Archive for January, 2011

Intermittent Fasting

I started experimenting with intermittent fasting about three weeks ago. Four or five days per week, I use the eight-hour window method, which for me means squeezing my meals into the period between noon and 8:00 PM. A few times I’ve forgotten to eat a snack at 8:00 PM, so the between-meal fast was extended by two or three hours. I’ve also been picking one day per week — Saturday or Sunday — to go without eating at all. As I noted in a couple of posts, it’s easier than I would’ve suspected. 

I ended up doing a 22-hour fast a couple of days ago without really intending to. Tom Monahan (the composer for Fat Head) and I are working on a music project together, and my old second-hand guitar isn’t up to snuff for recording. So in the early afternoon — after skipping breakfast, which I often do — I set out for Guitar Center in Nashville, planning to buy a particular acoustic/electric combo guitar, based on some positive reviews. I figured I’d be home an hour later.

The good news is that Guitar Center had that particular guitar in stock. The bad news is that when I played it, I wasn’t impressed with the sound. Rather than let budget-consciousness seduce me into buying one guitar that would serve as a mediocre acoustic and a mediocre electric, I accepted that I’d need to buy one of each.

So my one-hour shopping trip ended up lasting four hours, as I tried out several acoustics, then several electrics, narrowing down the choices until I was satisfied with the final two. That put me in rush-hour traffic on the way home. Rush hour in Nashville isn’t anything like rush hour in Los Angeles, but nonetheless it after 5:00 PM by the time I got home. My last meal had been at 7:00 PM the previous evening. It wasn’t exactly a total fast because I’d had coffee with cream in the morning, but still pretty close.  I was only aware of feeling truly hungry for the last hour.

I weighed 200 pounds when I began the intermittent fasting experiment. Yesterday at the gym (we don’t have a scale at home), I was at 194. I wouldn’t label that as rapid weight loss, but considering that I eat quite heartily during my non-fasting periods, I’m pleased.

Netflix

I just received word yesterday that thanks in part to the popularity of Fat Head on Hulu, our internet distributor was able to strike a deal with Netflix to offer the film in the Instant Play lineup. I’ll make an announcement when it’s actually available. A sincere thanks to all of you who helped Fat Head make a splash on Hulu.

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In a Weight Watchers discussion group, someone recently posted this advice:

The key to successful weight loss is simple mathematics . . . ingest fewer calories than calories expended in a day.

That second part of that sentence is, of course, correct. Your body won’t tap the energy reserves in your fat cells unless the energy is needed.  You have to expend more than you ingest.  But that doesn’t mean successful weight loss is all about “simple mathematics.”  Biological systems aren’t simple.

Unfortunately, too many people grasp (again, correctly) that gaining or losing weight requires an imbalance between the energy consumed and the energy expended, but then take a leap in logic and conclude that:

  1. Consuming additional calories is the root cause of becoming fatter (as opposed to a response to storing more calories as fat).
  2. Everyone who becomes fatter is either eating more or moving less than before.
  3. Consuming fewer calories will automatically lead to a lower weight and less body fat.

In other words, they think it’s about simple mathematics, just like a savings account.  To dispute any of these conclusions, we’re told, would be to ignore the laws of thermodynamics. So let’s see how that contention holds up in the face of controlled research.

In a study published earlier this year, researchers conducted two experiments, each lasting three or four weeks, in which obese mice were divided into two groups: a control group that ate freely (ad libitum) and a calorie-restricted group. In the first experiment, researchers first recorded the average caloric intake of the mice when they were allowed to eat freely, then limited the calorie-restricted group to 95% of that intake. In the second experiment, researchers observed the on-going caloric intake of the mice allowed to eat freely, then limited the calorie-restricted group to 95% of that intake. In other words, if the mice eating freely ate more, the calorie-restricted mice were given more food … but they were still eating 5% fewer calories than their freewheelin’ cousins.

