How To Save Zero Lives For The Low, Low Cost Of Two Million Dollars And Change

In our previous episode, we saw that statins – in addition to a number of other horrors – may be triggering ALS (commonly known as Lou Gehrig’s disease) in a small percentage of people taking them. Yes, the data came from an observational study, but the risk ratios are as high as those that tied lung cancer to smoking. We’re talking about people on some statins being more than 20 times as likely to develop ALS than people not on statins.

But what if risking ALS, cognitive decline, liver damage, diabetes, joint pains and permanent muscle damage just doesn’t provide that Russian-roulette adrenaline rush you want?  Or what if your darned LDL just refuses to drop to an insanely low level even though you’re chugging high-dose Lipitor every day?

Modern pharmacology to the rescue!

You’ve probably heard of PCSK9 inhibitors, the newest (ahem) wonder drug in the never-ending war against your body’s stupid tendency to produce cholesterol. Here’s how WebMD describes them:

PCSK9 inhibitors are proteins made in a laboratory. They target other proteins in your body, specifically your liver.

Your liver cells have receptors that sweep away excess cholesterol. But another protein called PCSK9 destroys them. That’s where inhibitors come in. They latch onto PCSK9 proteins and block them from acting. The result: More receptors are able to do their job. This lowers the amount of LDL cholesterol in your blood.

And here’s how the makers of Repatha, one of the PCSK9 inhibitors on the market, explain why you may need the drug:

Different types of treatments are used to lower high LDL bad cholesterol. Statins are the most commonly prescribed treatment, but sometimes your LDL is still too high.

Meaning you still have some LDL in your bloodstream.

You may need additional help or a different treatment option to lower your LDL.

Oh yes indeedy, you need that additional help. Because as we all know, beating your LDL cholesterol down to almost non-existent levels will save your life.

Additional is the key word here. The clinical studies have tested statins plus PCSK9 inhibitors vs. statins plus placebo. The subjects typically have familial hypercholesterolemia, which is why statins alone haven’t reduced their LDL cholesterol scores to a level that makes doctors smile.

And what do those studies show? Here’s the money quote from a meta-analysis of several studies published in the Journal of the American Heart Association (that would be the organization that wants us all to get our LDL cholesterol levels as low as possible:

Compared with no PCSK9 inhibitor therapy, treatment with a PCSK9 inhibitor was associated with a lower rate of myocardial infarction (2.3% versus 3.6), stroke (1.0% versus 1.4), and coronary revascularization (4.2% versus 5.8). Overall, no significant change was observed in all‐cause mortality or cardiovascular mortality.

Very much like studies of statins. A slight reduction in heart attacks and other cardiovascular events, but no reduction in deaths from heart attacks or any other cause.

A reader sent me a PDF describing the results of a study on Repatha specifically. The study, named FOURIER, included nearly 28,000 subjects. Half took their statins plus evolocumab (brand name Repatha), and the other half took their statins plus a placebo.

The drug did what it’s designed to do: beat down LDL. Whereas most of these people couldn’t get their LDL much below 100 (the supposed magic number) on a statin alone, adding Repatha into the mix drove LDL levels down to an average of 30. Wow! Almost no LDL left in the bloodstream at all! Boy, that must have really saved some lives, eh?

I’ll quote from the PDF:

Myocardial infarction, stroke, hospitalization for unstable angina or coronary revascularization occurred significantly less frequently in those taking evolocumab than in those taking placebo.

Well, okay then. Sign me up. But wait … I checked the numbers and ran some calculations in Excel. I’ll skip the detailed math and cut to the chase: we’re talking about possibly preventing one heart attack in every 100 people who took the drug. For strokes, it works out to possibly preventing four strokes for every 1,000 people taking the drug.

But here’s the result that really matters:

The two groups did not differ significantly in rates of cardiovascular mortality or all-cause mortality.

No lives saved. Actually, the mortality rates were slightly lower in the placebo group – just not enough to be statistically significant.

If you’ve already heard of PCSK9 inhibitors, you’ve probably also heard they’re expensive. The PDF included a cost-to-benefit section:

The authors estimate that 74 patients similar to those in the trial would need to be treated with evolocumab for two years in order to prevent one cardiovascular death, myocardial infarction or stroke.

