• 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.

What Is The Peat Approach To Atherosclerosis?

stargazer1111

Member
Joined
Feb 16, 2017
Messages
425
What was the data he used to show Trans Fats caused atherosclerosis? I got interested in Trans Fats a while back, and every study I saw was either observational, or also used an oil that had a much higher level of PUFA than the control. All of the increases in atherosclerosis could have been due to increased PUFA intake. I'm thinking the fact that a lot of places stopped using hydrogenated versions of these high PUFA oils actually made problems much worse, as now there is more PUFA and fewer protective saturated and trans fats in the oils.




Pretty good summary, but you missed one big factor- high body iron stores. Jerome Sullivan even proposed the iron hypothesis back in 1981. Iron stores are elevated in almost every degenerative disease. It also dovetails perfectly with everything you mentioned. Excess iron also promotes PUFA peroxidation. It will also lower vitamin C and E levels in the body. There is research that shows that simply donating blood will increase levels of C, E and other antioxidants in the body.

Good point. Not just iron, but all of the redox active metals are potentially problematic here as they will steal electrons from PUFA creating toxic radical byproducts and then donate those electrons to oxygen creating the superoxide radical. That then creates a chain of events that creates the reactive oxygen and nitrogen species which then kill cells.
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
What was the data he used to show Trans Fats caused atherosclerosis? I got interested in Trans Fats a while back, and every study I saw was either observational, or also used an oil that had a much higher level of PUFA than the control. All of the increases in atherosclerosis could have been due to increased PUFA intake. I'm thinking the fact that a lot of places stopped using hydrogenated versions of these high PUFA oils actually made problems much worse, as now there is more PUFA and fewer protective saturated and trans fats in the oils.




Pretty good summary, but you missed one big factor- high body iron stores. Jerome Sullivan even proposed the iron hypothesis back in 1981. Iron stores are elevated in almost every degenerative disease. It also dovetails perfectly with everything you mentioned. Excess iron also promotes PUFA peroxidation. It will also lower vitamin C and E levels in the body. There is research that shows that simply donating blood will increase levels of C, E and other antioxidants in the body.


That's a good point, and I'd like to add to that.

On a deeper level, high iron stores as indicated by high ferritin can be due to chronic bacterial infection. The body will try to keep iron from these bacteria and as a protective mechanism store body iron to keep it away from bacteria. In doing so, ferritin levels increase because more iron is being stored.

It's easy to think we don't have any bacterial infection ongoing because we base this conclusion on our temperature. If we don't have a fever, we don't have bacterial infection. But that's only looking at it when bacteria is very active because our immune system was weakened, allowing opportunistic bacteria to multiply and spread. The body responds by increasing temperature in order to be more effective in killing bacterial. But when our immunity is working well, bacteria is suppressed. There is still infection ongoing, but it's ably suppressed to a low level. This low-level infection is under the radar, and we think because there's no fever, we're healthy.

But if we take a CBC test, we can examine our wbc and neutrophil count. If these values are high, it means the innate immune system is working more to contain low-level infection. The amount of bacteria in our vascular system, would be much higher when the innate immune system has to produce more wbc and neutrophils to contain it. If this situation has been chronic, over time dead neutrophils would accumulate and this would be part of the plaque that forms. This would also cause atherosclerosis.

Atherosclerosis come in many forms. Some may not have a strong bacterial element to it and some do. You have to know what form of atherosclerosis you're dealing with.
 

tankasnowgod

Member
Joined
Jan 25, 2014
Messages
6,824
On a deeper level, high iron stores as indicated by high ferritin can be due to chronic bacterial infection. The body will try to keep iron from these bacteria and as a protective mechanism store body iron to keep it away from bacteria.

True, but the causality can also be the inverse- high body iron stores can invite (or enhance) a chronic bacterial infection. It was a simple experiment in a petri dish conducted in E.D. Weinberg's lab where he discovered that iron (and no other known vitamin or mineral substance) could completely neutralize the antibiotic effect of tetracycline that started him on his career focusing on iron research. The fact that the body has an entire defense system to keep iron specifically away from pathogens.
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
They are intertwined I guess.