A legitimate criticism of many diet studies is that the researchers relied on food-recall surveys or diet journals to determine how much people ate. Those methods can be notoriously inaccurate. Realizing this, the researchers on this study elected not to allow the mice to keep their own diet journals. Instead, the researchers precisely measured and recorded how much each mouse ate — even going so far as to examine the little critters’ cages and subtracting any bits of food they found from the food-intake totals.

In both experiments, researchers took precise before-and-after measurements of weight, lean body mass, and adipose-tissue mass. In the second experiment, they also used infrared sensors to track locomotor activity levels (“moving around” to us laypeople), and measured oxygen consumption and carbon-dioxide output to calculate how much energy the mice expended. I’d say that’s about as precise as a diet study gets.

Now, according to Jillian Michaels and the other leading experts in thermodynamics, there are only a couple of possible outcomes for these experiments:

  1. The calorie-restricted mice, who were prevented from making little pig-mice of themselves, ended up weighing less and were leaner.
  2. If the calorie-restricted mice somehow ended up fatter, it could only be because they were far less active than the mice who ate freely.

Yup … if you get fat, by gosh, it means you’re either eating more or moving less. Now let’s look at the actual results:

At the end of first experiment (four weeks), the calorie-restricted mice weighed a teeny bit less than their free-eating counterparts — the difference was not statistically significant, but it was there. However, the calorie-restricted mice also had 68.5% more fat mass, and 12.3% less lean mass.

Being put on a diet made them fatter.

At the end of the second experiment (three weeks), the average weight for both groups was virtually identical — it was also virtually identical to their baseline weights. But the calorie-restricted mice had 43.6% more fat mass and 6.4% less lean mass than the free-eating control mice. Once again, being put on a diet made them fatter.

Well, clearly, those fat little calorie-restricted mice must’ve spent too much time sitting around watching reruns of The Biggest Loser while their free-eating cousins were whipping themselves into shape by running on the big wheel, right?

Nope. According to the study data, there was no difference in locomotor activity levels between the two groups.

The calorie-restricted mice ate less, they moved around just as much, but they ended up weighing the same as the mice allowed to eat freely, and also ended up with more fat and less muscle. Oh, dear me … did these mice find a way to violate the laws of thermodynamics?

No, heck no, for the thousandth time, NO.

The researchers didn’t take body-heat measurements (too bad), but reported that the calorie-restricted mice expended significantly less energy: 5% less overall, and 20% less while at rest. Simply put, their metabolisms slowed down, even though they were just as physically active.  No laws of thermodynamics were violated in the process.

I once sent a link to this study to someone who insisted that according to the laws of thermodynamics, weight gain is caused by eating more or moving less, period.  His reply was something like, “That doesn’t prove anything!  I’m not a mouse.  I’m talking about people.”

Well, I agree that mice aren’t little furry people, which is why I’m not concerned when this-or-that food is shown to trigger cancer in mice.  (Mouse chow probably wouldn’t agree with me either.)  But remember, we’re talking about The Laws of Thermodynamics here.  They don’t apply to one species, but not another.  If mice can become fatter without eating more or moving less, yet somehow avoid violating the laws of thermodynamics in the process, then so can people.

The researchers were at a bit of a loss to explain why the calorie-restricted mice grew fatter, but I’m pretty sure we can rule out gluttony and sloth. They suggested perhaps the mice were reacting to the stress of a limited food intake.

“Reacting,” of course, means something hormonal was going on. (It wasn’t thyroid hormone. The researchers checked.) Perhaps the calorie-restricted mice produced more cortisol. Perhaps evolution geared the mice to respond to the threat of starvation by accumulating more fat, even if it means sacrificing lean tissue.

The point is, they didn’t get fatter by eating too much, and they didn’t get fatter because they decided to expend less energy. They began to expend less energy (in spite of being just as active) because they were being hormonally driven to accumulate more fat, even on less food.

Doesn’t that sound something like the process described by a best-selling science journalist who supposedly doesn’t understand that his hypothesis would violate the laws of thermodynamics?

