My Buddy LDL

Not all LDL particles are created equal!

That’s it! I’m sticking up for my friend poor, old LDL cholesterol (mind the pun of course. Get it – sticking up for…sticking…). From now on Dr. Oz or Ornish, if you want to bad mouth my little buddy, you’re gonna have to go through me:

Let's see your guns Oz!

Anyhow, LDL cholesterol (the so called “bad” cholesterol) the stuff that clings to your arteries like a barnacle to a pier isn’t exactly bad per se. It’s actually a good friend and serves a very useful purpose.

LDL has two main sizes – small dense and large “fluffy.”

They look like planets or suns - the beauty of nature

Both are very different, serving very different purposes.

Question for y’all: When was the last time your doctor told you at your yearly physical that there are sub-classes of LDL and that some are responsible for turning your arteries into sticks of solid margerine and some are not? What’s that you say? She never told you?

My doctor (sweet as she is) was completely unaware that the difference in LDL particles size mattered. All that did (and still does) matter to her was that my total LDL number was low. But a low LDL reading alone doesn’t tell you squat. You need more information.

It’s sort of like a police captain being radioed by an undercover cop that there are 20 criminals robbing a bank he’s in. The captain asks “How many of them have guns?” He replies, “I don’t know.” This lack of information forces the captain to assume that all the criminals have weaponry when maybe none do or just one does. He has to go overkill with armament and risk killing them all – some that are not killers and never have been.

It is generally accepted that the small dense LDL particles are the ones that stick to your arteries and the large buoyant ones don’t. In other words, the small dudes are packing and the large ones aren’t. So what you want is very little small, dense LDL particles floating around in your blood stream.

You want your LDL pattern to look like this:

My pattern is similar to this but a tad more towards the A side.

Ask your doctor for a VAP test at your next physical so that you can see what your pattern is.

Truth is, without any nasty, beastly, gooey, sticky, LDL cholesterol, you’d croak. You need these little dudes in the same way you need plaster when the walls of your home get damaged. Imagine that the walls of your house could bleed when damaged and if you didn’t plaster the walls quickly enough, your house would die. But also imagine that the plaster pushes the walls a little closer together than before. Imagine this happening over and over again until you can’t get in the house. (You’ll see why I say “pushes the walls closer together” a bit later in this post.)

So, what’s good is when small, dense, LDL cholesterol comes to your rescue and “patches up” your damaged artery walls. What’s bad is when too much of this goo builds up and either A: breaks off and sends itself careening down your arteries to who knows where:

This is bad news!

or B: the build up is so great it occludes (disallows) blood flow.

Arterial occlusion by cholesterol

This is how cholesterol actually builds up in your arteries:

[youtube=https://www.youtube.com/watch?v=KdVOIu0Fe40&w=540&h=360]

See how the build up doesn’t occur on top of your arteries but rather, builds up from within? This is why I said that the walls of your house get closer together rather than the plaster building up on the outside of the walls.

However, what’s really bad, bad, bad, is when gurus like Dr. Oz and Ornish and movies like Forks Over Knives misinform you and the rest of the universe about the role LDL (and about cholesterol in general).

Dr. Oz actually said in a recent Times magazine article that a Paleo Diet can cause ketoacidosis. Incredibly, he mistakes ketosis with ketoacidosis. Tells you a lot about what he knows. I’ll be blogging on the Time article soon.

So the $64,000 question is WHY? Why is cholesterol – a substance vital to life – hell bent on killing us all? First let’s learn a bit about cholesterol. From Wiki:

Cholesterol is a waxy steroid of fat that is produced in the liver or intestines. It is used to produce hormones and cell membranes and is transported in the blood plasma of all mammals.[2] It is an essential structural component of mammalian cell membranes and is required to establish proper membrane permeability and fluidity. In addition, cholesterol is an important component for the manufacture of bile acids, steroid hormones, and vitamin D.

Yeah, it sure is bad stuff.

So, why does it sneak around looking to settle in our arteries attempting to kill us? Is it angry that we ate it? Some gurus say well, sure – cholesterol is an important substance but eating too much of it is no good. Really? I didn’t know that when too much is eaten, it sails through your body of blood like a Spanish Galleon looking to land and stake claim on the continent of Artery. If that were the case, Atkiners would be dropping like flies in the middle of the street on a daily basis.

And what about the vegans and vegetarians that get heart attacks and heart disease? They do you know. Oh yes, I forgot – it’s just their genetics. They’d have died even sooner had they not adopted a plant-based diet. (Well, not plant based – plant only diet. It’s a sneaky little term “plant-based.”) Yeah, right.

