Cancer Is A State Of Chronic Stress With Elevated Lipolysis And Ketogenesis

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
I am posting this study because it invalidates one of the central dogmas of modern oncology - i.e. that cancer is a localized, organ-specific disease that is best handled by attacking/destroying/removing the affected organ/tissue. Most doctors would flatly deny/reject the statement that a cancer patient is under chronic systemic stress as a result of their disease, and as such they see no problem with subjecting the patient to even more systemic stress as a result of radiation, chemotherapy and surgery.
This study shows that all organisms with a tumor burden experience increased lipolysis and ketogenesis. Mainstream medicine recognizes these metabolic abnormalities in cancer patients but claims that they are the result of poor appetite and anorexia in the patient. This study found that it is the tumor presence and not dietary abnormalities that change the patient's metabolism from carbohydrates to fatty acids. Perhaps more importantly, just as Peat has said, the brain plays a central role in directing this change of metabolic fuel preference. Given the recent studies I published that blocking fat metabolism can treat cancer, I think it confirms once again one of Peat's main points - any prolonged stress skews metabolism in favor of fatty acids, and conversely elevated lypolysis/ketogenesis/NEFA are a sign of systemic stress and not something that is desirable to maintain long term.
Just as an additional example, diverse conditions like depression, diabetes, schizphrenia, dementia/Alzheimer, Parkinson, ALS, liver disease, kidney disease, infection, etc are all also characterized by increased fatty acid level and metabolism and consequently reduced glucose oxidation. It is really all one disease under different names, and it comes down to blockade of proper oxidation of glucose. So, anything that improves glucose oxidation should be therapeutic regardless of the specific named "condition" a person has been diagnosed with.

[Activation of lipolysis and ketogenesis in tumor-bearing animals as a reflection of chronic stress states]. - PubMed - NCBI
"...In order to elucidate the peculiarities of brain metabolism in tumour-bearing organisms, the arterio-venous (A-V) content of glucose, acetoacetate (Ac-Ac), beta-hydroxybutyrate (beta-HB) and non-esterified fatty acids (NEFA) in growing Zajdela ascite hepatoma (ZAH) and solid hepatoma 27 (H-27) was compared. Analysis of metabolic patterns of healthy, starving and fed recipients (ZAH and H-27) revealed the inadequacy of the concepts on anorexia as being the cause of carbohydrate-lipid metabolic disturbances. In tumour-bearing organisms lipolysis and ketogenesis reflect the tumour-induced chronic stress. Absorption of beta-HB and release of Ac-Ac by brain were observed at all stages of malignant growth. This is probably due to a partial switch-over of brain metabolism to non-carbohydrate energy sources. Besides, certain stages of tumour growth are associated with active assimilation of NEFA by brain. A correlation between the A-V difference with respect to glucose and Ac-Ac as well as between the glucose and NEFA contents was established. It was assumed that the A-V difference in glucose is the main regulator of ketone body metabolism."
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe

Thank. I am posting the quote from the link below as most people may not have the patience to go through the entire script. It also emphasizes the role of excess iron in cancer and infections. Most people do not realize this but the purpose of fever in infection it to deplete serum iron and tryptophan (serotonin) as both are required for infection to persist. A drop in one or the other often resolves the infection rather quickly. That is why anti-serotonin drugs or tetracycline antibiotics (chelate iron) are so effective even in cases where no obvious mechanism of action exists or there is bacterial resistance to the antibiotic.
"...Georg Wondrak: Well we work with anti-malarials that are working through induction of oxidative stress. So, these are called artemisinins and it turns out that cancer cells are sensitive to the same mechanisms as malarial parasites being killed by these anti-malarial drugs. So, it’s about these drugs being able to induce oxidative stress. These are peroxides that can decay with the formation of free radicals and they find the targets, because the target is iron rich. Targets with a lot of free iron, such as malaria parasites or cancer cells that mishandle iron, they’re more sensitive to theses drugs. So it is sort of a common denominator that malaria parasites and cancer cells share."
 