It's interesting I had hemachromatosis before. Now I don't have that anymore, but I have higher ferritin. If I'm not mistaken, I had high serum iron and that was enough to be called hemachromatosis.

Before, I didn't have high blood pressure. Now I do.

If my high BP was due to atherosclerosis, and my atherosclerosis was due to chronic bacterial infection, it would be reasonable for me to surmise that my ferritin would be high, and my serum iron to be. normal. Only because the body wants to keep iron away from bacteria. Perhaps if I didn't have chronic bacterial infection now, my ferritin levels would be low and my serum iron high. And I would have hemachromatosis again.

That's something I would have to find out much later, assuming I'm able to fix my current condition.
 

tankasnowgod

Member
Joined
Jan 25, 2014
Messages
6,824
They are intertwined I guess.

It's interesting I had hemachromatosis before. Now I don't have that anymore, but I have higher ferritin. If I'm not mistaken, I had high serum iron and that was enough to be called hemachromatosis.

Before, I didn't have high blood pressure. Now I do.

If my high BP was due to atherosclerosis, and my atherosclerosis was due to chronic bacterial infection, it would be reasonable for me to surmise that my ferritin would be high, and my serum iron to be. normal. Only because the body wants to keep iron away from bacteria. Perhaps if I didn't have chronic bacterial infection now, my ferritin levels would be low and my serum iron high. And I would have hemachromatosis again.

That's something I would have to find out much later, assuming I'm able to fix my current condition.

Weird, I have never heard of a diagnosis of hemochromatosis like this. It really doesn't make any sense. Ferritin is far and away the best marker of body iron stores. You can raise serum iron simply by having a meal. Not a good indicator at all. Simply eating a steak doesn't mean you have hemochomatosis, but that same act will indeed spike serum iron. If anything, they should at least be using TSAT, where serum iron is part of the calculation.
 

Terma

Member
Joined
May 8, 2017
Messages
1,063
Iron certainly causes problems but it appears necessary for NADPH oxidase to work. Here's a counter-example pathogen where iron gains importance:
https://sci-hub.tw/http://www.eurekaselect.com/86981/article
H. pylori disrupt NADPH oxidase targeting so that O 2 • is released into the extracellular milieu and is not accumulated inside phagosome. The nascent H. pylori phagosomes ac- quire flavocytochrome b558, while p47 phox and p67 phox are not efficiently recruited on the phagosome membrane [15].

Iron chelation by desferrioxamine inhibited NADPH oxidase-dependent reactive oxygen species production in mice . It is plausible that iron chelator directly inactivates NADPH oxidase by chelating the active site heme iron thus blocking the transfer of electrons from NADPH to oxygen and its re- duction to O 2 • . It was showed that chelation of host Fe in vivo exacerbates murine salmonellosis and that iron depriva- tion results in an inability to induce the NADPH oxidase – dependent production of ROS. Thus, altering the equilibrium of intracellular Fe influences the course of infection to the benefit of the pathogen [16].

To evade oxidative killing H. pylori prevents NADPH oxidase assembly at the phagosome, with release of NADP + and large amounts of superoxide anions into the extracellular milieu . The NADPH oxidase complex causes a massive increase in non- mitochondrial oxygen consumption due to one electron reduction of oxygen to generate superoxide ani- ons and a strong stimulation of the pentose phosphate path- way (PPP). Generated supehe OPP is the major provider of reducing equivalents while the NOPP provides C3-C8 glycolyl units which serve as cellular assembly units and as reserve energy metabolites [24,25]. The key enzyme of OPP, glucose-6-phosphate dehydro- genase has main role in production of NADPH needed for reductive biosynthesis and maintenance of cellular redox state [26]. The activity of glucose-6-phosphate dehydro- genase regulates the level of glutathione, the most important antioxidant of gastric mucosa [27]. Exposure of glutathione to ROS oxidizes it and forms glutathione disulfide which is reduced to glutathione by glutathione reductase. The NADPH reducing equivalents utilized for this reaction are produced by glucose-6-phosphate dehydrogenase [25,28].

