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January 30, 2006
What did you eat last December 12?
Stephen Daniells, Ph.D., the food science reporter for NutraIngredients.com, wrote an excellent article today entitled Time to Ditch the FFQ that should be read by all scientists doing nutritional research (and all readers of this blog).
The premise of his piece is that the FFQ (Food Frequency Questionnaire) should be abandoned in favor of the 24 hour dietary recall or the three day food diary as a means for compiling nutritional research.
As Dr. Daniells points out, a food frequency questionnaire, a set of forms that
may contain up to 100 questions, and ask people to remember what they ate up to a year before.
And he asks the question:
Pause for a moment to reflect on what you ate last Tuesday, and on Monday 12th December.
Did you drink a small quantity of fizzy drink, a medium quantity or a large one? My small is half-a-glass. How small is your small?
So was that a small amount of fizzy drink you drank in December, or a large amount?
See the problem?
In some cases, in what are called case-controlled studies, people may be asked what they ate 10 or even 20 years before.
If they are inherently inaccurate, why are FFQs even used at all?
Because they are cheap compared to the other alternatives.
It has been estimated that a basic assessment of diet for 160 000 women would cost $1.2m using an FFQ, but over $23m for either of the two alternatives.
But, as the old saying goes, you get what you pay for. If you want to publish a paper and not spend a lot of money, then the FFQ is your tool. If you're striving for accuracy and producing meaningful research, then you need to choose another method.
As Dr. Daniells points out
It is better to spend $20m on a study that shows something real, than $1.2m on a study that will mislead and may even harm.
I've always distrusted studies using FFQ's as their means of accumulating data: now, after reading Dr. Daniells' article, I distrust them just a little more.
Posted by mreades at 04:15 PM | Comments (3)
January 29, 2006
Missive from the road
I apologize for not posting over the past few days, but MD and I are on one of those multi-city trips we plan from time to time. We went to the Nutrition & Metabolism meeting in Brooklyn, then over to Manhattan for a few days to do some book stuff. We were wrapped up in a frenzy of activity there what with meeting with our agent, a number of friends, and a few business partners. We left from there a few days ago and came to Michigan for my mother’s 80th birthday.
Since arriving here it has been a non-stop visit-a-thon from early in the morning until 1 or 2 in the morning. We leave here on Tuesday to head for Dallas and our youngest grandson’s 4th birthday, then to Austin where we meet face to face with our website guru to take our website—including bulletin board—live. Until we get back from all this craziness, I can’t promise faithful posting, but I’ll give it my best.
It’s frustrating for me because I have about a million things to post on. I took a bunch of medical papers with me to read critically while on the numerous flights, many of which will be of interest to readers. I also have a ton of stuff to post on about the Nutrition & Metabolism meeting, but I need some time to organize the info to present it coherently. Just to give you a taste, at the meeting we learned that low-carb diets: decrease headaches, decrease fatty infiltration of the liver, decrease the incidence of prostate cancer, reduce progression of diabetes, improve lipid parameters, decrease atherosclerosis, and a host of other improvements in health. Stay tuned and I’ll bring you up to date on it all.
I slipped out for a few minutes today and got a copy of the New York Times. I haven’t read the whole thing yet, but in reading the first section, The Week in Review, I came across an interesting editorial by Nicholas Kristoff about the governor of Arkansas Mike Huckabee about whom I posted recently.
I have a real love/hate relationship with Kristoff, but I never fail to read his columns because I think that, unlike Paul Krugman, he is evenhanded. If he finds someone he doesn’t agree with politically doing something he likes, he will laud him (or her) for it. Krugman would never do such a thing. (I defy anyone to show me one Krugman column in which he says anything positive about any Republican or conservative politician).
The thrust of Kristoff’s piece is that obesity is a major health problem confronting America (and the word, for that matter) today that most politicians are choosing to ignore. Arkansas’s Huckabee, since he lost 110 pounds, is making the prevention of obesity a major part of his administration. Huckabee realizes that sooner or later the chickens are going to come home to roost in the sense that obesity will ultimately cause government a fortune to deal with. Already health issues are causing huge expenses to industry.
"This year, G.M. will spend more on health care for employees and pensioners than on steel," Mr. Huckabee noted. "Starbucks will spend more on health care than on coffee beans."
I think the Huck is absolutely correct. And, especially after the Nutrition & Metabolism meeting, I believe that somewhere down the line (sooner rather than later, I hope) people are going to have to realize that the low-carbohydrate diet is the single best tool to prevent and treat obesity and its related disorders. When that happens, I think that we will start making strides in the right direction. Until then, I think we’re in for more of the same.
In an interesting take on the situation, Kristoff wrote the following paragraph:
Imagine if Al Qaeda had resolved to attack us not with conventional chemical weapons but by slipping large amounts of high-fructose corn syrup into our food supply. That would finally rouse us to action — but in fact it’s pretty much what we’re doing to ourselves.
I hadn’t thought about it that way before, but Kristoff is right. If an outside, hostile force introduced something as toxic as high-fructose corn syrup into the food supply, we would consider it an act of war. As it is, all the politicians on the payroll of Archer Daniels Midland keep it coming.
Posted by mreades at 02:50 PM | Comments (2)
January 24, 2006
We never failed to fail...
A couple of days ago somewhere in our travels I happened to catch a few minutes of Rachael Ray’s show on the Food Network. On this particular episode Rachael was being her chirpy self, prattling on about one of her 30-minute meals when (I was only about half listening) I heard the words: low-carb. I tuned in a little more and realized that Rachael was making a low-carb 30-minute meal. As I watched, it slowly dawned on me that Rachael doesn’t have a clue as to what low-carb really means. She was making a dish that was pasta-based (not the low-carb variety) and was adding dried apricots and other fairly high-carb stuff here and there along the way. After watching the remainder of the show closely, I realized that Rachael’s idea of low-carb is to avoid bread and potatoes - everything else seemed to be okay. Then I figured that if Rachael doesn’t know any better and really believes she’s cooking low-carb, so must many other people.
If many other people are doing low-carb in the same way Rachael is, then they’re in for some bitter disappointment.
The whole idea brings to mind an article I wrote for the now-defunct Low Carb Living magazine a year or so ago. Here it is in its entirety. Copy it and give it to someone who believes he or she is truly on a low-carb diet.
We Never Failed to Fail
We never failed to fail; it was the easiest thing to do, so say Crosby, Stills and Nash in their terrific song Southern Cross. Unfortunately, multitudes of low-carb dieters today will be crying these same words if they’re not careful because low-carb diets, if followed in a half-hearted manner will fail, and the resultant regain of lost weight will be the easiest thing to do.
Recently the NPD Group, a marketing research company that provides information to industry, tracked the eating habits of 11,000 people who were cutting carbs as part of a strategy to lose weight. The results of this study found in the report Carbohydrate Consumption Patterns show that virtually none of the 11,000 subjects, and by extrapolation, few to none of the population at large represented by the study subjects, were cutting carbohydrate intake to a meaningful degree. Instead of the 20-50 grams of carbohydrate per day recommended by us in our book Protein Power or by Atkins, South Beach, Sugar Busters, etc. men were consuming an average of 145 carbs per day while women were eating around 109 grams per day. Although these carb-consumption figures are less than the 210 grams of carbohydrate eaten by the non-low-carb dieter, they are not nearly low enough to bring about the benefits of low-carb dieting. We fear that the people making a modest stab at lowering carbohydrate intake are in for major disappointment.
Low-carb diets bring about a host of positive changes. Along with ditching excess fat followers of sound low-carbohydrate regimens see their triglycerides fall, their blood pressures normalize, their lipid profiles improve, and their blood sugar levels stabilize. They sleep better, get rid of bad indigestion, even GERD if they have it, have more energy and are much, much less hungry. And, seemingly magically, low-carb dieters can even consume more calories than their brethren on low-fat diets and lose more weight. But, and here’s the big but"¦low carb diets must be followed correctly to bring about all these benefits. If not, there is no magic.
Most cells in the body can use glucose or fat or even protein, for that matter, for energy, but certain cells can use glucose only. Those glucose-only cells are some of the cells in the brain, the red blood cells, cells in the kidney and cells in the retina. All these glucose-using cells consume about 120-150 grams of glucose per day (about 3/4 of a cup), so if we’re eating 210 grams of carbohydrate per day as the Carbohydrate Consumption Report shows, then we have plenty of glucose (most carbohydrates convert to glucose in the body) to feed them with 60-90grams left over. As long as we’re getting the carbohydrate in our diet to meet the needs of these glucose-only cells, then nothing much happens metabolically. If we get these carbs and more and eat a lot of calories, we gain weight; if we get these carbs, but cut our calories, then we can lose a little. But we have no low-carb magic. It’s only when we get the carbs significantly down below the 120-150 grams we need that the metabolic changes that make low-carb diets work kick in. But, you may be wondering, what about all those cells that have to have glucose? What happens to then when we cut our carbs way back? Let’s take a look.