Um … let’s correct that. According to both this study the AHA journal’s meta-analysis, the drug might prevent a heart attack or stroke once in a great while, but doesn’t prevent any deaths.  Zero. None. Again, the death rate was actually slightly lower in the placebo group.  So suggesting the drug would prevent any cardiovascular deaths at all is speculative at best and dishonest at worst.  Anyway, to continue:

The estimated cost of treating 74 patients with Repatha for two years is $2,149,400.

So there you have it. For the low, low cost of just over two million dollars, modern pharmacology allows doctors to treat 74 people with a drug that beats their LDL down to unnatural levels — and save zero lives as a result.

Ain’t it wonderful?

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More Very, Very Bad News For Statins

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As if you need another reason to avoid statins …

A couple of readers sent me a link to the latest post by Dr. Malcolm Kendrick, which is titled Statins and Amyotrophic Lateral Sclerosis. (You may have heard ALS referred to by its more common name, Lou Gehrig’s Disease.) Let’s take a peek:

With ALS, your brain remains unaffected, whilst your body dies around you. People suffering ALS are often the ones you see in front of the High Court asking for a change in the law, so that they can be assisted to die, rather than suffocating to death. Thus far, in the UK, the courts have remained impervious to basic, caring, humanity. [You may infer what my views are on this matter].

Now, I have known for many years that statins are likely to cause damage to nerve cells. Probably through a direct effect on inhibiting cholesterol synthesis. Synapses are made, primarily, of cholesterol. Cholesterol is required to maintain the health of the myelin sheath, that surrounds and protects neurones. Glial cells in the brain, sustain the myelin sheath by synthesizing their own cholesterol and transferring it across to neurones, and suchlike.

A couple of weeks ago I was sent the following paper that was published in the Journal Drug Safety. ‘Amyotrophic Lateral Sclerosis Associated with Statin Use A Disproportionality Analysis of the FDA’s Adverse Event Reporting System.’

You can read a summary of the study Dr. Kendrick analyzed here. He apparently has the full-text version and pulled out some interesting (or horrifying, if you prefer) findings. The paper lists the relative risk of developing ALS among statin-takers compared to the general population. As Dr. Kendrick explains:

An odds ratio, basically means increased (or decreased) risk of something happening relative to the standard risk of one. An odds ratio of two (2) means something is twice as likely to happen. An odds ratio of nine (9) means something is nine times as likely to happen. This can also be represented as 900% increase in risk.

Stripping these figures out, we find the following increased risk of ALS associated with the use of different statins. Some statins are more likely to enter the brain than others (atorvastatin, simvastatin and lovastatin) because they are lipophilic (attracted to lipids), these ones had higher ROR.

He listed the odds ratios in a table, so let me just summarize in words: compared to the general population, people taking Rosuvastatin (brand name Crestor) are nine times as likely on average to develop ALS. Horrifying, right? Actually, that’s on the low end of the spectrum. For Atorvastatin (Lipitor), the odds ratio is 17. For Simvastatin (Zocor), the odds ratio is 23 – again, that means people taking it are 23 times more likely on average to develop ALS. But wait, it gets even better. For people taking Lovastatin (Mevacor), the odds ratio is 107.

Two questions may have already popped into your mind. Here’s the first: since this is just an observational study, should we be concerned? I’ll let Dr. Kendrick answer that:

It is often said that association does not mean causation. However, this is only true up to a point. Most statisticians agree that an odds ratio > 6 represents proof of causation. When you find that people taking atorvastatin have a seventeen-fold increase in risk of ALS, this is proof of causation. The effect is too massive to be due to anything else.

A lot of the scary headlines produced by observational studies are based on what looks like a high risk (people who eat bacon are 20% more likely to develop bunions!) but isn’t – 20% more likely in this case would mean an odds ratio of 1.2. Nowhere close to 6.0.  We can and should ignore associations of that variety.

But in this study, we’re talking about odds ratios ranging from 9.0 to 107. I’d pay attention.

The second question: why aren’t doctors beating down the doors of health agencies to scream that statin patients are developing ALS at an alarming rate? I’ll let Kendrick answer that as well:

Now, you may think this is one hell of a lot of people, surely someone would notice. In truth, an increase like this is unlikely to be spotted by anyone. Looking at the UK, each year you might expect to see an extra 3425 cases of ALS each year.

There are around fifty thousand General Practitioners in the UK. So, each GP might expect to see an extra statin related ALS case every sixteen years or so. Or a maximum of two in their working life. You would have to be exceptionally alert to associate one extra case of ALS every sixteen years to statin use.

