A quick recap in case you couldn’t play the video: Dr. Delgoofy tells us that dietary fat causes insulin resistance and diabetes. To prove the point, he swallows a half-cup of olive oil and – horrors! – his triglycerides nearly double. Then he consumes a big ol’ sandwich and some pizza and – double horrors! – his triglycerides rise to 214, and his glucose shoots up to 131. This, he assures us, proves that dietary fat causes diabetes.

As I often say about journalists after reading slanted news stories, I can’t tell if this is guy is intentionally dishonest or merely stupid.

Let’s start with that shocking rise in triglycerides after Dr. Delgoofy cannonballs a half-cup of olive oil. The horror music was a nice touch, but the result is about as horrifying as drinking a gallon of water and then discovering that the volume of urine in your bladder has doubled an hour later. In fact, if you ever swallow a half-cup of oil and your triglycerides don’t rise dramatically, check yourself into a hospital pronto and ask them to find the blockage in your digestive system.

The reason you find a long list of “essential fatty acids” listed in biochemisty textbooks is that — surprise! — your body needs fats. Your hair, your nails, your brain, your nervous system, your cell walls, your hormones, etc. — they’re all fat-dependent. Now, I suppose in theory you could fill a hundred syringes with fat and inject the stuff where it’s needed, but that would probably hurt. Plus your body likes to break nutrients down into little-bitty pieces before using them.

Consequently, most of us prefer to get our essential fats by eating them. The digestive system then does the work of breaking them down into itty-bitty pieces and packaging them as triglycerides — three fatty acids bound up with a glycerol molecule. Then the triglycerides are delivered to your tissues through your bloodstream.

So when Dr. Delgoofy showed us that the triglycerides in his blood doubled after a big belt of oil, all he proved is that his liver and bloodstream are in working order. If Dr. Delgoofy is a real doctor, then he surely knows that eating always raises triglycerides. That’s why doctors measure your triglycerides after a 12-hour fast. To give you an idea of how dramatically eating a meal can affect the measurement, here’s a tidbit I found online:

My blood triglyceride level was alarmingly high 497 mg/dL. It turned out to be a false result. A nurse sent to my home by my life insurance company had taken my blood sample just a few hours after I ate lunch. When my doctor drew my blood after an overnight fast during my annual physical a few months later, my triglyceride level was 97.

Larry Lindner
Tufts University School of Nutrition Science & Policy

If your fasting triglycerides are high, then you do have a problem. But it’s not dietary fat that causes high fasting triglycerides. Rather than explain it myself, I’ll quote Dr. William Davis:

One of the most common triglyceride myths is that eating fats increases triglyceride. But that’s only a half-truth, since fats do indeed increase triglycerides - but only if triglycerides are measured after eating. Depending on the quantity of fat consumed and other factors, triglyceride levels can reach around 300 mg/dl after a fat-containing meal, only to descend rapidly.

In contrast, carbohydrates can increase triglyceride levels many times higher, increasing levels to 300, 400, 500 mg/dl or more, even occasionally in the thousands, after many weeks to months of carbohydrate-excess. But carbohydrate excess leads not just to after-eating high triglycerides, but high triglycerides all the time.

The real story is that fats in the diet decrease triglycerides - at all other times except after a meal. The higher the fat content of your diet, the lower your triglycerides will be in a fasting blood draw. This has been well-established in numerous diet trials comparing low-fat with low-carbohydrate diets.

After demonstrating a perfectly normal rise in triglycerides after swallowing olive oil, Dr. Delgoofy continues his anti-fat demonstration by chowing down on a big sandwich and some pizza. Lots more fat, of course, but now he’s also consuming a heapin’ helpin’ of refined flour. Surprise, surprise … when he checks his blood levels awhile later, his triglycerides are up again, and so is his blood glucose level.

Once again, if he’s a real doctor, he knows perfectly well the rise in glucose was caused by the bread and the pizza crust, not the cheese and the meats. If he wanted to prove fat spikes blood sugar, he could’ve simply shown us a glucose reading after the olive oil. But nope … he stuffs himself with white flour, measures his glucose, then hopes to fool us into blaming the fat.

After seeing Dr. Davis give a lecture on the low-carb cruise, I got into the habit of checking my glucose after meals. Meats, eggs and cheeses barely cause a blip. But one white potato pushed my blood sugar up to 162. A small serving of pasta kicked it up to 174. After reading the latest book by Drs. Eades & Eades, my mom was finally persuaded to go on a low-carb diet. A few weeks later, her fasting glucose was down by 20 points. Her blood pressure and triglycerides dropped as well.

If her current diet is going to cause type 2 diabetes, I’d sure like for Dr. Delgoofy to explain the biochemistry of how that’s going to happen. I’d also like for him to point out the people who ate low-carb, high-fat diets and became diabetic in the process. I can certainly point to type 2 diabetics who were able to stop taking insulin shots after going low-carb.

Dr. Delgoofy tells us we should limit our dietary fat to 15% of total calories. Let’s back up to the beginning of his presentation and see how that’s working for him. Take at look at the fasting blood-work he showed us before consuming the olive oil:

The triglycerides are impressively low, so I’m guessing he doesn’t eat much sugar or other refined carbohydrates. But his HDL is an anemic 37. Mine was 64 last time I had it measured. As I found while digging through the American Heart Association’s data some months back, it’s low HDL that’s associated with heart disease, not high LDL. Here’s what the AHA itself says about HDL:

With HDL (good) cholesterol, higher levels are better. Low HDL cholesterol (less than 40 mg/dL for men, less than 50 mg/dL for women) puts you at higher risk for heart disease. In the average man, HDL cholesterol levels range from 40 to 50 mg/dL. In the average woman, they range from 50 to 60 mg/dL. An HDL of 60 mg/dL and above is considered protective against heart disease.

So even according to a kindred-spirit, fat-phobic organization, Dr. Delgoofy’s HDL is too low. Mine’s great. That’s because I eat plenty of fat. While we’re at it, let’s compare more of our cardiovascular markers.

Dr. Delgoofy told us his LDL is too low to be measured. The word to describe that claim rhymes with “tullpit.” Unless you want to spend a lot of money for a complicated lab test, LDL isn’t measured; it’s calculated by something known as the Friedewald equation, which looks like this:

LDL = Total cholesterol - HDL - (Triglycerides/5)

The reason we didn’t get an LDL reading for Dr. Delgoofy is that his triglycerides were inconclusive and simply shown as < 45. Dr. Eades and others have pointed out that the Friedewald equation tends to overestimate LDL for people with triglycerides below 100, but with that caveat in mind, let’s estimate Dr. Delgoofy’s LDL. For the sake of argument, I’ll assume his triglycerides are 40. We know his total cholesterol is 182 because his cholesterol ratio (total cholesterol/HDL) was listed as 4.9.

182 - 37 - (40/5) = 137

His LDL is probably lower than that because of the limitations of the Friedewald equation. But if he walked into a doctor’s office and had his lab work done, he’d be told his LDL is too high and his HDL is way too low. Meanwhile, here’s how my LDL would be calculated:

203 - 64 - (70/5) = 125

Mine would also over-estimated. But going by the standard tests, I win that contest. Now let’s look the other ratios commonly used to predict heart trouble.

