Search Results for: cholesterol

Insane Clarity – Cholesterol, Ketogenic, and Low Carb Myth Busting

I was just going to leave it at that. And this one too, even though I had a follow-up post planned initially. Then I got this comment from "FormerBlogger."

A few of us quit blogging (fairly prominent sites) because we were tired of being associated in any circles with Jimmy Moore. You just could never win. If you didn’t affiliate with him, people thought you were a hater; if you did, you just didn’t sleep well at night knowing you were acknowledging a doughy dufus who made money marketing himself. At the end of the day, some of us chose to sleep at night, and put our sites to rest (we had a combined running total of well over two decades).

I asked recently why Jimmy Moore was so fat. I was met by the excuses of accolytes, from “his book writing made him gain weight” (funny, I wrote two and never gained weight), and “I choose to support Jimmy” (which isn’t even a response). People refuse to hold him to the standards we should hold marketers and salesmen to. Now that he’s jumped into paleo, it’s even more incomprehensible this new crowd is looking the other way. Why isn’t anyone calling this chubby guy out? Why are people funding a lie? Are we saying there are no better alternatives out there? And if not, why not? Where’s the common sense leadership?

And from "AnotherFormerBlogger."

There are many of us! Jimmy Moore is obese again, nothing new, I just won’t participate and haven’t in a few years. Not my monkeys, not my circus.

Along the way, there have been a number of mildly dissenting voices; that after years of supporting Jimmy Moore and standing up for him many, many times, I'd finally had it with him. And, I understand their dissent. The old "baby with the bathwater" thing.

Well, yea, but this has become Rosemary's Baby, now. It's high time for infanticide.

...I recall first getting wind of Jimmy in about early 2008, I think. It was also a time where he'd maintained his LC-diet weight loss for a decent while but was beginning to experience problems. As a guy on the decline from 245+ to an eventual 175 myself (then at perhaps 220), I overlooked it, largely because of the podcast. I never read his blog regularly—I have my own. But the podcast was quite something in those days. So much cool info that really helped me gain a wide perspective.

And, it was quite something to initially be a guest, then another appearance or two, and finally, guest hosting it about a year ago. Now, I see the podcast as an endless array of The Usual Suspects to prop up his sycodouche, peppered with the occasional dissenting voice to manipulatively lend a sense of integrity to people who are only looking for authority figures anyway. I choose to not feed into any sense of Guru seeking, going forward. Rather, I wish to declare open season on all Gurus, for whateverthehell reason you like.

It's difficult to regret any of it, however. I'm more of a life goes on kinda guy, and don't ever agonize over couldashouldawoulda. Humans are very bad at integrating the context of the time with actions at that time. Give yourself a pass, and just don't do that shit anymore once you come to your proper senses.

...Someone else pointed me to Jimmy's "I Will No Longer..." post, where he's going to let himself off the hook in terms of adhering to pretty much every standard that's logically, critically integrated into everything his Low-Carb Business is about.

I was talking to a trusted friend this week about what’s been happening in my life over the past year that has had a direct impact on my weight. I’ve been very open and honest about this and working diligently behind-the-scenes to create strategies that will help control the stress that is raising my cortisol and blood sugar levels making it next to impossible to lose weight right now despite faithfully eating low-carb, high-fat. With so many people writing to me sharing their own frustrations about the lack of weight loss despite everything being right in their diets, I wanted to offer up some encouragement to them and myself that all hope is not lost. Keep in mind there are so many non-diet reasons why your weight is stuck or going up, including stress-induced cortisol spikes (what I believe I’m dealing with), lack of sleep, hormonal imbalances, getting older, and more. I’m always amused by those who say the ketogenic diet must not work because people like me don’t have the “perfect” body and weight. Despite our cultural obsession with this, there are many other markers of health besides weight–triglycerides, HDL cholesterol, minimal small, dense LDL particles, A1c, fasting insulin, hsCRP (key inflammation marker), CT heart scan, and many other tests. The fact that these markers are still all excellent for me is what keeps me motivated while still working through the weight challenges.

Shorter Jimmy: I'm so stressed about not losing, but gaining weight instead, that I can't lose weight, only gain weight.

Do you even need to unpack that? It is too ridiculous; it is to laf. It is designed for his cadre of fucktard sycophants—who are now beyond excuse for their own selves. Read the bolded sections again. Essentially: it's got to be something else, and not that one thing we can't speak of, lest it tarnish the LC/Ketogenic magic appeal of gluttony.

Jimmy gained about 60 pounds AGAIN!, in a year or two—an incredible rate of gain in a SAD world where it typically creeps up on people 10 pounds per year—and it could be anything or everything except the one thing that actually caused it: he ate too fucking much, too fucking often.

The CICO guys are once again vindicated. You can't fool mother nature; you can't fool physics or thermodynamics. Now, WHY he ate too much too often IS a valid question, and it's my particular area of interest. In that, all of his excuses might play a role, and others, such as the gut microbiome. But, the role is contributory to making the conscious or unconscious decision to eat too much, too often: the absolute cause of his gobsmacking weight gain over a relatively sort period of time is simply eating too much over that period of time than he expended in energy over that same period of time—and even the Eadesian metabolic advantage of 300 kcal/d doesn't matter.

People get stupidly confused about this, because they weigh themselves every day and lose the forrest through the trees. The bod doesn't work like that. Every long-term weight gain is comprised of a wave function with days of weight gain and weight loss, in an overall upward trend. Every long-term weight loss is comprised of a wave function with days of weight gain and weigh loss, in an overall downward trend. The difference is that in the former, it's higher highs and higher lows. In the latter, lower highs and lower lows.

So, you can count all the fallacious ways Jimmy got fat yet again, if you like, but there's really only one reason, you silly cunts. Nonetheless, he's going to let himself off the hook—that people are rightfully holding him to account for—because it's inexplicable and, "despite everything being right in [his] diet." That's called an A priori falsehood. You don't even need to get up off the couch to know and understand that virtually nothing is right with his diet.

...This is nothing new, though, and guys like Dr. Michael Eades paved the ad hoc way. They taught acolytes well in Atkinianity. Here's Eades' modus operandi:

  1. You haven't read the studies.
  2. Oh, you have? Well, you might want to look at the full text, not just the abstract.
  3. Oh, you did that too? Well, you need to understand how to interpret them.
  4. ...Oh, BTW, it's either observational, it's old, or the researchers don't understand basic biochemistry, or they're not serious anthropologists, or whatever.
  5. Oh, still not satisfied? Well, OK, then it's basic biochemistry. I'll post about it in a year or more.
  6. What? A genetic mutation that makes some people different? Dismissible. "Stef," and Basic Biochemistry.
  7. Oh, BTW, there are experts in the field. An expert is someone I think I agree with.