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It still amazes me … Gary Taubes wrote an entire chapter in Good Calories, Bad Calories titled Energy Conservation, which explains how the laws of thermodynamics apply (because they do) to his hypothesis that elevated insulin makes us fatter. In Why We Get Fat And What to Do About It, he explained the concepts again in two short chapters titled Thermodynamics for Dummies. It’s all right there. And yet a reviewer of Why We Get Fat offered up this criticism:

There is no question that the science of nutrition needs critical review, but Taubes is just wrong. Calories-in-calories-out is the law of thermodynamics.

Anxious to share similar insights, a reader once left me this encouraging comment:

You should take your own medicine and stop posting until relatively basic concepts like thermodynamics cease to elude you.

I do, in fact, understand the “relatively basic concepts” the reader insists are eluding me. He was referring to the First Law of Thermodynamics, which Wikipedia summarizes as:

The law expresses that energy can be transformed, i.e. changed from one form to another, but cannot be created nor destroyed.

Since energy cannot be created or destroyed and we store energy as fat, the “it’s all about counting calories” crowd believes the amount of weight we gain or lose is a function of calories-in vs. calories-out. Guess what? They’re correct. I’ve never disputed that, and neither has Gary Taubes. What Taubes does dispute is that “calories-in vs. calories-out” means gaining and losing weight works like a simple bank account.

With a bank account, deposits and withdrawals are independent variables … that is, they both affect the account balance, but have no effect on each other. If I deposit $100, my account grows by $100, period. If I withdraw $25, my account shrinks by $25, period. Depositing $200 and then withdrawing $100 has exactly the same effect on my balance as depositing $100.

It’s because of the bank-account mentality that the calorie-counting crowd offers up useless advice such as, “If you just cut 100 calories per day from your diet, you’ll lose 10 pounds per year!”

What Taubes has tried to explain is that the bank-account analogy doesn’t work because in human biology, calories-in and calories-out are dependent variables — that is, when we change one of them, our bodies make compensating adjustments that affect the other. He’s also tried to explain that hormones — chronically elevated insulin in particular — can cause our bodies to store more calories as fat, which in turns affects our appetites (calories in), metabolisms (calories out) and activity levels (calories out).

Nothing he wrote in either book disputes or ignores the laws of thermodynamics. To illustrate, let’s expand on the simple bank-account idea and create a fictional banking scenario where things are a little more complex.

My arrangement with the fictional bank works like this:

1. I’m expected to make daily deposits.
2. The bank pays all my bills electronically, including a large, daily heating bill.
3. If my account runs low, the bank will call and ask me to make bigger deposits for awhile, and I’m expected to comply.

I like this arrangement. I deposit some cash and checks every day but don’t track the exact amounts, because the bank is handling my bills and I don’t like paperwork. I’m dimly aware that my average balance is somewhere around $2,000 and that’s fine by me.

In the real world, of course, we love big bank accounts. So to make our fictional banking world serve as an analogy for weight loss, let’s suppose FDR is serving his 20th term as president and just passed a new stimulus bill declaring that anyone who maintains a bank account of more than $2000 for six consecutive months is hoarding “undistributed profits,” and will face federal prosecution. So I actually open my next bank statement instead of shredding it, and — yikes! — my balance is $2234.

Unsure how to deal with this problem, I visit a financial consultant who explains that there’s a fundamental, unbreakable, empirically proven law of banking known as The First Law of FiscalDynamics. Here it is:

Money can be transformed, but cannot be created or destroyed.

(Of course, the Federal Reserve creates new money out of thin air all the time, but just go with me on this.)

The consultant explains that when The First Law of FiscalDynamics is applied to a savings account, it works like this:

The balance of a savings account is always determined by the dollars in minus the dollars out.