If pathogens are a worry NADPH and NADPH oxidase are the first places to look. Evolution noticeably relied on NADPH when building defensive measures.
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
Weird, I have never heard of a diagnosis of hemochromatosis like this. It really doesn't make any sense. Ferritin is far and away the best marker of body iron stores. You can raise serum iron simply by having a meal. Not a good indicator at all. Simply eating a steak doesn't mean you have hemochomatosis, but that same act will indeed spike serum iron. If anything, they should at least be using TSAT, where serum iron is part of the calculation.
It was a while back when I was diagnosed for hemachromatosis. I wasn't collecting my blood test records then, and I was where I left everything to the doctor. I don't recall perfectly, but it seemed that my serum iron was so high it left no doubt I had hemachromatosis. Is that possible? I don't know. But I would guess if my serum iron were that high now, I would be so much sicker beyond my imagination.
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
Iron certainly causes problems but it appears necessary for NADPH oxidase to work. Here's a counter-example pathogen where iron gains importance:
https://sci-hub.tw/http://www.eurekaselect.com/86981/article


If pathogens are a worry NADPH and NADPH oxidase are the first places to look. Evolution noticeably relied on NADPH when building defensive measures.
The pentose phosphate pathway isn't much discussed by Ray Peat nor in this forum. I think it may have its roots in a disdain for anything that has to be supportive of the production of ROS. That has changed as we now know the importance of its role in producing NADPH, and its use in producing ROS, which is needed in the respiratory burst of phagocytosis to kill pathogens. I could count this as another reason why we need glucose and must rely on glucose metabolism more than fatty acid metabolism.

Good to know iron is needed for the PPP.
 

Terma

Member
Joined
May 8, 2017
Messages
1,063
The pentose phosphate pathway isn't much discussed by Ray Peat nor in this forum. I think it may have its roots in a disdain for anything that has to be supportive of the production of ROS. That has changed as we now know the importance of its role in producing NADPH, and its use in producing ROS, which is needed in the respiratory burst of phagocytosis to kill pathogens. I could count this as another reason why we need glucose and must rely on glucose metabolism more than fatty acid metabolism.

Good to know iron is needed for the PPP.
Yeah something like that lol. But in fact (won't bother to link right now) in mainstream research it's simply thought that when cells become fat-adapted by turning off PDH and other enzymes - notably as part of the FOXO program (most quoted in life extension) - that spares glucose to go toward ROS handling.
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
Yeah something like that lol. But in fact (won't bother to link right now) in mainstream research it's simply thought that when cells become fat-adapted by turning off PDH and other enzymes - notably as part of the FOXO program (most quoted in life extension) - that spares glucose to go toward ROS handling.
That's got my interest piqued. Do you agree with the mainstream research on this? Is there much contention on this?
 

Terma

Member
Joined
May 8, 2017
Messages
1,063
There's going to be some contention about quantifying the contributions of all pathways to life extension - in a natural setting (I say we can do better than "natural") - for quite a while. NADPH will certainly contribute since it seems it's one of the purposes of the FOXO survival program (as I said + e.g. FOXOs support the metabolic requirements of normal and tumor cells by promoting IDH1 expression). How much compared to other factors? I can't say or I haven't read it yet. Then again, in discussions with Travis he was not impressed with the ROS theory of aging, and it's certainly not the whole story.
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
There's going to be some contention about quantifying the contributions of all pathways to life extension - in a natural setting (I say we can do better than "natural") - for quite a while. NADPH will certainly contribute since it seems it's one of the purposes of the FOXO survival program (as I said + e.g. FOXOs support the metabolic requirements of normal and tumor cells by promoting IDH1 expression). How much compared to other factors? I can't say or I haven't read it yet. Then again, in discussions with Travis he was not impressed with the ROS theory of aging, and it's certainly not the whole story.
Thanks for the link. I'd have to save it for later to read. It's another set of acronyms to deal with and I'm brain-dead now lol

I thought that atherosclerosis Is due to low grade inflammation.
It could also be due to low-grade infection which generates an inflammatory response from the innate immune system.
 