J

jb116

Guest
Thank. I am posting the quote from the link below as most people may not have the patience to go through the entire script. It also emphasizes the role of excess iron in cancer and infections. Most people do not realize this but the purpose of fever in infection it to deplete serum iron and tryptophan (serotonin) as both are required for infection to persist. A drop in one or the other often resolves the infection rather quickly. That is why anti-serotonin drugs or tetracycline antibiotics (chelate iron) are so effective even in cases where no obvious mechanism of action exists or there is bacterial resistance to the antibiotic.
"...Georg Wondrak: Well we work with anti-malarials that are working through induction of oxidative stress. So, these are called artemisinins and it turns out that cancer cells are sensitive to the same mechanisms as malarial parasites being killed by these anti-malarial drugs. So, it’s about these drugs being able to induce oxidative stress. These are peroxides that can decay with the formation of free radicals and they find the targets, because the target is iron rich. Targets with a lot of free iron, such as malaria parasites or cancer cells that mishandle iron, they’re more sensitive to theses drugs. So it is sort of a common denominator that malaria parasites and cancer cells share."
The malarial connection also highlights K2 as potent anti-cancer as well, would you say?
 

nbznj

Member
Joined
Oct 4, 2017
Messages
287
awesome post. Does this mean that elevated triglycerides (which can be seen in young subjects) are a first sign of future disease? Also what are your preferred methods of raising glucose oxidation?
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
The malarial connection also highlights K2 as potent anti-cancer as well, would you say?

Yes, it does. Not just K2 but any quinone capable of raising ROS and changing redox indicators like NAD/NADH and especially GSSG/GSH as the latter one if the primary defense method of cancer cells against apoptosis and ROS.
 

Whataboutbob

Member
Joined
Apr 16, 2017
Messages
103
Cancer Insights at ASU » Blog Archive » Cancer: The Beat of An Ancient Drum – Paul Davies (Video)More interesting insight from Dr. Davies at ASU into cancers ancient roots and its similarities to early embryo development (same genes up regulate down regulate ....I like the phrase dedifferentiate or revert back to ancient cell like “critters”)....anyway @haidut it gets really interesting at about 30 min in till about 50 min...around 45-50 min. he mentions Warburg/glycolysis/fermentation....early life forms lack of oxygen (U get the picture)He might not end up / not yet anyway where Dr. Peat does...but he is open and is just asking some big questions , says we have throwing billions of dollars at cancer research with nothing to show for it, over 1,000,000 research paper and 90+ % can’t be replicated ....sad ...very sad! Anyway.....Enjoy
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
Cancer Insights at ASU » Blog Archive » Cancer: The Beat of An Ancient Drum – Paul Davies (Video)More interesting insight from Dr. Davies at ASU into cancers ancient roots and its similarities to early embryo development (same genes up regulate down regulate ....I like the phrase dedifferentiate or revert back to ancient cell like “critters”)....anyway @haidut it gets really interesting at about 30 min in till about 50 min...around 45-50 min. he mentions Warburg/glycolysis/fermentation....early life forms lack of oxygen (U get the picture)He might not end up / not yet anyway where Dr. Peat does...but he is open and is just asking some big questions , says we have throwing billions of dollars at cancer research with nothing to show for it, over 1,000,000 research paper and 90+ % can’t be replicated ....sad ...very sad! Anyway.....Enjoy

Thanks. I posted a thread on this a few years ago and it seems that the idea is finally becoming more mainstream. See below.
https://raypeatforum.com/community/...-cheaper-for-dividing-cells.8805/#post-113153

Cancer is the lack of restraint on growth. Inhibitory mechanisms like GABA, glycine, progesterone, pregnenolone, magnesium, vitamin E, DHEA, T, DHT, etc is what keeps cells from reverting into a shapeless, hungry mass that loses its morphostasis and consumes the host. Conversely, estrogen, cortisol, aldosterone, prolactin, serotonin, NO, etc are "growth" and de-differentiating agents. Stress, toxins, chronic infections and perceived inability to escape from restrictive environments is what activates the second group.
 

Regina

Member
Joined
Aug 17, 2016
Messages
6,511
Location
Chicago
Thanks. I posted a thread on this a few years ago and it seems that the idea is finally becoming more mainstream. See below.
Warbug Effect Revisited - Glycolysis Is "cheaper" For Dividing Cells

Cancer is the lack of restraint on growth. Inhibitory mechanisms like GABA, glycine, progesterone, pregnenolone, magnesium, vitamin E, DHEA, T, DHT, etc is what keeps cells from reverting into a shapeless, hungry mass that loses its morphostasis and consumes the host. Conversely, estrogen, cortisol, aldosterone, prolactin, serotonin, NO, etc are "growth" and de-differentiating agents. Stress, toxins, chronic infections and perceived inability to escape from restrictive environments is what activates the second group.
Epic!

