haidut

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A fascinating study, which highlights once again not only the role of one of the "youth" steroids in human health but also demonstrates that the protective/therapeutic mechanisms of DHEA against cancer are due to increase in metabolism and ROS generation. The primary restrictive mechanism on ROS generation in humans is the enzyme glucose-6-phosphatase dehydrogenase.
Glucose-6-phosphate dehydrogenase - Wikipedia

Excess activity of this enzyme strongly dampens ROS levels, while excessive inhibition may lead to hemolytic anemia. Androgens are well-known inhibitors of the enzyme, and in higher doses are known to lead to hemolytic anemia. Other inhibitors include progesterone, long chain saturated fatty acids (SFA) and a redox state in favor of oxidation. Activators of G6PD include estrogen, hypoxia (HIF-1) and redox state in favor of reduction. It just so happens that DHEA is one of the most potent inhibitors and perhaps the primary endogenous inhibitor after puberty.
The authors describe the almost perfectly negative correlation between DHEA levels and increase in cancer incidence in both humans and animals. They also openly state that the current direction of efforts for cancer cure are likely dead-wrong, that cancer has little to do with mutations, and that DHEA may just be the simple, master "kill switch" for most cancers that keeps young/healthy people so resilient to this disease. A progesterone/DHEA or pregnenolone/DHEA combination likely potentiates the anti-cancer effects, considering the role of pregnenolone, progesterone and other androgens as G6PD inhibitors.


Detection of a novel, primate-specific ‘kill switch’ tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53 : Endocrine-Related Cancer

"...The activation of TP53 is well known to exert tumor suppressive effects. We have detected a primate-specific adrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has been inactivated. DHEA is an uncompetitive inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell. Uncompetitive inhibition is otherwise unknown in natural systems because it becomes irreversible in the presence of high concentrations of substrate and inhibitor. In addition to primate-specific circulating DHEAS, a unique, primate-specific sequence motif that disables an activating regulatory site in the glucose-6-phosphatase (G6PC) promoter was also required to enable function of this previously unrecognized tumor suppression system. In human somatic cells, loss of TP53 thus triggers activation of DHEAS transport proteins and steroid sulfatase, which converts circulating DHEAS into intracellular DHEA, and hexokinase which increases glucose-6-phosphate substrate concentration. The triggering of these enzymes in the TP53-affected cell combines with the primate-specific G6PC promoter sequence motif that enables G6P substrate accumulation, driving uncompetitive inhibition of G6PD to irreversibility and ROS-mediated cell death. By this catastrophic ‘kill switch’ mechanism, TP53 mutations are effectively prevented from initiating tumorigenesis in the somatic cells of humans, the primate with the highest peak levels of circulating DHEAS. TP53 mutations in human tumors therefore represent fossils of kill switch failure resulting from an age-related decline in circulating DHEAS, a potentially reversible artifact of hominid evolution."

"...The p53 gene was discovered almost 40 years ago (Kress et al. 1979, Lane & Crawford 1979, Linzer & Levine 1979), and its role as a major tumor suppressor was identified a decade later (Baker et al. 1989, Takahashi et al. 1989). The p53-knockout mouse model of human cancer has been a staple of cancer research for some 26 years (Donehower et al. 1992). The depth of infiltration of this model into the fabric of human cancer research is demonstrated by the fact that it has been accepted by the FDA as a preclinical model for human drug development for more than 20 years (FDA 1997). The use of this model system over this long period of time has created a paradigm in which mutations in p53 are considered to be linear initiators of carcinogenesis with virtually universal application independent of species, such that results in one species, e.g., the mouse, are thought to accurately translate to another, e.g., the human. Yet, new research in non-murine species (dog, elephant, naked mole rat, etc.) suggests that while p53 may be a universal sensor of mutagenic insult, many animals, including humans, adopt species-specific solutions to such insult and those species-specific solutions triggered by p53 inactivation appear frequently to converge mechanistically upon lethal inhibition of G6PD. These observations suggest that the focus of nature’s anti-cancer effort is the singularity. In this way, nature suppresses cancer at its most vulnerable point, at the level of the initial, potentially transformed cell, before it has initiated the explosion of diversification that has made clinical cancer incurable up to now. This appears to be how the elephant suppresses cancer throughout its long life, with its species-specific method to enhance its p53-mediated kill switch system. It also appears to be how chimpanzees and other great apes suppress cancer (McClure 1973, Hill et al. 2001, Brown et al. 2009), capitalizing upon primate-specific circulating DHEAS and G6PC promoter motifs, as well as the uncompetitive G6PD inhibition kinetics of DHEA. We believe that the species-specific DHEAS-mediated kill switch is fundamental to cancer suppression in humans."