LDL / HDL
Dr. Delgoofy: 137 / 37 = 3.7  (average risk)
Fat Head: 125 / 64 = 1.95  (low risk)

Total Cholesterol / HDL
Dr. Delgoofy: 182 / 37 = 4.92  (average risk; over 5.0 isn’t good)
Fat Head: 203 / 64 = 3.17  (very low risk; anything below 3.5 is excellent)

Triglycerides / HDL
Dr. Delgoofy: 40 / 37 = 1.08
Fat Head: 70 / 64 = 1.09

A virtual tie on the last one. But on every other ratio, the guy whose diet is more than 50% fat is kicking the pants off the guy who tells us to limit our fat to 15%.  And by the way, my fasting glucose level is better too. His was 96. To prepare for this post, I checked mine this morning. It was 85.

Given his low triglycerides, Dr. Delgoofy’s heart is probably healthy. I sincerely hope so. But after seeing this video, I have doubts about his brain.

Dear Sirs,

Thank you for your interest in our article. Please let me clarify that we were not writing tongue in cheek, nor were we joking. Heart attacks are serious for our patients and those that suffer them often wish they could have been prevented.

What we are asking is why is it routine in fast food restaurants to have unhealthy condiments provided free (e.g. salt) which have no beneficial properties, and yet no access at that location to statins?

It can’t be because salt (for example) is healthier than statins.

Statins do not prevent many deaths in primary populations, i.e. people who seem healthy. They do convincingly prevent heart attacks but, since heart attacks are usually with modern care not fatal, these prevented heart attacks cannot be expected to translate into lives actually saved in a quantity that would be convincing to a neutral observer.

As for side effects of statin, they are few, when the genuine statin muscle abnormalities are compared to the blank placebo tablets. The power of the human imagination is gigantic: more than most people imagine (if that is not a self-defeating statement).

Daily statin tablets are now routine therapy for patients whose future diet and exercise are considered permanently irreparable; how can that be right and yet an individual statin an individual unhealthy meal be wrong?

How can it be right to hand out salt to people who may have high blood pressure (without checking or even asking), sugar to people who may be diabetic (without checking or asking), and excess calories to people who may be overweight (even obviously obese); and YET wrong to even make available statins for those who wish to exercise their free choice to have them? Let me reiterate that it is not the presence of the former that I object to, nor the lack of the latter, but the conjunction of the former being routine but the latter forbidden.

I do appreciate your good-humoured look at life, and at science. Keep it up. Somebody has to ask awkward questions - and you are definitely doing that. But that, too, is what I am doing in my own way.

Best wishes from London,

Darrel Francis

So there you have it, straight from the source.  Statins are better for you than salt, so we should allow people to self-medicate.

Last week, I wrote about the two-year study that compared low-fat and low-carb diets. Low-carb won the comparison as far as raising HDL, but other than that, the results were the same — at least according to the researchers. I noticed right away that the Atkins dieters essentially went on a maintenance program within the first year, but it was Fat Throat who confirmed that the researchers included the drop-outs in their final numbers to even up the weight-loss score for the low-fat diet.

Fat Throat also believes the researchers included the drop-outs in their calculations to help even up the cardiovascular scores.  As he told me, “Follow the triglycerides.” (Okay, he didn’t use those exact words, but the meaning is the same.)

Here’s what he’s talking about.  At the beginning of the study, these were the average triglyceride levels:

Low Fat: 124
Low Carb: 113

Now look at the change in triglycerides over the course of the study:

Within three months, the low-carb group had reduced their triglycerides by a whopping 40 points.  That result held up at six months.  At the one-year mark, the low-carb group was backsliding but still had a much more impressive reduction in triglycerides.  And then, wouldn’t you know it, by the time the study ended, the low-fat group actually had an edge — because the reduction in triglycerides for the low-carb group had dwindled from 40 points to just 12 points.

As Fat Throat explained during a follow-up phone call, it’s highly unlikely a group of people sticking to a low-carb diet would experience a 20-point rise in triglycerides in the last year of the study, and even less likely they’d end up with a smaller drop in triglycerides than low-fat dieters over the course of two years.  I believe his words were something like, “It’s not biochemically plausible.”

In my own experience, triglycerides are remarkably stable on low-carb diet. I’m not on a zero-carb diet by any means, but I probably keep my carb intake below 60 grams on most days. Every time I’ve had a checkup in the past three years, my triglycerides were right around 70.  The people in the Atkins group reached that level, then averaged nearly 30 points higher by the two-year mark.

So I’m guessing either they weren’t on much of a low-carb diet by the end of the study, or we’re seeing the results of creative calculations performed on the estimated end-points for the drop-outs. Perhaps a bit of both.

If we could just take a peek at the actual food intake for both groups of dieters, we could clear up this mystery. That would also address my suspicion that the low-carb dieters reached maintenance level within the first year. But as I noted in the previous post, the full text of the study (slipped to me by Fat Throat in a plain manilla email) doesn’t list any food-intake figures.

This weekend, I received another email from Fat Throat to explain why:  There aren’t any food-intake figures.  The researchers didn’t track or record anyone’s actual diet.  Yes, you read that correctly.  Their reasoning apparently goes like this:  food journals are often inaccurate, so we won’t ask the study subjects to keep them. Instead, we’ll just counsel them regularly about the importance of sticking to their diets, then assume both groups stayed within their fat-and-calorie or carbohydrate limits … then estimate data for the drop-outs.

In a two-year, $4 million study with “weight loss” listed as the primary outcome, there’s no recorded information about food intake … and yet I’m supposed to believe this study actually tells us something?

I’m starting to wonder if this group of researchers — all with long histories of praising low-fat diets in their previous works — didn’t track the data for fat, calories and carbohydrates because they were afraid they wouldn’t like the results. Perhaps they didn’t want us to see that the low-carb dieters — with no restrictions on calories — would only regain weight after increasing their carb intake to, say, half of what the government recommends.  (This was a government-funded study, by the way.)

Or perhaps they intended to test the results of dietary advice instead of actual diets.   If so, those Low-Fat, Low-Calorie Diets Equally Effective For Weight Loss headlines are looking pretty shaky.

All I know is, something doesn’t pass the smell test here.  Fat Throat probably has an opinion on that, but he didn’t say.  Next time, I may offer to meet him in an underground garage so I can ask more questions.

With no warning one weekday morning, investigators entered an organic grocery with a search warrant and ordered the hemp-clad workers to put down their buckets of mashed coconut cream and to step away from the nuts.

Then, guns drawn, four officers fanned out across Rawesome Foods in Venice. Skirting past the arugula and peering under crates of zucchini, they found the raid’s target inside a walk-in refrigerator: unmarked jugs of raw milk.

Yup, guns drawn and everything.  Apparently the police were warned about the extreme violence that breaks out when hemp-clad owners of organic-food stores are facing arrest.   I heard one cop who raided an organic  joint required a small band-aid on his nose after an angry employee threw a sandal at him.

You can see some footage of the raid as well as some interesting discussion in this video:

Since this incident involves governments and regulations, I’m gong to step up on my political soapbox for moment.  You’ve been warned.