Speaking of vegans, here’s a pic of President Clinton when he was eating plenty of cell-building cholesterol:

Bill looking robust

Here’s a pic of him now, bereft of dietary cholesterol:

Poor Bill.

But of course, the zeitgeist that fat and cholesterol are evil is so deeply embedded in his brain, even looking at himself in the mirror and seeing that he’s a shadow of his former self isn’t enough to wake him up and smell the lipids. Sigh.

Anything that causes damage to your artery walls gives your body a reason to create SDLDL (small dense LDL) and send them on their merry way to fix the problem.

You can’t blame policemen for riots or firemen for fires.

Doctors who give you drugs to keep your liver and intestines from making LDL cholesterol are like mayors firing their policemen to handle crime better or laying off their firemen to stop fires.

Yes, it’s better to have very little small, dense LDL floating around inside your body. But it’s only better if you are taking measures to keep your body from needing these particles. Capeesh?

So, stop smoking. Stop drinking like a fish. Handle your stress better. Eat a real food, fat-based diet. (Wait I think I coined a phrase there…). Research shows that a low carb, real food diet alters the LDL particle size/pattern from SDLDL to LBLDL. Why? ‘Cuz it’s a healthful way to eat that significantly decreases systemic stress and inflammation that’s why!

Take a look-see.

So the next time you hear Dr. Oz, Ornish and all the other cholesterol bullies spouting their vitriol against our little friend, tell them to stick it .

Forks Over Knives

[youtube https://www.youtube.com/watch?v=O7ijukNzlUg&rel=0&hl=en_US&feature=player_embedded&version=3]

Here’s my blog for today – read Denise Minger’s critique of the movie Forks Over Knives.

I am in AWE of her brain.

‘Nuff said.

Charts, Charts, Charts…

I was tooling around online and found something interesting.

Take a look at this chart:

As you can see, since the 1970’s, we’ve been chowing down more on carbs and less on fat. And the types of carbs we’ve been imbibing more of are not (and I think we all agree), more carrots and kale.

Take a look at this one:

This is the NHANES data for macronutrient intake from 1970 to 2000. NHANES stands for National Health and Nutrition Examination Surveys. This chart supports the chart above on macronutrient intake till 2000. More carbs, less fat.

As you can see from this next chart, we’ve been getting fatter since 1980 – after roughly a decade of increased carb consumption and decreased fat consumption.

US Weight trends over the past four decades

So it’s pretty clear from these charts that eating fat doesn’t make you fat. So those of you who still hold that eating fat makes you fat, ditch that idea now and forever. It just ain’t so.

Here’s another NHANES chart showing the same. Round about 1980, BAM!

Dang!

Now, it’s easy to jump to the conclusion that carbs are to blame for this. Bad carbs, bad! Tsk, tsk.

But take a look at this chart:

"Food, food, food, everything is food..."

So it appears we have been slowly and gradually eating more calories as well (of course those calories are all from carbs), about 250 calories per day max from 1980 to 1990 where it levels off. Calories – you know, those little gadgets that our bodies have no receptors for. Think about that for a sec or two or three, or…

We hear the same R.D./fitness guru mantra in our sleep explaining fat regulation: “Calories in = calories out…yaddya, yaddya, yaddya…” “The law of thermodynamics, yaddya, yaddya, yaddya…”

Hey meng – jour body doesn’t know from no stinkin’ calories, meng.

We are living entities. Our bodies do different things with different macronutrients (fat, protein and carbohydrates), in different ratios, at different times and in different states (cooked, not cooked, etc.). It ain’t just in/out, open/shut, up/down, fat/thin. Badda bing, badda boom.

Take a hypothetical pair of identical twins – one eats 2000 calories a day (assume this is the amount of calories is what they both need to maintain their body weight. This is a totally bogus concept mind you, but I’m too dim to explain it any other way) of fatty meat. The other twin eats 2000 calories a day of rice. Do you think that at the end of a decade of eating like this their bodies would look exactly the same (aside from the fact that the rice-twin would be dead)?

Fahgettaboutit.

Now, look at the total caloric intake chart again and eye-spy the total calorie intake between 1970 and 1980. By gum, it goes down! But if you look at the chart above the energy intake chart, you’ll see obesity rose during this time. Do tell! The law of thermody-what? As a nation, we were eating LESS total calories but were still getting fatter. Wassup wit dat?