"...Such data do not encourage a ‘stay the course’ approach to cancer research, but rather suggest that something is fundamentally wrong with the paradigms that have been guiding this endeavor for at least three decades. The unanticipated existence of an essentially human-specific adrenal androgen-mediated kill switch tumor suppression mechanism clearly undermines much of the research that has been performed ex vivo, in vivo and in vitro over this long period of time:"

"...The slow, very meager progress in prolonging cancer survival, the fact that such survival appears to be at an asymptotic boundary beyond which any further progress may be impossible, and the extreme, accelerating and clearly unsustainable costs of new cancer drugs that only minimally extend life (Sidduqui & Rajkumar 2012, Cohen 2017, Davis et al. 2017, Jackson & Nahata 2017, Prasad & Mailankody 2017, Carrera et al. 2018, Dranitsaris et al. 2018), all indicate the necessity for reappraisal of the current paradigm in which developed tumors are the target for virtually all of our anti-cancer research efforts. It may be time to redirect our labors and research expenditures toward understanding the singularity, the apparent focus of nature’s major effort at tumor suppression. If tumor complexity has been the Gordian knot of the cancer problem, preventing real progress in cancer treatment, then reactivating a kill switch made latent by an age-related decline in DHEAS may represent Alexander’s blade. The adrenal androgen-mediated kill switch tumor suppression system has the singularity as its target, and its evolutionary programming for a prehistoric, not a modern life span, may be responsible for the anomaly of an exponentially increasing rate of cancer with increasing age in our species. Singularities occurring in aging modern humans experience a diminishing capacity to undergo irreversible G6PD inhibition because of the dramatically declining levels of circulating DHEAS and consequent inability to trigger the kill switch mechanism. While this was not problematic for our ancestors who rarely reached the age of 30 years, it is problematic for modern humans who regularly live into and beyond their ninth decade. The life-long low, flat cancer risk observed in other long-lived animals that employ parallel, but life-long species-specific tumor suppression strategies, suggests that a similarly life-long low, flat cancer risk may be achievable in humans; that is, there appears to be no a priori reason, such as accumulated genomic damage, that makes an age-related increase in human cancer unavoidable. Rather, an approximately 4% lifetime cancer risk may be the norm for all species, including Homo sapiens. The lesson from other long-lived species appears to be that kill switch mechanisms that function throughout life extinguish almost all potentially tumorigenic damage at the level of the singularity. If pharmacological maintenance of DHEAS at peak levels establishes life-long functionality of the adrenal androgen-mediated kill switch, humans might join the majority of the animal kingdom in which death from cancer is a rare event and has little to do with advancing age. Determining what the true background risk of cancer is in the presence of such a fully functional, life-long adrenal androgen-mediated kill switch tumor suppression system should therefore be a primary goal of our species."
 

Dobbler

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I've always though that ROS is a very bad thing that is basicly other name for inflammation. I've read from many places that low metabolism is caused by high ROS aka inflammation. Hmm...