Therefore, if my account is growing, the root of the problem is that I’m making too many large deposits. The consultant estimates that the bills the bank is paying on my behalf add up to $200 per day. So if I just rigorously count my deposits and limit them to $180 per day, my account will drop below $2000 within one month. If I want to shrink the account even faster, he explains, I can sign up for aerobics classes and the bank will pay for them out of my account.

I follow his advice, but when I open my statement a month later, I discover that my balance is $2158. Frustrated, I reduce my deposits to $170 per day, but a month later my balance has shrunk to just $2122.

Worse, a bank manager named Marta keeps calling to say I don’t have enough liquid funds to pay my bills, and I’d better start making larger deposits again. Mystified, but unable to resist Marta’s request, I increase my deposits to $175, only to discover a month later that my account has grown to $2285. Something is clearly wrong here. I’m following the expert’s advice, but it’s failing.

So I do something nobody outside the banking industry has ever done before: I dig out the DISCLOSURE OF TERMS document I was required to sign when I opened my account, and I actually read it. I also read books on banking practices. I interview people who work at the bank.

After completing my research, I write a document titled Good Dollars, Bad Dollars in which I propose an alternative explanation for what’s causing my savings account to become bloated and why the financial consultant’s advice failed. It’s complicated, but here is the basic scenario:

The bank, as it turns out, is not a passive organization that simply takes deposits and then pays my bills. In fact, the bank is quite interested in having me maintain my savings account at the level it prefers. This is largely because the bank manager, Marta Bolism, has been around long enough to remember some serious bank failures and is therefore obsessed with cash flow. However, she’s also aware of the undistributed-profits law and knows my account shouldn’t grow too large.

For most of her long career, Marta has handled my account quite well. If my balance dips, Marta worries that I may eventually run short of funds to pay the daily heating bill …  and as I discovered on page 87 of the DISCLOSURE OF TERMS document, she not only pays the bill, she can adjust my thermostat from her office. So if I forget to make a few deposits, she responds by turning down the thermostat to reduce my bill. She also calls and reminds me to make bigger deposits, and since I’m unable to resist her, I comply.

On the other hand, if I make occasional big deposits, she turns up the heat for a couple of days to generate a bigger bill. She also has the discretion (as I discovered on page 119 of the DISCLOSURE OF TERMS document) to divert a portion of my deposits into the bank’s Building And Repair Fund as a service fee. So when I make big deposits, Marta decides the bank should replace a few loose bricks and makes a contribution to the Building And Repair Fund on my behalf, thus keeping my account below $2000.

In other words, Marta exerts rather a lot of control over my account. My deposits and withdrawals don’t affect my balance independently, because Marta adjusts my withdrawals based on my deposits, and alters her requests for deposits based on my withdrawals. She does all this to keep my account high enough to pay the bills, but not so high that I risk the wrath of the feds.

Unfortunately, Marta’s previously-effective methods for maintaining my balance have been slowly undermined by changes in the deposits I’ve been making. I used to make most of my deposits in cash. Since cash is available as soon as it’s deposited, Marta was never concerned about my ability to pay my bills, even though my average deposits weren’t very large and my average balance was below $2000.

But nowadays, most of my deposits are out-of-state checks. At first glance, this doesn’t appear to be a problem — after all, a dollar is a dollar, as the financial expert informed me. But as it turns out, my deposits are processed by an elderly account manager named Ian Sulin, and being somewhat old-school, he treats cash and checks differently. When I deposit what Ian considers too many checks, he become suspicious and puts on a hold on a big portion of the funds.

The result is a small but consistent trend towards excess savings accumulation. After I deposit several checks, my account balance may be $2205, but Ian tells Marta the available balance is only $1100. So Marta grows worried and turns down my thermostat to conserve funds. Then she calls and tells me I’m low on available funds and should make larger daily deposits.