More and more, I see people's behaviour through a Peat-inspired lens--which helps with compassion and understanding. Now, I think the de-differentiating agents of the second group also de-differentiate the people that the afflicted interacts with. Sometimes, I think, "why is this person doing this (negatively thing to me)? I have nothing to do with this." The second "de-differentiating" group is catabolizing the afflicted and "wills" (if you will) them to de-differentiate and attrit their environment and anyone they can attach to.
Wish there was a mister of inhibitory mechanisms that could halt the second group to give them a bridge back to connection and coherence.

Ah, I see in your former post, you say, "And yes, I meant restraining mechanisms ARE working properly." So yes, no restraint.
 
Last edited:

Whataboutbob

Member
Joined
Apr 16, 2017
Messages
103
Thanks. I posted a thread on this a few years ago and it seems that the idea is finally becoming more mainstream. See below.
https://raypeatforum.com/community/...-cheaper-for-dividing-cells.8805/#post-113153

Cancer is the lack of restraint on growth. Inhibitory mechanisms like GABA, glycine, progesterone, pregnenolone, magnesium, vitamin E, DHEA, T, DHT, etc is what keeps cells from reverting into a shapeless, hungry mass that loses its morphostasis and consumes the host. Conversely, estrogen, cortisol, aldosterone, prolactin, serotonin, NO, etc are "growth" and de-differentiating agents. Stress, toxins, chronic infections and perceived inability to escape from restrictive environments is what activates the second group.
thanks Haidut it was that post that got me started down this rabbit hole, I think the article was written in 2011 and this talk was 2014......I was fortunate and had 10 days of vacation to burn over the holidays.....(just me and the wife at home, I have 3 daughters .....twins are 30 [identical but different... size /temperament /female issues how they sleep handle stress, they are my “up close living experiment”.. context/$/environment is everything... younger daughter is 26, they have all moved out one is married but they live close .
Had a lot of free time....sat under my lamp took walks in the woods and did a ton of reading/thinking/watching and contemplating the many ideas I have read here on the forum and elsewhere.....o and cleared the driveway (snow) ..Michigan got a bunch of ☃️ In Dec....anyway grace2u Haidut and everyone here at the forum for all you have done and continue to do for the “common folk” ...

Epic!

More and more, I see people's behaviour through a Peat-inspired lens--which helps with compassion and understanding. Now, I think the de-differentiating agents of the second group also de-differentiate the people that the afflicted interacts with. Sometimes, I think, "why is this person doing this (negatively thing to me)? I have nothing to do with this." The second "de-differentiating" group is catabolizing the afflicted and "wills" (if you will) them to de-differentiate and attrit their environment and anyone they can attach to.
Wish there was a mister of inhibitory mechanisms that could halt the second group to give them a bridge back to connection and coherence.

Ah, I see in your former post, you say, "And yes, I meant restraining mechanisms ARE working properly." So yes, no restraint.
Thanks Regina for reminding me to have more “compassion”.......”understanding”,(especially at work/stressful environment been here 17 years... I’ve grown older with many here...sickness/pain/heart aches disease and death)we’re all on a journey/self discovery and many are stuck or going backwards (de-differentiated) ...as I was ....I’m 60 and from about 45-50 I was a mess....job stress [still] ......raising 3 daughters, marriage...been married 36 years....paleo diet, no sugar☹️ on SSRI for almost 10 years,... anxiety/insomnia/depression....went cold turkey from all this....O according to my Dr/blood work-weight I was in great shape..yada yada yada....that was 5 years ago......[what a ride]....someday I will post my journey.....all this to say “been there bought the shirt”...... “me too”...anyway thanks Regin for pointing out once again that Peats ideas are soooooooo much more than aspirin/caffeine/progesterone ....etc and that everyone has their own context and maybe are in a “de-differentiated state” but just maybe we can become part of their context and they part of ours and with the “catalyst/enzymes” we call love, friendship, compassion wisdom-understanding (of which takes a lot of energy) ....maybe we can help them differentiate and become more of warm human being. .....grace2U
 

Regina

Member
Joined
Aug 17, 2016
Messages
6,511
Location
Chicago
Thx Whataboutbob.

If only Nietzsche did not use the unfortune vocabulary "slave" morality and "master" morality. He may have been observing this very thing.
Thankfully Peat shines a huge light with his metabolic bioenergic interpretation of say, the insanities or all the other classifications of behaviors; i.e., narcissism (projection = de-differentiating self/non-self).
 

rei

Member
Joined
Aug 6, 2017
Messages
1,607
How do you settle this finding with the fact that numerous diseases are found to be treated if not cured by ketogenic diet? Is the point to shift the metabolism so far over to ketones to overpower direct fatty acid source for energy in tissue other than liver?
 