Doctors aren’t noticing because a 23-fold increase in a very small number is still a small number.  Dr. Kendrick did the math:

In short, in a population of fifty million people, not taking statins, we can calculate that around 1,250 would develop ALS every year.

On the other hand, in a population of fifty million people taking statins (atorvastatin and simvastatin) we can expect that figure to be multiplied by around twenty. Now instead of 1,250 people developing ALS, we can expect to see 20 x 1,250 = 25,000.

Still a very small number in absolute terms. Divide 25,000 by 50 million and you get 0.0005, or one in every 2,000 statin-takers.  The study isn’t saying if you take a statin, you’re highly likely to develop ALS.  It’s saying the small odds are multiplied.

But then again, the supposed life-saving benefits of statins are also very small. Even the most positive studies (which are certainly cherry-picked) suggest perhaps 1 in 100 people taking statins will avoid a heart attack – but only if they belong to a narrowly-defined group at high risk.

Here’s what one study said about how long statins actually prolong life:

The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.

Wow. A few extra days on average. Now balance that against the risks of muscle and joint pains, permanent muscle damage, diabetes, liver damage, memory loss and perhaps ALS.

And that’s why I once told a doctor who suggested I might try a statin to lower my (ahem) “high” cholesterol, “I wouldn’t take a statin unless you had a gun to my head and I was convinced you’d pull the trigger.”

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Rethinking Exercise And Weight Loss

Exercise is great for your health, but it doesn’t do much for weight loss.

I’ve said it. Plenty of people I respect have said it. You might have said it. But based on recent experience, I’m not so sure it’s true.

That is, of course, what the research suggests. In my Science For Smart People speech, I mentioned a study in which middle-aged women were enrolled in a pretty intense aerobic exercise program: 45 minutes per session, five sessions per week. According to the published study, compliance was quite good. Women in the exercise group average 3.6 sessions per week. That works out to an average of 162 minutes per week.

And yet after a year, these women had lost an average of a whopping 4.4 pounds of body fat compared to a control group of women who didn’t exercise. Hardly a ringing endorsement of exercise as a fat-loss tool. (I mentioned the study in the speech because the researchers touted the results as proof that exercise is good for weight loss. Seriously? A year’s worth of effort to lose 4.4 pounds of body fat?)

The scientific literature is full of similar studies. People enroll in exercise programs, put in the time and effort, but lose very little weight.

And yet I have to balance that against my own experience. Exercise does seem to accelerate weight loss for me. I just proved that to myself again recently. Well, perhaps proved is too strong a word, so let’s just say I have n=1 evidence I find compelling.

For the past several years, my weight has generally hovered around the 200 mark. In the summer I’ll typically weigh 197 pounds or so, and in the winter I might weigh more like 202. I fattened myself up during the 2016 holiday season by indulging in too much good scotch and good food, but lost the extra bloat once I went back to my usual diet.

Then came the surgery in November. I didn’t think I’d gain any significant weight during the long recovery, but I did. A big part of that was diet. I’d been cut open, had bone shaved away, and had a torn tendon re-attached. I didn’t want to be in a catabolic state when my body was trying to rebuild damaged tissues. So I ate rather freely, including more potatoes and other starches I’d normally limit. My physical activity, of course, went down to zero after the surgery.

We don’t have a scale at home, so the first time I weighed myself was in January, when I went to the gym just to work my legs. The scale said I was at 213 pounds. Yikes.

I tightened up the diet, went back to limiting the carbs to somewhere in the 50-75 gram per day range, watched my portions, fasted until dinner two days per week, limited my alcohol consumption to two beers on Friday night, etc. Yeah, that should do it.

Six weeks ago, I went to the gym to work my legs and stepped on the scale. I was at 212 pounds.

What the f…? I tightened up my diet for nearly six weeks and lost one pound?! Well, that’s just awesome. At this rate, it will only take me until sometime in 2019 to be back to what I consider my normal weight.

When I was hitting the gym regularly and putting in farm-work sessions on weekends, that same diet kept me at or below 200 pounds.  I wasn’t cleared yet for lifting weights or doing heavy outdoor work, so I made one additional change to my routine: I started diligently using the treadmill I bought myself after the surgery. This one:

For the past six weeks, I’ve been putting in hour-long walking sessions four or five nights per week. I actually find them quite pleasant. The treadmill has a little shelf to hold a tablet and a connection jack to built-in speakers. I watch documentaries on my iPad while walking (the latest is Wild Wild Country on Netflix) and the hour goes by quickly.