Broken man

Member
Joined
Sep 11, 2016
Messages
1,634
Thanks for the link. I'd have to save it for later to read. It's another set of acronyms to deal with and I'm brain-dead now lol


It could also be due to low-grade infection which generates an inflammatory response from the innate immune system.
Did you have success with enzymes you tried?
 

yerrag

Member
Joined
Mar 29, 2016
Messages
8,795
Location
Manila
Did you have success with enzymes you tried?
It's too early to tell. Will know in a month as I try to tweak my protocol. It seems that I have to keep fine-tuning my dosage in response to an ever-changing protagonist. It's a dynamic tug-of-war as we try to outsmart each other.
 

Broken man

Member
Joined
Sep 11, 2016
Messages
1,634
It's too early to tell. Will know in a month as I try to tweak my protocol. It seems that I have to keep fine-tuning my dosage in response to an ever-changing protagonist. It's a dynamic tug-of-war as we try to outsmart each other.
I understand, thing is that I am not doing progress with peat advice And my cvd.....
 

nbznj

Member
Joined
Oct 4, 2017
Messages
287
I thought this was a classic from ray...

Thyroid: Therapies, Confusion, and Fraud

Administering a thyroid supplement, blood cholesterol came down to normal exactly as the basal metabolic rate came up to the normal rate. The biology of atherosclerotic heart disease was basically solved before the second world war.

For some reason many here shoot for elevated LDL and think they are superior to what’s a healthy level in humans - as seen in non westernized tribes, all fairly consistent with ldl in the 50-70s range even the high saturated fat Masai.

Ldl above range is the cheapest way to diagnose hypothyroidism and it’s been this way for close to a century now.

https://chrismasterjohnphd.com/blog/2011/08/28/central-role-of-thyroid-hormone-in/

Statins are a fraud, PCSK9 inhibitors make sense, t3 is king...

Thyroid extract reduced the incidence of heart attacks by four-fold in the older office patients and by seven-fold in the younger business men. Stated another way, it reduced the incidence of heart attacks by 76% among the older office patients and by 85% in the younger business men. This effect is much more powerful than that seen with any drugs that are currently on the market and suggests that correcting thyroid deficiency may be able to nearly abolish the risk of heart disease if done so early enough.

Kountz published his results in 1951, over two decades before Brown and Goldstein discovered the LDL recpetor pathway. Thus, Kountz had no way of knowing the role of thyroid hormone in regulating the expression of this receptor, and no way of knowing the critical role of this receptor in governing the risk of heart disease.
 

lampofred

Member
Joined
Feb 13, 2016
Messages
3,235
I used to believe this too but I'm suspicious that there is something missing from this picture.

Dr. Fred Kummerow was the first scientist to propose and successfully show that trans fats can cause atherosclerosis and he agreed with Ray Peat that it was the consumption of polyunsaturated fats (along with cigarette smoking) that caused atherosclerosis in most people. He lived to be over 100 years old and his diet consisted of: fruits, vegetables, whole grains, red meat, butter, and eggs. So, his long-term diet was relatively low in PUFA.

However, Dr. Kummerow had an artery blockage at the age of 89 and had to have bypass surgery. So, despite the fact that he actively avoided PUFA for most of his life, he still developed advanced atherosclerosis.

I wonder if Linus Pauling's unified theory of heart disease was correct and if Kummerow was low in vitamin C.

Linus Pauling's hypothesis actually dovetails nicely with the hypotheses of both Broda Barnes and Dr. Kummerow.

Broda Barnes believed that it was hypothyroidism that caused athersclerosis.

Dr. Kummerow believed it was peroxidized PUFA.

Linus Pauling believed it was vitamin C deficiency.