I agree with Mr. Hemminger that the big agri-business corporations push for these regulations to shut down independent suppliers and limit our choices. But what Mr. Hemminger didn’t mention is that the real problem here isn’t corporate power; it’s government power. Without government, corporate power is pretty limited.

A few years ago, I watched a stupid left-wing documentary that compared corporations to sociopaths. As an example, the filmmakers showed how a company that builds water systems moved into a small country and then (according to their narrative) made it illegal for people to collect their own water.  This prompted me to scream at the TV, “How the @#$% can a corporation make anything illegal?!  Corporations can’t pass laws!  The @#$%ing government passed the law!  The @#$%ing government enforced the law!”

The filmmakers’ preferred solution, naturally, was to turn water collection over to “the people” … in other words, the government — the same government that already proved itself corrupt by making it illegal for citizens to collect water. Yeah, that’ll make a difference.

The same principle applies in this case. It doesn’t matter if evil executives at MegaMilk, Inc. want to shut down raw-milk producers; without government, they can’t do it.

The bigger the government, the more opportunity there is for corruption, because corruption is the bastard child of government power.  Power gives you something to sell.  Has a corporation ever tried to bribe you? Your grandmother? Your best friend? Of course not, because you don’t have the power to do anything for them — such as outlaw their competition and call it a “health and safety” regulation. But get yourself appointed to a regulations-writing committee and suddenly your phone will never stop ringing.

It’s not a matter of just convincing the regulators to write the “correct” laws. If they have the power to outlaw products you don’t like, they also have the power to outlaw products you do like. The reality of the situation is that MegaMilk will always be able to offer them a sweeter deal than you or I can. The solution is to take away their power to regulate which products supposedly free adults in a supposedly free country can buy, period. Until we wise up and do that, we’d better get used to scenes like this one.

But in the meantime, I have an idea for how we can make these onerous regulations work in our favor:

Prohibition made The Mafia. Yes, organized crime existed before, but it was Prohibition that made previously small-time gangsters rich and powerful. Legal or illegal, people wanted liquor and were willing to pay for it. So when our government made it illegal for Anheuser Busch and Johnny Walker to take money from drinkers, Al Capone took it instead. He and the other gangsters soon became wealthy enough to hire their own armies and bribe the police to look the other way. (After all, the police had the power to shut them down and were therefore worth corrupting.)

So, here’s what we do: we need to make raw milk incredibly popular, albeit in an underground sort of way. At social gatherings, we can slide up next to the movers and shakers and offer them a hip-flask of the stuff. Raw milk is irresistibly delicious, so we know they’ll want more. After they’re hooked and spread the word, we can open a few Milkeasys in the big cities, complete with milk taps, jazz bands, and a nice selection of raw-milk cheeses.

Once raw milk becomes the new bootleg liquor, today’s small-time producers will become the new Milk Mafia. Newspapers will run scandalous stories about the crimes and extravagant lifestyles of Joey “Milk Moustache” Bambano and Harold “Baby Burp” Nelson. There might even be a shootout or two in Chicago, with raw milk flying everywhere.

Oh, sure, the government will put together a special task force of G-men to harass the new milk lords, but their successes will probably be limited to a few P.R. stunts … the G-men taking an axe to some confiscated jugs of raw milk, that sort of thing. (Let’s just hope they don’t poison the milk and kill a few thousand unsuspecting drinkers, like they did with liquor in the 1930s … yes, our government actually did that.)

The point is, the Milk Mafia will make sure we get our raw milk.  Everyone will know who the local supplier is. (Okay, buddy, just walk over to that door, tap on the sliding window and say “Cream rises to the top.”)  Eventually, raw-milk farmers will be rich enough to bribe the politicians and police to look the other way.  We might even learn a few cops are drinking the stuff when no one’s looking. 

Best of all, the Milk Mafia will have the money to recruit some armed thugs as enforcers.  That way, when the police decide to kick down a door and bust someone for selling raw milk, they’ll actually need those guns.

Since you keep showing up on my blog and trying to convert me to the Church of the Holy Plant-Based Diet, I’ve decided it’s time to explain, once and for all, why you’re wasting your time. You seem like nice people and all, but really, this is getting tiresome.  Every time I answer the doorbell, you stand on my porch and repeat the same old sermons by the same old preachers:   Joel Fuhrman, John McDougall, Dean Ornish, T. Colin Campbell, etc.  This may surprise you, but I don’t find those sermons any more convincing on the 100th repetition than I did on the 10th.

Perhaps if I actually heard a new sermon now and then, I might pay attention, but sadly that’s never the case.  So in the future, when you ring the bell, I’m going to simply refer you to this post and bid you good-day. 

I know some of you will label this as closed-minded.  That’s because to an evangelist, the definition of “closed-minded” is “does not agree with me.”  The truth is, I’m being polite.  Even though I believe your religion is based on a mixture of emotions and faulty reasoning, I don’t show up on your doorstep and try to talk you out of it.  Unlike you, I don’t get emotionally involved in other people’s dietary choices.  If you believe it’s better for humans to shun animal foods, please do so.  I don’t really care.

But you obviously care very much that I eat meat, since you keep trying to convince me I shouldn’t.  Sometimes it seems as if you all got together and said, “There’s a meat-eater who lives in that blog over there!  We must take turns showing up on his doorstep and preaching to him until he sees the light!”  I give you credit, by the way, for attempting to cloak your arguments in something resembling science.  You apparently noticed the “Meat is Murder!” tactic just makes me laugh, so you’ve taken to presenting the same sentiment as a health issue.

Nice try, but it isn’t going work, and I’m going to explain why.  I’m not foolish enough to think I’ll change your minds — evangelists aren’t swayed by evidence, as Eric Hoffer explained brilliantly in his book The True Believer – but I figure there’s an outside chance you’ll finally realize I don’t find your arguments the least bit persuasive, in which case you actually might give up and go away. 

WHY I’M AN EX-VEGETARIAN … AND WHY I THINK VEGETARIAN EVANGELISTS ARE FULL OF BEANS.

I’ll start with the reason that’s the least valid scientifically, but frankly the only one that ultimately matters to me:  my own experience.  I was a vegetarian for several years (yes, I’m a fallen-away believer) yet somehow never experienced all the magic health benefits promised to me by your preachers.  I did, however, experience arthritis, asthma, psoriasis, gastric reflux, restless legs, lower back pain, irritable bowel, fatigue, slow but consistent weight gain, listlessness, depression, frequent colds, canker sores, cavities, and receding gums that required grafts.  None of those ailments were caused by sugar consumption, because I already knew sugar was a sin and didn’t indulge except on very rare occasions.  I’ve since learned that some of those ailments were caused by a lack of fat and cholesterol in my diet, while others were likely caused by the lectins found in grains and beans.

Now that I’ve gone over to the dark side of low-carb/paleo eating, I don’t suffer from those ailments anymore — not one.  It’s also no longer a battle to keep my weight down.  I’m 51 years old, but feel better than when I was 30.  I moved to Tennessee a year ago and haven’t even bothered to look for a doctor yet, since I’m never sick. 

Given my personal history, I don’t really care how much cherry-picked evidence bean-eaters like Fuhrman and McDougall can cite,  because my body told me they’re wrong.  I listen to my body.  If I whack myself in the head with a rubber mallet and my body says, “You know, that gave me a headache and made me dizzy,” I’m not going to do it again –  even if you cite a Fuhrman study concluding that head-whacking improves mood and prevents sexual dysfunction.

I also have to consider the experiences of my friends and acquaintances.  I’ve known plenty of vegetarians over the years, and as far as health status goes, I wouldn’t trade places with any of them.  They’re all on prescription drugs.  I’m not.  I’ve seen them suffer from arthritis, auto-immune diseases, spinal degeneration and cancer, to name just a few.  One vegan friend in Los Angeles had to undergo extensive dental surgery because she lost half the bone mass in her jaw.

But of course, those are mere anecdotes and therefore aren’t scientifically valid.  Now, you and I both know you’re only interested in the so-called “science” that supports your religion, but since you insist on pretending otherwise, I’ll deal with your science (ahem, ahem) as well.

First, let’s look at some basic principles of science.  In real science, we control for confounding variables when testing a hypothesis.  We also don’t consider a hypothesis valid unless the results are consistent and repeatable.

The studies you cite when you show up to preach at me are observational studies, which are notoriously awful when it comes to controlling variables.  So Fuhrman and McDougall can cite a few studies that linked saturated fat to heart disease and cancer … so what?  I’m sure that’s true to an extent, at least in America.  But some of the biggest sources of saturated fat in the American diet are grain-based desserts (sugar and refined flour), dairy desserts (sugar), pizza (refined flour) and Mexican dishes (refined flour).  Do you see any possible confounding variables there?

If animal fats are the culprit, then the supposed link between heart disease and saturated fat would hold up across time and across the world.  But it doesn’t.  Humans have been meat-eaters for hundreds of thousands of years, and yet heart disease and cancer are referred to as “diseases of civilization.”  As researcher Peter Cleave told the McGovern committee back in the 1970s, blaming modern diseases on ancient foods is ludicrous.

There have been native peoples all over the world who lived primarily and sometimes exclusively on animal flesh and animal fat — the Masai tribes, our own buffalo-hunting tribes, the Inuits, etc. — but heart disease was nearly non-existent among those people.  Doctors who visited them were stunned at how healthy they were.   The buffalo-hunting tribes didn’t become fat, diabetic, and plagued with heart disease until they stopped hunting and started living on sugar and flour.

A century ago, Americans consumed four times as much butter and lard as we do now, but again, heart disease was quite rare.  We didn’t see a surge in heart disease until we began eating a lot more sugar and substituting processed vegetable oils for animal fats.   Even today, the French and Swiss consume far more cream, butter, cheese and pork than Americans, but have a much lower rate of heart disease.  (They do, however, consume far less sugar, soda, processed vegetable oils, and white flour.)

In other words, the observational evidence that Fuhrman and McDougall cite isn’t consistent.  It doesn’t hold up across time or geography.  Not even close.

Clearly something other than animal fat causes heart disease — my guess is sugar and refined carbohydrates, because that result does hold up.  Go around the world, look at different cultures throughout time, and you’ll see that heart disease, cancer, and other “diseases of civilization” show up shortly after sugar and white flour become dietary staples.

Many of you have preached to me that the Fuhrman-McDougall-Ornish diet is superior because it lowers cholesterol.  I’ve got news for you:  That’s one of the least convincing arguments you can make, because I don’t want my cholesterol lowered.  Check the longevity figures against various cholesterol levels.  People with low cholesterol have shorter lifespans.  They’re more likely to die of cancer, stroke, infections and suicide. 

Yeah, yeah, yeah, I can sense you reaching for that chapter from the prayer book already:  “No, you see, cancer CAUSES low cholesterol!”  Uh-huh.  If high cholesterol is linked to heart disease, it must mean cholesterol is causing the disease.  But if cancer is linked to low cholesterol, by gosh, it must be the other way around — because preacher Fuhrman says so.  Since the low cholesterol often shows up years before the cancer, that’s quite a trick.  And good luck explaining how strokes and suicide cause low cholesterol.

But about that link between high cholesterol and heart disease:  it doesn’t actually exist, except in males below the age of 65 living in a few countries.  It certainly doesn’t hold up around the world.  Some of you have quoted McDougall as saying he’s never seen a heart attack in anyone with cholesterol below 150.  (Notice he didn’t say he’s never seen cancer or a stroke.)  Well, if that’s true, it merely means McDougall has never visited Australia.  Aborigines have one of the lowest average cholesterol levels in the world.  They also have one of the highest heart-disease rates.  Autopsies have shown plaque-filled arteries in heart-attack victims whose total cholesterol was as low as 115.   If high cholesterol causes heart disease and low cholesterol cures it, how is that possible?

Some months ago, I dug up the WHO data on average cholesterol levels and heart-disease rates around the world.  If high cholesterol causes heart disease, then plotting those figures against each other would produce a nice, recognizable trend-line.  And as it happens, I did plot them against each other.  You can see the result below:

Do you see a trend-line there?  I certainly don’t.  When I ran the CORR function in Excel, it showed a very slight negative association between cholesterol and heart disease — in other words, higher cholesterol was correlated with a slightly lower rate of heart disease.

I found a similar result when I ran an analysis on the American Heart Association’s own data:  people with LDL over 130 actually have a slightly lower rate of heart disease than people with LDL below 130. 

So once again, the observations your preachers made that you keep quoting don’t hold up.  They’re not consistent, and they’re not repeatable.  Therefore, they’re not scientifically valid.

Many of you have offered yourselves as evidence that the Fuhrman-McDougall-Ornish diet works.  Some of you have even sent me pictures of your now-skeletal bodies, apparently thinking I’d be impressed.  I wasn’t.  I have no desire to look like I take my meals in a concentration camp.

If your health improved, I’m happy for you.  But you might want to ask yourself which aspect of the diet improved your health.  Your preachers insist you give up animal foods, but also sugar and refined carbohydrates.  Then when your health improves, they offer it as proof that animal foods were the problem and only the Holy Plant-Based Diet can lead to eternal health and happiness.

But I also gave up sugar and refined carbohydrates, and my health also improved, despite adding more animal fat to my diet.  Hey, ya know … perhaps it’s the sugar and refined flour that are the real problem here.

You’ve preached about how Ornish and Furhman have reversed heart disease in their patients.  Fine, I believe you.  But so have doctors like William Davis and Al Sears, and they don’t tell their patients give up animal foods; they tell their patients to give up sugar and refined carbohydrates.  A friend of mine went on the Atkins diet — no sugar, no refined carbohydrates — and his labs improved so much, his doctor took him off his statin and said, “Whatever you’re doing, keep doing it.”

Notice anything consistent about the diets that reverse heart disease?

If merely giving up animal fats and switching to all plant-based foods were the key to avoiding heart disease, that result would hold up around the world.  But it doesn’t.  Vegetarians in India have one of the highest rates of heart disease in the world — higher than the Indians who aren’t vegetarians.  They don’t eat meat, but they do consume sugar and flour.

Since your religious tracts are full of cherry-picked observational evidence, I’m going to close by asking you to make an observation for me …  just one, and if your preachers are correct, this should be easy:  Find me a culture, now or in the past, where people subsisted on a diet high in animal foods and animal fats but consumed little or no sugar and flour, yet had high rates of heart disease and cancer.  If you can do that, I’ll answer the bell and listen to you preach the next time you feel like asking me to join the Church of the Holy Plant-Based Diet.