I had my final follow-up session with the surgeon a few days ago and finally got clearance to do full workouts at the gym again, with a few caveats: 1) start at half the weight I used to lift on all upper-body machines, 2) don’t go to a higher weight until I can do 15-20 reps with good form, and 3) don’t ignore pain and try to work through it.

Yeah, okay, I’m fine with those. I’ll turn 60 in November and have had my shoulder surgically repaired twice now, with a bicep surgery and a knee surgery tossed in for good measure. I shouldn’t expect to work out like a 25-year-old jock.

On Sunday, I went to the gym and worked my upper body for the first time in six months. The bad news is that I’m a lot weaker than before the surgery. I thought dropping to half the previous load would make each exercise seem ridiculously easy, but, uh, no. It was real work.

The good news is that when I stepped on the scale, I weighed 205 pounds. That means I’ve lost seven pounds in six weeks – on the same diet that previously produced a one-pound weight loss in a similar span. The only difference I can see is the time I’ve been putting in on the treadmill.

Keep in mind, I’m not suggesting it’s a simple matter of calorie math. In fact, the usual calorie math doesn’t account for it. The treadmill has a feature that displays how many calories you burn during a session based on your weight, the incline, the speed, the distance, etc. If the feature is accurate, I’m burning around 300 calories per session. At five sessions per week, that would translate to 1500 calories, or less than half a pound. But I’ve lost just over a pound per week.

Back in my low-fat, high-carb diet days, I jogged for lord-only-knows how many miles and spent countless hours on treadmills, but never lost any significant weight. If it were a simple matter of losing weight by burning calories through exercise, I should have gotten leaner. But I didn’t.

So why do I believe exercise is working as a fat-loss tool now, when it failed me before and has failed so many times in clinical research? I’m just spit-balling here, but I think it probably comes down to hormones.

To explain, I’ll quote from the Fat Head Kids book. In the chapter on why we get fat, we introduce Marty Metabolism, the chief engineer for the biological starship known as The Nautilus. Getting fat, we explain, is the result of Marty receiving commands delivered by chemical messengers called hormones:

Since Marty is under orders to store more fat, he’ll trigger the Get Hungry! program to make you eat more. But if that doesn’t work, he’ll slow down your metabolism to burn less fuel. Either way, you end up consuming more calories than you burn … The commands from hormones are so powerful, Marty can’t just ignore them.

Trying to lose weight by burning calories through exercise is just the flipside of trying to lose weight by eating a bit less. Both assume your body works like a simple bank account, with your weight determined by the simple math of deposits vs. withdrawals. Cut your calories by 500 per day, and by gosh, you’ll automatically lose half-a-pound per week and all that.

But of course, our bodies are nowhere near that simple. Marty has to be willing to go along with the plan. Otherwise, he’ll respond to that attempt at creating a calorie deficit by slowing your metabolism to match the lower food intake.

When I used to go jogging for miles, I was still eating a diet that commanded Marty not to burn away stored fat. So he didn’t. I suspect that in many of the studies on exercise and weight loss (or lack thereof), the subjects were also consuming a diet that worked against burning away stored fat.

But suppose we switch to a diet that tells Marty, through a change in hormonal signals, that it’s perfectly fine to tap the fat stores. Now eating less works. Now exercising works.

And of course, the right kind of exercise also affects the hormonal balance. It improves insulin sensitivity, to name just one benefit. To name another, I’ll quote from the excellent book Primal Endurance, by Mark Sisson and Brad Kearns:

Exercise not only increases the size and number of mitochondria, but also makes them more efficient by increasing the number of oxidative enzymes found in mitochondria. These enzymes improve metabolic function of your skeletal muscles, boosting fat and carbohydrate breakdown for fuel, and speeding energy formation from ATP.

Dr. Bill Lagakos, author of the poor, misunderstood calorie, has also written about how walking lowers fasting glucose and fasting insulin levels.  (I believe you have to be a Patreon of his site to read the full article.  If you’re not a Patreon, I’d urge you to become one.  He puts out a heckuva lot of good material.)

