Peat Got The Fats Quite Wrong

Steffi

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Hi folks! I have some strong points against some of Rays ideas:

So all started because my blood lipid levels have gone bad from being spot on average before I started "peating". LDL is high now.

I was looking around once more and found quite shocking information. It is quite obvious and contradictory to things Ray said. I did my body wrong with all the coconut oil and butter rather than olive oil and fish. There's an effect just like Ray describes that harms the body through fatty acid composition for a long time, but it's not about PUFA but the most common SFA in dairy, palmitic acid - which is evil (see at the end).

A great summary and mountain of information can be found on
http://edubily.de/2014/10/fette-das-der ... n-teil-iv/
but it is in German.

I thought Ray said that babies are all created saturated - which of course would SFA seem quite optimal.
http://www.ncbi.nlm.nih.gov/pmc/article ... 6-0016.pdf
What's true is that there's always at least 40% UFA in fatty tissue, also PUFA, but mostly the MUFA Oleic Acid.

Coconut oil isn't all that great according to this paper:
https://gupea.ub.gu.se/bitstream/2077/3 ... 2909_1.pdf

It can be concluded that coconut fat as the main fat in the diet led to significantly higher TC
levels and LDL levels in adults compared to diets rich in HUFA, which is today
not considered to be beneficial when it comes to blood cholesterol in relation to health.

And now to the worst fact I learned. Palmitic Acid (which is abundant in dairy and coconut oil) is outright evil:

In contrast, when palmitic acid reaches the liver after absorption, it simply recirculates as palmitic acid in lipoproteins. Thus, dietary palmitic acid, along with lauric and myristic acids, elevates plasma cholesterol and LDL concentrations by down-regulating the hepatic receptor for LDL (5). (Connor, 1999)
The same author also writes how stearic acid, another SFA, lowers "the good" HDL levels.

Here is about which fats are being metabolized preferredly - and it's definitely not PUFA:

The oxidation of laurate was the highest of all fatty acids tested (Figure 4⇓). The next most highly oxidized fatty acid was linolenate (18:3n−3), followed by elaidate, linoleate, and oleate, which showed similar rates of oxidation. The oxidation of elaidate (trans 18:1n−9) appeared to be slightly higher than that of oleate (cis 18:1n−9) and the peak oxidation appeared to be delayed by ≈30 min (Figure 5⇓). The 2 long-chain saturated fatty acids were the least oxidized, with only 13% of stearate oxidized over the 9-h test. (DeLany, 2000)

Palmitic acid causes insulin resistance:

Palmitate-induced cellular insulin resistance was clarified by the reduced Akt phosphorylation, glucose uptake and Glut4 expression. Palmitate-caused myotube loss was clearly observed under microscope and proved by myotube counting and expression analysis of myotube marker genes. Moreover, palmitate-induced transcriptional suppression of three health benefit myokine genes (FNDC5, CTRP15 and FGF21) was found, and the different involvement of p38 and PI3K in the transcription of these genes was noticed. (Yang, 2013)

And causes diabetes even further by killing insulin making ß-cells of the pancreas (Maedler, 2001).

Oleic Acid seems to be the one king of FAs that is really only good (it can even reverse damage caused by palmitic acid):

Importantly, oleic acid, but not other long chain fatty acids such as palmitate, increased the expression of genes linked to fatty acid oxidation pathway in a SIRT1-PGC1α-dependent mechanism. As a result, oleic acid potently accelerated rates of complete fatty acid oxidation in skeletal muscle cells. These results illustrate how a single long chain fatty acid specifically controls lipid oxidation through a signaling/transcriptional pathway. Pharmacological manipulation of this lipid signaling pathway might provide therapeutic possibilities to treat metabolic diseases associated with lipid dysregulation. (Lim, 2013)


Further I was quite taken aback finding out that babies born to moms with untreated gestational diabetes (what Ray kind of describes as positive cause it supposedly makes the babies smarter) is also making them likely to develop diabetes later in life!
http://care.diabetesjournals.org/conten ... 6.abstract

So please be careful with Rays advice. And I'm curious if anyone can argue against this with positive studies. The ones mentioned surely can be attacked from certain angles, but there's a lot more that support these findings.
 