After 1980, we started eating more food – for whatever reason (I have my hunches as to why) and as the chart shows, we continued to get fatter still. How can this be? Since it clearly has nothing to do with the total amount of calories, might it be the type of calories we are eating? Perhaps? Maybe? Possibly? Hypothetically? And what then did the increase in carbs and the decrease in fat do to some of our metabolisms and hormonal profiles?

OK, it’s time for another chart. Here ya go:

The carb-tide is turning...

Kinda looks like Americans went to the library and pulled out a copy of The Protein Power Lifeplan! (BTW, this is an affiliate link.) Less carbs, more fat and adequate protein. Calories? Who cares, as we learned above.

I think that the title of the book – Protein Power – is a tad misleading. It really should be called Fat Power because this is the macronutrient you want to swap the carbs for, not more protein necessarily.

I’m not criticizing my co-authors mind you. I’m just pointing out that many people think low carb diets are high protein diets and that is not so. Americans have always eaten adequate protein more or less.

It’s nice to see that people are slowly realizing that fat is not so bad after all and that it’s the carbs that have to be curtailed – specifically the refined carbs. Obviously no one is denigrating spinach and cabbage.

The change in American’s macronutrient intake is due, in large part, to all the low carb/sugar, high fat bloggers out there who continuously shove science down the gen pops gullets. These would be folks like:

Gary Taubes
Jimmy Moore
Mike Eades, M.D.
Dana Carpender
Tom Naughton
Andreas Eenfeldt, M.D.
William Davis, M.D.
Laura Dolson
Richard Feinman, Ph.D

And a host of others.

But what’s really interesting here is this. Carb consumption is going down and fat consumption is going up and, at the same time obesity rates have somewhat plateaued starting around 2004-5. (I think sugar consumption also plateaued a few years earlier). Take a look-see:

You can see that in both the obese and the overweight, things have slowed down here and there. Obviously not ALL people have dropped their carb intake and increased their fat intake. All these charts reflect a national average.

I put to you that, if you put 2 and 2 and 2 and 2 and 2 and 2 together, you’ll see what I’m seeing. That as calorie intake plateaued and carbs consumption fell, weight gain halted too. Again, the increase in calories over 10 years by a max of 225 calories cannot account for the obesity epidemic because from 1970 – 1980 calorie consumption fell and weight gain continued.

Given this fact, I think it’s pretty clear that the increase in carb consumption along with the decrease in fat consumption, which drives up blood sugar and thus drives insulin which then drives insulin resistance which then drives excessive fat storage which then drives hunger which then drives more fat storage is to blame.

You are what your body does with what you eat.

Have you ever met a person who was obese and has never eaten refined carbs and has always kept total carb intake low? No you haven’t and you never will. The only way you can become obese from food intake is by eating most of your calories from carbohydrates, specifically, refined carbs and starches.

This is not to say that there aren’t some people who can and do eat most of their calories from carbs who aren’t fat (usually, if not always, the carbs these people eat are predominantly veggies and fruit). But that is beside the point. You can smoke and not get emphysema or lung cancer. But smoking directly causes these two maladies.

There’s a reason why it’s not called a “meat belly!”

I’ll be blogging on the bogus concept of food reward soon – a hypothesis that is just the calories in, calories out concept in disguise.

Fat Regulation: Insulin or ASP?

insulin_influence

When we eat and get fatter, how does that work exactly? What mechanisms are at play that turn the things we eat into the goo that gets stuffed into our fat cells?

: Fat inside a fat cell called a lipocyte

Many nutritional experts say obesity is caused by eating and drinking too much – taking in too many calories in other words. Well, OK, but when we do overindulge, how does the excess turn into fat? Why doesn’t it turn into muscle, bone or organ tissue?

Insulin or ASP
There’s been some debate about the role of ASP in the regulation and storage of fat tissue. Some argue that Acylation Stimulating Protein (ASP) is the main regulatory lipid hormone and not insulin. Based on a series of papers and this one from late 1998, some have taken these papers to mean that ASP plays not only a critical role in fat storage and retention, but the critical role.

If it is ASP, this means significant amounts of body fat can be gained and retained merely by eating fat; that carbohydrates are unnecessary to stimulate insulin secretion, because ASP will do the fat storing and imprisoning job all by its lonesome.

But is it? Is it ASP or insulin that is the “boss” of fat?

This is what the current edition of Lehninger Principles Of Biochemistry says about fat storage in adipocytes:

“High blood glucose elicits the release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen and triaglycerols, while inhibiting fatty acid mobilization in adipose tissue.”

Seems like an open and shut case for insulin being the boss of fat regulation. But perhaps there’s more to it than this.