I don't hate Jimmy, though I can't bring myself to well wishes, anymore. I'm a bit disgusted by Michael Eades. I think he's lying an manipulating—which is why I'm glad he went into the appliance business. I'm a sucker for redemption and even though you can do a decent sous vide on the cheap, his creation is cool and I paid for it, so he can't take it away.

Look here. It's but one tiny example of what The Duck Dodgers have been dealing with in terms of Eades' Intransigence for well over a year—though we started off in a very honest attempt to get him to come along with new discovery. Valhalla proved too enticing.

This is from Peter's blog, last November. The snark goes substantially up the thread, but here's where it gets funny. Eades:

No dishonesty on my part at all. You once again are getting confused by Draper's speculation versus what was actually measured.

It is true that Draper did write the above line in the paper in question. But here is where critical reading of the literature comes in. In Table II on page 314 (for those of you who want to follow along from home), in the far right column, it shows the glycogen content of the native foods (meat) to range anywhere from 0.1-0.9 grams. I averaged it to 0.5 grams. Remember, these are not speculative - they are measured. And measured in the native foods. Which is what, I have assumed, we've been talking about all along - the native Inuit diet of meat. [condescension emphasized]

Uh, oh.

LOL, so you are having trouble reading. You read it wrong!

Table II is not measured in grams. Table II is a measurement of percent of nutrients obtained from native foods.

In other words, each column is just the percentage of that nutrient that was obtained from native foods.

Try reading a little more closely next time, Dr. Eades!

Did that humble him in any way? Bitch, please: He's Doctor Eades! And here's a more recent Dr. Eades (his blog doesn't have comment hyperlinks, so hit that link and do a Find on a relevant string). He still must assume—and show his congregation of blind-believing, cock-sucking, groupie-whore fucktards—that any interlocutor isn't aware of studies; only read the abstract if he is aware; or doesn't know how to "interpret" them if both prerequisites have been satisfied (rather like a Supreme Court interpretation of the plain English U.S. Constitution). In other words, the very only way that you and Mike Eades could ever see eye to eye on any study ever done anywhere, by anyone, at any time, is if you agree with him on its findings.

Your comments make it patently obvious that you have little understanding of the stable isotope literature. [...] you need the 15N studies for that. All of which you carefully ignore.

You’re interested only in promoting a specific viewpoint that bears little resemblance to scientific reality. And, like Team DD, you’re fond of cutting and pasting large swaths of text without really knowing what they mean or how to interpret them. And, like Team DD, you’ve drifted into repetitive troll territory.

So (BTW, his interlocutor was just another in "Team DD"):

Right back at you. You are apparently unaware that the 15N values are misleading for determining meat consumption:

“Nitrogen isotope values in particular can be misleading. First, because of the complex nonlinear relationship between food source and consumer, it is not possible to accurately estimate the proportion of meat versus plants in the diet, since large changes in the percentage of meat are indicated only by small increases in 15N values (Ambrose et al., 2003; Hedges and Reynard, 2007). Second, unlike herbivores that acquire all of their protein from plant leaves, foraging humans usually eat plants for their carbohydrate content, and therefore focus on the starch- and sugar-rich storage organs of plants, such as USOs and seeds (Lee, 1979; Marlowe, 2010). These storage organs may have higher nitrogen values (Hedges and Reynard, 2007), and in any case provide a smaller amount of protein to the body and are therefore relatively swamped by the meat protein signal.” –

Therefore, you won’t be able to conclude much about meat consumption from 15N values.

But there’s no need to be rude and terse with me. Do you always talk like that to anyone who disagrees with you?? It seems we are talking about different hominid species. I was referring to the dramatic shift from C3 foods to C4 grasses and sedges around ~3.5 million years ago, as explained by the National Academy of Sciences. Nowhere in any of the studies does anyone conclude that high-meat consumption was the most likely source of that shift for early hominids. You are inventing such conclusions if you think that’s what the studies said.

He published the comment, but it's crickets after that. I'm sure all his Usual Eades Groupie Fucktards took note of that. Not.

I'm not sure if you knew this, but rumor has it that Mike Eades has a Low-Carb, Fire-Breathing, Ketogenic Dragon in His Garage.

"A fire-breathing dragon lives in my garage." [...]

"Show me," you say. I lead you to my garage. You look inside and see a ladder, empty paint cans, an old tricycle--but no dragon.

"Where's the dragon?" you ask.

"Oh, she's right here," I reply, waving vaguely. "I neglected to mention that she's an invisible dragon."

You propose spreading flour on the floor of the garage to capture the dragon's footprints.

"Good idea," I say, "but this dragon floats in the air."

Then you'll use an infrared sensor to detect the invisible fire.

"Good idea, but the invisible fire is also heatless."

You'll spray-paint the dragon and make her visible.

"Good idea, but she's an incorporeal dragon and the paint won't stick." And so on. I counter every physical test you propose with a special explanation of why it won't work.

Now, what's the difference between an invisible, incorporeal, floating dragon who spits heatless fire and no dragon at all? If there's no way to disprove my contention, no conceivable experiment that would count against it, what does it mean to say that my dragon exists? Your inability to invalidate my hypothesis is not at all the same thing as proving it true. Claims that cannot be tested, assertions immune to disproof are veridically worthless, whatever value they may have in inspiring us or in exciting our sense of wonder. What I'm asking you to do comes down to believing, in the absence of evidence, on my say-so.

In this context, the ad hoc, goal-post-moving is a concerted effort by Moore, Eades, et al, to prop up a sense of wonder in the ability to fool mother nature by being a quotidian glutton—only just keep the carbs low. It does work for some, perhaps many people. It worked marvelously for me at 25-30. Doesn't at 54. But, perhaps the real reason it worked for me at 25-30 is that it satiated me, and I focussed on various active things that took time away from sitting around, wondering what was in the cupboard or fridge.

Again, WHY you eat too much—too often for your level of activity—is the issue you ought best be dealing with. Or, think of it this way: it's not eat less, move more. Perhaps, it's move more less 'cause you're engaged. Think about the difference.

Well, all is apparently right with the world. Jimmy wrote Cholesterol Clarity to explain away very high cholesterol numbers that normal people don't have and might want to be concerned about—this is way apart from the Cholesterol Con. Then, he wrote Keto Clarity to explain away his and others' dietary failure on Atkins. And since it's now Atkinianity, it can't be wrong. Explanations, qualifications, and interpretations are always needed to keep the catechism sound for all the children.