CoolTweetPete

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Hi Steffi,

Have you read any of Andrew Kim's work? He clarifies many of Ray's ideas with physiological mechanisms rather than studies. Studies can be misleading, and can be used to prove almost anything. Many are funded by the particular food industry.

For example, study showing gluten is a health promoting food.

http://www.jneb.org/article/S1499-4046% ... 8/fulltext

Here is one of Andrew's articles on UFA and SFA. He has many more on his blog.

http://www.andrewkimblog.com/2013/01/sa ... -fats.html
 

johns74

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Well, I guess this is it. Time to close this forum and move to other things.
 
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When are people going to realize that fat is the least important macronutrient. Carbohydrates equal energy and protein equals structure. Fat just gets in the way of things and causes problems. But SAFA can be used in context to help with the unstoppable onslaught from pufa, so that is SAFA's ultimate role, to protect you from pufa because you're a warm-blooded animal who doesn't have the lipid metabolism as a cold water fish:

"The results demonstrate that supplementing the diet with n-3 fatty acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which was not suppressed by vitamin E supplementation."

http://www.functionalps.com/blog/2012/0 ... oxidation/

There's your fish fat. Do you really want to play the PubMed pissing contest game?

Steffi said:
post 99562 I did my body wrong with all the coconut oil and butter rather than olive oil and fish.

All of that butter and CO? How much are you talking about here? Peat eats a little bit of butter daily but he's also warned about its over consumption in audio interviews. The same with milk fat which is essentially still butter, thus his comments on low fat milk: viewtopic.php?f=17&t=7402&p=93284#p93284

The same with coconut oil. It's a therapeutic tool, not something to be gorged on ad libitum:

Q: "How beneficial are coconut oil and coffee to a healthy person with a good diet?"

Peat: "If the basic foods were chosen for minimal unsaturated fats, then coconut oil wouldn't add much of value. Coffee is a good source of magnesium and niacin, and has smaller amounts of other essential nutrients, besides the caffeine and antioxidants."

He's written a lot about coconut oil and most people should be using it simply because of having a history of high pufa. But it's still something to use correctly.

Ray is not against oleic acid. He has mentioned that olive oil has good anti-oxidants and similar to how he uses butter, a small amount can be used daily but olive oil has accompanied pufa.

The problem with PUFA is PUFA Breakdown products - acrolein, malondialdehyde, hydroxynonenal, crotonaldehyde, lipid peroxides, isoprostanes, prostaglandins, neuroprostanes, eicosanoids, leukotrienes. The true cause of heart disease.
 
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LucH

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Forget the studies for a while and put this question to yourself: What makes cholesterol elevate? What's the use of LDL cholesterol?
You won't blame the fireman to be responsible for a disaster, just because the fireman is always present on the place when fire has started ...
LDL cholesterol is the witness of a problem. If you eat 50 % SFA, no processed food, and a lot of greens with one spf olive oil and fruits + vitamin E (and b-caroten from fruit) (+ vit C because synergy) you will lower your LDL.
LDL cholesterol acts as a bandage when the arteries are weakened and oxidized.
:hattip
LucH

PS: eat also some fish when too much cholesterol. I take one gel chlorella (500 mg) when I eat fish. Only one. to neutralize toxins.
Don't forget selenium to neutralize mercury. As long the ratio is under 1, there is no problem with fish.
 

Steffi

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Hi guys!
I'm not trying to do a study-pissing game. It's about a wholesome theory. It's about thinking and forming your opinion and I appreciate anyones constructive input. The way Ray and others around here portray fats is incomplete and outright wrong - at least what I concluded.

You cannot say SFA is good and UFA is bad. It is much more complicated. If anything, one can say MUFA is good, SFA neutral with some bad and PUFA, well, bad if lots. And then there is the shorter chain FAs as in MCTs. They are a different thing altogether.

PUFA are a very small part of fatty tissue in humans - and you can't have none. They are not preferrably stored nor preferrably released - the opposite is true.