So I do … and then I’m surprised and frustrated when my next statement shows my account balance is at $2260. I decide to ignore Marta and reduce my deposits to $170. Unfortunately, those deposits are almost entirely in the form of checks, and Ian puts a hold on most of the funds. Marta panics at my low available balance and turns my heat down even more. She cancels my aerobics classes to avoid paying for them. She decides the bank can live with the cracked bricks and stops diverting any of my deposits to the Building And Repair Fund.

I finally lose my will to ignore her increasingly desperate calls for larger deposits and raise them to $185 per day, figuring that’s still below my daily expenses. Unfortunately, Marta has reduced my bills more than enough to make up the difference, and when I open my next statement, I see a balance of $2287.

After figuring out how this all works, I realize the only way to prevent Ian and Marta from pushing my account slowly higher is to switch back to making most of my deposits in cash. So I do. The funds in my account are readily available, so Marta stops calling and asking for bigger deposits. She turns up my thermostat. She withdraws funds to re-enroll me in exercise classes and diverts some of my deposits to the Building And Repair Fund. A few months later, I find that I’m happily making deposits whenever Marta asks for them, but my average daily balance is right around $1900.

Now … suppose I present this explanation to the financial expert who told me to simply make smaller deposits. He could disagree with the explanation. He could claim Marta Bolism doesn’t manage accounts in the manner I’ve described. He could deny that Ian Sulin puts a hold on checks. He could insist that people who end up with bloated savings accounts just don’t have the discipline to count and limit their deposits, and remind me that when people are put in prison for 10 years, they end up with no savings whatsoever.

That’s not the point. The point is that nothing in my hypothesis requires money to be magically created or destroyed. Nothing in my hypothesis disputes that the size of my savings account is determined by the dollars in minus the dollars out. So no matter what other criticisms the financial consultant may raise, he can’t simply dismiss my hypothesis by claiming it violates the First Law of FiscalDynamics.

Well … he could claim that, of course. He could roll his eyes, shake his head, and say, “Dollars-in-dollars-out is the Law of FiscalDynamics. You should stop commenting on financial matters until relatively basic concepts like FiscalDynamics cease to elude you.”

But if he did, I’d seriously doubt his intelligence.

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Statins in our drinking water?! 

I’ll never drink tap water again if this happens.  In fact, I won’t drink any water I don’t catch my own tank.

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Let’s hope this is the beginning of the end for statins. The so-called wonder drugs have been a cash cow for pharmaceutical companies for decades now, mostly because doctors bought into the idea that high cholesterol causes heart disease, therefore any drug that reduces cholesterol must also reduce heart disease. I’ve lost count of the people I know who don’t have atherosclerosis, but were prescribed statins simply because their cholesterol was above the supposedly magic number of 200. Their doctors weren’t treating heart disease; they were treating a cholesterol score.

While researching Fat Head, I became aware of quite a few doctors who insist that giving statins to people who don’t already have heart disease simply to beat down their cholesterol is worse than worthless … Al Sears, Mike and Mary Dan Eades, Uffe Ravnskov, Malcolm Kendrick, etc. I found the evidence they presented quite convincing. Unfortunately, the medical establishment and the media have tended to either ignore the anti-statin doctors or write them off as a bunch of kooks.

Not anymore … at least I hope not. A new meta-analysis of the effectiveness of statins (and lack thereof) was just released by the Cochrane Collaboration, and it’s bad news for the statin-makers — partly because the analysis itself isn’t flattering, and partly because the Cochrane Collaboration is a highly-respected organization whose work is considered both thorough and unbiased. Consequently, their report has generated quite a bit of media coverage. I’ve already read articles in the UK Telegraph (two), TIME’s online version, the Los Angeles Times, Miller McCune, and Reuter’s Health, among others.

If we piece together quotes from the articles, we end up with a nice summary of the statin story. Let’s start with how and why they became the best-selling drugs of all time:

Back in 1975, Henry Gadsden, the chief executive of the drug company Merck, expressed his frustration that the market for his company’s products was limited to those with some treatable illness. Ideally, he said, he would like to “sell to everyone”.