Mike: call your office. Childrens needs interpretations.

The ABC Australia Pulls Catalyst Show On Cholesterol & Statins. So See It While You Still Can.

When I was alerted to this last week my reaction was "it's a good thing." It's always a good thing when the government (no typo) censors something they don't want you to see.

I make no meaningless distinctions between the State, Media, and Mega Business—particularly when it comes to the food and drug multinationals. One in the same, pretending to be different. Hell, there's isn't even investigative journalism, anymore. Whether right or wrong, deep investigative journalism into the affairs of State serves a good purpose. Witness that there are still some who see this. I give you Sheryl Attkisson and Michael Isikoff.

Here was the ABC's press release concerning their own shame.

Today, the ABC’s independent Audience and Consumer Affairs Unit has released its findings regarding a controversial Catalyst program on statins and heart disease.

The detailed investigation was prompted by a number of complaints into two Catalyst programs, collectively titled Heart Of The Matter, aired in October last year. The report of the investigation is available here.

While acknowledging the importance of public health issues relating to the efficacy of heart disease treatment and the contrasting opinions of highly-qualified scientists, the A&CA has concluded that the second episode breaches ABC standards on impartiality.

Because of the interlocked nature of the two programs, both will be removed from the ABC website. Information will be added to the program website and the ABC Corrections page to advise of the steps that have been taken.

Ah, isn't that sweet. Don't let people decide for themselves. Protect your advertising revenue coming from big drug and food companies under the guise of "protecting the public from reporting that 'breaches ABC standards on impartiality.'"

What an hlarious laf at pipsqueaks and clown whores for ad revenue. I'm talking to you, Mark Scott, whore.

But, in the end this is a good thing, because information can't be contained. These programs and transcripts probably exist in a number of places, but are actually still on The Way Back Machine.

So here's what I need you to do for planet earth today.

  1. Put on your hats of objectivity. Whether or not you agree with the message, realize that the shenanigans that gets a message banned that you disagree with is the same shenanigans that will get the message banned you agree with.
  2. Everyone gets to decide for themselves, and everyone has an opportunity to persuade or dissuade others. This is the nature of the Internet, of unfettered access to information anyone in the world who cares enough can upload or publish for everyone's consideration.
  3. Watch the programs and/or read the transcripts while you still can.
  4. Get this message out, that I've just written, to as many folks as you can.
  5. Admonish anyone you have contact with, who has the tech and tools, to preserve these programs and transcripts, forever. The Way Back Machine is pretty cooperative in removing stuff at the request of originators, so get on it.

With any luck, far more people will end up seeing these programs now, as a result of the ABC's shameful actions, than otherwise ever would have.

Update: I would be remiss to not shout out for Dr. Maryanne Demasi, the lovely peach who put this together. I can only imagine her disappointment at having it pulled. She'll win in the end.

Don’t Worry About Cholesterol

A comment by Dr. Charlie, biochemist.


Sorry for delay in getting back to you re TC/ apoB and Gabriella’s concern over a patient who had a blip in her LDL readings. In a way I’m glad that I did because just by chance I watched again the Wisdom of Clouds speech by Tom Naughton and the lecture by Prof Tim Noakes on YouTube, entitled “The Great Diet Controversy: UCT taught me to Challenge Beliefs”.

Although we could discuss the size and shape of the cholesterol bearing particles and whether it’s the number or total quantity that should be considered, I think that it is more important to consider whether the whole concept of the cholesterol hypothesis is correct. In the early days of the hypothesis many trials attempted but failed to establish a clear link between cholesterol and CHD – yet the medical profession were eventually persuaded that there was a very positive relationship.

I would agree with Noakes’ response to a question concerning cholesterol levels and say that women should not pay any attention to them – no work has shown any link for them and for men over 50, high cholesterol levels have been shown to be protective. For example, many studies, including the famous Framingham study begun in 1948, have shown that in people over 50/60, higher levels of cholesterol are protective (ie the death rate comes down with higher cholesterol). I just happen to have to hand the results of a recent Scandinavian study. This study published in the Scandinavian Journal of Health Care [I think that's the one - Ed] looked at the levels of cholesterol and risk of death in almost 120,000 adults living in Denmark.

The researchers found that having higher than recommended levels of total cholesterol was associated with a reduced risk of death. So they looked at the death rates amongst men who had a total cholesterol level of less than 5 mmol/l and compared that figure with the death rates of men who had total cholesterol levels between 5 and 5.99, and those between 6 and 7.99, and those with levels of 8 and above.

  • They found that in men aged 60-70 when compared to those who had a total cholesterol level of less than 5...
  • those with levels of 5.00-5.99 had a 32% reduced risk of death; and
  • those with levels 6.0-7.99 had a 33% reduced risk of death.

Even in individuals with levels of 8.00 mmol/l and above, the risk of death was no higher than it was for those with levels less than 5.0 mmol/l.

The results were similar for women too. In women aged 60-70, levels of 5.0-5.99 and 6.0-7.99 were associated with a 43 and 41 per cent reduced risk of death respectively.

In individuals aged 70 and over, the results were similar, except here, levels of total cholesterol of 8.00 mmol/l or more were associated with a reduced risk of death too (in both men and women).

Together, these findings suggest that the current total cholesterol recommended by medics and other health professionals are way off beam. And the authors of this study suggested –rather meekly that - these associations indicate that high lipoprotein levels do not seem to be harmful to the general population.

So I hope you appreciate that for me the minutiae of particles may be of academic interest but not of medical interest – apart from the fact that higher levels are protective!


It has been 2007 since I have blogged on this topic, saying essentially the same thing, and nothing seems to change.

Thanks, Dr. Charlie!

Saturated Fat & Cholesterol Worries are so 2009

I love evolution, but particularly in thinking. It's not an issue of right vs. wrong but a process hallmarked by honesty. Evolution happens in large swaths of time, such that discrete changes at any point in time are hard to identify short of outright re-evolution. Then one day, you realize that everything has changed. To my mind, the job of historical scholarship is to relate those seeming gulfs, such that people laf at the way they think today, realizing it's likely fleeting.

Going back to 2007/8 when I first jumped on this bandwagon, perhaps the most helpful thing was to dismiss the dogma of limiting saturated fat and its cholesterol, or cholesterol changing properties. I still remember being part of the whole gig, as blogging about saturated fat and cholesterol in those first few years was an everyday staple. I touted HDL test results as high as 133 mg/DL. Even the Wife Unit got up to 93. No idea what either of us test, today. I'm not interested in such tests anymore.