Insufficient vitamin C causes a relative deficit of collagen. When this occurs, the arterial walls are not properly repaired when they are damaged. What damages arterial walls? Lipid peroxidation of PUFA and its byproducts. Vitamin C levels and lipoprotein A levels are negatively correlated. When vitamin C is high, lipoprotein A is low and vice versa. Lipoprotein A is significantly correlated with atherosclerosis. Pauling believed that lipoprotein A evolved as a backup mechanism to repair the arteries in animals that lost the ability to produce their own vitamin C. What else raises lipoprotein A levels? Hypothyroidism.

I also wonder if calcium is simply an innocent bystander in this process since we know that the Maasai get several grams of calcium per day from their traditional diet of milk, blood, and meat but have low rates of heart disease. Kummerow showed that what happens when peroxidized PUFA damages the artery is that sphingomyelin builds up as part of the plaques that patch up the arterial holes. Sphingomyelin is negatively charged and attracts the 2+ calcium ions which stabilize the plaque thereby calcifying it. Vitamin K2 helps to break up the plaques by taking away calcium and putting it into the bones so that the negatively charged sphingomyelin is no longer stabilized by the positive calcium ions.

Vitamin C has the added benefit of reducing lipid peroxidation. Obviously, vitamin E will be helpful too.

So, my flow chart for atherosclerosis incorporates all 3 hypotheses into this:

Vitamin C deficiency + PUFA --> low collagen + hypothyroidism --> unrepaired arterial damage --> increased lipoprotein A + oxidized PUFA to patch up arterial holes --> negatively charged sphingomyelin build up --> attraction of calcium ions to stabilize sphingomyelin negative charge --> plaques are formed --> eventual blockage as the plaques build up --> heart attack

That diet is very low in calcium. I don't have a hypothesis for the mechanism but I suspect that a low calcium:phosphate ratio plays a large role in heart problems, metabolic syndrome, obesity, diabetes, things of that nature (but probably doesn't have much to do with multiple sclerosis, lupus, autoimmune type of issues).

I do think low vitamin C also played a role, as you mentioned.
 

stargazer1111

Member
Joined
Feb 16, 2017
Messages
425
That diet is very low in calcium. I don't have a hypothesis for the mechanism but I suspect that a low calcium:phosphate ratio plays a large role in heart problems, metabolic syndrome, obesity, diabetes, things of that nature (but probably doesn't have much to do with multiple sclerosis, lupus, autoimmune type of issues).

I do think low vitamin C also played a role, as you mentioned.

That's a great observation. I also wonder about magnesium levels because a diet rich in fruits, vegetables, and whole grains is too vague. Grains have antinutrients that rob the body of calcium, magnesium, and other minerals and the particular types of each category have varying amounts of magnesium and calcium. I suspect his diet was low in both but more so in calcium.

Calcium is definitely not the cause of heart disease. The Maasai demonstrate that.
 
Last edited:
Joined
Jun 16, 2017
Messages
1,790
That diet is very low in calcium. I don't have a hypothesis for the mechanism but I suspect that a low calcium:phosphate ratio plays a large role in heart problems, metabolic syndrome, obesity, diabetes, things of that nature (but probably doesn't have much to do with multiple sclerosis, lupus, autoimmune type of issues).

I do think low vitamin C also played a role, as you mentioned.
I agree, it also seems like a low calorie diet. Those whole grains scraping against the intestines also doesn't sound nice...
 