J

jb116

Guest
How do you settle this finding with the fact that numerous diseases are found to be treated if not cured by ketogenic diet? Is the point to shift the metabolism so far over to ketones to overpower direct fatty acid source for energy in tissue other than liver?
I see it as a metabolic deficiency where an alternative fuel source becomes helpful. But I also see it as temporary. If that metabolic issue can be addressed, it would be possible to resort to normal oxidative metabolism. A good indirect evidence for that is Peat mentioned for seizures for example, treated with ketogenic diets can also be controlled with progesterone. We actually had somebody here control his daughter's seizures I believe with progesterone.
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
for the “common folk”

There is nothing else but "common folk". Anybody that tries to sell you on the idea that there is a "special" breed/class/layer of humans is...well...selling you something, and sometimes not voluntarily :):
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,798
Location
USA / Europe
So inject insulin, eat starch and protein, and cansa finally goes bye bye?

It is interesting that you mention insulin as it is one of the most potent activators of the enzyme PDH, which is downregulated in every cancer. And insulin is actually being actively studied as cancer treatment.
Insulin treatment in cancer cachexia: effects on survival, metabolism, and physical functioning. - PubMed - NCBI

Starch would be good only if it does NOT stimulate endotoxin release, so this means staying away from "resistant" starches.
 
Joined
Feb 1, 2016
Messages
384
Location
NY
It is interesting that you mention insulin as it is one of the most potent activators of the enzyme PDH, which is downregulated in every cancer. And insulin is actually being actively studied as cancer treatment.
Insulin treatment in cancer cachexia: effects on survival, metabolism, and physical functioning. - PubMed - NCBI

Starch would be good only if it does NOT stimulate endotoxin release, so this means staying away from "resistant" starches.
Well, if I had cancer, I would avoid any growth factors (insulin, sugar, protein) like the plague, probably fast/do gerson diet and allow my immune system to get rid of those junk cells. Yeah my ketones would be high, good, they aren't growth substrates for cancer. Activating PDH is not a cancer cure, its an anabolic pathway for normal healthy cells, irrelevant in the whole body context of cancer.
 

Koveras

Member
Joined
Dec 17, 2015
Messages
720
How do you settle this finding with the fact that numerous diseases are found to be treated if not cured by ketogenic diet? Is the point to shift the metabolism so far over to ketones to overpower direct fatty acid source for energy in tissue other than liver?

I see it as a metabolic deficiency where an alternative fuel source becomes helpful. But I also see it as temporary. If that metabolic issue can be addressed, it would be possible to resort to normal oxidative metabolism. A good indirect evidence for that is Peat mentioned for seizures for example, treated with ketogenic diets can also be controlled with progesterone. We actually had somebody here control his daughter's seizures I believe with progesterone.

How about this mechanism?

@haidut has talked about alternative methods to raise NAD+

Front Mol Neurosci. 2017 Nov 14;10:377. doi: 10.3389/fnmol.2017.00377. eCollection 2017.
Ketone-Based Metabolic Therapy: Is Increased NAD+ a Primary Mechanism?
Elamin M1, Ruskin DN2, Masino SA2, Sacchetti P1.

The ketogenic diet's (KD) anticonvulsant effects have been well-documented for nearly a century, including in randomized controlled trials. Some patients become seizure-free and some remain so after diet cessation. Many recent studies have explored its expanded therapeutic potential in diverse neurological disorders, yet no mechanism(s) of action have been established. The diet's high fat, low carbohydrate composition reduces glucose utilization and promotes the production of ketone bodies. Ketone bodies are a more efficient energy source than glucose and improve mitochondrial function and biogenesis. Cellular energy production depends on the metabolic coenzyme nicotinamide adenine dinucleotide (NAD), a marker for mitochondrial and cellular health. Furthermore, NAD activates downstream signaling pathways (such as the sirtuin enzymes) associated with major benefits such as longevity and reduced inflammation; thus, increasing NAD is a coveted therapeutic endpoint. Based on differential NAD+ utilization during glucose- vs. ketone body-based acetyl-CoA generation for entry into the tricarboxylic cycle, we propose that a KD will increase the NAD+/NADH ratio. When rats were fed ad libitum KD, significant increases in hippocampal NAD+/NADH ratio and blood ketone bodies were detected already at 2 days and remained elevated at 3 weeks, indicating an early and persistent metabolic shift. Based on diverse published literature and these initial data we suggest that increased NAD during ketolytic metabolism may be a primary mechanism behind the beneficial effects of this metabolic therapy in a variety of brain disorders and in promoting health and longevity.
 

Similar threads

Back
Top Bottom