Human body fat composition is rather independent of what you eat and the body regulates it rather tight and there will always be 35% UFA in there. Sport and nutrition can change composition only by a few percent.

All these statements I have heard the opposite of around the Peat circle. The evidence paints a different picture.

If you want to do something good and assure complete FA oxidation without peroxidation and incomplete oxidation - increase your oleic acid. That one promotes it.

Some PUFA have very strong effects in the body, like lowering inflammation and lowering LDL while increasing HDL and also increasing insulin sensitivity. However, I haven't concluded a good or bad for these yet - too much differing information.

And before I started eating implementing Ray's philosophy I had "perfect" blood lipid levels despite being clinically hypo! Now after almost 2 years and being clinically euthyroid my total cholesterol is up, LDL is up and HDL is down - so worse in every way.
 

MCF

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Hi Steffi

I am sorry for your distress. Through months of research on articles on raypeat.com I learned that Dr Ray Peat pays attention to the total cholesterol. Do you perhaps have that number? I have learned that for Dr Peat there is not a "good" or a "bad" cholesterol, he views that as a myth or invention if you will. The "good"-"bad" number might have been created by drug companies in order to promote their agenda and to sell drugs. This is not to demean in any way your concern regarding fats in any way. That is a different issue and I would not pretend to know enough to address the matter. I am writing to you because a while back, a cardiologist prescribed 4 drugs to my partner after a cholesterol blood test that was interpreted as him having "high" LDL. It took countless hours of research for me to realize that his total cholesterol was on the low side. His total cholesterol was 160. He was put on dangerous drugs, one of the drug prevent his body from making cholesterol, the very protective and vital substance we need. In the case of my partner "conventional wisdom" was rather unwise.
 

Tarmander

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I am glad you brought this topic up. I definitely think there is more to fats then SFA good, everything else bad. Context is obviously very important.

I do want to share one personal experience. I used to eat a lot of chips, really liked them, craved them. I cut them out a couple years ago, along with all PUFA about 9 months ago. Nothing earth shattering happened, but I do feel better not eating PUFA. Just yesterday I took my mom out on a birthday lunch, and I had an omlette which I assume was fried in some type of vegetable oil. Within a couple hours of eating it, I felt pretty depressed. I was depressed in a way that I usually associate with inflammation. I got home and took some anti inflammatories and felt better. This is no science experiment, but I am pretty positive given this experience and others that PUFA is just not something I should eat.

However PUFA is so confusing because it can definitely do things that seem to be helpful, like lower blood sugar. I have talked to so many people happy about their cholesterol after consuming large amounts of fish oil. IT is just confusing without proper context.
 

Steffi

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The distress comes more from finding out that SFA are much worse than I thought, MUFA much much better und PUFA can have beneficial effects.

I totally agree that cholesterol is widely "misused" and I'd never take or recommend cholesterol lowering drugs. But it doesn't matter if the cholesterol is the problem or there because of a problem - it is indicating a problem. Especially when it was "perfect average" before. Maybe my eating has nothing to do with it - but there is a lot of knowledge out there that would explain the reason well. And I am now very comfortable trying out a different path, including especially MUFAs preferred in my diet.

Fortunately my blood sugar seems to be absolutely unchanged (irregardless of thyroid status). I'd expect nothing else looking at my family history. But if it did change I'd have a few things to blame it on and consuming SFAs would be a pretty important one.
 

MCF

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Steffi

Your quote:
"I am now very comfortable trying out a different path, including especially MUFAs preferred in my diet".

May you benefit greatly in the path that works for you. The best we can do as humans is to be conscious and present in our own life's journey. You have done that by doing research for yourself and reached an answer that you resonate with. At the end of the day it is your health, wellbeing and peace of mind that matters.

Thank you for sharing your findings with us.
 

jyb

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Steffi said:
And causes diabetes even further by killing insulin making ß-cells of the pancreas (Maedler, 2001).