Three decades later, his dream would seem to have come true – epitomised by the most profitable class of drugs ever discovered, the cholesterol-lowering statins that are taken by an estimated seven million people in Britain, and tens of millions worldwide.

Yup, Merck and the other pharmaceuticals wanted to sell drugs to healthy people, and by gosh, they finally figured out how to do it.

The story starts with the arrival of “cholesterol consciousness”: the thesis that those indulging in (for example) bacon and eggs for breakfast boosted the cholesterol level in the blood, causing the arteries to become narrow, and making a heart attack more likely.

Although this idea has its critics, there is no doubt that the small proportion of the population with a genetic predisposition towards high cholesterol levels are at greater risk of circulatory disorders. Encouraging them to switch to a healthy diet had failed to lower that risk – so the idea gained ground that cholesterol-lowering drugs might be the answer.

The small proportion of the population with a genetic predisposition are those with familial hyperlipidemia. Their LDL is extraordinarily high because their LDL receptors don’t work and therefore don’t remove LDL from the bloodstream. Cholesterol-lowering drugs were shown to reduce their rate of heart disease by a teeny, tiny bit. From that result, the medical community decided cholesterol is a killer and we should all stop eating bacon and eggs — even though low-fat diets didn’t do diddly for the people with hyperlipidemia. Go figure.

An even more important factor, especially in the US, was the drive to establish “clinical practice guidelines”, under which panels would set the optimal treatment for any given condition. Successive guidelines have forced the “normal” level of cholesterol ever lower, resulting in leaps in the numbers deemed eligible for treatment. In the US, the figure went from 15 million to 40 million.

That’s how you sell drugs to healthy people: redefine normal cholesterol levels as dangerous. Among the un-medicated population, average total cholesterol was around 220 a few decades ago. Doctors rarely warned patients about heart disease unless their cholesterol was 250 or higher. But if 220 was the average, how did the new “normal” end up being 200?

After it was pointed out that those responsible for the most recent guidelines had failed to declare any potential conflicts of interest, it subsequently emerged that most of them had received research grants or consultancy fees from the drug companies involved in manufacturing statins.

That’s how. By declaring 200 to be the target level for cholesterol, the researchers (ahem, ahem) who wrote the guidelines guaranteed their paymasters millions of new customers.

Not surprisingly, quite a few clinical studies eventually concluded that statins prevent heart disease. I say “not surprisingly” because nearly all the studies were funded and conducted by the pharmaceutical companies. According to the Cochrane review, the studies might’ve been (surprise!) skewed to exaggerate the benefits and minimize the side effects:

In particular, while all the studies focused on benefits, only half provided information on the side effects of the drugs, said Dr. Shah Ebrahim, whose group’s findings are published by the Cochrane Collaboration, an international organization that evaluates medical research.

“There is evidence that the reports cherry-picked the best outcomes for presentation,” he added, “which will tend to inflate apparent benefits of treatment.”

While there appeared to be no difference in side effects between trials participants taking dummy pills and statins, the researchers say those results aren’t credible.

“Any appraisal we can make of adverse events is biased by failure to report these events,” Ebrahim said in an e-mail to Reuters Health. “We believe that trial funders, investigators and journal editors have failed to provide adequate information to doctors and their patients to assess the benefits and harms of statins in primary prevention.”

The good news is that while Merck and Pfizer may not report on negative side effects, more media outlets are:

Dr. Greg Burns (not his real name) is a 72-year-old retired radiologist living in Connecticut. Until early last year, he ran with his dog at canine agility meets, skied, ice skated and played 18 holes of golf. He is now unable to walk and is taking a course of medication that will postpone, by a few months, his death.

Burns’ rapid decline began in December 2007 when he suffered a short-acting stroke from which he fully recovered. His cholesterol level was elevated and so as a preventative measure his doctor prescribed a 20mg daily dose of Crestor, a cholesterol-lowering drug in the “statin” class.