To find out more, I figured I’d do the obvious and actually ask the man who wrote the series of papers I mentioned earlier. His name is Dr. Keith Frayn. Dr. Frayn is from Oxford University and is considered one of the world’s leading experts on fat metabolism. If anyone knows anything about what regulates fat in the human body, it’s him.

But before I tell you what Dr. Frayn said, here are a couple of snippets about ASP written by a blogger known as Carbsane. She is one of several bloggers who believe that the carbohydrate/insulin hypothesis of obesity is bogus, meaning, not the primary cause and that those who support it are misinforming the gen pop:

“ASP is mentioned in Frayn’s latest version of Metabolic Regulation, but unfortunately texts are woefully outdated. They are NEVER considered better references than peer review journal articles. Read my latest blog on a Frayn article: Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein. ASP is a more potent stimulus to fatty acid uptake and esteriﬁcation in adipocytes than is insulin.”

“ASP is a potent agent in triglyceride clearance from circulation, insulin less so, although it can stimulate ASP. But this study did demonstrate that IF we are to point to fat accumulation, ASP is the big Kahuna. Insulin is not, as far as I know, directly involved in fatty acid uptake (as in transporting it).”

Really? Insulin is not directly involved in fatty acid uptake?

What’s interesting about this statement is that in Dr. Frayn’s 2010 textbook Metabolic Regulation (3rd edition) there’s still very little mention of ASP and the section on fat accumulation says nothing about it.

Carbsane has suggested in her blogs that Gary Taubes, author of Good Calories, Bad Calories and Why We Get Fat has committed intellectual dishonesty by stating that insulin is the main fat-regulating hormone and not ASP.

“I am increasingly convinced that Taubes deliberately maintains a state ignorance on such matters as ASP. Because it pretty much demolishes his hypothesis.”

She says this because she thinks (stated in her blogs) that Taubes and others who support the insulin/obesity hypothesis purposefully ignore the work done by Dr. Frayn (and others) on ASP subsequent to the printing of his 1998 text book. You can read her statement here in the body of the blog and in the comments section . In fact, if you are really interested in this issue, please read her blog post before continuing with this one. If I’ve got it wrong, reading her blog will set the issue straight. You be the judge.

If Carbsane (and others) are right in thinking that Dr. Frayn believes ASP is the main fat regulating hormone and not insulin, it seems really odd that Dr. Frayn would choose to exclude this information in his 2010 textbook. Why would he omit such a discovery? You’d think that such a fact would have Dr. Frayn penning much about it.

Let’s see if she (and others) are right about insulin not being the main fat regulating hormone. Let’s see if ASP is really the “big kahuna,” as Carbsane puts it, of fat regulation and find out the reason why Dr. Frayn made so little mention of ASP in the new edition of his textbook.

As I mentioned earlier, contacting Dr. Frayn seemed like the obvious thing to do. Here is the word for word email exchange that resulted. It’s true that our conversation is a half year old now, but I’ve been busy and the points are clear.

From: Fred Hahn [[email protected]]
Sent: 11 February 2011 18:49
To: Keith Frayn; [mailto:[email protected]]
Subject: A question on ASP
Dear Dr. Frayn,

I was wondering if you could answer a question for me on insulin and acylation-stimulating protein (ASP).

Of the two, which is a more potent stimulator of fatty acid uptake? A biochemist said that it is not controversial; that ASP is a more potent stimulator of FA uptake/esterification than insulin. I gleaned from your textbook that insulin was by far the main regulating hormone of fat storage and release and at best ASP was secondary. Am I correct? Any clarification is greatly appreciated.

Thank you very much for your time.

Sincerely,
Fred

His response:

From: Keith Frayn [mailto:[email protected]]
Sent: Saturday, February 12, 2011 3:47 AM
To: Fred Hahn
Subject: RE: A question on ASP

Hi Fred

The ASP story is very controversial. A number of people have not been able to reproduce the claimed effects of ASP. So I think we’re still in the dark. But insulin definitely does work! I can’t say for certain but my bet is that insulin is the major regulator of this step, with maybe some local ‘fine-tuning’ by ASP.

Hope that helps. Have you seen edition 3 of my textbook? Out in 2010. (https://eu.wiley.com/WileyCDA/WileyTitle/productCd-1405183594.html?productCd=1405183594 )

Best,

Keith

I wanted Dr. Frayn to be a bit more specific. So I sent him another email. He replied promptly.