Until you can do that, go away.  You don’t stand a chance of converting me.

Over the long term, a low-carb diet works just as well as a low-fat diet at taking off the pounds - and it might be better for your heart, new research suggests.

Both diets improved cholesterol in a two-year study that included intensive group counseling. But those on the low-carbohydrate diet got a bigger boost in their so-called good cholesterol, nearly twice as much as those on low-fat.

Given all the nonsense over the years along the lines of “Sure, you might lose weight on the Atkins diet, but all that fat will give you heart disease!” I was of course pleased to see this study make the news.  But at the same time, something about either the study itself or the reporting of it didn’t feel quite right.  We were told that the low-carb group lost more weight initially, but both diets performed equally well for weight loss after two years … and yet this bit of information didn’t make it into the Associated Press version of the story:

The 153 participants in the low-carb group followed guidelines set out in Dr Atkins’ New Diet Revolution. For the first 12 weeks, they were told to limit carbohydrate intake to 20 g per day in the form of low-glycemic-index vegetables. After this, they could gradually increase their intake of carbohydrates by 5 g per day per week by adding more vegetables, a limited amount of fruits, and later small quantities of whole grains and dairy products until a stable and desired weight was achieved.

The 154 participants assigned to the low-fat diet limited their energy intake to 1200 to 1500 kcal per day for women and 1500 to 1800 kcal per day for men, with approximately 55% of calories from carbohydrate, 30% from fat, and 15% from protein.

Are there alarm bells going off in your head?  Notice any problems with the comparison here?  We’re looking at one group that was told to restrict fat and calories for two years, and another group that was told to strictly limit carbohydrates for just three months, then gradually raise them until a stable and desired weight was achieved! 

If you’re consuming 20 grams of carbohydrates per day at three months and then starting adding an extra 5 grams per day each week, at six months into the study you’d be consuming 80 grams of carbohydrates per day.  At 12 months, you’d be up to 210 grams per day. 

Ask anyone who’s lost weight and kept it off by restricting carbohydrates what happens if the carb count starts drifting up.  The answer:  first you stop losing, then start gaining again.  Most of us find the magic number is somewhere below 100.  So at some point in the first year, the low-carb dieters most likely hit their limit and stopped losing weight.  From then on, it was merely a maintenance diet.

Meanwhile, I couldn’t find anything suggesting that the low-fat/low-calorie group was told to start eating more once they’d achieved a stable and desired weight.  A limit of 1200-1500 calories for women and 1500-1800 calories for men sure sounds like an ongoing weight-loss diet to me, unless we’re talking about people who aren’t very big to begin with. 

But as it turns out, the study subjects were big.  After digging around and sending out distress signals, I managed to obtain a copy of the full study.  According to the researchers, the subjects all had a BMI of over 30.  Two-thirds of them were women, and yet the average starting weight was 226 pounds.  After 12 months, the average weight in the low-fat/low-calorie group was still over 200 pounds.  At that weight, a diet of 1500-1800 calories is a weight-loss diet.

So in theory, we’re comparing a low-calorie weight-loss diet that lasted for two years with a low-carb diet that reached maintenance level within a year.  Strange design for a study in which weight loss was listed as the primary outcome.  The fact that the low-carb dieters still lost the same amount of weight after two years should have been a major headline — especially since they weren’t told to count calories at any point in the study.  But in his press interviews, lead researcher Gary Foster seemed to determined to give low-fat/low-calorie and low-carb diets equal ratings:

Foster, the study leader, said dieters should be less concerned about which diet to use, and focus on finding the support or technique - like writing down what they eat - that keeps them on track.  “It doesn’t make a difference for weight loss how you get there,” he said.

When I read the statistical analysis part of the paper, I ended up scratching my head and trying to make sense out of gobbledygook like this:  (Don’t give yourself a migraine trying to interpret.  I’ll get to that.)

A parallel longitudinal model structure based on main effects for visit, treatment group, and baseline value and visit-treatment interactions was implemented with logistic regression for binary outcomes. We did estimates by using generalized estimating equations under the logistic regression model for correlated longitudinal binary outcomes implemented in the GENMOD procedure in SAS, version 9. Predicted values for each treatment and visit combination at the mean level of the baseline outcome, with corresponding lower and upper confidence bounds, were produced under each model for the figures. The previously mentioned longitudinal models preclude the use of less robust approaches, such as fixedimputation methods (for example, last observation carried forward or the analysis of participants with complete data [that is, complete case analyses]). These alternative approaches assume that missing data are unrelated to previously observed outcomes or baseline covariates, including treatment (that is, missing completely at random). The longitudinal models implemented for this study relax this missing-completely-at-random assumption in different ways.The generalized estimating equation- based longitudinal logistic models assume that missing data are unrelated to previously observed outcomes but can be related to the treatment because it is a covariate in the model. (that is, covariate-dependent missing completely at random) (18). The likelihood-based mixed-effects models further relax the covariate-dependent missing-completely-at-random assumption by allowing missing data to be dependent on previously observed outcomes and treatment (that is, missing at random). To assess departures from the missing-atrandom assumption under informative withdrawal-that is, the missing weights are informative for which patients chose to withdraw or continue to participate in the study-we present sensitivity analyses. As such, we assume that all participants who withdraw would follow first the maximum and then minimum patient trajectory of weight under the random intercept model.

I thought I knew what they were saying, but to make sure, I asked someone who deals with statistics.  My suspicions were confirmed.  Here’s what all that Engfish means:

WE INCLUDED THE DROP-OUTS IN OUR NUMBER-CRUNCHING BY ESTIMATING WHAT THEIR DATA POINTS WOULD HAVE BEEN.

Yup … they guessed.  So at the end of the day, we’ve got them declaring that low-fat/low-calorie and low-carb diets produce equal weight loss after two years based on estimating the values for the people who quit the study.  Nowhere in the paper do we find statistics based solely on the subjects who actually finished.  Nowhere in the paper do we find any statistics at all on the actual calories or carbohydrates consumed.  Did the low-carb group adhere to the low-carb diet?  Did the low-calorie group keep their calories restricted?  Since both groups regained some weight between the first and second year, the answer to both questions is almost certainly No. 

But the data isn’t there for us to read.  That makes me a little suspicious.  I couldn’t help but wonder if these people set out to prove the superiority of low-fat diets, didn’t care much for the results, then got creative with their statistical analysis to blur the lines.  So I put Google Scholar to work and looked up previous papers by the same researchers.  What I found were studies written by people who clearly believe that weight loss is all about calories and that low-fat diets are the best way to keep calories in check.  Here are some choice quotes.  (I’m not going to italicize them because it’s a lot of text to read.)

“These results show that energy intake increases as dietary fat content increases across the usual range of dietary fat consumed in the United States. Even small reductions in dietary fat could help in lowering total energy intake and reducing weight gain in the population.”

“Our current food supply is high in fat, and high fat diets have been suggested to promote obesity by increasing energy intake, thus increasing the probability of positive energy balance and weight gain.”

