? I had my mom drink 2 cups of ozonated water every morning after chemo for her breast cancer ---in addition to pau d'arco tea (as she would not take supplements --discouraged by the oncologist..) Not sure if it helped but my hopes (prayer) was that it made the chemo slightly more effective while stimulating her immune system to step up and deal with some of the toxic chemicals.....It took her a while to lose her hair but it has grown back and she looks great. Hoping she can live cancer/care free from here on out :) Easier said then done for somebody with the monkey on the back but it's about mindstate, intention and prayer (also a form of intention)... JMO

 

[Obi-wan]

Interesting article: NAD+ in Cancer Prevention and Treatment: Pros and Cons | SciTechnol.

"NAD+ has multiple and diverse cellular functions. Changes in NAD+ metabolism have been associated with several pathologies, including cancer. In the hypothesis presented NAD+ is shown as an important factor related to cancer formation and prevention. It is not only the NAD+ as the cofactor in redox reactions that has important role in cancer biology, but also the NAD+ as the substrate for sirtuins and PARP signaling. How exactly NAD+ metabolism is regulated in the human cancer cells still remains to be fully elucidated as well as different metabolic changes that can take place following pharmacological supplementation with NAD+ precursors and NAD+ inhibitors. NAD+ levels can be influenced with sport activity, caloric restriction and ingestion of NAD+ precursors. PARP and sirtuin inhibitors are used also as anti-cancer agents. Namely, by decreasing intracellular PARP and sirtuin’s level apoptosis can be influenced. Additionally, cancer preventive strategies presented could have dichotomous roles in the later stages of the disease (once tumor has developed and progressed), namely they could be tumor preventive for healthy (non-mutated cells) or tumor suppressing at early stages of tumorigenesis and could be tumor promoting later on. Increased amounts of NAD+ may contribute to the development and/or progression of cancer once the cells already have cancer-like properties."

The article concludes that increasing NAD+ is great for cancer prevention but might not be good once cancer is formed. I am starting to think that treating cancer is the opposite mindset of preventing cancer. Cancer is a mitochondria defect and per @Mito uses Complex 1 of the ETC only for biosynthesis and redox control during proliferation, resistance to cell death, and metastasis of cancer cells. Maybe increasing OXPHOS is not the answer and the answer lies in keeping the redox state in a highly oxidative state, activating P53 and creating cancer cell death.

 

[Taotatoes]

Following.