Around 2010 I developed a nagging nag that I'd gone from unnatural in one direction to unnatural in the other. Saturated fat from animals and some plant oils (coconut & palm) may not be deleterious in the slightest, but why process, concentrate and chow down so much? Moreover, while fats in general are a bunch of lipids, that's about all they are. Check it out.

I got too sick of—and especially low carbers—postings and Tweetings about eating spoonfuls of [processed and concentrated] "nutritious" fats as though it's a superfood (no such thing except offal). Why? That's just going too far in a benign dietary direction to prove IT'S THE RIGHT DIRECTION!

Alas, that's the one thing I've learned from this path: Everyone has to be right, such that everyone else is wrong.

Meat. Fish. Fowl. Vegetables. Fruits. Nuts, perhaps. Get 'em yourself. Cook 'em yourself. And you don't need to essentially deep fry everything—where it's OK, 'cause you're using a skillet! I still have a few ounces left of a 1-lb tub of leaf lard I got almost 3 months ago.

All that said, it does serve to review from time to time. Dr. Greg Venning, always looking out for me, shot me a video the other day. It's an Aussie production, and has as its mainstay authorities Dr. Michael Eades, Dr. Jonny Bowden and Gary Taubes, amongst a couple of others I'm not as familiar with.

It's pretty remarkable how the Doktors in the interview, those from the Australian Heart Whores for the Statin Drug Industry (AHWSDI), appear as dear in headlights.

The video is about a half hour and I enjoyed it a lot. (Good job, Gentleman Mike!)

Heart of the Matter Part 1 Dietary Villains from Michael Eades on Vimeo.

This is a good time to pimp for Tom Naughton, again. Fat Head Director's Cut is to me the go-to in this realm, and it's all done in a sometimes serious, sometimes comedic presentation that begins by debunking The Queen of Fear Porn, Morgan Spurlock, who still won't release his actual food journals from Super Size Me (because he lied his ass off).

So go get Fat Head and watch for a screen clip of this blog in the Director's Cut....

Hey, Mothers: Saturated Fat and “Bad” Cholesterol; Off the Hook

So, a happy special day to all you mothers out there. None of us would be here without you.

Just a brief note before heading off to visit my own mom and family, and what better gift to you all than to let you know that the decades long scam to implicate saturated fat and cholesterol -- such that drug companies can make big bucks selling you drugs to combat nature, multi-national BigAgra can make big bucks growing and selling unnatural, crap commodities, and processed "food" giants can make big bucks manufacturing and selling crap-in-a-box, calling it wholesome and healthy -- maybe just might be coming to an end.

Now, even someone as mainstream as Dr. Andrew Weil is singing a different tune.

You're correct that my thinking on saturated fat has evolved. One catalyst was a scientific analysis of 21 earlier studies, which showed "no significant evidence" that saturated fat in the diet is associated with an increased risk of coronary heart disease. The 21 studies analyzed included nearly 348,000 participants, most of whom were healthy when they were enrolled. They were followed for five to 23 years, during which 11,000 developed heart disease or had a stroke. Looking back at the dietary information collected from these thousands of participants, the investigators found no difference in the risk of coronary heart disease, stroke, or coronary vascular disease between those individuals with the lowest and highest intakes of saturated fat. This goes completely against the conventional medical wisdom of the past 40 years. It now appears that many studies used to support the low-fat recommendation had serious flaws.

Yea, and who has been saying that forever? Lots of us lowly bloggers, that's who. The article isn't perfect, as you'll see toward the end of it, but I hate to bash a serious step in the right direction, so I'll just leave it at that.

The next article is the sort of thing I'm seeing more and more, chipping away at the cholesterol con bit by bit. In ScienceDaily'Bad' Cholesterol Not as Bad as People Think, Study Shows.

The so-called "bad cholesterol" -- low-density lipoprotein commonly called LDL -- may not be so bad after all, shows a Texas A&M University study that casts new light on the cholesterol debate, particularly among adults who exercise.

Steve Riechman, a researcher in the Department of Health and Kinesiology, says the study reveals that LDL is not the evil Darth Vader of health it has been made out to be in recent years and that new attitudes need to be adopted in regards to the substance. His work, with help from colleagues from the University of Pittsburgh, Kent State University, the Johns Hopkins Weight Management Center and the Northern Ontario School of Medicine, is published in the Journal of Gerontology.

Riechman and colleagues examined 52 adults from ages to 60 to 69 who were in generally good health but not physically active, and none of them were participating in a training program. The study showed that after fairly vigorous workouts, participants who had gained the most muscle mass also had the highest levels of LDL (bad) cholesterol, "a very unexpected result and one that surprised us." ...

"LDL serves a very useful purpose. It acts as a warning sign that something is wrong and it signals the body to these warning signs. It does its job the way it is supposed to.

"People often say, 'I want to get rid of all my bad (LDL) cholesterol,' but the fact is, if you did so, you would die," the Texas A&M professor adds. "Everyone needs a certain amount of both LDL and HDL in their bodies. We need to change this idea of LDL always being the evil thing -- we all need it, and we need it to do its job."

It doesn't surprise me and it shouldn't surprise you. The notion that LDL is in any way a problem is rather like concluding that police are the cause of crime, since they always seem to show up at the scene. No, what's happening is that other dietary factors, such as replacing saturated fats and cholesterol laden foods with "fortified" crap-in-a-box, jacks up inflammatory factors and the LDL is simply there to repair the damage. The additional problem is that the damage is so chronic that LDL sits around too long, becoming oxidized.

So there, mothers. Have your sons & daughters treat you to a nice big steak, chock full of saturated fat and cholesterol. Resolve to stop starving yourself on rabbit food and eat luxuriously and healthfully, just as nature intended.

“High Cholesterol,” Statins & Diabetes

My mom went to the doc yesterday. As a Type 2 diabetic who controls it pretty well, she nonetheless still does regular visits. She's very low-carb Paleo-ish, and while she was able to be off insulin for a time completely, still finds she needs very small doses now and then.

To the endocrinologist's credit (a new doc), she did acknowledge being impressed with my mom's diet and supplement regime. But there was one little problem: mom's total cholesterol is 217. The doc asked her if she wanted cholesterol lowering meds. But my mom reads this blog and was thus prepared, indicating that for women, higher cholesterol is associated with increased longevity (lowest all-cause mortality and not just an overly reductionist tunnel vision, zeroed in on cardiovascular mortality).

But the doc retorted with something I can't recall reading or hearing about, specifically. She asked my mom if the studies and information she's relying on concerned women with diabetes and not just a general cross-section, as diabetes is associated with twice the heart disease and stroke as for non-diabetics (according to the doc).

Hmm.... So I did some initial digging around. I ended up writing this in a reply email.

The problem is: what level of diabetes? You control yours pretty well, so there is no comparison between you and someone who doesn't.

There is ZERO benefit to lowering cholesterol, especially in women (indeed, the greater chance is it's harmful). Cholesterol doesn't cause heart disease; inflammation does and this is how statins, when they work, work. But keeping grains, legumes, sugar, and vegetable/seed oils out of your diet has an even more anti-inflammatory influence I suspect. Actually, it simply allows your body to go back to its natural, non-inflammatory state.

I added links to an article by Dr. Duane Graveline at Spacedoc, as well as Chris Kresser's 2-part video series on statins at The Healthy Skeptic. The problem is, neither of those seemed to address the issue specifically, and moreover, there's this quote from the first link.

The fact that there is no statistically proven cardiovascular benefit from the use of statins for cholesterol reduction in women was first publicly disclosed by Uffe Ravnskov in his book, Cholesterol Myths and has been corroborated repeatedly by numerous longitudinal clinical studies.

The ASCOT study, the largest randomized clinical study of statin effectiveness in women, found that the women who took Lipitor, developed more heart attacks than women in the group given placebo.

While not statistically significant this finding hardly supports cardiovascular benefit. In this ASCOT study, 2,000 women were included among 10,000 patients having elevated blood pressure and at least three other cardiovascular risk factors.

Again and again, clinical studies have failed to show that the use of statins lowers cardiovascular risk in women who do not already have coronary heart disease or diabetes.

So just when you think it's all settled, there's that D word, right at the end. This is off the top of my head but as I recall, statins have only been shown statistically beneficial to men who have had a previous coronary event (statins reduce the rate of subsequent events). But is there another category of benefit out there I don't know about?

So I did more digging and came up with this:

Is diabetes a coronary risk equivalent? Systematic review and meta-analysis


Aims To determine whether patients with diabetes without prior myocardial infarction (MI) have the same risk of total coronary heart disease (CHD) events as non-diabetic patients with previous myocardial infarction.

Methods Using MEDLINE, EMBASE, Cochrane and MeSH in this systematic review and meta-analysis, extensive searching was carried out by cross-referencing from original articles and reviews. The study consisted of cohort or observational studies with hard clinical endpoints, including total CHD events (fatal or non-fatal myocardial infarction), stratified for patients with diabetes but no previous myocardial infarction, and patients without diabetes but with previous myocardial infarction. Studies with less than 100 subjects, follow-up of less than 4 years and/or without provisions for calculating CHD event rates were excluded. The review of articles and data extraction was performed by two independent authors, with any disagreements resolved by consensus.

Results Thirteen studies were included involving 45 108 patients. The duration of follow-up was 5–25 years (mean 13.4 years) and the age range was 25–84 years. Patients with diabetes without prior myocardial infarction have a 43% lower risk of developing total CHD events compared with patients without diabetes with previous myocardial infarction (summary odds ratio 0.56, 95% confidence interval 0.53–0.60).

Conclusion This meta-analysis did not support the hypothesis that diabetes is a ‘coronary heart disease equivalent’. Public health decisions to initiate cardio-protective drugs in patients with diabetes for primary CHD prevention should therefore be based on appropriate patients’ CHD risk estimates rather than a ‘blanket’ approach of treatment.

So on the one hand, statins are of no benefit to women, even those who have had a previous coronary event (unlike for men), and on the other, even men & women with diabetes who have never had a coronary event are far less likely to have one than non-diabetics who've had one.

While that's not a direct study of the question (do statins lower coronary events in women with diabetes?), putting 2 and 2 together seems to imply to me that given the rate of serious side-effects experienced by those on stains, combined with what seems like a very dubious benefit to a woman with well controlled diabetes, equals not much reason to take them and lots of reasons not to.

Anyone have anything contrary, or better. Either way.

Exposing the Cholesterol Con

[Just a quick off-topic aside. Darya Pino at Summer Tomato did a mildly critical but fair & balanced post on paleo dieting. Go take a look and drop a comment about your own experience if it suits you. From my perspective, we out to be able to take fair criticism to refine & strengthen our message.]

This is just a rather quick hit & run with some excerpts and commentary that I wanted to post because it's nice to finally see something in the mainstream news that echos what I and my fellow bloggers have been saying all along, for nearly three years in my case. From MSNBC:

Bad cholesterol: It’s not what you think

Yea, no shit. And it never was. And there was little justification to ever create the "tidy narrative" in the first place.

For decades, a tidy narrative about the relationship between LDL cholesterol and heart disease has affected everything from the food we eat to the drugs we take to the test results we track and the worries we harbor. This oversimplified view of cholesterol — that all LDL is the same and that all LDL is bad — has enabled the adoption of an accompanying oversimplified dietary belief, that all saturated-fat consumption raises your risk of heart disease.

Oversimplified view of cholesterol --> oversimplified view of diet --> complex and dangerous drugs --> obesity --> diabetes --> more complex and dangerous drugs --> lots of drug company profits --> lots of assholes still out needlessly scaring people to death.

The LDL hypothesis has also encouraged many of us to swallow the most-prescribed class of drugs in recent history. Americans spent more than $14 billion on LDL-lowering medications in 2008. Whether that money came out of their own pockets — straight up, or through ever-escalating co-pays — or out of the hemorrhaging U.S. health-insurance system known as Medicare, it's a huge expenditure. Twenty-four million Americans take statins, and the latest health directives suggest that those numbers should be higher. And why stop at grown-ups? Some pediatricians want to start feeding Lipitor (and the like) to kids.

$14 billion for something with tons of side-effects and of dubious, nonexistent value for all but a small subset: men under 65 who've already had a coronary event. Sure, if you've had a heart attack already, go right ahead and "trust your heart to Lipitor."

LDL comes in four basic forms: a big, fluffy form known as large LDL, and three increasingly dense forms known as medium, small, and very small LDL. A diet high in saturated fat mainly boosts the numbers of large-LDL particles, while a low-fat diet high in carbohydrates propagates the smaller forms. The big, fluffy particles are largely benign, while the small, dense versions keep lipid-science researchers awake at night.

But here's the problem: The typical LDL test doesn't distinguish between large and small LDL particles — it can't even spot the difference. And people can have mostly large LDL or mostly small LDL in their overall LDL, depending upon a host of genetic, lifestyle, and environmental factors. Your own personal mix may make all the difference between living to a heart-healthy old age and becoming a Monday-morning casualty at your desk.

Right. And Americans are spending $14 billion per year on statins and it's based on irrational, uncorrelated, unproven associations with a measurement technology that "can't even spot the difference." I'll bet the drug companies are all over getting this new measurement technology into wide usage. Yea, right.

Now, to heap even more outrage on the deal, how long back has it been since it was known that the small-dense sub-particles associated and reasonably predicted heart disease risk? 1976, almost 35 years ago. Dr Krauss recounts:

The heart-disease community was not impressed. "It took me 4 years to publish that paper," he says, recalling his early work on sub-particles in the late 1970s. "That's beginning to tell you some of the obstacles I was going to face."

Big surprise, eh? There's more.

But during experiments, Dr. Krauss discovered that while a diet high in saturated fat from dairy products would indeed make your LDL levels rise, "saturated fat intake results in an increase of larger LDL rather than smaller LDL particles," as he wrote in an American Journal of Clinical Nutrition review he co-authored in 2006. A diet heavy in full-fat cheese and butter — but not overloaded in calories — triggered the relatively harmless health profile described as pattern A. [...]

Not only is dairy fat unlikely to increase heart-disease risk, Dr. Krauss and others have learned, but reducing saturated fat in a way that increases carbohydrates in a diet can shift a person's LDL profile from safe to dangerous. That's pretty much what happens whenever some well-meaning person with "high LDL" starts eating "low-fat" frozen dinners filled out with corn-derived additives, all the while engaging in the customary ravaging of a basket filled with dinner rolls.

Well that should do it. You might want to check out the inane comment from Dean "Chubby Faced Diet" Ornish.

Can Cholesterol Get Any More Complicated?

I might have to put updates up as I continue to gather information (emails out to vetting sources) but I thought I'd put this up as a starter, maybe generate some conversation.

I've posted a lot about cholesterol and how and why I don't generally see it as a problem for most people on a good (paleo-like) diet. In other words, the diet is the problem causing the inflammation markers, small dense LDL, low HDL and high triglycerides (fat in the blood, caused by sugar, not dietary fat). So fix the diet. The problem, of course, is that the standard from-on-high dietary advice is precisely what's behind those aforementioned problems. A Paleo diet doesn't seem to work for everyone to get the sort of lipid numbers I enjoy, so that leaves the question open as to whether "bad" lipids are generally only a concern with a bad diet of processed foods, high sugar and omega-6 polly unsaturated fats. That's where I've placed my bet.

But what about familial hypercholesterolemia? Does that not substantiate if not prove the lipid hypothesis? After all, even children and infants afflicted with this genetic disorder get heart disease. But is it the high LDL itself, or what it's able to act upon? For an amazing education in all things cholesterol, take a listen to Jimmy Moore's recent interview of Chris Masterjohn who specifically addressed this disorder and argues that it's rather like having a ton more cars on the road (LDL) and the real problem is that because they're on the road so much longer that it makes them far more susceptible to oxidative stress; and combined with chronic inflammation caused by a nutritionally deficient, low fat, high sugar, high omega-6 diet, that's the real underlying cause of the plaque buildup. Give it a listen.

Added later: Think of the causal chain mixup like this when it's claimed that LDL is causal. It's like having a gunman shoot you through the heart and you die, and cause of death is that your heart can't stop bullets. So, when the underlying cause is inflammation and oxidized small-LDL, the "cause" is claimed to be that your heart can't withstand small-LDL, inflammation and oxidation.

Now comes the added complication. Via reader Dexter I got a link to an article about this very recent study today. Be warned: it's not a light read, at least not for me.

Strongest evidence yet that Lp(a) causes heart disease

Oxford, UK - New genetic research has identified two relatively rare single nucleotide polymorphisms (SNPs) that explain just over a third of the variance in lipoprotein(a) (Lp[a]) levels in individuals of European descent. The work confirms unequivocally that Lp(a) is a causal factor for coronary disease, say Dr Robert Clarke (University of Oxford, UK) and colleagues in their paper in the December 24, 2009 issue of the New England Journal of Medicine.

"This is the most convincing evidence so far that this protein [Lp(a)] is directly part of the pathway that causes heart disease rather than a bystander. If we can target it through treatment, we might expect to lower the risk of disease," coauthor Dr Hugh Watkins (University of Oxford) told heartwire.

Well I've known for sometime that high Lipoprotein(a) -- Lp(a) -- is a strong risk factor for CHD (mine is 4 mg/dl with "standard range" <30, so presumably low risk on that score), but that's based on association, not causation. But now they're saying it's unequivocally causal. OK, good, and I'll get to how you can naturally lower your Lp(a) in a bit. But first, here's what really struck out at me, making my head spin around and around a bit. From the article.

In a press release issued by the British Heart Foundation [3], which describes Lp(a) as a "third type of cholesterol," senior author of the new paper, Dr Martin Farrell (University of Oxford), tries to put the findings into perspective: "The increase in risk to people from high Lp(a) is significantly less than the risk from high LDL-cholesterol levels. So Lp(a) doesn't trump LDL, which has a larger impact. The hope now is that by targeting both we could get an even better risk reduction."

Say what? Here's what I'll state unequivocally: high LDL is only associated with CHD and even that's tenuous because I have many times (check the cholesterol links above) demonstrated that very low LDL is also associated with CHD (as well as increased all-cause mortality, particularly in the elderly and slam dunk in women). So let me get this straight: the risk from high Lp(a) that they are calling "unequivocally causal" is a significantly less risk than a mere association?

What say you, experts? I'm confused.

At any rate, and again not a light read by any means, but one blogger and good friend, Dr. BG really stands out in blogging about Lp(a) and other risk factors.

Cardio Controversies: Lp(a) Dangerous at ANY Value (link removed)

Can Lp(a) create more damage than we previously thought?

Dr. Hecht has apparently showed it with his examination of lipoprotein, cardiac and metabolic parameter comparisons with the real measure of heart disease risk: EBCT-determined plaque burden. Lp(a) was 3rd after HDL and LDL particle diameter in being highly associated with coronary calcifications. See below. Free PDF HERE. Normally at TrackYourPlaque we consider Lp(a) greater than 20 mg/dl as a high contributor toward accelerated plaque burden. When I look at Dr. Hecht's graphs, what I notice is that indeed this may not be true.

It appears to my observations that at ANY Lp(a) value, plaque burden is quite high reaching even 97th, 98th or 99th calcium percentile for CAD risk (of population norms) at severely low Lp(a) levels of 5 mg/dl or 10 mg/dl.

OK...what the heck?

I can make the same observations for my CAD (heart), PVD (peripheral), or CVD (stroke) patients and individuals with extensive diabetic complications. At any Lp(a), the extent of disease can still be quite pronounced.

What other factors are correlated to vascular damage?

1. Low HDL2b

2. High small dense LDL.

These THREE factors determine almost entirely the extent of disease. Both visionaries Dr. Davis and Dr. Hecht focus on these predominantly to control and halt the progression of calcifications.

How are these 3 metabolic parameters created in the first place?
--low fat SAD AHA low cholesterol low saturated fat diet
--saturated fat deficiency
--excessive carbs (>10 g/d, >20 g/d, >50 g/d, >100 g/d -- depending on a person's insulin and insulin sensitivity and pancreas/adipose/hormone status)
--inflammation (excessive omega-6 oils)

But she has a lot of stuff on Lp(a), so here's a search link (link removed) for those wanting to dig super deep. For those of us wanting to cut to the chase, how best to lower Lp(a) and keep it low? You know what I'm gonna say, dontcha? You guessed it: high saturated fat from natural sources, i.e., animals, butter, coconut oil. The Doctor again, from another post (link removed):

Lp(a) Reduced By Saturated Fatty Acids and Raised by Low-Sat-Fat Diets

Benefits of Krauss high-saturated fat diet cannot be overstated. Saturated fats control CETP and thus control the amount of Lp(a) individuals produce. In fact, when an experiment group was put on a low fat, high veggie diet, Lp(a) increased significantly by as much as 9% (Silaste ML et al Arterioscler Thromb Vasc Biol. 2004 Mar;24(3):498-503. Free Full Text)

Additionally, the low fat diet produced HIGHER oxidized LDL (OxLDL) by 27%. Recall the small dense LDL are less resistant to oxidation than buoyant large LDL and transform to OxLDL rapidly.

Not good.

For. Plaque. Burden.

OxLDL causes fatty/calcified organs: arteries (atherosclerosis); endothelium (hypertension); liver (NASH); pancreas (diabetes, MetSyn); thyroid (Hashimoto's), visceral fat (obesity); etc.

Saturated fat lowers and controls Lp(a) and coconut oil is one great example (Muller H et al . J Nutr. 2003 Nov;133(11):3422-7. Free PDF HERE). In this study by Muller et al women with elevated Lp(a) in the 30s mg/dl were provided a coconut oil-rich diet (22.7% sat fat; 3.9% PUFA) was compared with a high PUFA-diet (15.6% PUFA !!yikes). Lp(a) was reduced 5.1% compared to baseline habitual diets with the high saturated fat diet whereas in the high PUFA diet, Lp(a) increased a whooping 7.5%. The difference between Lp(a) on the high sat fat compared to the high PUFA diet was 13.3%.

Here are the conclusions from those two study links above, respectively.

The question remains as to why the Lp(a) levels increased in response to the dietary changes. The basal levels of Lp(a) are primarily genetically determined, but some data suggest that Lp(a) may act as an acute-phase reactant under some situations.40 In a previous study, a diet high in SAFA was found to produce approximately 10% lower plasma Lp(a) concentration than diets high in oleic acid or trans-fatty acids.41 This observation is consistent with our study in that both diets led to lower SAFA and consequently increased Lp(a).

In conclusion, we found that a diet traditionally considered to be anti-atherogenic (low in saturated fat and high in polyunsaturated fat and naturally occurring antioxidants) increased plasma levels of circulating oxidized LDL and Lp(a). The question of whether the changes observed in the present study are, in fact, pro-atherogenic or anti-atherogenic remains to be solved.


The connection between Lp(a) and atherosclerosis is not entirely understood. Different studies have provided strong evidence that Lp(a) level is an independent risk factor for developing coronary artery disease in men (47,48), but the question of causality continues to be debated. Recent data suggest that Lp(a) might be atherogenic (49), in particular when combined with other risk factors. High levels of Lp(a) combined with other risk factors such as the ratio of plasma total/HDL cholesterol have been shown to increase the risk for coronary heart diseases (50). It has also been reported that when substantial LDL cholesterol reductions were obtained in men with coronary heart disease, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening (51).

In conclusion, the present results show that the HSAFA- diet lowered postprandial t-PA antigen and thus potentially improved fibrinolysis compared with the HUFA-diet. Diets with either high or low levels of saturated fatty acids from coconut oil beneficially decrease Lp(a) compared with a HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy may be of importance if the goal is to decrease Lp(a).

Alright, so for us KISS folks, it all just comes down once again to a natural, Paleo-like diet plenty high in delicious and healthful saturated fats.

Is Cholesterol a Problem to Be Managed?

I'm going to begin by saying that via this blog I've likely contributed to the notion that it should. I've posted my own cholesterol numbers a few times, have written many posts on it, argued how the paleo-like diet improves the numbers, and so on.

For decades, likely since Ancel Keys, there has been a focus on reducing cholesterol, under the presumption that high cholesterol causes heart disease. And, so, there's all sorts of dietary advice, and now prescription medications to lower cholesterol. In fact, no such causal link has ever been even close to being proved. And, in fact, even the associations once thought to be solid, aren't there.

Want proof of that? Got 77 seconds?

Let's just sum it up beyond what's given in the video: about half the people who die of heat disease have low cholesterol, half high. For women, higher cholesterol seems to be associated with higher longevity. For older people too.

In spite of this, many of us on paleo like to tout our great lipid numbers. Why? If none of these "associations" are even very sound, and a causal link has never been established, then what's "good" or "bad" in these numbers?

The thing about a paleo like diet is that we operate from a principle that has tons of basis in fact: we know what we evolved to eat. We know the archeological record of excellent health for pre-agricultural humans. We know that dozens, even hundreds of primitive hunter-gatherers, pastoralists, and other non-industrial peoples have been observed by physicians and other scientists going back 200 years, and virtually none of the diseases of civilization show up. We know all this, yet then go get our lipids tested to confirm that we're eating right.

Shouldn't we just know that we're eating right? How do you feel? Very nearly everyone raves about how great they feel; that is, until they get their cholesterol numbers and they aren't in the club with the rest of us who have "good" numbers.

I've come to believe that there's a lot of silliness going on and I'm sorry to have been a part in promoting it.

Cholesterol is not a problem to be managed, a diet of real foods is what is to be managed and the cholesterol numbers are the numbers.

Let's dive into a couple of examples. I had three, but I have misplaced one and can't find it. If the reader who wanted his numbers looked at by other readers for comment would still like that, please email it again and I'll append it to this post. I previously did a post on a reader Patrik's MNR LipoProfile.

