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I Dont Know What To Call This Thread But Its A MUST SEE

dbh25

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Jul 29, 2016
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653
Lab tests are always a picture of what’s going on in your body at a defined time (when you get bloods drawn). The idea behind them is to make them useful through giving an accurate picture, meaning don’t try to game them just show up after some day to
How is he gaming the test by tracking results based on what he eats?
I think it shows these tests are useless
 
L

lollipop

Guest
Good for him but advocating low carb and/or ketogenic diets is ignoring all the evidence against them. There’s no evolutionary advantage to a high fat / ketogenic diet and no population thrives on it. It’s a short term strategy only. Going from 300+ to 200+ TC means nothing at all from a health standpoint, besides that his metabolism is slow.

Being insulin sensitive is much more desirable, having high LDL receptor activity and high (cholesterol) metabolism and therefore low lipid numbers is much more desirable, not being hypothyroid is much more desirable.



Lab tests are always a picture of what’s going on in your body at a defined time (when you get bloods drawn). The idea behind them is to make them useful through giving an accurate picture, meaning don’t try to game them just show up after some day to day routine is set. Then ask a capable doctor to read a blood test, which is the technical part, although what they prescribed is a strong indicator to whether you should look for another doctor or not.

Edit - and yeah the AHA is an awful bunch of policital morons who wanna pay their bills being in bed with big pharma. As a pharmacist I can safely say a large number of doctors MDs or pharmDs aren’t fools and have the basis that engineers don’t. But we’re in a day and age where people want magic pills to cure their lifestyle nonsense, and wanna feel good about eating more fat. So what shall we say that isn’t perceived as boring at best, or threatening to most?
This makes sense to me. Can’t ignore that truth that ketogenic is only a short term strategy. I totally agree that Long term no one can thrive on it.
 
L

lollipop

Guest
I think it shows these tests are useless
Maybe not useless but only able to show a particular snapshot in time and not able to give a whole picture. I remember Haidut saying something like this. Take them, but be cognizant that they are only a snapshot of one particular time and could rapidly get another measurement with a test taken at a different time.
 

Travis

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Never forget that 'high cholesterol' quite often simply means a function of serum cholesterol, which says nothing about cholesterol at other locations. Saturated fat doesn't 'raise cholesterol' in the sense that it increases de novo synthesis, but raises serum cholesterol on account of changing the lipoprotein/chylomicron saturation index. Unsaturated fatty acids take up more space, are less dense, have higher kinetic energies, and have higher water solubilities: all of the aforementioned properties tend to reduce their affinity for cholesterol. Conversely: the saturated fatty acids have higher cholesterol affinity, density, lipid-solubility, etc. For these reasons, long-chained saturated fatty acids will predictably raise serum cholesterol concentrations which, incidentally, are higher in the low density lipoprotein fraction (LDL) simply because that is where the saturated fats necessarily are; if they were made of α-linolenic acid (18∶3ω−3), they simply wouldn't be 'low density.'

By since cholesterol doesn't even cause cardiovascular disease it doesn't need to be worried about; if a person still worries about it, for some odd reason, they taking DHA (22∶6ω−3) will predictably (1) increase the HDL∶LDL ratio, (2) decrease the serum cholesterol concentration on account of the high kinetic energy and relatively low (for a lipid) oil solubility, and (3) be distributed into the brain where it can serve to repel cholesterol from the grey matter towards the white matter—it becomes myelin—where it belongs, serving to increase glucose flux in the process by lowering cell membrane density. Although Ray Peat tends to marginalize polyunsaturated fatty acids in general, docosahexaenoic acid—or is precursor α-linolenic acid—is (are) the only real essential one(s). Without DHA in the brain: glucose flux, mylelination, and IQ decrease very quickly (see Zellweger's disease).