The problem is that these kind of cell culture palmitic acid studies are subject to discussion and you can reach an opposite conclusion depending on the study. Peter from Hyerlipid has written a lot about different studies on palmitic acid. Palmitic acid is typical of dairy, so I personally feel very safe eating it and I increased my consumption after reading Peter. There's probably a dozen entries about palmitic acid, but here are 3 to get going:
http://high-fat-nutrition.blogspot.co.u ... mmoll.html
http://high-fat-nutrition.blogspot.co.u ... -ends.html
http://high-fat-nutrition.blogspot.co.u ... ia-in.html

I wonder if diabetes even exists in populations following a rich dairy tradition. Obviously that's a rare tradition now for the last 50 years as sat fats have been gradually replaced with stuff like margarine, even in the healthier Europeans countries that have been heavy dairy consumers.
 

tara

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As far as I can tell, Peat says the main benefit of having a little SFAs regularly is that they can dilute and displace some of the PUFA. So you can't make a balanced assessment of Peat's attitude to SFAs without also considering the PUFAs.

It seems to me that Peat has pointed to pretty strong evidence that PUFA are anti-metabolic toxins. Some of these hazards are well-known in the mainstream, too, e.g. PUFAs are sometimes used to deliberately suppress immunity when people need transplants to not be rejected.

Steffi said:
post 99562 Coconut oil isn't all that great according to this paper:
https://gupea.ub.gu.se/bitstream/2077/3 ... 2909_1.pdf

It can be concluded that coconut fat as the main fat in the diet led to significantly higher TC levels and LDL levels in adults compared to diets rich in HUFA, which is today
not considered to be beneficial when it comes to blood cholesterol in relation to health.
The line you quoted above is just a restatement of common perception. We know that PUFA have been promoted over SFA for decades.

They show reduced total cholesterol after using more HUFA/PUFA. I'm not sure that this is news. It seems to be the main argument for PUFAs over SFAs.

There is little information about the rest of the participants diets and initial or subsequent health, and in some cases less than half the dietary fat is ascertained:

The fats provided from the three different diets were approximately 36 E%. In the Coconut fat diet, 46% of the fat content was from coconut. The same ratio of butter was given in the Butter fat diet. In the Safflower oil diet, 29% of the fat content was from safflower oil.

This seems to me to be the big leap of faith (logic):

Cardiovascular disease
In this systematic review the relationship between the consumption of coconut fat and blood cholesterol levels, and not the relationship between coconut fat and CVD, has been examined. It has not been investigated in what way an intake of coconut fat may
increase the risk of CVD, but only the extent to which it affects cholesterol levels in the blood. To be able to express how coconut fat would affect the incidence of CVD, research has to be divided into two steps: the first being coconut fats effect on blood cholesterol and the second being cholesterols effect on CVD. Regarding the second step, a comprehensive international study, named the INTERHEART study, concluded dyslipidemia as a major risk factor for CVD (31).

As far as I can tell, the meaning of risk factor is correlation, not necessarily causation. The causation could be some third factor that causes the first two.

Separating out these two steps seems to invalidate the point of the study - it does not show the effect of the fats on CVD, only on cholesterol levels. I think Peat's point (and Broda Barnes') would be that low metabolism and other factors can cause both CVD and higher than normal cholesterol levels. I'm fairly sure I read of at least one study of men with CVD that had to be stopped because the intervention group, who had PUFA margarine replacing butter, were dying faster than the non-intervention (ie still eating butter not marg) group were. In terms of what's good for us, I count mortality effects as a lot more significant than changes in risk factors.

Just for the sake of illustrating the (il)logic:
Step 1. Grey hair is a risk factor for death.
Step 2. Dye can largely eliminate grey hair.
Conclusion: Dying hair significantly reduces mortality.

Also, dislipidemia is a risk factor for CVD, but low cholesterol is correlated with worsened mortality from several causes for significant chunks of the population, and there seem to be reasonable causal explanations for these links.

There are other poisons that can lower TC, too. Some of them are big business.

Do the other studies you linked use sounder logic?

Have you taken a look at Haidut's several threads pointing to studies related to fats?

Steffi said:
post 99562 Further I was quite taken aback finding out that babies born to moms with untreated gestational diabetes (what Ray kind of describes as positive cause it supposedly makes the babies smarter) is also making them likely to develop diabetes later in life!
http://care.diabetesjournals.org/conten ... 6.abstract

That the offspring of mothers with diabetes (gestational or otherwise) are more likely to develop diabetes, does not seem surprising or contradictory to Peat's views. Peat has suggested that metabolism can be inherited epigenetically, and that diabetes tends to be associated with hypothyroid states, so I don't see why this wouldn't include a greater risk of diabetes if mum had this metabolic imbalance.

The conclusion of the linked study suggests that it is Mum's blood sugar levels themselves that are causal. I may not have read the study thoroughly enough, but I see they controlled for various factors that may well be relevant, including class, but I see no mention of thyroid. I see no method to distinguish whether the results arise from the hyperglycemia, itself, or the impaired glucose metabolism.

I don't think Peat suggests that diabetes is generally a good thing, pregnant or not. He favours restoring glucose utilisation to resolve the problem, rather than just avoiding sugar. He is opposed to blinding and strictly controlling lood sugars without adressing more fundamental causes. Peat has talked about it being hopeful that people may sometimes be able to correct metabolism, and avoid passing such burdens on to their offspring.
Is there anything in that study showing (rather than just assuming) that strictly limiting diabetic Mum's blood sugar (without curing the diabetes) would reduce the risk of the offspring inheriting the condition? I didn't see this, but I may have read too hastily.
 
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Giraffe

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Ray Peat said:
The fetus produces saturated fats such as palmitic acid, and the monounsaturated fat, oleic acid, which can be turned into the Mead acid, ETrA (5,8,11-eicosatrienoic acid), and its derivatives, which are antiinflammatory, and some of which act on the "bliss receptor," or the cannibinoid receptor. In the adult, tissues such as cartilage, which are protected by their structure or composition from the entry of exogenous fats, contain the Mead acid despite the presence of linoleic acid in the blood.
Ray Peat said:
When dietary PUFA are not available, the body produces a small amount of unsaturated fatty acid (Mead acids), but these do not activate cell systems in the same way that plant-derived PUFAs do, and they are the precursors for an entirely different group of prostaglandins.
Ray Peat said:
If we didn't eat linoleic acid and the other so-called "essential fatty acids," we would produce large amounts of the "Mead acid," n-9 eicosatrienoic acid, and its derivatives. This acid in itself is antiinflammatory, and its derivatives have a variety of antistress actions. The universal toxicity of the polyunsaturated fats that suppress the Mead fats as they accumulate, and the remarkable vitality of the animals that live on a diet deficient in the essential fatty acids, indicate that the Mead fats are important factors in the stability of our mammalian tissues. This protective lipid system probably interacts with cellular proteins, modifying the way they bind water and carbon dioxide and ions, affecting their electrons and their chemical chemical reactivity.
https://en.wikipedia.org/wiki/Mead_acid
Mead acid is an omega-9 fatty acid, first characterized by James F. Mead. As with some other omega-9 polyunsaturated fatty acids, animals can make Mead acid de novo. Its elevated presence in the blood is an indication of essential fatty acid deficiency. Mead acid is found in large quantities in cartilage.
 

tara

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Steffi said:
post 99562 So all started because my blood lipid levels have gone bad from being spot on average before I started "peating". LDL is high now.

What did you change from and to when you started "peating"?
Had you been suppressing cholesterol with lots of PUFA or other means before?
Did you actual health (as opposed to your/yr drs interpretation of your lab tests) get better or worse?
If your health got worse, that seems like a good reason to change something. There are lots of variables to consider.
If you've now changed things again, are you noticing any health improvements from the changes?
 
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James IV

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The real flaw is evaluating your health based on random numbers established as "healthy" perameters.
 

burtlancast

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schultz

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You seem to be really hung up on your cholesterol level. I'm curious as to what it actually is?

So you had a normal cholesterol level and low thyroid and you started taking dessicated thyroid and eating sat. fa?. Your thyroid normalized but you're upset because your cholesterol went up? It sounds to me like you got healthy and your body normalized. Did you feel healthy on the thyroid and sat. fat?
 
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