Exercise suppresses insulin via sympathetic nervous system. This doesn’t matter because a contracting muscle, or rather the contraction itself, recruits GLUT4 to the surface of contracting muscle to suck up glucose, to fuel the contraction. It doesn’t need insulin to do this. Glucose-lowering this way also contributes to reduced need for insulin. This is a very healthy thing.

As Sisson and Kearns emphasize in their book, crappy foods can easily cancel out those benefits. That’s why there’s an entire section on diet in what’s otherwise an exercise book.

But if you don’t cancel them out, the benefits are real. I’m pretty sure that’s why I’m no longer stalled on losing the post-surgery fat.

Add it all up, and I’m not sure we’re doing anyone any favors by insisting exercise doesn’t do much for weight loss. Combined with a diet that creates a favorable hormonal mix, perhaps it does. It sure seems to be helping in my case.

But that’s my n=1 experience. I’d like to hear how exercise has or hasn’t worked for the rest of you.

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Now For The Good News: Young Doctors Want To Learn About Nutrition

If you’re a health and nutrition nerd (and if you’re reading this blog, you probably are), you may have had a frustrating experience that goes something like this: a friend mentions an ailment … say, irritable bowel syndrome, or high blood sugar. You start to suggest how a change in diet could relieve the ailment, only to have the friend interrupt with, “But my doctor said …”

In that situation, I’m tempted to reply, “Yeah? And what does your plumber say? Because your plumber has probably spent as much time studying nutrition as your doctor.”

To be fair, I also used to believe doctors are experts in nutrition. When I wrote for a small health magazine in the 1980s, we regularly called doctors for quotes on dietary issues. Most of the major media reporters still run out and find a doctor to comment on any story that involves diet and health. After all, doctors know almost everything about how to stay healthy, right?

Heh-heh-heh. Yeah, a lot of us have learned that’s not true. Doctors aren’t trained to keep us healthy; they’re trained to treat us when we’re sick or injured. The treatments nearly always involve drugs or surgery or both –- and I’m grateful both are available when they’re needed. Take drugs and surgeries out of the equation, and I’d be hobbling around with a bad left leg and barely using my left arm. I’d also be deaf in my left ear, which wouldn’t exactly help with all the sound and music mixing I’ve been doing lately for the Fat Head Kids film.

So thank goodness for what medical doctors do well.

It was only when I got to know some doctors personally while making Fat Head that I learned how little they’re taught about nutrition in medical school. Dr. Mike Eades knows as much about diet and health as anyone I’ve met, but he explained to me that he learned it on his own, long after medical school. Same goes for Dr. Bill Davis, Dr. Eric Westman, Dr. Jay Wortman, etc., etc. If nutrition is taught at all in medical school, it’s usually a brief detour through the usual artercloggingsaturatedfat! and hearthealthywholegrains! nonsense. Then back to learning about drugs and surgery.

In my previous post, I quoted Chris Kresser on why that approach leaves so many patients these days unhappy with their medical care:

Conventional medicine evolved during a time when acute, infectious diseases were the leading causes of death. Most other problems that brought people to the doctor were also acute, like appendicitis or gall bladder attack.

Treatment in these cases was relatively simple: the patient developed pneumonia, went to see the doctor, received an antibiotic (once they were invented), and either got well or died. One problem, one doctor, one treatment.

Today things aren’t quite so simple. The average patient sees the doctor not for an acute problem, but for a chronic one (or in many cases, more than one chronic issue). Chronic diseases are difficult to manage, expensive to treat, require more than one doctor, and typically last a lifetime.

I ended that post by saying that if people are going to trust the health-care profession again, it’s the profession that needs to change, not the rest of us. I’m happy to say some future doctors feel exactly the same. As the BBC reported in an online article, medical students want more training in … wait for it … nutrition. Here are some quotes:

Medical students say they currently learn almost nothing about the way diet and lifestyle affect health – and they should be taught more. They say what they are taught is not practical or relevant to most of the medical problems they see in GP surgeries, clinics and hospitals.

A leading GP estimated that up to 80% of his patients had conditions linked to lifestyle and diet. These included obesity, type 2 diabetes and depression.

Exactly what Kresser pointed out: most people these days visit doctors for chronic conditions that can’t be eliminated with a pill. But diet can sure help in many cases.

While reading the BBC article, I thought about a girlfriend I had more than 30 years ago. Sheri was sweet and pretty, and we were together for more than a year. I remember driving her several times to a doctor to be treated for irritable bowel flare-ups -– she of course didn’t want to drive while doubled over in pain. Each time she had another attack, her doctor tried some different combination of drugs. Each fix was temporary.