A few months after beginning Crestor, Burns developed muscle cramps. He was assured by his doctors that these were not serious side effects of taking the drug. But in December 2008 when tests showed that his creatine phosphokinase – an enzyme that is released into the blood stream when muscle cells are damaged – was elevated, Dr. Burns stopped taking Crestor. When his enzyme levels returned to normal, he began taking Pravachol, another statin drug. He quickly developed weakness in his lower legs and a right foot drop.

Mayo Clinic cardiologists acknowledge that the side effects of statin drugs can include muscle pain, extreme fatigue, liver damage, digestive problems and neurological damage including memory loss.

Of course, not everyone who takes statins will experience side effects, so it’s a question of balancing benefits and risks, just like with any other drug. So let’s look at the supposed benefits.

If you’ve seen Lipitor ads on TV (and if you haven’t, it means you don’t watch TV), you know Pfizer claims Lipitor reduces the rate of heart attacks by 36%. As I’ve explained in previous posts, that figure may sound impressive, but basically it means that during the clinical trials, three out of every 100 men who took a placebo had a heart attack, while slightly less than two out of every 100 men who took Lipitor had a heart attack. So for every 100 men treated for ten years, we’re preventing (in theory) one heart attack.  That’s one heart attack, not necessarily one death. 

But even those unimpressive results were found only among with men with existing heart disease or multiple risk factors for heart disease — not among women, and not among otherwise healthy people who happen to have high cholesterol.

But of course, statins didn’t become the most profitable drugs in history by being prescribed solely to men with existing heart disease. Nope, statins became a cash cow when doctors started prescribing them to pretty much everybody whose cholesterol is above 200.  (In the UK, you can even buy your future muscle or memory problems over the counter — yippee!)

The theory, of course, was that statins could prevent heart disease from developing in the first place, otherwise known as “primary prevention.”  The Cochrane report casts more than a little doubt on that theory, as several media articles pointed out:

An authoritative review shows there is little evidence that the cholesterol-lowering drugs protect people who are not already at a high risk of heart disease.

Experts who advocate the use of statins say they have helped prolong thousands of lives by preventing heart attacks and other cardiovascular events. But a wide-ranging review of previous studies, published today in the journal The Cochrane Library, urges “caution” among GPs who prescribe them. It concludes that there is no “strong evidence” to suggest that statins reduce coronary heart disease deaths among those who have not suffered a heart attack or other cardiovascular event in the past.

Shah Ebrahim, a professor of public health at the London School of Hygiene and Tropical Medicine, who co-wrote the report, called on doctors to stop giving patients the drugs unnecessarily.

Just one life is currently saved for every 1,000 people who take them each year, the report says.

Great … so to prevent (in theory) one fatal heart attack among every 1,000 people who take statins, we’ve created lord-only-knows-how-many cases of muscle degeneration, memory loss, kidney failure, erectile dysfunction and liver damage. Of course, that works out well for Big Pharma — they sell drugs to treat those conditions, too.

I’ve said it before, and I’ll say it again: statins are some of the worst drugs ever. I’m just happy to see more people in the news media are catching on.

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Saturday was our first big night out in a long time. (A “big night,” of course, means “the children were at home and we weren’t.”) A couple of months ago, we bought tickets for a Bill Cosby concert at the Tennessee Performing Arts Center in downtown Nashville, and earlier this week I made dinner reservations at what looked to be a nice restaurant with interesting items on the menu, such as bison sandwiches.

I’d like to try a bison sandwich someday, but we ended up walking out of the place. I’m not a hockey fan and didn’t think to check if the Predators were playing that night at the Bridgestone arena, which is three blocks from the restaurant. They were.

The restaurant was jammed with hockey fans, the staff was racing around trying to keep up, and nobody even acknowledged us for the first 10 minutes we stood there. The Cosby concert was at 8:00, so I’d made a 6:30 reservation, but we weren’t seated until nearly 7:00. We sat for another five minutes before a waiter dropped a couple of menus on the table and dashed off again. No “Let me tell you about the specials” or “May I get you something from the bar?” Just plop, plop, gone.