But what is actually capable of causing increases or decreases in de novo cholesterol synthesis is surprisingly the Zn²⁺∶Cu²⁺ ratio.
 

benaoao

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Apr 21, 2018
Messages
368
Saying ”cholesterol doesn’t cause heart disease” is dangerous because it makes people fine with high cholesterol. High cholesterol means a low liver metabolism of cholesterol, quite simply. Whether someone’s had X or Y fatty acid in the mix the days before or ate Z meal that increase de novo genesis, it’s up to themselves but not significant

I agree that DHA shouldn’t be avoided. I don’t understand Ray/some posts in this forum on the matter. DHA is good. 10% Of the fatty acids are polyunsaturated.

Also giving a reminder that PUFAs form cholesteryl ester which make it seem like total cholesterol is lowered but those esters are then found in plaques.

IMO, PUFAs and statins to decrease cholesterol are the wrong approaches to lowering it back to optimal levels. Unfortunately that’s what medicine favors because that’s easily quantified through studies and blood tests. But I’m optimistic and I believe some day doctors in their majority are going to connect the dots.
 

benaoao

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Optimal levels of cholesterol as seen in mammals and non western humans are in the low 100s

It doesn’t matter that it’s not backtracking for more than 3, 30 or 300 days. What this topic shows is “have you done anything special or out of ordinary the last 3 days?” - If the answer is no and your cholesterol is high then you have to fix the lifestyle.

What this topic also shows is besides one person in this video, they may try as hard as they want to lower LDL on a test, their cholesterol is still one of a >60-70yo person
 

tara

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Optimal levels of cholesterol as seen in mammals and non western humans are in the low 100s
But AIUI, in Western humans, cholesterol levels in the low 100s seem to correlate with increased mortality rates, especially in older people.
And I'm not sure about the mortality/longevity rates in the non-Western countries you refer to - do they really make a strong case for such low cholesterol levels?
 

benaoao

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Like okinawans?

Correlation isn’t causation. High cholesterol however, is slow metabolism. It’s fine as one age, I guess*. Definitely not as a younger person. It’s the one thing I’ve been saying again and again in this thread, overall mortality is secondary when you’ve got a 30yo implying hundred of grams of SFA should be eaten on the regular .

*and I’m not even sure of this.

Relationship between serum cholesterol and the risk of acute myocardial infarction in a screened cohort in Okinawa, Japan. - PubMed - NCBI


0 E06 A7 E3 3520 475 E 9441 6 F0 EC37503 FD
 
Last edited:

tara

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Correlation isn’t causation.
I quite agree.
High cholesterol however, is slow metabolism.
Indeed there seem to be some strong indicators that slow metabolism can be a causally contributing factor for elevated cholesterol levels. Broda Barnes, amongst others, wrote about this, and his patients seemed to benefit from his approach.

Cholesterol is a necessary and useful substance - and we can sometimes have higher levels because we need more of it, or because it's conversion to downstream substances is not functioning well for some reason. I would guess that optimal cholesterol levels in a human depend on the context - the state and conditions they are in may require more or less cholesterol. Forcing cholesterol level down in someone who needs it to be higher could be potentially harmful. Forcing it up in someone who doesn't need it may not be great either.

I guess you've come across the firefighter analogy.

Comparing with other primates, I'd note that whatever one may say about their health, and I imagine this would vary a great deal depending on the conditions they are in etc, they don't generally live as long as humans.
 

Mito

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Birdie

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Do you have the study that contains that graphic? I’m not sure Peat would agree with total cholesterol in the low 100s as optimal.

The Paukapuka and Tokelau had much higher cholesterol levels than your examples.
Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies | The American Journal of Clinical Nutrition | Oxford Academic
View attachment 9152
I remember Peat's mentioning a study where people in a convalescent home did better with a 250+ cholesterol level than with lower.
 