When I thought of her today, it was one of those if only I knew then what I know now moments. She was lactose intolerant, so she drank soy milk and poured it on her morning cereal. We both thought grains were health food and ate plenty of them.

I’ll bet you dollars to donuts (and you can keep the donuts) she could have cured the irritable bowel syndrome with a change in diet.  Plenty of people have.  In fact, when we had a premiere party for Fat Head back in 2008 (on my 50th birthday), the sound mixer thanked me for changing his life. After watching the film, he gave up the cereals and breads, started eating bacon and eggs for breakfast … and the irritable bowel syndrome that had made him miserable for years vanished.

If he hadn’t seen Fat Head and talked about diet and health with me during mixing sessions, lord only knows how much longer he would have continued taking drugs and continued suffering. I was delighted to hear watching the film gave him the answer, but of course he shouldn’t have heard it from me. He should have heard it from his doctor.

You may be familiar with Dr. Michael Mosely, who created the 5:2 diet that’s popular in the U.K. Here’s what he told the BBC about nutrition and medical school:

“Unfortunately it’s not part of the traditional training. At medical school I learnt almost nothing about nutrition. And I have a son at medical school and it’s again not part of his key curriculum.”

But that’s changing:

A hotbed of the new revolution is Bristol University where, in 2017, third year medical students Ally Jaffee and Iain Broadley founded Nutritank.

It’s an online organisation created for and by medical students to share nutrition science research and organises events and lectures on campus. This summer, it will welcome GP, author and podcast host Dr Rupy Aujla to Bristol to lead the first UK course in culinary medicine for medical students.

From one society in Bristol, Nutritank has now spread to 15 other student-led groups at universities across the country.

Student-led groups … well, that figures. Meaningful change tends to bubble up from the bottom, not rain down as a gift from on high. But however it’s happening, if more young doctors and doctors-to-be are insisting on being educated about nutrition and health, that’s a very good sign indeed.

Personally, I’d love to have a doctor someday who’s read more about nutrition and health than I have.

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If You Don’t Trust Doctors, You’ll Die From Ebola. Or Something Like That.

One of the best books I’ve read in the past few years is Undoctored by Dr. William Davis. As I explained in my review, I drove up to Wisconsin to interview Dr. Davis for the Fat Head Kids project while he was still working on Undoctored, and he told me about it over dinner.

So the new book (which was untitled at the time) would include two major sections: The first section would explain to readers why the “health-care” system is more interested in their dollars than their health. The second section would arm readers with the knowledge and tools to monitor and improve their own health, and thus avoid ending up in the belly of the health-care beast. With all the bad advice coming from the medical establishment, people need to do their own research and direct their own health instead of relying on doctors to do it for them.

As a reminder, here’s a quote from the introduction of Undoctored:

I propose that people can manage their own health safely and responsibly and attain results superior to those achieved through conventional healthcare – not less than, not on a par with, but superior.

Naturally, that doesn’t sit well with many doctors. In fact, a doctor named Dhruv Khullar recently wrote an op-ed in the New York Times titled Do You Trust The Medical Profession? And in case you have any doubts about where Khullar stand on the issue, the subtitle is A growing distrust could be dangerous to public health and safety. Let’s take a look:

Trust, in each other and in American institutions, is vital for our social and economic well-being: It allows us to work, buy, sell and vote with some reasonable expectation that our behavior will be met with fairness and good will.

But trust has been declining for decades, and the most tangible and immediate damage may be to public health and safety. Mistrust in the medical profession — particularly during emergencies like epidemics — can have deadly consequences.

In 1966, more than three-fourths of Americans had great confidence in medical leaders; today, only 34 percent do. Compared with people in other developed countries, Americans are considerably less likely to trust doctors, and only a quarter express confidence in the health system.

I’m going to step out on a limb here and say that if trust in the medical profession is less than half of what I was in 1966, there’s a good reason for that — reasons Dr. Davis spelled out in Undoctored. But let’s read on:

Trust is the cornerstone of the doctor-patient relationship, and patients who trust their doctors are more likely to follow treatment plans. One study found that nearly two-thirds of patients with high levels of trust always take their medications, but only 14 percent of those with low levels of trust do.

