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Cholesterol Logic

12 Sunday Aug 2012

Posted by John Hanson in Cholesterol, Diabetes, Food, Literary, Nutrition, Science

≈ 3 Comments

Tags

asociation, carbohydrates, cholesterol, faith, food, insulin, LDL, nutrition, saturated fat, science, studies, sugar, sugar kills

Cholesterol is a hot and complicated topic. It’s not easy to wrap your head around it, especially when you consider that even the experts haven’t so far.

Here’s a bit of proof: The National Heart Lung and Blood Institute is in charge of cholesterol treatment policy. It tells the rest of the world what to do. Nevermind for now that Big Pharma tells the NHLBI what do do. The fact is the NHLBI does not know what causes atherosclerosis. They cannot say without reasonable doubt that cholesterol causes it. In fact, they say outright “The exact cause of atherosclerosis isn’t known.”

For the logically feeble readers: if you do not know what causes something, you cannot say what causes something.

“Bill, somebody egged our windows again.”
“It’s those damned Pentecostals, Martha.”
“How do you know it’s them and not the Catholics?”
“Because I see them driving up and down the street all the time in their bus!”

This is cholesterol logic. It’s thinking like this that has made the western world fat and sick. It’s this type of logic that has made it okay to drink Coke and Pepsi, to add sugar to 87% of the 600,000 food products in America *Dr. Lustig Rumor from #AHS12*, and to consider bread a household staple because it tastes good and is full of added vitamins which many think we only pee away.

The path to cholesterol policy has not been paved with good science. We fed excess cholesterol to rabbits, herbivores, and they developed atherosclerosis. Nobody asked why. Nobody speculated if that cholesterol was sitting in a box for three months that it might be somewhat rancid. Nobody asked whether feeding a foreign substance to a herbivore was valid. Nobody asked whether no dead rabbits was important.

“Eating cholesterol hardens arteries, and that’s all that matters.”

Apparently that’s not all that matters. Anything that raises or lowers cholesterol also matters. *palm-plant* Eating saturated fat raises cholesterol; therefore it’s bad for you. Oatmeal lowers cholesterol; therefore it’s good for you.

“But the Presbyterians also drive their bus up and down the street, Bill.”
“It can’t be them. We’re Presbyterians.”

Cholesterol logic.

There have been lots of studies about the associations between cholesterol and heart disease, and there have been many studies on associations between foods and cholesterol. By extension, either directly or implied, there are also associations between food consumption and death by cause. Which of these is most important?

The answer is none of them. All association studies do is raise questions. We cannot assign cause to associations. I don’t care how good your math is, statistics do not form physical links between two things. This has been written about time and again, and I’ve argued it with mathematical geniuses. But the fact remains: math can never explain a cause of anything. You always need to proceed with scientific experiments to validate the questions.

Scientific experiments have never proven cholesterol or saturated fat causes heart disease; therefore the NHLBI’s assertion that we do not know its causes is correct.

And we should, therefore, not be saying what is or isn’t dangerous based on such evidence. The Seven Countries Study, The China Study, the Nurses Health Study, The Farmingham Study, and countless others should only raise questions; they do not provide any answers. Anybody who makes a conclusion about cause based on an association study is either totally incompetent or biased, take your pick.

Let’s quickly take a look at a confounding study: Dr. Ronald Krause’s 2010 Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. This study basically says all the other food studies are wrong: they do not prove there’s an association between saturated fat consumption and heart disease.

“But it’s obvious that eating animal fats and meats raises cholesterol; therefore it must be bad.”
“I hope you don’t bet on the races much.”
“The races? They have nothing to do with this discussion.”
“Exactly!”

Cholesterol logic.

I won’t get into metabolism much; because I am not a biologist, but I do know enough to be a little dangerous. Please correct me if I’m wrong here.

Dr. Peter Attia states that LDL-P is the problem, not LDL-C. Let’s first look at the “science” of fat metabolism without getting into the details. Fats are packaged in our guts into chylomicrons which utilize an APO-B 48 protein. The liver packages available carbon energy into triglycerides utilizing the APO-B 100 protein. The 100 means it expresses 100% of an LDL particle. Fats do not contribute directly to LDL counts. Period. This simple gap should exclude all such discussion, but of course it doesn’t. We have to place our trust in more remote, black box effects like studies.

“These people ate more fat and their LDL-C went up. Therefore, fat cause cholesterol to rise.”
“Couldn’t something else cause it to rise?”
“What kind of stupid question is that? You get a C for your grade.”
“Sorry, I thought science programs encouraged stupid questions.”
“Only stupid questions that make us rich and famous.”

Cholesterol logic.

Possible explanations: Eating high sugar degrades LDL quality. The resulting particles are smaller, and since the Friedwald Calculation is based on volume, the LDL-C looks lower. And when sugars [fuel for TG production] are eliminated, the rise in LDL-C is due to large, fluffy, benign particles. We are pretty sure that high triglyceride production results in low LDL particle size, but I do acknowledge that this is an association as is small LDL particle size with increased risk of atherosclerosis. But if you want to trade association punches, I submit that mine are stronger than yours. Let’s go! Actually, the smallness theory lives in somewhat of a doubtful house. The whole retention-response theory holds very little attraction due to scarce and conflicting evidence. Still, it seems likely that whatever causes small particles may also cause heart disease, just like whatever causes obesity also causes diabetes [not all type 2 diabetics are obese].

“That makes perfect sense John, but your LDL-C is still higher than I want. Take this statin.”
John sits in stunned silence for a few moments. “No.”

Cholesterol logic.

Here’s an interesting study on Iranian women. These women had very low levels of triglycerides and when their LDL-P was measured, it was discovered the value was far lower than their LDL-C values. It even prompted a proposed new calculation of LDL-C when triglycerides are very low. By the way, if triglycerides are very high, LDL-C isn’t performed because the calculation isn’t reliable. Just sayin’.

Another interesting study shows glycation [attack by sugar] directly decreasing cholesterol size and quality making it atherogenic. To me this is very damning evidence against sugar.

What does John know? Well, his cholesterol numbers are outstanding on a high saturated fat diet, so all of you saturated fat causes cholesterol causes heart disease good can bugger off. John’s eye-artery issues have gone away with his diet. We might say they’ve gone away with his lower blood sugar levels, that’s still a possibility, but it’s more sure with his diet. Zero signs of eye disease in last four years of LCHF. My good BGs have lasted six years. Those first two years were hell. And of course less sugar consumed equals fewer blood sugar problems. Back to logic. If fat was a cause of arterial issues, wouldn’t John’s eyes be getting worse? There’s been zero new blood vessel growth, zero bleeding, zero background retinopathy, and zero artherosclerosis seen in his eyes in four years of LCHF eating. And when I say high fat, I do mean high fat. 60-70 percent of my calories come from fat. I drink a quarter to a half litre of whipping cream every day and use two to six tablespoons of coconut oil plus fatty meat, butter, high fat cheese, olive oil, and more.

Examination of the small blood vessels (arterioles) in the retina of the eye with an ophthalmoscope is valuable for diagnosis. Atherosclerotic arterioles reflect light (emitted by the ophthalmoscope), giving them a “silver wire” appearance.

I am living my life on faith. I am following an ancestral style of eating and dispensing with modern man’s conclusions of what a healthy diet is. I do this largely because what man has said doesn’t add up but also because the results of my forays have been spectacular. I’ll be honest here: I don’t trust humans. They are biased, corrupt, and stupid. I raised my kids by telling them that 80% of people were idiots. “Be in that top 20%,” I said. They said I was wrong. It’s more like 90% are idiots. The biggest fault I see is the populations’ lack of sound logic. They think with Cholesterol Logic.

Won’t That High Fat Diet Raise Your Cholesterol?

26 Thursday Jul 2012

Posted by John Hanson in Cholesterol, Diabetes, Food, Nutrition, Science

≈ 84 Comments

Tags

carbohydrates, cholesterol, fat, lipids friedwald

I’ll try to stay focused today. I need to write some serious fiction tonight.

Background:

I
– am a type 1 diabetic in my 37th year of battle.
– am 51 years old.
– ‘ve worn an insulin pump since 2006
– have battled diabetic proliferative retinopathy since 1994
– have received 4,000 plus lasers that kill the peripheral regions of my eyes
– experienced major bleeds in 2006 resulting in blindness and surgery (vitrectomy)
– suffered subsequent bleeds for two years
– decided I needed to risk a major change, so I tried a high fat low carb style of eating in 2008
– have been 911’d nine times while sleeping
– have experienced over 100 major hypoglycemic events [I’m thick headed]
– I’ve fought HBP at 145/80

Current Status:

I’m still at it and doing very well. I now run an A1C hovering 6%, my optho hasn’t seen any signs of damage since I started this way of eating, I’m down 20 pounds, I have much more energy, and I feel great, my BP is normal now with no meds.