Over the time we’ve been on earth as humans nature has endowed us with some pretty amazing metabolic protective features. Many times in our evolutionary history, in fact, during most of it, we probably didn’t get much more than 50 or 60 grams of carbohydrate per day, if that many. Most of the cells in our bodies respond to this carbohydrate restriction by kicking the sugar habit (for at least as long as there is no sugar around) looking to fat for their energy. Other cells, particularly the brain cells, learn to love ketone bodies; in fact ketone bodies become a substitute for glucose for the brain. The heart also uses ketone bodies, and, in fact, uses them much more efficiently than it does either glucose or fat. This switch from glucose to ketone bodies and fat leaves the small amount of ingested carbohydrate for the cells that absolutely have to have it. But, a sound low-carbohydrate diet restricts the carbohydrate intake to the point that even with the switch over to fat and ketone bodies for fuel there still isn’t enough incoming carbohydrate to meet the needs of all the glucose-dependent cells.
Not to worry, the body can make glucose from protein and, to a small extent, even from fat in a process called gluconeogenesis (making new sugar) that takes place in the liver. In fact, when it gets going the liver can crank out 200+ grams per day (a little over a cup), which is more than enough for all the glucose-dependent cells even if we weren’t eating any carbs at all. This ability of the liver to make plenty of sugar is what allows the Inuit, the Masai, and other groups of hunter populations to survive nicely for most of their lives on almost no carbohydrates at all. And it is this same ability that makes low-carb diets work as well as they do.
When the carbs quit coming in, blood sugar starts to fall slightly, which throws the switch for the whole sugar conserving process to begin. Insulin levels fall and glucagon levels rise, sending the signal to the liver to start making both ketone bodies and glucose. As the ratio of insulin to glucagon falls the fat cells (the very ones we want to get rid of) start releasing fat to be used by all the tissues switching to a higher-fat, lower-glucose diet and to be used by the liver to convert to the glucose-pinch-hitting ketone bodies. It takes more energy to convert either fat or protein to glucose then to burn the glucose than it does to burn the fat or protein directly. It is this extra energy-consuming step that increases the number of calories a low-carbohydrate diet burns.
As long as the carbohydrate restriction is in place, insulin levels stay low so that all these glucose-preserving and glucose-making processes continue because these metabolic processes can’t take place when insulin is high. And since elevated insulin levels are a driving force behind high blood pressure, elevated triglycerides, lowered good cholesterol, glucose intolerance and all the rest of the problems associated with obesity, then lowering these elevated insulin levels undoes all these problems. But to get the insulin levels down and bring about all these benefits you’ve got to get your carb intake down to significantly below the 120-150 grams per day required by the glucose dependent cells. That’s why all the 11,000 people who think they are on low carb diets while consuming an average of 145 grams of carbohydrate per day will "never fail to fail" because it is indeed "the easiest thing to do" when you don’t keep your carbs low enough.
We and all the other authors of low-carbohydrate plans recommend that dieters reduce their carb consumption to the 20-50 grams per day level. We do that because we’ve all learned that the low-carb diet works at those levels, and now you know why. If you pussyfoot around with your carb restriction, you’ll go nowhere; if you commit, then you’ll bring all the wonderful metabolic pathways nature has endowed you with into play and you will experience the low-carb magic.
Posted by mreades at 07:48 PM | Comments (7)
January 19, 2006
Travel update
MD and I are running to catch an early morning flight to New York for the Nutrition & Metabolism sponsored low-carb meeting.
I'll try as best I can (as will MD) to blog on any exciting and interesting presentations during this meeting.
If you are at all interested in supporting and furthering research on low-carbohydrate dieting, you can join the Nutrition & Metabolism Society for only $25, none of which, unfortunately, will ever find its way into my pocket. It's all spent on forwarding the goals of the society.
Posted by mreades at 05:37 AM | Comments (0)
January 18, 2006
Statistical humbug
A paper appeared in last weeks JAMA that I just now got around to reading, but had already read about in a number of other publications. The study looked at the effect early-in-life obesity has on death from heart disease decades later. The paper is a real treasure trove of information worthy of a longer, more comprehensive blog later on. For now I want to use it as an example of how statistics can be used to humbug the non-statistically inclined.
In brief the JAMA study was done with data pulled from the monster-sized Chicago Heart Association Detection Project in Industry that was begun in 1967. Subjects who were at least 31 years old were evaluated for a number of parameters including BMI, blood pressure, elevated cholesterol, and history of smoking. The researchers re-evaluated these subjects over the next several decades.
Researchers divided the subjects into five groups: low risk, moderate risk, intermediate risk, elevated risk, and highest risk. It's not important to the point of this post to get into what specifically constituted these varying levels of risk, but in general, the greater the number or the more severe the risk factors, i.e., elevated cholesterol, high blood pressure, etc., the more high-risk the category. The researchers then divided the subjects into three other groups based solely on BMI: normal weight, overweight, and obese. Within each of these three weight-related groups were spread subjects with varying degrees of risk. In other words, the normal weight group contained subjects who were low risk, moderate risk, intermediate risk, elevated risk and highest risk as a function of their cholesterol levels, blood pressures, smoking history, etc. It was the same for all the groups. The obese group was composed of obese subjects who ranged from low-risk to highest risk. The object of the study was to follow these subjects for many years to see if obesity was truly a risk factor for death from heart disease or if obesity led to elevated cholesterol, high blood pressure, and all the rest, which in turn caused the heart disease mortality.
If the subjects in the normal weight, low-risk group had no more heart disease than those in the obese, low-risk group, then it could be inferred that obesity by itself may not cause heart disease. If, on the other hand, the subjects in the obese, low-risk group had a much higher death rate from heart disease than did those subjects in the normal weight, low-risk group, then at least some of the heart disease could be attributed to the excess fat.
(There is really much, much more under the surface of this paper worthy of exploration, but it will have to wait.)
So what did the study show? It depends upon where you get your information.
According to a statistical analysis of the data, the odds for death by heart disease in the obese, low-risk subjects was 1.43 times that of the normal weight, low-risk subjects implying an almost half again greater risk simply for being obese. And that's how it was reported in the lay press.
WebMD allowed as to how
The researchers found that the risk of dying from heart disease was 43% higher for study participants who were obese but also met these qualifications for low cardiovascular risk than for normal-weight, low-risk participants.
It appears to be a pretty clear indictment against obesity.
But not if the statistics are analyzed correctly.
Before I get into that I want to produce a quote from Judge Samuel Alito that he uttered during his confirmation hearing before the Senate Judiciary Committee last week. Said he
Well, the analogy went to the issue of statistics and the use and misuse of statistics and the fact that statistics can be quite misleading. ... And that's what that was referring to. There's a whole - I mean, statistics is a branch of mathematics, and there are ways to analyze statistics so that you draw sound conclusions from them and avoid erroneous conclusions from them.
Truer words were never spoken. But you've got to analyze the statistics, not take them at face value.
So let's analyze the statistics used in our study under discussion to see if and how anyone went wrong.
Here is how the 1.43 ratio was written in the paper:
the odds ratio (95% confidence interval) for CHD [coronary heart disease] death for obese participants compared with those of normal weight in the same risk category was 1.43 (0.33-6.25).
What does this really mean?
First, it means that 143 people who were in the obese, low-risk group died from CHD for each 100 people who were in the normal weight, low-risk group, giving the risk ratio of 143/100 or 1.43. It seems reasonable that if that were really the finding, then the risk of dying if you are obese with low-risk (as these researchers define low risk) is 1.43 times greater than if you aren't obese. Right? Not necessarily, and here's why.
If you flip a coin 10,000 times the odds are that you will get about 5000 heads and 5000 tails since the odds are 50-50 of the coin landing on either side. But what about if you only flip it 40 times? Are you going to get exactly 20 heads and 20 tails? Probably not. What about if you only flip it six times? Will you get three and three? Maybe, but probably not. In fact I just flipped a coin 10 times and got five heads in a row, two tails, one head, and one tail, giving me seven heads and three tails. Now if this were a study on coin flipping I could confidently predict based on my data that if I flipped this same coin 10,000 times I would get 7000 heads and 3000 tails. But we all know this isn't really true because the sample size I used (ten) was too small to be used to accurately predict the outcome for 10,000 flips. The fact that I went 7 heads and 3 tails came about strictly by chance, which plays a smaller and smaller role as the sample size gets larger.
Statisticians realize that virtually any outcome can be influenced by chance and have developed equations to quantify just how much chance is involved. One of the terms they have come up with (after some pretty complex mathematical maneuvers) is the confidence interval. Pretty much the gold standard for confidence intervals is what's called the 95 percent confidence interval. What this means is that once a confidence interval has been established (a range between two numbers) you can be confident that your result will fall into that range 95 percent of the time. Since chance can't be totally eliminated, there will still be a 5 percent chance that our result will fall outside the range.
Let me digress a little here to define what we mean by our result falling into or outside of this range. In our study the data showed that 43 percent more people died in the obese, low-risk group than in the normal weight, low-risk group. But so what? As callous as it seems, we don't care about those people; they're already dead. What we care about is how the data provided by all these dead people affects you and me and our loved ones and all the other people who aren't dead yet. We all want to know if this 43 percent is just a chance finding like my flipping 7 out of 10 heads, in which case it's meaningless, or do I really have a 43 percent greater chance of dying of heart disease if I'm obese even though I don't have any other risk factors? Those are the questions the confidence interval addresses.
In this study the 95 percent confidence interval is (0.33-6.25). It's usually stated like it is in this case 1.43 (0.33-6.25). This means that the risk ratio as applied to the population at large should come in 95 percent of the time between 0.33 and 6.25. So this means that the risk of dying if you are obese with no other risk factors could be anywhere from 1/3 as much to 6.25 times as much.
Say what? 1/3 as much?
Yep. Even though the middle of this range is around 1.43 the actual risk is just as likely to be 0.5, which would mean you have half the chance of dying as someone who is normal weight without risk factors. In other words, you would be better off being fat.
These numbers in the parenthesis are critical. If you've got a positive number in front of the parenthesis as we do with the 1.43, then you want to make sure that both numbers within the parenthesis are above 1. If the first number is below one that means that the risk is actually greater the other way, which negates your analysis.
In this case since the first number is less than 1, indicating that the risk ratio is meaningless and can be ignored. What it means in this specific case is that it makes no difference whether or not you're overweight early in life as long as your other risk factors (as identified by the researchers in this study) are normal in terms of your risk of dying of heart disease later in life. Not the 43 percent that the authors and the press that picked the story up proclaimed. Too bad the authors and all the medical press people weren't a little more statistically honest.
But to tell you the truth, I suspect that the authors of this paper (and I know that the medical writers) don't have the same understanding of the confidence limits and what they really mean that you do after reading this post. Most researchers run their data through a computerized statistical program and simply look at the risk ratio (the 1.43 in this case) without really having a clue what the numbers inside the parenthesis mean.
I swear that over the next few weeks I'll post in as simple a way as I can a basic (very basic) primer on statistics. If I don't do this in a timely fashion you may write and cancel your subscription to this blog, and the unused portion of your subscription fee will be cheerfully returned.
Posted by mreades at 03:53 PM | Comments (4)
January 17, 2006
See what happens when we leave the state
Check out this new report on childhood obesity in Arkansas. And this under Mike Huckabee, who I'm sure the only governor in history who has written and gotten published his own diet book
I commend Gov. Huckabee for undertaking this first-of-its-kind study and reporting the results despite making his state look bad. I'm quite sure that if other states would belly up to the bar with similar testing, the results would be the same.
Childhood obesity is an enormous problem that we as a nation are going to have to deal with in the years to come.
Posted by mreades at 08:56 AM | Comments (1)
January 16, 2006
Another take on the Splenda nonsense
The Cato Institute did a piece on the Sugar lobby's attack on Splenda. In my opinion, Doug Bandow, the author of the article entitled "A Sweet Deal for the Sugar Industry," hits the nail on the head when he says of the sugar industry's tactics:
You can never get enough from consumers and taxpayers. That apparently is the sugar industry's motto. Collect subsidies. Ban trade. Outlaw your competitors. Let the American people pay.
In further contemplation on my previous post, I would guess that people get more chlorine from treated municipal water or from a dip in a chlorinated swimming pool than they do from consuming a typical amount of Splenda. I haven't actually done the calculations, so I'll leave that for someone else with more time on his or her hands.
Oh, and by the way, if you want to see a real piece of propaganda, go to the sugar lobby website and navigate around. Sugar doesn't cause obesity? Sugar is a brain food? Sugar is part of a healthy diet? I guess if they say so.
Posted by mreades at 11:24 AM | Comments (6)
January 15, 2006
Splenda misinformation
Do you know what your children are eating?
So asks the ubiquitous anti-Splenda advertisements.
These ads go on to say:
Splenda's advertising claims that it is "Made from Sugar, so it Tastes Like Sugar." What it doesn't tell you is that Splenda is not natural, it's a chlorinated artificial sweetener.
Since rational people don't want to send their kids off to school with a lunch box full of swimming pool disinfectant, these ads have gotten a lot of attention.
What is the real truth behind the Splenda and chlorine? Let's look at the evidence.
But before we do, I want to lay out my position. First, MD and I don't own any stock in the companies that manufacture or sell Splenda. We don't sell it. We have no financial involvement with Splenda in any way. Second, we do use it. We don't use a ton of it because we would rather do without sweets of any kind as much as possible. But, when we do want to sweeten something, we use Splenda as our artificial sweetener of choice. Unlike aspartame Splenda is heat stable so we can cook with it, and unlike aspartame it doesn't break down into toxic substances. In fact, very little of it is absorbed. And we have never had patients who had problems with Splenda as we have had with aspartame. We first found out about Splenda in Canada back in the mid 1980s when we attended a medical conference in Toronto. Splenda was in use at that time in Canada and has subsequently been approved for use here in the U.S., and since then tens of millions of people have used it without major problems showing up. We have never seen anything in the medical literature showing that Splenda is in any way harmful. So, we don't have a problem with Splenda, and until we find something that changes our minds, we'll continue to use it as our artificial sweetener of choice.
Now on to the Splenda attack ads.
These ads are the brainchild of Rick Masters, a former Democratic operative who has gone into the public relations business. He was profiled last March in the Atlantic Monthly in an article entitled "J-School for Jerks," which was a piece about how Mr. Masters conducts a course for people who want to be the next Bill O'Reilly. Mr. Masters works for Qorvis Communications, a large, Washington, DC based public relations firm.
Qorvis Communications and Mr. Masters were hired by non other than the sugar lobby to mount an attack against Splenda. Why the sugar lobby would want to attack the folks who make Splenda, I can't imagine.
Mr. Masters and "a group of concerned consumers, led by sugar cane and sugar beet farmers across America" (read: Sugar Association, the sugar lobby) put up a website purporting to tell the horrible truth about Splenda. But does this website tell the truth or is it simply sugar lobby propaganda? Let's take a look.
We can forget about all the posturing and all the doctors and others who are on the site claiming that Splenda is a menace because that's all lip service. Let's cut to the chase, to the real nitty gritty.
The main attack against Splenda is that it is a chlorinated artificial sweetener. Is that true? Well, yes and no. It is chlorinated, which, as we'll see shortly, doesn't mean squat. And it is really a sugar molecule, so it really isn't an artificial sweetener as is, for example, saccharine. It's artificial in the same way a bowl of ice cream with artificial flavors added is artificial. The bulk of the ice cream is made with cream, milk, and sugar, so does the little bit of artificial vanilla extract make the whole shebang artificial? I don't think so. But in Splenda's case, the additive isn't even really artificial.
But what about the chlorine? That sounds like the real problem. It can't be good to consume chlorine.
First of all, every time you eat salt, half of what you are eating is chlorine. Common table salt is sodium chloride, half sodium and half chlorine (since the chlorine is in its ionic form it's called chloride). Chloride is a natural substance. In fact chlorine is one of the elements in the periodic table. No one would consider salt artificial, so how can chloride - a natural element - be artificial?
So, Splenda isn't really an artificial sweetener. If anything it would be more accurately called a chemically altered sweetener.
Splenda is made by replacing three hydroxyl groups (and oxygen-hydrogen combination) on a sucrose (common table sugar) molecule with three chloride ions. By doing so, the sweetening power of the sugar is increased by a factor of about 600. So, in actuality, when you consume Splenda, you consume real sugar, but because of the huge increase in sweetening power only about 1/600th of what you normally would . Instead of a teaspoon it would be a tiny grain.
But what about the extra chlorine? Doesn't that cause any kind of problem.
Well, you do eat salt don't you. A teaspoon of salt contains many thousands of times more chlorine than you would get from the teaspoon of sugar equivalent of Splenda.
If you want even more evidence that the tiny amount of chloride in the Splenda is harmless consider that like with blood sugar you have about a teaspoon of chloride circulating in your blood at any given time, which is more than 20,000 times the amount you would get from a dose of Splenda. How do we figure this?
A normal value for chloride as a component of an electrolyte panel (common lab measurement of blood that doctors often look at) is about 100 mEq/L. One mEq of chloride equals about 35 mg. 35 mg times 100 equals 3500 mg. One teaspoon is about 4000 mg, so 100 mEq of chloride is a little less than one teaspoon.
So, knowing what we now know, it's easy to see who is telling the truth about Splenda. With the above in mind, let's look at a particularly egregious example of truth stretching on the sugar lobby-underwritten, anti-Splenda website:
Fiction: The chlorine found in Splenda is similar to that found in other foods we eat.