Well, yes, if you have blind faith in the medical profession, you’re more likely to take that statin your doctor prescribed. That’s why I don’t want you to have blind faith in the medical profession. Dr. Khullar is simply assuming that taking your prescribed medication is always the best decision.

Trust is also critical for patient satisfaction, and makes it more likely that patients keep seeing the same doctor.

Well, duh! Of course I’m more likely to keep seeing a doctor I trust. But that doesn’t mean I should just blindly trust any ol’ doctor.

Perhaps most concerning is evidence that low levels of trust can weaken the ability of governments and public health agencies to respond to epidemics.

Researchers surveyed people in Liberia about their knowledge of Ebola, about how much they trusted the government, and how likely they were to take recommended precautions against Ebola. These precautions included adopting safe burial practices; abiding by restrictions on travel, social gatherings and curfews; keeping a bucket of chlorinated water at home; and avoiding physical contact with those displaying symptoms.

People who didn’t trust the government were much less likely to take recommended precautions.

So to prove how dangerous it is not to trust doctors, governments and public health agencies, he had to reach across the ocean and find an example of people ignoring advice about Ebola — in Liberia. Sorry, but that doesn’t convince me I should trust the USDA’s dietary advice, or the CDC’s sodium advice, or my doctor’s advice on the need to lower my cholesterol.

To his credit, the doctor writes that trust needs to be earned:

But there are steps medical leaders and public health officials can take to show they deserve to be trusted. People’s trust depends fundamentally on three questions: Do you know what you’re doing? Will you tell me what you’re doing? Are you doing it to help me or help yourself?

I think the first question is where the rubber meets the road when it comes to trusting doctors. Does the doctor know what he or she is doing? I’d say that depends. If I’m diagnosed with an acute condition such as pneumonia, or appendicitis, or a torn bicep tendon, I’m going to trust the doctor. But if I’m diagnosed with “high” cholesterol, or “high” blood pressure, or type 2 diabetes, or any other chronic condition, I’m going to do some research before I just blindly follow the doctor’s advice.

To explain why, I’ll quote from a recent blog post by Chris Kresser:

Conventional medicine evolved during a time when acute, infectious diseases were the leading causes of death. Most other problems that brought people to the doctor were also acute, like appendicitis or gall bladder attack.

Treatment in these cases was relatively simple: the patient developed pneumonia, went to see the doctor, received an antibiotic (once they were invented), and either got well or died. One problem, one doctor, one treatment.

Today things aren’t quite so simple. The average patient sees the doctor not for an acute problem, but for a chronic one (or in many cases, more than one chronic issue). Chronic diseases are difficult to manage, expensive to treat, require more than one doctor, and typically last a lifetime. They don’t lend themselves to the “one problem, one doctor, one treatment” approach of the past.

Unfortunately, the application of the conventional medical paradigm to the modern problem of chronic disease has led to a system that emphasizes suppressing symptoms with drugs (and sometimes surgery), rather than addressing the underlying cause of the problem.

Just today, I heard about another case of doctors not addressing the underlying cause of a problem. A co-worker told me his daughter suffered from irritable bowel syndrome for years. Doctors treated her with drugs, of course, which sometimes worked and sometimes didn’t. It was a family friend who finally suggested the daughter try a diet devoid of grains. You can guess the happy ending: no more irritable bowel syndrome. How many times have we all heard similar stories?

And of course, modern medical doctors sometimes want to treat a “problem” that isn’t a problem in the first place. Here’s an example I’ve mentioned before: Some years ago, I had a checkup that included (of course) a lipid panel. After viewing the results, the doctor told me I needed to go on a low-fat diet and consider taking a statin. I asked why.

“Your cholesterol is elevated.”

“Put a number on that, please.”

“It’s 203.”

“Uh-huh. And what’s my HDL?”

“Let me see … it’s 64.”

“What about the triglycerides?”

“Hang on … 71.”

“So what you’ve just told me is that for a guy my age, my cholesterol profile is excellent. I’m not going on a low-fat diet, and no, I’m not taking a statin.”

This doctor knew less about how to interpret a cholesterol panel than I did. He saw one number — 203 — and decided my heart was at risk. Strike one. He thought the solution would be a low-fat diet. Strike two. Or a statin. Strike three.

Not trusting that doctor was the right decision. Same goes for my mom’s doctor, who recently put her on statins — again. My mom called and asked why she might be taking something spelled A-V-O-R-A—

“Statin,” I finished. “Avorastatin. It’s a statin. It’s to lower your cholesterol, and no, you don’t need it. There’s never been a single study proving that giving statins to women in your age group prevents any deaths.”

And yet there she was, taking a worthless drug that can screw up a person’s memory, despite the fact that she’s been having memory issues for the past couple of years. Doctor’s orders.

So let’s put two and two (plus one more) together: Dr. Khullar complains that trust in the medical profession is less than half what it was 40-some years ago. Chris Kresser notes that most people these days see doctors for chronic conditions. I’m pretty sure those are related. Too many doctors suck at treating chronic conditions. They mean well, but the advice still sucks.

Dr. Malcolm Kendrick put it nicely in his terrific book Doctoring Data:

The sad truth is that most of the advice we are now bombarded with varies from neutral to damaging. In some cases it can be potentially very damaging indeed. Advising people with diabetes to eat a low fat, high carbohydrate diet, for example. As a piece of harmful idiocy, this really could hardly be bettered.

No wonder patients aren’t happy and full of trust.

Then there’s this additional problem, as described by Dr. Davis in Undoctored:

There is a continual push to medicalize human life. Shyness is now “social anxiety disorder” to justify “treatment” with antidepressant medication; binging in the middle of the night is now “sleep-related eating disorder” to justify treatment with seizure medication and antidepressants; obesity, declared a disease by the FDA, justifies insurance payments for gastric bypass and lap-band. Don’t be surprised if sometime soon, bad dreams, between-meal hunger and excessive love of your cat are labeled diseases warranting treatment.

I read recently that 20% of American boys are diagnosed with ADHD by the time they reach high school and two-thirds of them end up being prescribed drugs — apparently for being energetic males who annoy teachers. Talk about medicalizing what used to be considered a normal part of life.

Here’s another quote from Dr. Kendrick:

As for the elderly, it has become virtually impossible to find anyone taking fewer than four or five separate medications. One of my jobs is working in Intermediate Care where I help to look after elderly people, many of whom have suffered an injury or fracture of some sort. When patients enter this unit, the average number of medications taken is ten. That is ten different drugs, to be taken each and every day, some of them three or four times each day. I suppose it saves on buying food.

Yes, it’s true: people don’t trust doctors like they once did. But it’s not because people are stupid. It’s because they’re smart. It’s because they can do their own research and share experiences with others online. It’s because they’ve learned the hard way that far too often, simply following the doctor’s orders doesn’t heal what ails them.

Personally, I think it would be great if surveys 30 years from now show a renewed faith in the health-care profession. But for that to happens, it’s the profession that needs to change, not the rest of us.

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We Now Return (Again) To Your Regularly Scheduled Program … And I Think I Mean It This Time

Obviously I spoke too soon when I announced just over a week ago that the blog was back up and running. The old site kept getting automatically shut down because of suspicious traffic. I thought our previous provider had the problem solved. The techs switched the site to PHP 7, which was supposed to include better security, but the automatic shutdowns continued. So they offered to move the site to a newer and more powerful server and suggested I use a service named CloudFlare to cut down on bogus traffic.

I was willing to do that, but days went by and the site was never moved to the newer server. Since everything (including the WordPress control panel) was unavailable, there was nothing I could do. I called several times and was told the techs were having difficulties moving the site.  That’s it.  No apologies, no promises, no timelines, no suggestions for ways to get the blog back online while waiting.

So I finally gave up and went looking for another hosting service. The one I chose has quite a few positive reviews online and is optimized specifically for WordPress – our previous host wasn’t. CloudFlare and other security doo-dads are included automatically – again, not the case with our previous provider. I’ll even save a few bucks over the course of a year.

At some point, I’ll move my other blog as well — no big hurry, since I’ve written exactly one post on that blog in the past several years. I had to face reality and let that one go dormant when full-time programming work, part-time farm work and producing a book and film ate up my time.

Anyway, it appears that we really are back up and running this time. Unfortunately, we haven’t yet gotten my Fat Head emails and email folders moved. Apparently there’s some kind of hiccup involved there. If you send an email to my Fat Head account and don’t hear back from me, it probably means I haven’t received it. But I’m sure we’ll get all that straightened out soon.

Chareva also noticed, in the brief time the blog was available last week using the new template, that the purchase page for DVDs didn’t make the transition.  We’ll have to fix that as well.

And then I can actually get back to blogging instead of dealing with technical issues that make me want to break things and say bad words.

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