From wikipedia:

In a biological context, ROS are formed as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis.[3] However, during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically.[3] This may result in significant damage to cell structures. Cumulatively, this is known as oxidative stress. The production of ROS is strongly influenced by stress factor responses in plants, these factors that increase ROS production include, drought, salinity, chilling, nutrient deficiency, metal toxicity and UV-B radiation. ROS are also generated by exogenous sources such as ionizing radiation.[4]
 

Obi-wan

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Glucose-6-phosphate dehydrogenase (G6PD or G6PDH) (EC 1.1.1.49) is a cytosolic enzyme that catalyzes the chemical reaction

D-glucose 6-phosphate + NADP+ ⇌ 6-phospho-D-glucono-1,5-lactone + NADPH + H+

G6PD is negatively regulated by acetylation on lysine 403 (Lys403), an evolutionarily conserved residue. The K403 acetylated G6PD is incapable of forming active dimers and displays a complete loss of activity. Mechanistically, acetylating Lys304 sterically hinders the NADP+ from entering the NADP+structural site, which reduces the stability of the enzyme. Cells sense extracellular oxidative stimuli to decrease G6PD acetylation in a SIRT2-dependent manner. The SIRT2-mediated deacetylation and activation of G6PD stimulates pentose phosphate pathway to supply cytosolic NADPH to counteract oxidative damage and protect mouse erythrocytes.[15]

Acetylation refers to the process of introducing an acetyl group (resulting in an acetoxy group) into a compound, namely the substitution of an acetyl group for an active hydrogen atom. A reaction involving the replacement of the hydrogen atom of a hydroxyl group with an acetyl group (CH3 CO) yields a specific ester, the acetate

Proteins are typically acetylated on lysine residues and this reaction relies on acetyl-coenzyme A as the acetyl group donor.

-From Wikipedia

Back to Acetyl CoA...which is produced by an acetate and CoA

Apple Cider Vinegar/Baking soda is an acetate

"the protective/therapeutic mechanisms of DHEA against cancer are due to increase in metabolism and ROS generation."

"a redox state in favor of oxidation"...
which occurs when Acetyl CoA enters the Kreds Cycle and produces NADH which turns the ETC to produce ADP/ATP...and ROS

Pyruvate is supposed to produce acetyl CoA via PDH but sometimes PDK prevents it...

 

haidut

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I've always though that ROS is a very bad thing that is basicly other name for inflammation. I've read from many places that low metabolism is caused by high ROS aka inflammation. Hmm...

From wikipedia:

In a biological context, ROS are formed as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis.[3] However, during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically.[3] This may result in significant damage to cell structures. Cumulatively, this is known as oxidative stress. The production of ROS is strongly influenced by stress factor responses in plants, these factors that increase ROS production include, drought, salinity, chilling, nutrient deficiency, metal toxicity and UV-B radiation. ROS are also generated by exogenous sources such as ionizing radiation.[4]

Not really. ROS levels correlate very well with mitochondrial function. Inflammation is primarily driven by PUFA and endotoxin. I do not see anything in that quote you provided that ROS can cause low metabolism. All it says is that some exogenous stresses like radiation can increase ROS. That is why radiation and chemotherapy are used for cancer - i.e they increase ROS but destroy the entire organism in the process due to their systemic toxicity. The ROS is not the villain.
If cancer cells have very LOW levels of ROS and are known to have LOW mitochondrial metabolism then high ROS and low metabolism do not really go hand in hand, do they?
 

Hans

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Not really. ROS levels correlate very well with mitochondrial function. Inflammation is primarily driven by PUFA and endotoxin. I do not see anything in that quote you provided that ROS can cause low metabolism. All it says is that some exogenous stresses like radiation can increase ROS. That is why radiation and chemotherapy are used for cancer - i.e they increase ROS but destroy the entire organism in the process due to their systemic toxicity. The ROS is not the villain.
If cancer cells have very LOW levels of ROS and are known to have LOW mitochondrial metabolism then high ROS and low metabolism do not really go hand in hand, do they?
Would this make MCT oil an inferior fat source compared to other saturated fat sources, because it generates less ROS?
 

haidut

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Haidut, is the connection between dhea and dhea-s that clear?