First up is Tim, who we first saw right here. Then we saw his transformation photos. He decided to do a 90-day experiment with eating meat only. He sent his latest numbers.

You have my earlier cholesterol numbers from that previous post you did.  I did a 90 day Zero Carb test with a sample of one (me, 41 year old, white male) from May 1 to August. Primarily ate beef from a free range, hormone free local ranch.

Got some numbers back.  You have my previous from that post.  In a nutshell:

c-Reactive Protein unchanged at .3 mg/L
HbA1C unchanged 5.2%
mean plasma glucose unchanged 119 mg/dl

So no changes, and liver and kidney function all remained unchanged/fine

My Lipid Panel this time is an NMR Lipoprofile, so the proper thing, I suppose.  I can rattle off the numbers:

Total Cholesterol 288 mg/dl
Triglycerides 50 mg/dl
HDL 93 mg/dl

So, I had a Total increase, a slight Triglyceride increase and a pretty good HDL increase.

More NMR Nitty Gritty I'll need help sorting out as the units of measure are odd to me, but here it is:

Total LDL Particle Concentration 1348 nmol/L  (considered borderline high)
Small LDL Particle Concentration sub 300 nmol/L (with sub 600 optimal)
Total HDL Particle Concentration 34 umol/L (considered intermediate)
Large HDL Particle Concentration 17.9 umol/L (with above 9 optimal, so banger)

And they threw in my calculated LDL at 185 mg/dL which is a guess using the Friedewald equation?

SO, I don't understand how to convert units, nmol/L and umol/L, but I gather that my LDL is indeed up, but it is pretty much all the non-threatening A type larger.  And my HDL is also about as big and protective as it gets.  Couple all that with the low low low inflammation markers, the low glucose levels, and I'm sitting pretty happy.  Would like help converting and interpreting the NMR nmol/l and umol/L numbers..... got any experts at hand?

I think my LDL is classified "borderline high" but conventional wisdom still does not take particle size (mine are large and fluffy) into consideration.  My lab results even have this little pro- "statin-ator" comment:

"...studies have shown that elevated LDL particle concentration is associated with increased risk for coronary heart disease.  Statins effectively reduce the number of LDL particles, but DO NOT GENERALLY INFLUENCE THE SIZE DISTRIBUTION OF THE LDL PARTICLES...."

So, I could spend a ton of money to get likely smaller LDL particles, AND less protective HDL, and muscle cramps, cancer, and neurological disorders, but I think I'll stay statin free, and keep on pouring in the animal fats.

My one comment would be that the LDL particle number of 1348 nmol/L corresponds to an actual LDL of 134. Notice that his Friedewald measured LDL (the kind 99% of people get) is 185, an error of 40%. I recently blogged about this and a new formula some Iranian researchers came up with for when triglycerides are under 100. There's a calculator too. Well, under that formula, Tim's calculated LDL comes out to 145, a very reasonable calculated approximation of his actual of 134.

OK, great, right? paleo diet -- even a near zero carb one -- confirmed. Tim has the cholesterol numbers to prove it. No slight to Tim at all, and yea, anyone is going to be pleased to get these results. But what if you don't?

The next reader is "John." Rather than an MNR, he has pre and post paleo VAP tests. I've uploaded the files for reference.

Now, for those who don't want to dig deep, here's the summary from John:

I just got a blood lipid panel from my first 3 months of Paleo.  Very, very few cheats in that 3 months.
LDL direct went to 396 from about 150
Triglycerides went from 114 to 150
HDL didn't budge, mid 60s
Total Cholesterol went from 240 to 485

After a few questions, he ads further:

1. I am 5'11", started the diet at about 162, am about 150 now, stronger than ever in recent memory (22 pullups this morning).  I tend to be lean, my weight until my mid-20s was 130 lbs, I was a fanatic distance runner.

2. Pretty normal diet, not too much crap compared to average.  I was not a dessert freak or anything.  Lots of chips (doritos, etc.) was my main weakness.

3. I'm trying to eat mostly meat.  We usually have a vegetable or salad with the meal, my wife likes that.  Especially early on, I'd marinade the steak in soy/teriaki blends or something like that, but how much is going to soak in?  At least the last month or so, I've been using dry rubs instead.
I have been eating much less fruit than she has.  I'm trying to hold that to one or two servings a week.  I'm totally mystified by the triglycerides as well.  I can't see where they'd be coming from.  I thought lower triglycerides would be the slam-dunk effect of this diet right off the bat.

So, what do you make of that? Should John immediately stop paleo and go back to lots of Doritos? Anyone have any ideas? Anyone seen this huge of a jump in a paleo or low-carb dieter?

I have no idea, myself. But I do think that tremendous of a jump merits some attention, as it could be signaling something else going on. In the meantime, I'd still eat real foods. John should probably look into getting some sort of consultation with a reputable low-carb doc.

To close it up, I'm going to quote what my Hyperlipid UK veterinarian friend Peter told Tim about his cholesterol, as it's insightful and what really got me to thinking about this. See, John's was by far the most dramatic increase, but I've received many disappointed emails from new paleo dieters who didn't get into the "good cholesterol club" with myself and others.

I think you are pretty well in charge of understanding your lipids. The comment about statins reducing LDL count but not size is simply wrong, but this is about what you would expect in our statin culture.

Bear in mind it is perfectly acceptable to view your lipid panel as evidence you are eating an appropriate diet made of real food, which promotes health. The lipids reflect that diet and are secondary markers of the diet... It is not necessary to believe in good or bad cholesterol. Eat Food and never mind the lipids. The Kitavans have "awful" lipids because they eat a carb based real food diet. The real food results in health, the lipids are bad. But the lipids cause no badness because it's not the lipids which are the problem. It's the food that matters! Most real junk is carb based, which is why "carb" lipids are "associated" with ill health. Blame the food not the lipids...

That's just my cantankerous way of looking at things!

Exactly. It's not that it's an awful thing to view your lipids as some confirmation of eating a good diet. But it's probably just confirmation bias, because, what happens when you're John?

Exposing the Cholesterol Myth

I probably get more questions about cholesterol than anything else. But cholesterol is not a problem to be managed. Your diet is to be managed, it should be a natural diet of meats, fowl, seafood, good fats (animal, coconut, olive), vegetables, berries & nuts.

Take nine minutes for Dr. Ron Rosedale to expose the cholesterol scam.

Tomorrow I'll post a couple of advanced lipid panels from readers for discussion.