I now have hope I’ll live until my senior years and actually be able to enjoy some of them.

Cholesterol:

But this post isn’t about all of these changes. This diet I follow centers around animals as food, and not just the red, stringy muscle but the fat too. In fact, the more fat the better. My breakfast is usually a cup of two of coffee with coconut oil (a saturated fat) and heavy whipping cream, no sugah. My dinner tonight was a package of bologna, some cheddar cheese, and some raw pineapple. My lunch was a bag of garden kale.

I eat the diet everybody says is supposed to kill me. Well, that’s what they say. The curious part, though, is when you ask them to explain it, they backtrack a bit:

“We know that cholesterol causes heart disease, and your diet raises cholesterol.”

“But have you studied whether this diet really results in heart disease? I mean, that’s one big assumption you’re making here.”

Silence.

The standard response to this question is silence. Everybody believes so much in it that they feel there’s no need to support it to us radicals. The world is simply better off if we continued our suicidal paths — an estimated 10 million people worldwide have bought in to this plan.

The truth seems to be there’s no scientific evidence to support this belief that consuming fat and cholesterol kill. I could throw study after study after study at you, but honestly, I can’t even find a hint of science that supports it. Well, there is some.  I’ve pretty much convinced myself after my own reviews of the evidence, and I do ask supporters of the lipid hypothesis for their evidence, that this hypothesis actually has no sound basis. So far, nothing.

I’ll throw one little meta analysis at you. Dr. Ronald Krause has shown that there is in fact no association between saturated fat intake and heart disease. These are the studies this lipid hypothesis is based on, and they don’t even link to heart disease.

So back to cholesterol. Do I really care if fat makes my cholesterol rise if it doesn’t cause heart disease? Does fat even raise choelsterol? Studies used to arrive at this conclusion have also been debated, but I won’t get into those. Let’s assume studies show it’s true. I’m more curious about what it does to me. My records below go back four years, and when I started keeping track, I was taking a statin. This magic pill was supposed to produce magical cholesterol values, numbers I’d be able to write mom about if she were still alive. Numbers my endocrinologist was very happy with. Note that yellows are not on target — their targets. My ratios have all been optimal: they couldn’t get any better, yet he wanted me back on a statin because my LDL was not where a diabetic’s should be, never mind lowering it risks many things such as mental degradation and muscle [including the heart] damage.

Summary of targets: HDL should be high, LDL should be low, and Triglycerides (TG) should be below 150.

Debate: The low carb community wants TGs below 0.8 which indicates LDL particle size is large and fluffy and benign, the only measurement that really matters. I tend to agree. Low TGs will naturally increase LDL because of size increase: The Friedwald is a volume measurement, and particle size increases volume. As a test, throw ten grains of sand in a full glass of water. Then set ten larger pebbles or stones in it. That’s basically how the Friedwald test works to measure cholesterol.

So please, explain how my lipid profile has evolved into something that looks like I made it up it looks so good? I found a comment that said the highest HDL value ever seen was 117, and mine’s 112. Explain how this diet that is supposed to kill me does that? And now my LDL is lower than when I was on a statin. I’ll repeat that. My LDL, the value my doctor gets all worked up about, is as low as it was while I took his statin. Am I a freak of nature? Hopefully at a future appointment I’ll ask for my pre-2008 values. I’d really like to see what my numbers were before all this hoopla.

The bottom line: saturated fat is supposed to be deadly because it messes up cholesterol numbers. Right. You run with that people.

Chol History

Cardiovascular Risk:

John is a type 1 so falls into the high risk category. His LDL-C should be below 70 and his Non-HDL-C should be below 100.
http://www.mayomedicallaboratories.com/articles/communique/2011/11.html

Goal (mg/dL)
Risk category
LDL-C
Non-HDL-C
Very high riska <100 (optional <70) <130 (optional <100)
High risk: CHDb or CHD risk equivalentc <100 <300
Moderately high risk: ≥2 risk factorsd (10-y risk, 10% to 20%) <130 (optional <100) 160 (optional <130)
Moderate risk: ≥2 risk factorsd (10-y risk <10%) 130 160
Lower risk 160 190

 

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