The DHEA-S is just the long term storage form and gets metabolized back to DHEA when and where it is needed. It is hard to have normal DHEA-S but low DHEA unless there is a deficiency of the sulfatase enzymes, which is a very very rare condition.
Multiple sulfatase deficiency - Wikipedia

The study itself uses DHEA-S almost interchangeably with DHEA. They specifically say the high DHEA-S levels is what protects humans from cancer. Look at the second sentence from the top colored in red. Also, when you use DHEA transdermally, a good portion of it is absorbed unchanged (as plain DHEA).

@LeeLemonoil
 
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haidut

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Would this make MCT oil an inferior fat source compared to other saturated fat sources, because it generates less ROS?

MCT are metabolized almost like sugar and do not need special carrier to get to the mitochondria, unlike the longer chain fats which need carnitine. Look at Table 1 of this link.
https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2014/06/Parrish-February-17.pdf

So, in very precarious states it may be preferable as food due to its use of metabolism. The goal is not to generate as much ROS as possible but to raise the very low levels of ROS in cancer cells back to normal by restoring mitochondrial function. MCT and sugar should be able to do that.
 

haidut

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Glucose-6-phosphate dehydrogenase (G6PD or G6PDH) (EC 1.1.1.49) is a cytosolic enzyme that catalyzes the chemical reaction

D-glucose 6-phosphate + NADP+ ⇌ 6-phospho-D-glucono-1,5-lactone + NADPH + H+

G6PD is negatively regulated by acetylation on lysine 403 (Lys403), an evolutionarily conserved residue. The K403 acetylated G6PD is incapable of forming active dimers and displays a complete loss of activity. Mechanistically, acetylating Lys304 sterically hinders the NADP+ from entering the NADP+structural site, which reduces the stability of the enzyme. Cells sense extracellular oxidative stimuli to decrease G6PD acetylation in a SIRT2-dependent manner. The SIRT2-mediated deacetylation and activation of G6PD stimulates pentose phosphate pathway to supply cytosolic NADPH to counteract oxidative damage and protect mouse erythrocytes.[15]

Acetylation refers to the process of introducing an acetyl group (resulting in an acetoxy group) into a compound, namely the substitution of an acetyl group for an active hydrogen atom. A reaction involving the replacement of the hydrogen atom of a hydroxyl group with an acetyl group (CH3 CO) yields a specific ester, the acetate

Proteins are typically acetylated on lysine residues and this reaction relies on acetyl-coenzyme A as the acetyl group donor.

-From Wikipedia

Back to Acetyl CoA...which is produced by an acetate and CoA

Apple Cider Vinegar/Baking soda is an acetate

"the protective/therapeutic mechanisms of DHEA against cancer are due to increase in metabolism and ROS generation."

"a redox state in favor of oxidation"...
which occurs when Acetyl CoA enters the Kreds Cycle and produces NADH which turns the ETC to produce ADP/ATP...and ROS

Pyruvate is supposed to produce acetyl CoA via PDH but sometimes PDK prevents it...

Thanks. Another good take from this quote is that sirtuins activate G6PD, which is not surprising given the role of sirtuins in cancer. So, conversely, inhibiting sirtuins would inhibint G6PD. Another solid point for niacinamide, the most potent sirtuin inhibitor in clinical use.
 

LeeLemonoil

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Thanks Haidut for your explainations here.
I‘ve seen serum-measurements from people with either mental or other inflammatory diseases. DHEA-S was always lower than in controls while DHEA was higher than in healthy controls.
Could it be that the diseased organisms desulfatizate their DHEA-S reserves so that DHEA can perform its protective functions?
Theoretically, once the pathology subsides, DHEA would then be restored as its sulfate, that’s where supplementation of DHEA would come in helpful.
Still, I don’t think it can be excluded that DHEA-S on its own has important physiological functions in that it might interact differently with receptors/proteins/cells and membranes due to its different lipophilicity and charge than DHEA
 

Hans

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MCT are metabolized almost like sugar and do not need special carrier to get to the mitochondria, unlike the longer chain fats which need carnitine. Look at Table 1 of this link.
https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2014/06/Parrish-February-17.pdf

So, in very precarious states it may be preferable as food due to its use of metabolism. The goal is not to generate as much ROS as possible but to raise the very low levels of ROS in cancer cells back to normal by restoring mitochondrial function. MCT and sugar should be able to do that.
Thanks. Yes I'm aware of most of its benefits. Was just wondering in terms of ROS generation.
 