“Although there are many environmental factors promoting excess energy intake and discouraging energy expenditure, it is clear that consumption of a high fat diet increases the likelihood of obesity and that the risk of obesity is low in individuals consuming low fat diets. On the basis of the available data, the current public health recommendations to lower dietary fat intake appear to be appropriate.”

“Despite changes in the diet over time, the variables associated with long-term maintenance of weight loss were the same: continued consumption of a low-calorie diet with moderate fat intake, limited fast food, and high levels of physical activity.”

“People definitely lose weight on low-carbohydrate diets. However, there is no evidence that the weight loss can be sustained over time. In addition, there are concerns about the long-term nutritional quality and safety of the low-carbohydrate diet, especially in regards to its effects on cardiovascular health.”

“Weight loss occurs with low-carbohydrate diets because people restrict caloric intake on these diets, producing a short-term negative energy balance. It is less clear whether they can stay with these diets in the long term and maintain their weight loss. It is also not clear whether the diets are safe to use for years at a time.”

“Control of portion size, consumption of a diet low in fat and energy density, and regular physical activity are behaviors that protect against obesity, but it is becoming difficult to adopt and maintain these behaviors in the current environment.”

“Using data from national surveys, we estimate that affecting energy balance by 100 kilocalories per day (by a combination of reductions in energy intake and increases in physical activity) could prevent weight gain in most of the population.”

Read that last one again.  Cutting just 100 per calories per day would do the trick, because it’s all about the calories, right?  Now read this one:

“To determine the optimal energy intake of very-low-calorie diets, 76 obese women were randomly assigned, in a double-blind fashion, to one of three liquid-formula diets: 420 kcal/d, 660 kcal/d, or 800 kcal/d. Weight, body composition, symptoms, mood, and acceptability of the diet were assessed throughout the 6-mo study. There were no significant differences in weight losses or changes in body composition among the three dietary conditions at the end of treatment.”

The difference between 420 calories per day and 800 calories per day for six months is 69,000 calories.  If you believe every 3500 calories equals a pound of fat, the women in the 420-calorie group should have lost an extra 20 pounds.  But they didn’t.  So obviously the body can adjust, which means cutting 100 calories per day isn’t the solution to obesity.  Those last two conclusions are from two different authors on the Low-Fat vs. Low-Carb study.  Perhaps they should get together for a drink and compare previous findings.

I know I’m getting long-winded here, but bear with me.  Given this group’s previous enthusiasm for low-fat diets, I doubt they were excited about the new study’s results, which clearly favored low-carb.  That’s why I’m suspicious that the low-carb group ended up on what amounted to a maintenance diet within a year, and it’s why I’m doubly suspicious that the two-year results included estimates for dropouts.

So just for fun, let’s compare the results at 6 months.  At that point, the dropout rate was still low, both groups were trying to lose weight, and the low-carb group would have been on a true low-carb diet.

Weight Loss:
Low-fat:  25 pounds
Low-carb: 27 pounds

That result alone should be a wake-up call.  We’re talking about people — two- thirds of them women — who weighed an average of 226 pounds.  A 1500-calorie diet is pretty restrictive for someone that heavy.  And yet the low-carb group, with no calorie restrictions at all, lost a bit more.  Did they end up eating less even without a calorie limit?  We don’t know, because the investigators didn’t tell us.  But if they did eat less, that should tell us something about which diet controls appetite naturally, and if they didn’t eat less, somebody owes the country a huge apology for telling us to count calories.

Triglycerides:
Low-fat:  -24.3
Low-carb: -40.06

HDL:
Low-fat:  + 0.89
Low-carb: + 6.21

Those two results should have been the final nail in the coffin of the Lipid Hypothesis and the low-fat diet.  Total cholesterol and LDL are lousy predictors of heart disease and always have been.  But the ratio of Triglycerides/HDL is actually a pretty decent predictor, most likely because it serves a proxy for large vs. small LDL.  The lower the ratio, the larger and fluffier your LDL. Ideally, that ratio should be less than 2.0.  (Mine was 1.1 at last checkup.)  Here is the change in that ratio at six months for both groups:

Low-fat at baseline:  124 / 45.4 = 2.73
Low-fat at 6 months:  99.7 / 46.3 = 2.15

Low-carb at baseline:  113 / 46.2 = 2.44
Low-carb at 6 months:   73 / 52.4 = 1.39

After six months, the group not counting calories and eating unlimited amounts of “artery-clogging saturated fat” lost more weight and showed a much more dramatic improvement in cardiovascular markers.  After 12 months, the results still favored the low-carb group, although both groups backslid a bit. 

And then wouldn’t you know it, by the end of two years, results were similar across the board, except for the HDL.  And all the investigators had to do to achieve that convergence was instruct the low-carb group to increase their carbs and include estimated results for all the drop-outs.

I can’t help but wonder if they did that for a reason.

Just no pattern to it that I can spot.

So I went downstairs and worked on a programming project until about 10:00 a.m.  Then I finally fell asleep and stayed asleep until mid-afternoon.  Saturday night I fell asleep around midnight and slept until noon.  Last night I tried to sleep, couldn’t, and gave up.  I crawled back into bed at 6:00 this morning and woke up five hours later.

This has happened on and off for decades.  I’ve tried without success to spot a pattern, but apparently there isn’t one.  I’ve had insomnia on low-fat diets, low-carb diets, and when not dieting at all.  It’s happened when I haven’t had a drink for months, and it’s happened after a night of drinking beer or wine.  (That’s the worst:  feeling loopy and wide awake at the same time.)  I’ve gone to bed hungry and had insomnia.  I’ve gone to bed feeling full and had insomnia.  I’ve stopped drinking caffeine in the afternoon, but it hasn’t helped … which shouldn’t have surprised me, because I once I gave up caffeine completely and that didn’t help either.

All I know is that on some nights, my brain refuses to shut down.  Sometimes I’m thinking about a specific problem — programming challenges when I’m in the middle of a project are pretty much a guaranteed sleepless night.  You’d be surprised how often the eureka! moment comes at 3:00 a.m.  When it does, I don’t really have any choice except to go downstairs and try the solution.  If it works, then I usually sleep.

But on other nights, I’m relaxed, happy, not feeling any pressure, yet my mind seems to be a conveyor belt of random thoughts.  I watch them go by almost as a neutral observer.  “Hmm, that one’s interesting.  I haven’t thought about Doug Watkins since fourth grade.  I wonder what kind of guy he turned out to be.  That was cool when his mom took us the dolphin show.  Amazing.  Too bad his parents had that awful poodle.  That reminds me, the girls don’t want a boxer anymore.  What was that breed they said they liked?  I’m not getting a dog without a fenced-in back yard, though.  Hey, when was the last time the van had an oil change?  Was it Christmas?  We really should clean out the garage so we can park the van in there on hot days.”

Usually this goes on for a night or two, and then I’m over it.  However, in my mid-twenties, I once went five days without sleeping, save for brief naps.  Towards the end of that week, I was walking home from a diner two blocks from my apartment — I was too tired to cook — and stopped at the corner of Clark and Fullerton, a busy intersection in Chicago.  I looked to my right and saw a WALK sign, then responded by stepping off the curb onto Fullerton.  Someone behind me grabbed my belt or jacket and yanked me backwards just as a car zoomed past.  The car missed me by perhaps 12 inches.  I turned around and mumbled “thank you.”  To this day I can’t tell you anything about who saved me … male, female, young, old, nothing.  My brain had stopped processing information.

If there’s such a thing as an natural night-owl, I’m one of them.  I know paleo types believe in waking up with the sun and falling asleep well before midnight, but that’s never seemed to fit with my natural body clock.  I do most of my creative thinking at night.  Always have.  If I’m tired during the day, I start to feel better when the sun goes down.

I was perfectly happy with my sleep schedule during my days as a traveling comedian, when I rarely went to bed before 3:00 a.m.  If I finished a show at midnight and was within 200 miles of Chicago, I’d just drive home.  Once I drove from Nebraska to Chicago after realzing I wasn’t going to sleep.

This could be a bit genetic.  I’ve had a few bipolar relatives on my dad’s  side of the family.  Perhaps I caught a touch, but just enough to be occasionally unipolar.  I get wired up at times and can’t sleep, but fortunately I don’t get the depressions afterwards.  I just go back to being more or less normal.

I suppose the upside is that I’m capable of working around the clock if I have to.  While editing Fat Head, I was facing a deadline to deliver a sample cut to a distributor, and my computer decided to torture me by crashing several times per day.  (This was before I bought a Mac Pro with Final Cut, so you Apple fans can relax.)  I ended up working for three days and nights, leaving my office only for coffee and food, plus two quick trips home for a shower.  I delivered the hard drives to FedEx a half-hour before the last deadline, then went home and slept for 18 hours.

At times like this, I’m hugely grateful to be self-employed.  When I had office jobs, I had to just suck it up and go to work without sleep.  If the boss says working hours are 9:00 to 5:00, that’s what they are.  Now clients hire me to write programs and deliver them some weeks later.  They don’t know when I work and don’t care, as long as the software is finished on time.  So if I pop awake at 2:00 a.m. and know I’m going to be awake all night, I just go downstairs and work.  If I end up sleeping away most of the next day, no big deal.  My wife suspects I may be part vampire, but she’s understanding.

Anyway, I’m going to relax tonight, stay away from the programming so I don’t discover any problems that need solving, and try to fall asleep by midnight.  Wish me pleasant dreams.

I don’t blame Ronald McDonald for the rise in obesity and diabetes.  I made that clear in Fat Head.  But if he starts handing out statins with the burgers and fries, I may have to track him down and punch him right in his red nose.

No, scratch that.  It wouldn’t actually be Ronald’s fault.  I should track these people down and punch them in the nose instead:

Fast food outlets could provide statin drugs free of charge so that customers can neutralise the heart disease dangers of fatty food, researchers at Imperial College London suggest in a new study.

In a paper published in the American Journal of Cardiology, Dr Darrel Francis and colleagues calculate that the reduction in cardiovascular risk offered by a statin is enough to offset the increase in heart attack risk from eating a cheeseburger and a milkshake.

Those must’ve been some amazing calculations.  After several major clinical trials that lasted for years and cost hundreds of millions of dollars, researchers have been left with contradictory results.  At best, they can say that among people with previously identified heart disease — and no one else — statins might prevent one heart attack for every 100 people who take them.

And yet this group in Britain fired up a copy of Excel and precisely calculated that one dose of statins offsets the coronary damage from a Double Quarter Pounder and a chocolate shake.  Their study (ahem, ahem) should’ve been laughed into instant oblivion.  Instead, it appeared in the American Journal of Cardiology (which next month will publish a study examining the heart-protecting effects of standing outside naked and howling at passing aircraft).

Good grief.  We’re finally seeing major media outlets like the Los Angeles Times openly question the supposed benefits of statins, and in the same week we’ve got doctors suggesting Ronald McDonald should serve them as a side dish … at least in Britain, where statins are already an over-the-counter drug.  Here’s part of what they wrote in their paper:

Routine accessibility of statins in establishments providing unhealthy food might be a rational modern means to offset the cardiovascular risk. Fast food outlets already offer free condiments to supplement meals. A free statin-containing accompaniment would offer cardiovascular benefits, opposite to the effects of equally available salt, sugar, and high-fat condiments.

Yeah, fabulous idea:

“Salt?  Ketchup?  Statin?” 

“How much is the statin?”

“They’re free, sir.”

“Really?  They cost money at the pharmacy.  Give me a dozen.”

An article about the study (ahem, ahem) in today’s Science Daily was so full of bologna, I ingested three days’ worth of saturated fat merely by reading it.  Here are some quotes:

Statins reduce the amount of unhealthy “LDL” cholesterol in the blood. A wealth of trial data has proven them to be highly effective at lowering a person’s heart attack risk.

What “wealth of trial data” would that be, exactly?  Let’s review what the Los Angeles Times said on the topic:

In the first of three studies published in the Archives [of Internal Medicine] last month, medical researchers found that, contrary to widely held belief, statins do not drive down death rates among those who take them to prevent a first heart attack.

Perhaps those researches forgot to limit their study group to people who’d just consumed a Big Mac.  But it’s not just the Archives of Internal Medicine that’s knocking statins lately.  In a paper published in a French medical journal, researchers examined the clinical trials and came to same conclusion:  several recent studies have been conducted to test the effects of cholesterol-lowering drugs.  Most were disappointing or inconclusive, some were stopped early (and never published) because the results weren’t flattering, and the only one that declared a clear benefit for statins — JUPITER — is highly suspect.  That’s the one where the investigators moved their end-point back in time to get a result they liked.

But back to the Science Daily article:

“It’s ironic that people are free to take as many unhealthy condiments in fast food outlets as they like, but statins, which are beneficial to heart health, have to be prescribed,” Dr Francis said.

Doctor, I’m going to step out on a limb here and suggest that any substance that messes with your basic biological functions probably ought to be prescribed.  And if they aren’t prescribed, people should be given all the information about them.  Before we put a dish of statins next to the ketchup dispenser, can we at least talk about side-effects?

Statins have among the best safety profiles of any medication. A very small proportion of regular statin users experience significant side effects, with problems in the liver and kidneys reported in between 1 in 1,000 and 1 in 10,000 people.

AAAARRGGHHH!!  No, damnit, I mean the real side effects!  One in a thousand?  Are you kidding me?  Dr. Beatrice Golomb has been tracking statin side-effects for years and says the rate could be closer to 30%.  Most doctors just don’t attribute the side effects to the statins they’re handing out.  My mom’s doctor certainly didn’t.

Studies have shown a clear link between total fat intake and blood cholesterol, which is strongly linked to heart disease.

So we’re back to that same old @#$%.  If A is linked to B and B is linked to C, then A must cause C.  Just one little problem:  nobody can produce a single study that shows that eating saturated fat causes heart disease.  Recent studies have concluded exactly the opposite:  there is no link between the two.

Recent evidence suggests that trans fats, which are found in high levels in fast food, are the component of the Western diet that is most dangerous in terms of heart disease risk.

No kidding.  Too bad the goofs in white coats convinced us we had to stop frying in tallow and lard … you know, like we did back when heart disease was rare.

Even if you buy the theory that saturated fat raises cholesterol and elevated cholesterol causes heart disease, this proposal is still almost charmingly stupid.  Heart disease is a chronic condition.  It develops over years.  To the minor extent that statins prevent a second heart attack, they do it over the long term.  They’re not condoms for your arteries. If you have the occasional one-nighter with a milkshake, you can skip the protection without receiving a surprise phone call a few months later.

But apparently these researchers are convinced that saturated fat clogs your arteries the way tobacco stains your teeth:  a little bit with every dose.  Eat a burger, grow some plaque — unless, by gosh, you pop a statin immediately to halt the process.

If, heaven forbid, we start serving fast food with a side of statins, here’s what will happen:  five or 10 years from now, you’ll see headlines about a new study that links fast-food consumption to muscle weakness, depression and memory loss.  The blame, of course, will be assigned to the burgers.  Michael Jacobson of CSPI will seek out the nearest TV camera and declare Quarter Pounders “Alzheimer’s in a bun.”

The researchers note that studies should be conducted to assess the potential risks of allowing people to take statins freely, without medical supervision.

This is coming from the same people who think it’s “ironic” that we dispense free ketchup in restaurants but require a prescription for statins?  What a nice little note of caution.

They suggest that a warning on the packet should emphasise that no tablet can substitute for a healthy diet, and advise people to consult their doctor for more advice.

No thanks.  The way doctors give out statins these days, I think white coats should come with a big warning label on them.

At the zenith of their profitability, these medications raked in $26.2 billion a year for their manufacturers.  The introduction in recent years of cheaper generic versions may have begun to cut into sales revenues for the brand-name drugs that came first to the market, but better prices have only fueled the medications’ use: In 2009, U.S. patients filled 201.4 million prescriptions for statins, according to IMS Health, which tracks prescription drug trends. That’s nearly double the number of prescriptions written for statins in 2001, four years after they arrived on the American pharmaceutical landscape.

It’s nice to know people can permanently weaken their muscles now without spending too much.  I knew people were popping statins like they’re tic-tacs, but 201 million prescriptions?!  That’s disturbing.  Worse, the statin-makers want doctors to prescribe these poisons to kids. 

But in recent months the drugs’ touted medical reputation has come under tough scrutiny.

Better ten years too late than never.

Statins were initially approved by the Food and Drug Administration for the prevention of repeat heart attacks and strokes in patients with high cholesterol who had already had a heart attack. And used for that purpose - called “secondary prevention” - the drugs are powerful and effective medications, driving down patients’ risk of another heart attack or stroke by lowering their levels of LDL (or “bad”) cholesterol.

AAARRGGHH!!  No, for @#$% sake, lowering cholesterol is just a nasty little side effect.  To the extent that statins do any good, they do it by lowering inflammation.  You can lower inflammation by cutting the garbage out of your diet.

Then physicians came to believe statins could also reduce the risk of a first heart attack in people who have high LDL cholesterol but are nonetheless healthy. This use of statins - called “primary prevention” - has driven the growth in the market for statins over the last decade.

It’s amazing what you can believe when a hot little pharmaceutical rep in a tight skirt gives you a sales pitch.  When we’re giving drugs to people who are “nonetheless healthy,” something is very, very wrong.

Today, a majority of people who use statins are doing so for primary prevention of heart attacks and strokes. It is this use of statins that has come under recent attack.

“There’s a conspiracy of false hope,” says Harvard Medical School’s Dr. John Abramson, who has cowritten several critiques of statins’ rise, including one published in June in the Archives of Internal Medicine. “The public wants an easy way to prevent heart disease, doctors want to reduce their patients’ risk of heart disease and drug companies want to maximize the number of people taking their pills to boost their sales and profits.”

False hope?  But Dr. Abramson, those Lipitor commercials are so convincing.  Every time I see the one where the guy is pleading with his older brother to take statins, it brings a tear to my eye.  (If I ever told my older brother to take statins, it would be to weaken him to the point that I could finally beat him in arm-wrestling.  But I don’t want to win that badly.)

Heart patients and their physicians are not the only ones to pin their hopes on statins. The drug companies that brought statins to the market have explored the medications’ benefits in prevention or treatment of such conditions as Alzheimer’s disease, rheumatoid arthritis, prostate and breast cancer, kidney disease, macular degeneration and diabetic neuropathy. Although clear proof that statins could forestall or treat any of these diseases might bring in millions of new, paying customers, results have largely been mixed, inconclusive or disappointing.

Well, I am just stunned that beating down your liver’s ability to produce cholesterol hasn’t turned out to be a cure for damned near everything.  Perhaps we need to start removing livers completely.  Tonsils at age 5, then livers a year or so later.  We’ll lie to kids and tell them they can rub all the ice cream they want on their bellies afterwards.

In an ideal world, debate over the clinical virtues or vices of a drug would be long settled by the time the medication saw a meteoric rise in use. But in a healthcare system that relies on commercial incentives to spur drug development, prescription medications are a product like any other.

Yeah, that’s bound to be a problem with our current system of direct-to-consumer sales by pharmaceutical companies.  If only we could place some kind of responsible intermediary between them … perhaps someone in a white coat.

Sometimes, by the time the deliberate pace of medical research and debate suggests that a drug is not all it’s been cracked up to be, it’s already become a bestseller.

That’s why I refer to Dane Cook as the Lipitor of comedy.

And yet, the relationship between cholesterol-lowering and heart disease is not perfectly understood.

Well, there’s an explanation for that.  I’ll use an analogy to clarify:  You could spend dozens of years and millions of dollars trying to understand the relationship between me and Salma Hayek and not get anywhere.  The reason?  We don’t have a relationship … other than the one time we passed each other in a hallway at Disney.

In the first of three studies published in the Archives last month, medical researchers found that, contrary to widely held belief, statins do not drive down death rates among those who take them to prevent a first heart attack.

And yet they lower cholesterol rather dramatically.  Hey, I’m starting to wonder if high cholesterol causes heart disease at all …

A second article cast significant doubt on the influential findings of a 2006 study, called JUPITER, that has driven the expansion of statins’ use by healthy people with elevated blood levels of C-reactive protein, a measure of inflammation. A third article suggested potential ethical, clinical and financial conflicts of interest at work in the execution of the JUPITER study and concluded the widely hailed trial was “flawed” and raises “troubling questions concerning the role of commercial sponsors.”

I’ve read critiques of JUPITER written by skeptical doctors who crunched the data.  Bottom line is that it’s one of worst studies ever.  Here’s just one example:  At one point, the statin-takers showed slightly better results.  Later, the difference between statin-takers and placebo-takers began to shrink to nothing.  So the researchers conveniently chose to place the study’s “end point” at a time when there was still a difference.  Those are the numbers they reported.

As many as three-quarters of patients currently taking statins haven’t yet had a stroke or heart attack; they have diabetes or high LDL cholesterol, conditions widely thought to put them at high risk of having one.

Those patients largely joined the ranks of statin consumers after 2001, when the National Heart, Blood and Lung Institute adopted guidelines on the treatment of patients with high cholesterol. The guidelines, updated again in 2004, suggested that as many as 36 million Americans should take statins - essentially tripling overnight the potential American market for the drugs. Of the nine experts involved in drafting the cholesterol treatment guidelines, the National Institutes of Health later acknowledged that eight had substantial financial ties to statin makers - links that may have predisposed them to view evidence of statins’ benefit in its most positive light.

I think that last sentence pretty much says it all.