At that point, I said to my wife, “I’ve got a bad feeling about this.” She agreed and we left. Walking north towards the Performing Arts Center, we passed a few restaurants where we could’ve gotten a quick meal, but most of them had big TVs showing the Steelers-Ravens game. I was recording the game, and I hate learning the outcome of games I plan to watch later, especially playoffs. So we ended up at Sbarro (a sort of fast-food Italian restaurant, for those of you who don’t know), partly because we knew we’d be in and out quickly, and partly because they didn’t have a big TV showing the game.

So imagine how overjoyed I was when a pimply-faced twenty-something walked through the door, spotted a friend with whom he’d apparently had a football disagreement, and announced, “Hey, ass****! Pittsburgh won! Ha!”

Oh, thank you, thank you, thank you so much, you @#$%ing pea-brained pimply-faced little #$%@.

No, I don’t expect people to stop and ask themselves if perhaps someone within shouting distance might have recorded the game .. but really, is there ever a reason to walk into a public restaurant and yell to someone sitting across the room? (I mean, besides something like, “The building next door is on fire and you all should leave.”)

Since I believe in letting my hair down (metaphorically, of course) one or twice per month and eating whatever I want, we split portions of lasagna with meatballs, chicken parmesan, and one slice of pizza. Then we walked to the concert, with me still grumbling about the pimply-faced Steelers fan.

If anyone can de-grumble me, it’s Bill Cosby. This was the third time I’ve seen him perform live, and all I can say is, he’s still the most delightful comedian ever. In one of the funniest bits of the whole show, he imitated how it sounded to him when his parents had an argument downstairs, while he listened to their muffled voices upstairs. He had the audience roaring for a full two minutes — without saying any real words. Just back-and-forth muffled voices, with all the laughs coming from changes in the vocal tones. (His father lost that argument, by the way.) Comic genius.

We walked the several blocks to where we’d parked and left just in time to run smack into bumper-to-bumper traffic leaving the hockey stadium. I now like hockey even less than before. For a little while there, it felt like being back in Los Angeles.

I had also recorded the Packers-Falcons game and decided I wanted a couple of Foster’s Lagers to go along with the game, so we stopped at a beer store on the way home. (In Tennessee, stores can either sell beer, or wine and liquor. I have no idea what that’s supposed to accomplish. Often the stores are side-by-side, with the same owner.) My wife went in to pick up the beer, because I figured if I did it, the clerk would surely greet me with something like, “Hey, how about that dramatic overtime win by the Falcons?  Uh, sir, why are you leaving …?”

So I finished my big Saturday night enjoying a combination of football, beer, nuts and cheese. Since I’ve been experimenting with intermittent fasting, that made Sunday the perfect choice for an all-day fast. Perhaps denying myself any food the day after indulging appeals to some part of my consciousness conditioned by years of Catholic schooling.

Most days last week, I adopted the 8-hour window method of IF, which for me means limiting my food intake to between noon and 8:00 PM. That’s no big deal. It just means giving up my usual late-night snack.

But once again, I was surprised at how easy it was to go all day Sunday without eating. No low blood sugar, no mental fog, no urge to take anyone’s head off — although when my wife started describing an interesting pork recipe she’d just seen, I did say, “Uh … would you mind not talking about the delicious meals you’re planning to make?”

I had hunger pangs for the last two hours before bed last night, but ignored them. I’d planned to go to the gym this morning and work out — exercising in a fasted state is supposed to spur muscle growth — but remembered it was closed for Martin Luther King Day. So I did calisthenics and some power-band exercises to work my muscles. I finally had my first meal of bacon and eggs around 11:00 AM.

Now that I know I won’t be miserable, I’ll probably go for an all-day fast every Sunday. But if the Bears make it to the Super Bowl, I reserve the right to eat whatever I want on February 6th.

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