LeeLemonoil

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It‘s really an intriguing paper. I‘m very open to phylogenetic extrapolations, they provide new approaches to many a „gordian knot“. The paper though is by one author only so I think he might be an original, rouge thinker and that doesn’t bode well for the impact this paper will have. Especially when this really means that routine supplementation of small doses DHEA for people about ~40/50 upwards might slash cancer risks manifold. Oh the profits....
If anyone can forward this to Dr. Peat himself and get his reactions to us that would be invaluable.
 

haidut

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Thanks. Yes I'm aware of most of its benefits. Was just wondering in terms of ROS generation.

I think it may generate less ROS than LCFT but is probably more beneficial for the mitochondria than the LCFT, especially in cases where mitochondria is damaged by things like radiation or chemotherapy.
 

haidut

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I don't know if the author of that book you posted earlier is the same guy, but the patent does seem to be by him. Here are his other publications.
Error encountered - PubMed - NCBI

Btw, he has some remarkable results with high-dose DHEA among those publications on Pubmed. Many dogs with metastatic cancer surviving for years or getting complete remission without much other treatment.
 

Wagner83

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The DHEA-S is just the long term storage form and gets metabolized back to DHEA when and where it is needed. It is hard to have normal DHEA-S but low DHEA unless there is a deficiency of the sulfatase enzymes, which is a very very rare condition.
Multiple sulfatase deficiency - Wikipedia

The study itself uses DHEA-S almost interchangeably with DHEA. They specifically say the high DHEA-S levels is what protects humans from cancer. Look at the second sentence from the top colored in red. Also, when you use DHEA transdermally, a good portion of it is absorbed unchanged (as plain DHEA).

@LeeLemonoil
Do you have any links on dhea-s being a mere storage form of dhea?
It's good to keep in mind that Peat seems to favor pregnenolone and progesterone on the account of higher levels of dhea found in alzheimer patients' brains. People on this forum often have a hard time with it. A knowledgeable member of this forum mentioned in a pm that this guy, a dhea-for-longevity advocate, didn't make it to old age Dr. William Regelson .
 

haidut

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Do you have any links on dhea-s being a mere storage form of dhea?
It's good to keep in mind that Peat seems to favor pregnenolone and progesterone on the account of higher levels of dhea found in alzheimer patients' brains. People on this forum often have a hard time with it. A knowledgeable member of this forum mentioned in a pm that this guy, a dhea-for-longevity advocate, didn't make it to old age Dr. William Regelson .

This was several years ago. Now he routinely recommends DHEA (especially in combination with progesterone), but cautions the DHEA has to be in lower doses to prevent estrogen elevation. For him a ratio of 2:1 for progesterone:DHEA apparently works best. For many people even massive pregnenolone doses do not raise DHEA because of "naturally" elevated cortisol/estrogen with age, both of which block 17,20-lyase - the crucial enzyme for DHEA synthesis.
The comment on DHEA and Alzheimer needs to be followed up with him IMO. Many subsequent studies found lower DHEA levels in Alzheimer patients and animal models show protective effect.
Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease. - PubMed - NCBI
A Potential Blood Test for Alzheimer’s Disease
Testosterone and DHEA are Directly Involved in Alzheimer’s Disease | Journal of Alzheimer's Disease

Direct intervention trials found mild benefit, but definitely no deterioration as a result of DHEA.
DHEA for Alzheimer’s disease
 
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