From: Fred Hahn [mailto:[email protected]]
Sent: 12 February 2011 20:56
To: Keith Frayn
Subject: RE: A question on ASP

Thank you Dr. Frayn.

A blogger I recently read (she is a research scientist) who quotes your textbook often, quoted your article on ASP (which confused me given what your response was to my question):

“Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein (ASP) and ASP is a more potent stimulus to fatty acid uptake and esteriﬁcation in adipocytes than is insulin.”

She goes on to say:

“ASP is mentioned in Frayn’s latest version of MR, but unfortunately texts are woefully outdated. They are NEVER considered better references than peer review journal articles. Read my latest blog on a Frayn article:

https://carbsanity.blogspot.com/2011/02/non-esteried-fatty-acid-metabolism-and.html

Here she is referring to your 1998 version. I assume that ASP is not mentioned in the 2010 version of your textbook as the main fat regulator (I know this because a friend has it and he looked) over insulin because, as you said, no one has been able to replicate ASP as the predominant fat regulating hormone?

I don’t want to take up too much of your time Dr. Frayn, but I and several other people are very interested in this subject and wonder if elevated insulin (and to a lesser extent ASP) levels are what is responsible for excessive fat accumulation in adipocytes.

I think we can definitely state that insulin’s the regulator of fatty acid release through its action on HSL. That’s enough evidence, wouldn’t you say, for it to be the primary regulator of fat accumulation? I say this because if insulin keeps fat in the fat tissue, it’s not all that important whether insulin or something else puts it there though I think high insulin levels caused by high carbohydrate intake sure seem to facilitate greater fat accumulation especially in the presence of high fat which is how most people eat.

So, I guess the bottom line question is, given what we currently know about insulin, is insulin the primary regulator of fatty acid uptake as well as the primary regulator fatty acid release, not ASP?

Thank you,
Fred

His response:

From: Keith Frayn [mailto:[email protected]]

Sent: Monday, February 14, 2011 2:45 AM
To: Fred Hahn
Subject: RE: A question on ASP

Hi Fred

My guess is that you are right: insulin is the primary regulator of both fatty acid uptake and fatty acid release. The ASP story was a nice one but I don’t think it’s been substantiated.

Best wishes

Keith

There you have it. ‘Nuff said.

Hobo Health – An Observation

Riding back from the Catskills the other day I observed a homeless man walking along the highway dragging his cart of things. Since traffic was slow, I had time to notice that his face was reddish brown, his bare arms were deeply tanned and he sported a full shock of hair. Other than his clothes, he looked kind of good actually. He was probably in his late 40’s or early 50’s.

Years ago, I used to see a particular homeless man on the Upper West Side of Manhattan all the time. I would always wonder what in the name of all that is holy is keeping this man alive. He smoked, drank, ate from garbage cans and clearly took drugs of all sorts. Yet, he lived for years like this. As I recall, he too had a full head of thick hair, thick beard and tan skin.

In the summer in NYC near where my gym is, I often see a particular shirtless homeless man walking around on Broadway. He’s in such good shape that he’d win a trophy in an amateur body building contest if he entered. He too has a full head of hair.

What is it that keeps these people alive – and with heads of hair to die for? (O.K., so I’m a little obsessed with head hair.)

Today it dawned on me (mind the pun) – it’s the sun. Yes, good old vitamin D.

These homeless men are outside all the time. They probably get more quality sun time in a week than many of us do in a year. And I don’t have to tell you how important vitamin D is for your immune system and overall health. Just read through the link I provided above or this link to find out all about how important vitamin D is and how deficient most people are especially vegetarians since they eat little fat and oils.

Experts today suggest that our serum vitamin D levels in our blood should be at least 40 ng/ml. A few clients of mine who I suggested have their vitamin D levels checked due to frequent illnesses were below 20! That is not good.

Cod liver oil is a good source. So too is salmon and mackerel. Beef or calves liver, eggs, sardines are also decent sources. Cheese contains little if any D. Ready to eat cereals are fortified with D, but you don’t want to put that sort of garbage food in your temple just to get some.

Vegetarians and especially vegans should take a D3 supplement in olive oil. From what I have read, D3 is better absorbed than D2.

But everyone should get more sun – sans sunscreen of course. You don’t need to slather on sunscreen when in the sun unless you are walking through the Mohave dessert. Talk about an industry that has freaked people into putting on a coating of chemical goo just to go to the park for a few hours. The best sunscreeen I know of is called a tree.

Lack of sun could have been the reason the Bubonic plague and other plagues took such a toll on people. Think about the dress of the 14th century – take a look: