“It’s no accident that we’re drug oriented, really. The drug companies got us that way and they’d like to keep us that way.  It’s a simple thing. They start you early with the oral habit. Little orange flavored aspirin for children. (pop, pop) Two in the mouth, son. Something wrong with your head? (pop, pop) Two in the mouth. Remember that:  head, mouth. (pop, pop) These are orange; there’ll be other colors later on.”
– George Carlin

I’m wondering what color the drug companies will choose for children’s statins.  Maybe they’ll produce cherry-flavored pills shaped like the American Heart Association’s logo.  Two in the mouth, son.

I was hoping against hope the anti-cholesterol hysterics would never be foolish enough prescribe statins for kids, but a recent news article suggests that’s where we’re headed:

More children should be screened for high cholesterol before puberty, beyond those with a family history of problems, according to wide-ranging new guidelines expected from government-appointed experts who are trying to prevent heart disease later in life.

Any call for wider screening is likely to raise concern about overdiagnosing a condition that may not cause problems for decades, if ever. Yet studies suggest that half of children with high cholesterol will also have it as adults, and it’s one of the best-known causes of clogged arteries that can lead to heart attacks.

High cholesterol is one of the best-known causes of clogged arteries?  Well, in that case, obviously most people who suffer heart attacks must have high cholesterol.  We’ll come back to that.

About a third of U.S. children and teens are obese or overweight. And government studies estimate that about 10 to 13 percent of children and teens have high cholesterol — defined as a score above 200.

Yup, that’s how high cholesterol is defined, all right.  It was defined that way for an important scientific reason:   the average cholesterol level among (non-statinated) adults is around 220.  By defining a normal cholesterol level as high, the National Cholesterol Education Program (whose members nearly all had consulting contracts with statin-makers) turned millions of adults into instant patients.  Now the statin-makers want to tap the kiddie market too.

A key change will be more aggressive recommendations for cholesterol screening and treatment in children, including a change in “the age at which we feel we can safely use statins,” said Dr. Reginald Washington, a pediatric heart specialist in Denver and member of the panel.

I wasn’t aware that the safety of statins for children was based on feelings.  I was thinking perhaps there should be some hard evidence involved.

The pediatrics academy already advises that some children as young as 8 can safely use these cholesterol-lowering medicines, sold as Lipitor, Zocor and in generic form. They are known to prevent heart disease and deaths in adults and are approved for use in children.

Statins are known to prevent heart disease and deaths in adults?  Let’s see what the science has to say on that.  Here’s the conclusion of a meta-analysis on the usefulness of statins for primary prevention – that is, preventing heart attacks in people who don’t already have heart disease:

A new meta-analysis of statins in the primary prevention of heart disease has not shown a significant reduction in all-cause mortality.

Here’s the conclusion of a similar study:

In patients without CV disease, statin therapy decreases the incidence of major coronary and cerebrovascular events and revascularizations, but not coronary heart disease or overall mortality.

Statins may slightly reduce your chances of having a heart attack (if you already have several known risk factors), but they don’t reduce heart disease or overall mortality.  So when a journalist tells you statins are known to prevent heart disease and deaths in adults, the journalist is making a statement that simply isn’t true.

Statins are worthless for primary prevention.  So at best, the kids would be taking a powerful drug they don’t need.  At worst (and I expect the worst), the statins would starve their brains of cholesterol and destroy the mitochondria in their muscles – at exactly the time when their brains and muscles are developing rapidly.  This is a disaster waiting to happen.  With their brain development stunted at an early age, the only career paths open to these kids will be running for Congress or working for the FDA.

But there aren’t big studies showing that using them in children will prevent heart attacks years or decades later.

Well then, by all means, let’s start giving statins to kids based on nothing more than anti-cholesterol hysteria  — and our feelings.  We needn’t bother waiting for those big studies.  To paraphrase George McGovern, we don’t have time to wait for every last shred of evidence to come in.

I said earlier that we’d come back to the statement that high cholesterol being one of the best-known causes of clogged arteries.  If that’s true, then we’d expect most heart-attack victims to have high cholesterol.  But that simply isn’t the case.  Several months ago, I posted about a study showing that nearly three-quarters of heart-attack victims have normal or even low LDL levels – and course, it’s LDL that statins beat into submission.

If you look at heart disease rates and cholesterol levels around the world, you won’t find any correlation whatsoever.  The French and the Swiss both have average cholesterol levels over 230.  They also have the first and second lowest rates of heart disease among industrialized nations.  Russians have an average cholesterol level of 190 – below that magic number of 200.  Russians also have the highest rate of heart disease in Europe.

In another recent news story warning that (eek!) up to one-fifth of people with heart disease aren’t being good little patients and taking their statins, the truth about cholesterol and heart disease slips out again  — although that wasn’t the intention of the article:

More than one in five people with heart disease aren’t getting life-saving statin drugs despite guidelines saying they should, a new study shows.  Researchers looked at nearly 39,000 people who had experienced a heart attack or undergone heart surgery, and found about 8,600 people weren’t prescribed the cholesterol-lowering medications.

Notice the reporter couldn’t resist referring to statins as “life-saving.”  Bias?  What bias?  We don’t see any bias.

Now for the paragraph where the truth slips out:

“Our study shows that half of untreated patients had low LDL levels,” said Dr. Suzanne Arnold of Saint Luke’s Mid America Heart Institute in Kansas City, who worked on the new findings. “This supports the assumption that some doctors may not think patients with low LDL levels need lipid-lowering medication,” she told Reuters Health.

The patients in this study were people who already had a heart attack – and half of them had low LDL levels.  If high cholesterol is one of the best-known causes of clogged arteries, then how the @#$% do we explain away the fact that at least half of the people who suffer heart attacks don’t have high cholesterol?  And how on earth do we justify giving statins to kids just because they have “high” cholesterol?

But even in people with low LDL cholesterol, statins can provide a benefit, according to Arnold. “Statins do more than just lower cholesterol,” she said. “They also play a role in reducing plaque and inflammation in arteries. That benefits people regardless of their cholesterol levels.”

Here’s a crazy idea, Dr. Arnold:  Given what you just said, perhaps high cholesterol isn’t the problem.   Perhaps inflammation is the problem, and the only reason statins provide any benefit at all is that they lower inflammation.    We don’t need drugs to reduce inflammation.  We can do that with a proper diet.  Beating down our cholesterol levels isn’t a benefit of statins; it’s a nasty side-effect.

In some people, statins can cause muscle pain and stomach problems such as nausea, gas, diarrhea or constipation. And their long-term effect on muscle tissue is unknown.

Yes, determining the long-term effect of statins on muscle tissue is tricky, especially since so many older people take statins.  As my mom discovered, if you’re a senior citizen who takes statins and you complain to your doctor about muscle pain, your doctor will probably attribute the pain to old age.

So here’s what we need to do:  Let’s prescribe statins to a whole generation of kids.  In just 20 years or so, we’ll finally know the long-term effects of statins on muscle tissue.  I’m sure all those 30-year-olds in wheelchairs will be glad to know they contributed to medical science.

The Older Brother’s oldest son (a.k.a. my nephew Eric) recently annoyed his (morbidly obese) doctor by refusing to take statins after a lab test flagged his total cholesterol as “elevated.”

Some snippets from an email Eric sent me:

The nurse called last night while I was driving home and only gave me my triglycerides and cholesterol readings, followed by the doctor’s (5 feet tall and a good 275lbs) recommendation to take a statin.

After verifying that she heard me correctly that “I’m not going to take a statin” and then informing me that cholesterol can lead to heart disease and stroke, I again declined and told her I would talk further with the doctor, recommending your movie and a couple books.

I called this morning to have the full results faxed to me.  After getting that fax from the machine with my greasy, McMuffin-without-the-muffin fingers (didn’t have time to make eggs this morning or a protein shake), I plugged them into excel to share.

Eric is 26 years old and (like his younger brother the Ranger) a strong, muscular guy who’s in excellent shape.  Here are the cholesterol numbers that prompted the obese doctor to recommend a statin:

Total Cholesterol:   219
HDL: 61
Triglycerides:  55
LDL:  147

The LDL, of course, is a calculated figure.  For those of you who don’t already know, LDL is usually calculated using something called the Freidewald Equation, which looks like this:

LDL = Total cholesterol – (HDL + (Triglycerides/5))

As Dr. Mike Eades explained in one his posts, the Freidewald equation has been shown to over-estimate LDL levels in people whose triglycerides are low.  The Freidewald equation also “rewards” you for having higher triglycerides – not something you want — by producing a lower calculated LDL figure.   Let’s create a couple of fictional examples to demonstrate:

Patient One
Total Cholesterol: 200
HDL: 45
Triglycerides:  150
Calculated LDL:  125

Patient Two
Total Cholesterol: 200
HDL: 50
Triglycerides:  70
Calculated LDL:  136

The most useful indicator of heart-disease risk you can extrapolate from a lipid panel is the ratio of Triglycerides/HDL.  You want that ratio below 2.0, because a ratio below 2.0 is a pretty good indicator that you’re mostly producing large, fluffy LDL.  At 3.0 or above, it’s more likely you’re producing small, dense LDL.

Patient One’s ratio is 3.33 — not horrible, but certainly not what I’d consider good, either.  Patient Two’s ratio is 1.4 –  pretty darned good.  Patient Two clearly has a much better cholesterol profile.  But because Patient Two’s calculated LDL (which is likely overestimated anyway) is above the supposed magic number of 130, she’s the one who’ll get a lecture from her doctor along with a recommendation to go on a low-fat diet – which will probably reduce her HDL and raise her triglycerides.

Eric’s Triglycerides/HDL ratio is 0.90 … in other words, it’s outstanding.  Even if his LDL is really and truly elevated, it’s almost certainly mostly the large, fluffy LDL.  That type of LDL not only isn’t dangerous, it protects us against infections and cancer, at least according to Dr. Uffe Ravnskov’s reading of the data.

And yet a doctor wants this strong, active, sports-nut of a 26-year-old man to go on statins because his total cholesterol is 219 and his calculated LDL is 147.  If Eric did go on statins, the only beneficiaries would be

• Pfizer
• The pitchers on opposing softball teams who would no longer have to watch Eric belt their fastballs over the fences

It’s a sad situation when we have to ignore our doctors’ advice in order to stay healthy.

Some interesting theories on Why We Get Fat and What to Do About It have been popping in the news lately – and no, I’m not talking about the book by Gary Taubes.  I’m talking about ideas proposed by … uh … well, let’s call them somewhat less-brilliant researchers.

A doctor in St. Louis, for example, has decided that the main cause of the obesity epidemic is pregnancy:

National experts have suggested that if a woman is obese, she should gain far less weight when pregnant than previously thought:  just 11 to 20 pounds.  But one local doctor says even that is far too much. Dr. Raul Artal, chairman of the obstetrics and gynecology department at St. Louis University School of Medicine, says an obese woman who gets knocked up shouldn’t gain so much as an ounce — and then adds that pregnancy, not an unhealthy affection for fast food and the La-Z-Boy, is “the main contributor to the obesity epidemic in this country.”

I believe the doctor is onto something.  While researching Fat Head, I was surprised to learn that back in the days when obesity was rare, the vast majority of women never became pregnant.  All the propagating of the species was accomplished by a small minority of women who then gave their babies to women who preferred to remain thin.  Pretty much every family was made up of kids who were adopted — which is how Puritans and the upper-class British managed to raise large numbers of children without ever engaging in sex.  It was also the reason that every individual bore a striking resemblance to at least 200 other individuals in their geographic area.  Sure, the gene pool was a little shallow, but people were thin and that’s what mattered.

Unfortunately, all that began to change in the late 1960s with the arrival of loose morals — which became even looser after disco music was invented in the 1970s.  Women who wanted to raise children began insisting on having their own babies, and the obesity epidemic was born.  (By pure coincidence, this was also around the time the McGovern committee told everyone to eat more grains and other carbohydrates.)

I know what you’re probably thinking:  if Dr. Artal is correct that pregnancy is the primary cause of obesity, why are so many men obese? All I can tell you is that both times my wife became pregnant, I got fatter.  I can’t explain the biological mechanism, but I expect science to provide an answer eventually.

Since women apparently plan to keep producing their own babies, the real question is what to do about all the obesity their pregnancies are causing.  A professor of bioethics has come up with a solution that was recently praised by a columnist for the Boston Globe:  we need to shame fat people into better eating habits:

“Hey, fatty! Pull that doughnut out of your pie hole! You look like a pig, and you are costing me, and every other taxpayer, billions of dollars in unnecessary health care each year!’’

How do you like my new public service ad campaign, designed to stigmatize the overweight and the obese in the same way smokers have been made to feel the knout of social opprobrium for the past quarter-century?

I got the idea when I heard Professor Daniel Callahan, the retired cofounder of the Hastings Center, a bioethics research institution, speak on a radio program about two weeks ago. Why aren’t overeaters subject to the same stigmatization as smokers?, he mused. Why not indeed?

Callahan makes a persuasive case: 67 percent of Americans are overweight, he writes. “Obesity is a leading cause of diabetes, heart disease, and kidney failure. There are some prima facie reasons for thinking about stigmatization as one more arrow in the quiver of possible solutions.

“It can hardly be said that obesity is beyond individual control,’’ he continues. “So, why not stigmatize [the obese], bringing social pressure to bear?’’

Boy, if only someone with Professor Callahan’s deep understanding of what causes body-fat accumulation had been around when I was becoming an obese adolescent, I would have remained lean.  When we had to play shirts vs. skins in gym-class basketball games, it just never occurred to me to feel ashamed of my fat belly, love handles and boy-boobs.  If the naturally-skinny boys in my class had cared more about me (and been armed with Professor Callahan’s insights), they could have helped me out by calling me names like Lard-Ass, Fat Boy, Pudge, Booby Boy, Porky Pig, or Butter Butt.  I now realize that with their kind-hearted acceptance of me (and the one other fat kid in class), they were inadvertently acting as enablers.

So to all you obese people out there who are happy with your bodies, it’s time to look yourself in the mirror and feel ashamed!  Don’t wait for Professor Callahan’s ideas to catch fire and inspire some do-gooders to shame you … be pro-active and take responsibility for shaming yourself.

I know what you’re probably thinking:  But what about all the fat babies being born these days?  Babies aren’t capable of shaming themselves … if they were, they’d  be more conscientious about where and when they fill their diapers.

Never fear.  The British government has an answer for the wee tykes:  get them to exercise more!

The British government says children under five — including those who can’t walk yet — should exercise every day. The new guidelines were issued Monday, partly to fight the obesity epidemic.

In them, the department of health says children under five who can walk should be physically active for at least three hours a day. For babies who can’t walk yet, the government says physical activity should be encouraged from birth, including infants playing on their stomach and swimming sessions with their parents.

I have to admit, I don’t know whether this advice will prove to be effective, since my only experience is with two little girls who are active even when I’d like to them slow down for a change.  Last night, for example, they grew bored with watching Man vs. Wild from a seated position and decided to construct a bridge between the sofa and an ottoman, using several household items as building materials.  When the bridge fell down under the older daughter’s weight, I thought they’d give up … but nope, they just built a new one.  When that one fell down, they changed designs and built yet another one.  When that fell down, they built another one.  I was expecting them to start whistling the theme from The Bridge on the River Kwai any minute.

But if the British government wants the “get your baby to exercise” advice to be truly effective, I’d suggest they combine it with Professor Callahan’s insights and shame babies into working out.  Then you’d have a sure-fire cure for childhood obesity.

“Come on, Junior!  Wiggle those arms!  One-two-three-four … you’re quitting at four reps?  What are you, some kind of baby?”

“Well, actually—“

“No wonder you’re so fat.  Look at you, you little butterball!  You’ve got thighs like canned hams!”

“That’s baby fat, coach!”

“Yeah, sure it is.  Listen, kid:  you’re fat because your mother listened to some old Bee Gees songs from the 1970s and then went out and got herself pregnant, so now everybody’s fat.  Well, not here in jolly old England, Butterball!  Not on my watch.  Now drop and give me twenty.”

“Twenty what?”

“Pushups!”

“WAAAAHHH!”

“Be quiet!  Hey, what did you just put in your mouth?”

“My thumb.”

“Is there any fat in that thing?”

“I’m a baby.  I’m fat all over.”

“Then take it out of your mouth, now!”

“WAAAAHHH!”

Yup, with all these brilliant new ideas being proposed, obesity will soon be nothing more than a bad memory – like disco.

About a month ago, a new study warning about the dangers of  “super-sticky cholesterol” made a bit of a splash in the media.  I ignored it at the time, but thought about it today when I received an email from a Fat Head viewer who’s raising a diabetic child.  We’ll come back to that in a minute.

The study, in case you missed it, produced headlines like this:

Super-Sticky ‘Ultra-Bad’ Cholesterol Revealed in People at High Risk of Heart Disease

When I was in journalism school, we were taught that many people don’t read much more than the headline and the first few paragraphs of a news story.  That’s why student journalists are taught to write in reverse-pyramid style:  get the important ideas in those first few paragraphs, then expand on the details.  Here are the first few paragraphs of a Science Daily article about the study:

Scientists from the University of Warwick have discovered why a newly found form of cholesterol seems to be ‘ultra-bad’, leading to increased risk of heart disease. The discovery could lead to new treatments to prevent heart disease particularly in people with type 2 diabetes and the elderly.

The research, funded by the British Heart Foundation (BHF), found that ‘ultra-bad’ cholesterol, called MGmin-low-density lipoprotein (LDL), which is more common in people with type 2 diabetes and the elderly, appears to be ‘stickier’ than normal LDL. This makes it more likely to attach to the walls of arteries. When LDL attaches to artery walls it helps form the dangerous ‘fatty’ plaques’ that cause coronary heart disease (CHD).

CHD is the condition behind heart attacks, claiming 88,000 lives in the UK every year (1).

If you stop there, the takeaway message is that evil ol’ cholesterol also comes in an especially evil form that’s even more likely to cause heart disease.  Yikes!   Better go on a low-fat diet and get your cholesterol down, maybe even take a statin just to be safe.  You have to read further to spot the true villain:

The researchers made the discovery by creating human MGmin-LDL in the laboratory, then studying its characteristics and interactions with other important molecules in the body.

They found that MGmin-LDL is created by the addition of sugar groups to ‘normal’ LDL — a process called glycation – making LDL smaller and denser. By changing its shape, the sugar groups expose new regions on the surface of the LDL. These exposed regions are more likely to stick to artery walls, helping to build fatty plaques. As fatty plaques grow they narrow arteries — reducing blood flow — and they can eventually rupture, triggering a blood clot that causes a heart attack or stroke.

What turns cholesterol into “sticky” cholesterol?  Sugar.

In 1976 a prominent researcher named Peter Cleave told the McGovern committee that if anything in our diets causes heart disease, it’s probably sugar.  McGovern sided with the researchers who blamed dietary fat, perhaps because he couldn’t imagine how sugar could produce fatty streaks in our arteries.  This study describes a plausible (and likely, in my opinion) mechanism:  high blood sugar produces small, dense LDL through glycation.

Glycation is what happens when sugars bind to proteins.  I’ve heard various descriptions, but the one that stuck with me (pun intended) is that glycation “caramelizes” your tissues.  The Wikipedia entry on glycation gives a good description of why you want to avoid being caramelized:

Endogenous (inside the body) glycations occur mainly in the bloodstream to a small proportion of the absorbed simple sugars: glucose, fructose, and galactose. It appears that fructose and galactose have approximately ten times the glycation activity of glucose, the primary body fuel. Glycation is the first step in the evolution of these molecules through a complex series of very slow reactions in the body … all lead to advanced glycation endproducts (AGEs).

Some AGEs are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as: cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer’s disease (amyloid proteins are side-products of the reactions progressing to AGEs), cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination).

Quite a horror show, eh?  As the article in Science Daily notes, pharmaceutical companies may use this information to develop drugs that help prevent heart disease by reducing glucose levels.

Yes, yes, I know … you’re probably sitting there, dangerously close to banging your head on your desk, wondering why doctors don’t just tell people to stop jacking up their blood sugar with too many carbohydrates.  Well, heck, they can’t do that because everybody just knows we need those carbohydrates –- which brings me back to the email I received today:

————————————————————-

Our son was diagnosed with type 1 diabetes a year ago this August. Doctors told us that we should feed him whatever he wanted, even after I pushed to speak with their staff nutritionist and nailed her about their suggested carb intake. Their response to our concerns was, “He needs to grow healthier and stronger and the only way to do this is to feed him more carbs and give him more insulin injections.”

This would be to any Fat Head unsatisfactory as best. Three months after beginning our son’s insulin regimen, we noticed he began to show signs of symptoms he had never had before.  The doctors again explained that he was fine in their opinion and his symptoms (while major and included loss of sight, balance, headaches, ear aches, and loss of cognitive function) were nothing more then simple effects of his disease and we would have to manage by continuing with their recommended treatment plan:  injections and carb counting.

We did some research — as good Fat Head parents tend to — and found that the insulin prescribed for our two year old son was only approved by the FDA for children age six and over. We stopped use and contacted his doctor’s office. After two days all our son’s symptoms vanished and he began to function normally again. When we confronted the doctor about this issue they claimed that this drug is being used world-wide among the same age group as our son and it wasn’t uncommon or irregular.

Then about two weeks ago we found Fat Head. I have been doing research to that (fat) end for months, but I was missing the key component that Fat Head was able to deliver:  Fat.  In all the information I’ve pored over, it is always the same story.  Stay away from sugar, carbs, processed foods, etc.  But no one said anything about adding animal fat.

Just as a kind of experimental joke my husband and I took the information in Fat Head literally and began to cut out two-thirds of the carbs from our family diet. In only two days our son’s sugar levels went from spiking randomly at 480-600 and fell to 140-160. Our daughter also began to show signs of improved health — which for us meant more trips to the time-out chair. Having more energy evidently means more Fat Head mischief. You might want to make that a disclaimer for unsuspecting parents *wink* … just a thought.

————————————————————-

Most doctors still believe high-fat diets cause heart disease, and diabetics are three times more likely to eventually develop heart disease.  Put those together, and you get the standard advice for diabetics:  go on a low-fat diet with plenty of complex carbohydrates, then take insulin to control your blood sugar.  Following that advice, this poor kid was getting glucose spikes of 600.  That’s major glycation territory.

Ignoring the standard advice, the same kid dropped his glucose to almost-normal levels.  Given more time on a low-carb / high-fat diet, he may even reach normal levels.  I certainly hope so.

Cholesterol isn’t the villain; “super-sticky cholesterol” resulting from too many carbohydrates is.  And by recommending low-fat / high-carbohydrate diets, doctors are putting diabetics and other people prone to heart disease in a sticky situation indeed.

In case you missed it in comments, Dana Carpender of Hold The Toast pointed me to this YouTube video.  Perfect comment on yesterday’s post about all the drug commercials on TV:

Even though I record all the TV shows I want to watch and skip through the commercials during playback, I’ve been half-consciously aware that pharmaceutical ads seem to dominate commercial airtime.  As I was watching a Biography Channel episode about Arnold Schwarzenegger a few days ago, it seemed as if every other commercial I skipped past was for some sort of drug.  So today, I played the episode again and tallied them.

There were 27 commercials, not counting promos for upcoming episodes on Biography.  Seven were for prescription drugs.  (There was also an ad for a cream to remove dark circles under the eyes, and one claiming that NutriSystem will help type 2 diabetes keep their blood sugar under control.)

Something is very, very wrong when a quarter of the prime-time ads on TV are directed at sick people.  And these aren’t even products you can just walk into a store and buy — you must, as the ads remind you, “talk to your doctor about …”

Here are some of the medical products I saw advertised, along with the conditions they’re intended to treat and abbreviated version of the obligatory warnings.

Advair (asthma).  May increases risk of death from complications of asthma.  May increase risk of hospitalization for asthma in children and adolescents.

Symbicort (chronic obstructive pulmonary disease).  Do not take more than twice per day.  Increases risk of lung infections, osteoporosis, and some eye problems.

Oracea (rosacea) Side effects include stomach upset, sore throat, sinus infections.  Stay out of direct or artificial sunlight while taking.  Talk to your doctor if you’re taking blood thinners or have kidney disease, as there may be serious side effects.

Nexium (heartburn, acid reflux).  Talk to your doctor about an increased risk of osteoporosis-related bone fractures if you take multiple daily doses.  Side effects include headache, diarrhea and abdominal pain.

Fabulous.  While you’re in traction because of an osteoporosis-related femur fracture, you’ll be delighted you’re not experiencing heartburn.

Cymbalta (chronic pain, osteoarthritis)  Taking with aspirin or blood thinners may increase bleeding risk.  Severe liver problems, some fatal, were reported, as were abdominal pain and yellowing of the skin or eyes.  Dizziness or fainting may occur upon standing.  Other side effects include confusion, dry mouth and constipation. Tell your doctor if you experience unusual changes in behavior, mood swings, or thoughts of suicide, as these can increase in children, teens and young adults.

By the time the announcer finished with the long list of warnings for Cymbalta, I was laughing out loud — mostly because I was seeing all these happy-looking people going by on the screen while hearing about fatal liver problems, confusion and suicides.  Look!  We’re happy!  Or maybe we’re just confused!

I half-expected one of the happy people to face the camera and say, “Let’s see … my chronic back pain is finally gone, but I’m constipated, I have yellow eyes, I faint when I stand up, I’m confused, my belly hurts, and I my liver isn’t working anymore.  You know what?  I think I’ll kill myself.”

I’m grateful drugs exist for the people who need them.  But we shouldn’t need so many of them, and as Dr. Mary Vernon emphasized in a recent podcast interview, taking a drug to mask the symptoms of disease isn’t the same as being healthy.  We learned that lesson again (well, some of us; many doctors and researchers won’t) a few days ago when yet another drug that artificially raises HDL failed to reduce heart disease:

The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health has stopped a clinical trial studying a blood lipid treatment 18 months earlier than planned. The trial found that adding high dose, extended-release niacin to statin treatment in people with heart and vascular disease, did not reduce the risk of cardiovascular events, including heart attacks and stroke.

During the study’s 32 months of follow-up, participants who took high dose, extended-release niacin and statin treatment had increased HDL cholesterol and lowered triglyceride levels compared to participants who took a statin alone. However, the combination treatment did not reduce fatal or non-fatal heart attacks, strokes, hospitalizations for acute coronary syndrome, or revascularization procedures to improve blood flow in the arteries of the heart and brain.

The DSMB also noted a small and unexplained increase in ischemic stroke rates in the high dose, extended-release niacin group. This contributed to the NHLBI acting director’s decision to stop the trial before its planned conclusion.

Triglycerides were pushed down, HDL was pushed up, but the rate of heart disease didn’t change.  Why?  Because chemically improving the markers for health isn’t the same as improving health.  As I pointed out in a previous post, my neighbor’s grass is a beautiful shade of green because he constantly fusses over his lawn to keep it healthy.  My lawn is patchy because I don’t care about lawns.  If I paint my lawn green, that won’t make it any healthier.  Sadly, many researches just can’t seem to grasp that concept:

“As we continue to search for new approaches to treating cholesterol problems, it is important to remember the value of existing treatments. The key to treating high cholesterol so patients can reduce their risk of cardiovascular disease is to lower the level of LDL cholesterol, through well-established drug treatments such as statins and lifestyle changes,” said Patrice Desvigne-Nickens, M.D., NHLBI project officer for the AIM-HIGH trial.

Head. Bang. On. Desk.

We just saw a drug that successfully manipulates cholesterol levels fail to reduce heart disease — while slightly increasing strokes — and yet the good doctor is still promoting chemical manipulation.  By gosh, if you change the risk factors, you must be changing the actual outcomes.  Riiiiight.  Paint your lawn green, and the grass becomes healthy.

This doesn’t even provide the entertainment value of being a new story.  Some years ago, Pfizer announced it had developed a combo drug that significantly improved cardiovascular risk factors.  The early press releases were breathless:  the miracle combo boosted HDL by 44 to 66 percent, while lowering LDL by 41 to 60 percent.  Wow!

The results were somewhat less spectacular:  Pfizer had to pull the plug on a clinical trial of the combo drug three years early because people taking the combo drug had a 60% higher mortality rate.  Hmmm … maybe Mother Nature, unlike NHLBI researchers, doesn’t think it’s a good idea to chemically manipulate our production of cholesterol.

We’re going to see this story repeated at least two more times.  Merck is currently developing and testing a drug that artificially raises HDL.  And earlier this week, a reader sent me a link to this online article:

Polypill ‘halves risk of stroke and heart attack’

A new 10p-a-day ‘polypill’ containing aspirin and statins halves the risk of heart disease and stroke, according to the world’s first international trial of the drug, reported The Daily Telegraph. The news story is based on a randomised controlled trial of a polypill in 378 people who all had a slightly increased risk of vascular disease. The researchers found that people who took the polypill had improvements in their blood pressure and levels of “bad” LDL cholesterol (equivalent to a 46% reduction in cardiovascular risk) over 12 weeks, compared to those who took a dummy pill.

If you’ve seen my Science For Smart People speech, you know what “lowers your risk” actually means.  So the polypill “halves the risk” of heart disease, does it?  Whoop-ti-do.  I’ve got news for you:  Pfizer’s combo drug dramatically raised HDL and lowered LDL, which means it dramatically “lowered the risk” of heart disease for the people taking it.  The only bad news is that more of those people died.

High HDL and low triglycerides don’t confer good health.  They’re markers for good health.  Chemicals that remove the blotches from your face, beat down your elevated blood sugar, or mask the pains of heartburn and arthritis don’t eliminate the underlying imbalances that caused those conditions in the first place.

If you want real health, eat real food.  Get some real exercise and some real sleep.  You’re not going to find real health in a little brown bottle, no matter how many times you “talk to your doctor about …”