Similar threads
Thread starter Title Forum Replies Date
S A Biophysical Approach To Altered Consciousness, Ray Peat Health 10
ddjd Peat Approach To Healing From Ciprofloxacin Damage? Ask For Help or Advice 9
ddjd Peat Approach To Gall Bladder Problems? Diet/ Nutrition/ Exercise? Ask For Help or Advice 23
bboone Introduction And Experience (so Far) With A Peat-inspired Diet Approach Meet & Greet 0
S Can't Eat Most Of Peat's Recommendation, Here's My Current Approach Diet, Recipes 38
S A Peat Approach To Unavoidable Testosterone Replacement Therapy Ask For Help or Advice 19
LUH 3417 An Orderly Approach To Ray Peat Ask For Help or Advice 1
B Peat Approach For My Cat Animals 52
W Newbee, Researching the Peat approach to eating. Meet & Greet 7
Vileplume I made an Instagram reel overviewing Ray Peat basics Miscellaneous 0
David PS Ray Peat Interview #74: Vaccine Shedding | Progesterone and Thyroid | Immunology, Ideology, and Power with Ray Peat 11/26/2021 Interviews 16
C Ray Peat advice on Ahus Cancer, Degenerative Diseases 0
J Peat: RNA treatments in animals suggests that they could be terrible Vaccines 5
G Peat on Novelty, Competition and Opportunities Ray Peat Quotes 0
CHEESEHEAD69 Does Ray Peat have an account on this forum? Ask For Help or Advice 17
ursidae Ray Peat’s Thoughts on the Appropriate Amount of Fat in a Diet Diet 72
B AHA releases 2021 Anti-Peat Recommendations Health 0
P Ray Peat Newbie Meet & Greet 4
Aimer Ray Peat Interview Health Odyssey:Ray Peat and what the Cells in our body are really made of Interviews 1
A Ray Peat right about Noam Chomsky, Chomsky says antivaxxers are killers and should be segregated from society Vaccines 43
K Covid nonsense and Pay Peat Health 131
K Covid nonsense and Pay Peat Health 1
Vileplume Ray Peat Philosophy Gems Ray Peat Quotes 18
PeatandPotatoes What is the most important and impactful lesson/information you have learned from Ray Peat Ray Peat Topics 29
K My Personal Version of Peat Diet - low protein and very little fat. Diet 15
G Vitamins/Minerals One Needs To Supplement On a "Peat" Diet? Ask For Help or Advice 25
PeatandPotatoes Your early Peat inspired diet vs. now Diet 4
Whats the "Peat guideline" that dont suit you health wise? Diet 16
nigma Ray Peat inspired health technologies Metabolism 17
L Recommended daily doses of vitamins and minerals according to Ray peat Ask For Help or Advice 18
H Job offer - need someone to help formulate Peat-friendly supplements The Ray Peat Forum Lounge 51
T Peat-Informed Practitioner for Hormones Female Issues 7
Acne and peat? Skin 10
Peat inspired Bodybuilding Log Logs 0
L Ray Peat Interview September 2021 - Ray Peat, Georgi Dinkov, Danny Roddy - #70 Interviews 36
Sertorius From Carnivore to Ray Peat - A repository to escape low carb hell Ask For Help or Advice 30
Ray peat grocery haul? Diet 38
RealNeat What's hiding in your staple "Peat" foods?.. Diet 16
L Is healthnatura’s progesterone inferior to Ray Peat’s ProgestE? Progesterone 6
L Ray Peat Interview July 2021 - Danny Roddy, Ray Peat, Georgi Dinkov - #64: Life | Energy | Estrogen | Fibrosis | Calcification | Process Theology | Altruism Interviews 0
Inaut Ray Peat Interview with Tucker Goodrich, David Gornoski on PUFAs, Seed Oils, Benefits of Sugar, Milk Interviews 3
M Has Peat talked about giants existing in the past? Ask For Help or Advice 94
RenaissanceMan Peat Wrong About Omega 3? DHA & EPA increase dopamine and lower serotonin Polyunsaturated Fats, Seed Oils 22
Sefton10 Ray Peat Interview Ray Peat on low carb podcast, August 2021 Interviews 12
M What does Peat use for transportation? what kind of car? Ask For Help or Advice 43
P Has Peat ever mentioned what happens when one takes too much levothyroxine? Ask For Help or Advice 19
ecstatichamster Lost Story of Vitamin E: Shute family that Dr. Peat referred to and estrogen research Ray Peat Topics 1
fr@ #64 @Ray Peat's comment about oils getting in the lungs Danny Roddy 17
T Where I can find/buy Ray Peat's old newsletters? Articles & Newsletters 3
G Aspirin and Androgens Compilation (Anti-Peat-ish) Scientific Studies 6

Similar threads

Top