Peater Piper

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Like okinawans?
Okinawans lived on chronic hypocaloric diets. Their diminutive stature is evidence of that. Unless you're going to place someone on a similar low calorie diet, I'm not sure how transferable their results are to someone with greater access to food. The same goes for all the rural Chinese in the China Study. I'm not saying low cholesterol isn't desirable, but are you aware of any populations with cholesterol in the low 100's who aren't undersized (evidence of lack of calories and protein)? Also something of note, pathogens and parasites are known to lower cholesterol, and they're not exactly uncommon in rural populations.
 

benaoao

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It’s absolutely true that larger people may benefit from more cholesterol so you guys are right to point that out. Older people too since their metabolism slows down and they still need some cholesterol so they will need “more firefighters “ to do the same job. I actually got my fathers off statins because I do want him to have higher levels of cholesterol instead of hammering his levels down (and his mood is much better already).

What I’ve been saying however, is that a sedentary unathletic 30-something guy with those levels of cholesterol does have an obvious faulty cholesterol metabolism, and that’s concerning, that happened to me when I was eating a high fat diet. Eater even more fats wasn’t the solution, going to a natural low fat high carbs whole foods diet was. As a 29yo very active man I want my levels in the 100-150ish range.

In a society with higher levels of “pregnenolone steal” I’d perceive a high cholesterol level (LDL and HDL alike) as a marker of inflammation and stress. It’s fine since cholesterol is a band aid, so to speak, I’m not saying it’s the big bad villain. I’d much rather have no need for increased levels of cholesterol, that’s my approach.

I have the same approach with DHT, NO, e2.... nothing the body produces is bad. But if it’s piling up there’s an issue that I’d believe is lifestyle related.

@Mito ill dig that up
 

Mito

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I’d perceive a high cholesterol level (LDL and HDL alike) as a marker of inflammation and stress.
Although cholesterol is protective, it seems useful to use it as a indicator of a slow LDL metabolism (i.e. thyroid) and/or inflammation. But I’m not sure TC in the range of 150-200 indicates a metabolic or inflammatory concern especially if eating a low PUFA/high saturated fat diet.

In a society with higher levels of “pregnenolone steal”
The Myth Of Pregnenolone Steal
 

benaoao

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Poorly worded but you know what I’m talking about; aka the up regulation of HSD enzymes leading to more Cortisol and less DHEA/sex hormones.
 

Gone Peating

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Never forget that 'high cholesterol' quite often simply means a function of serum cholesterol, which says nothing about cholesterol at other locations. Saturated fat doesn't 'raise cholesterol' in the sense that it increases de novo synthesis, but raises serum cholesterol on account of changing the lipoprotein/chylomicron saturation index. Unsaturated fatty acids take up more space, are less dense, have higher kinetic energies, and have higher water solubilities: all of the aforementioned properties tend to reduce their affinity for cholesterol. Conversely: the saturated fatty acids have higher cholesterol affinity, density, lipid-solubility, etc. For these reasons, long-chained saturated fatty acids will predictably raise serum cholesterol concentrations which, incidentally, are higher in the low density lipoprotein fraction (LDL) simply because that is where the saturated fats necessarily are; if they were made of α-linolenic acid (18∶3ω−3), they simply wouldn't be 'low density.'

By since cholesterol doesn't even cause cardiovascular disease it doesn't need to be worried about; if a person still worries about it, for some odd reason, they taking DHA (22∶6ω−3) will predictably (1) increase the HDL∶LDL ratio, (2) decrease the serum cholesterol concentration on account of the high kinetic energy and relatively low (for a lipid) oil solubility, and (3) be distributed into the brain where it can serve to repel cholesterol from the grey matter towards the white matter—it becomes myelin—where it belongs, serving to increase glucose flux in the process by lowering cell membrane density. Although Ray Peat tends to marginalize polyunsaturated fatty acids in general, docosahexaenoic acid—or is precursor α-linolenic acid—is (are) the only real essential one(s). Without DHA in the brain: glucose flux, mylelination, and IQ decrease very quickly (see Zellweger's disease).

But what is actually capable of causing increases or decreases in de novo cholesterol synthesis is surprisingly the Zn²⁺∶Cu²⁺ ratio.

Does higher zinc:copper increase or decrease cholesterol synthesis?
 

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