Fact: The manufacturer of Splenda claims that chlorine is naturally present in such foods as lettuce, mushrooms and table salt, but they never directly state that eating Splenda is the same as eating these foods. Remember, Splenda is not a natural substance, it is an artificial chemical sweetener manufactured by adding three chlorine atoms to a sugar molecule.
Would you trust your health to the sugar lobby?
Posted by mreades at 10:09 PM | Comments (10)
January 13, 2006
Read it and commit
A distressing editorial appeared in the Sacramento Bee (free registration) a few days ago. I feel that the point made in this piece is so important that I'm going to risk the ire of that paper's publishers and reprint it in its entirety here.
Editorial: Read it and weep
What's the cure for nation of weakly readers?
After years of handwringing about literacy in the United States, Congress passed the National Literacy Act of 1991. The aim was to make improved literacy a priority for the nation.
So the federal government did a baseline assessment of national literacy in 1992. Now, the government has released the first follow-up. The results are a big disappointment.
Overall, literacy has remained flat. In 1992, 83 percent of the population 16 and older were at basic literacy or above. That remained virtually the same in 2003 (84 percent).
The bigger disappointment is that literacy is slipping at every level of education. Educated Americans remain literate, but their capabilities in processing complex information, rather than simply basic information, is declining.
That presents a quandary. Should we put our efforts into bringing the 17 percent of illiterate or barely literate adults up to basic literacy? Or should we focus on improving the literacy of those who will graduate from high school, college or postgraduate institutions? In an ideal world, we would do both. But the more alarming dip is in the educated population. We can more easily reach those individuals in our system of education - with higher expectations and improved curriculum.
Part of the problem is that our culture is becoming more oral and visual. With television, cell phones, video games, iPods and other new media sources, people increasingly are dealing with flashes of information. Educational institutions must swim upstream in their effort to get students to interpret and analyze lengthy, difficult passages of words - and have them enjoy it and make it part of the habit of life.
To see the problem in stark form, look at what's happened to college graduates in the last decade.
They remain literate: 98 percent are at basic literacy or above (it was 99 percent in 1992). That looks like there's no problem. Basic means a person can perform simple and everyday tasks such as interpret instructions from an appliance warranty, write a letter explaining an error made on a credit card bill, determine the discount from an oil bill if paid within 10 days.
But then look at intermediate literacy or above: 84 percent are at that level, compared to 89 percent in 1992). That's a five-point slip in intermediate skills such as explaining the difference between two types of employee benefits, using a bus schedule to determine an appropriate route or using a pamphlet to calculate the yearly amount a couple would receive for basic supplemental security income.
But the biggest slip is at the proficient level: Only 31 percent are at this highest level compared to 40 percent in 1992. That's a nine-point slip in mastery of complex activities such as critically evaluating information in legal documents, comparing viewpoints in two editorials or interpreting a table about blood pressure and physical activity.
You see a similar slippage for high school graduates and, worse, for those who have done postgraduate work.
It's bad enough that we can't seem to improve basic literacy rates generally. But we cannot afford to have our most educated population drop in complex literacy levels. Ingraining the habits of literacy won't be easy, but it can be done. The task falls mostly to our schools, but they cannot do it alone. Others, from parents to libraries to communities, have to limit the video games and make reading fun again.
Those of us who aren't in school can't rely on others to ingrain our habits of literacy; we must do it ourselves.
I myself have fallen victim to a little mental laziness, and that's all it is: mental laziness. The brain is like any other muscle--it can be conditioned. But like muscle training, it's hard work, and so therefore avoided by most people (including Moi). I have a number of books I have been wanting to read, but I have put off simply because of the effort involved.
I am hereby making an addendum to my list of New Year's resolutions to include, in addition to my regular reading schedule, attacking and reading the following books over the next year.
1. The three volume biography of Graham Greene
this three-volume biography is incomparable; as an intellectual and political history of the 20th century it is invaluable; as a literary journey, as well as a journey across the world, it is masterly; as a source book and rogues' gallery it is fascinating.
Looks like I can have it all if only I will buckle down and work my way through these many formidable pages.
2. A biography of Charles Sanders Peirce
3.The Rainbow and the Worm
4.Order Out of Chaos
I challenge you to do the same thing. You can make public your commitment by sending in a comment with the books you plan to read in 2006. I'll post them all, then we can look back at the start of 2007 to see how we all did.
Remember, just like your biceps, your brain won't get any stronger unless you exercise it.
Posted by mreades at 08:50 AM | Comments (12)
January 12, 2006
1760 diet revolution
MD and I are still in the throes of our recent move. As I was unpacking another of the innumerable boxes still unpacked I came across a little pamphlet, a magazine more like, printed in 1760. It isn’t a reprint, it is an actual, honest-to-God, yellowed, crumbly issue of The London Magazine for May, 1760. It is in a plastic wrapper and is in remarkable condition. And I have no idea when or where I got it. In fact, I didn’t even know I had it until it emerged from a box of books.
I carefully took it out of the wrapper and paged through it, which was a remarkable experience. The London Magazine was the 1760 equivalent of Time or Newsweek. It was a magazine of current events, at least those current in 1760. For example, I found myself reading about the French and Indian War (it wasn’t called that then, of course; it was referred to as "the present war.") in a piece written as said war was taking place.
Immediately after the article on the "present war" I came upon an article written about the causes and cure of corpulency (obesity) written by one of the leading physicians of the day. I’m sure that this article inspired me to purchase this little jewel some time in the distant past, but I just can’t remember actually doing it.
This article was so intriguing and written in such a quaint fashion that I decided that as a treat for all my faithful readers I would type the thing in its entirety. It wasn’t an easy task, but I persevered.
Before I get to my modern typed version, however, I want to show you what I had to deal with. In 1760 the letter ’s’ was sometimes written as a ’s’ and sometimes as an ’f.’ In a blatant plea for sympathy for all my typing efforts, here is what a paragraph looked like in the original. Bear in mind that you are reading it in modern, clean type on a screen. I had to read it on yellowed, faded paper with not particularly good type impressions. It’s a wonder I didn’t go blind.
The fitteft foap for this purpofe is that from Alican in Spain, as being not only more cleanly and lefs difagreeable, but much more eafily diffolved in water than the home-made Caftile foap.
As you read this article think about some of the books and articles you’ve read on weight-loss in current times. Some things never change.
I hope you enjoy it as much as I did. (Note: all punctualtion, italics, spelling, grammar, etc. is exactly as published in 1760.)
Extracts from A Discouse on the Nature, Causes, and Cures, of Corpulency. Illustrated be a remarkable Case, read before the Royal Society, November 1757: and now first published, by Malcolm Flemyng, M.D.
Dr. Flemyng defines corpulency to be a too great accumulation of animal oil or fat, more or less over the whole body; but chiefly immediately under the skin, in the interstices of the muscles; and within the cavity of the abdomen or lower belly.
As for the cause of it, it may be occasioned, he says, either by the introduction of too much oil into the habit, through the channels of nourishment, whereby there is so much the greater chance of its being retained in too great a quantity—or by the over-laxity, or, perhaps, original over-largeness, of the cells in which it is reposited, disposing them to admit, and retain, an over-proportion of it—or by such a temperament of the blood, as renders it liable to part too easily with its oily particles, and let them be strained off in too great plenty by the secretory vessels—or lastly, by a deficient evacuation or expulsion, of oil already taken in and separated from the blood, and laid up in its cells.
With regard to the cure, the diet of corpulent persons ought to be moderate in quantity, and lean and plain, rather than rich and palatable.
Cold bathing (proper diet and exercise being supposed to go along with it) bids farewell to answer the second cause of corpulency: But it ought never to be used without great caution. There is scarce any remedy that is more generally, and more dangerously misapplied, than cold bathing.
The removal of the third cause of corpulency is to be attempted by with-holding, or at least diminishing, by a spare and plain diet, the daily fresh supplies of oily matter to the blood; that the solids, by whose action and energy the union, and as it were cohesion of the principles of the blood, is effected, may not have more work to do than enough: And, by exciting the action of the solids, by exercise, particularly friction of dry rubbing of the surface of the body, chiefly the trunk; for corpulent persons can scarcely use any other with remarkable effect.
The best way to remove the cause of corpulency assigned to the fourth and last place is to promote and increase the common natural excretions; to wit, urine, faeces, sweat, and insensible perspiration, which, in a healthy state, are always more or less charged with animal oil.
No great stress is to be laid on the insensible perspiration in our climate, mare than what friction may effect.
Frequent purging would no doubt be a speedy and effectual means of reducing corpulency; but it is dangerous to proceed far this way by art. What is most advisable in this respect is, to use such a diet and manner of living, as may prevent costiveness [constipation]. Walking, in a general way, promotes the evacuation per anum. Riding, as well as a sedentary life, encourages costiveness.
The fastest way of raising sweat is by increased muscular motion, as walking hard, playing at tennis, exercising some laborious mechanic deployment, or the like. The next fastest way, is by moist heat; as in a bagnio.
The excretion of urine may be promoted by a variety of diuretics, with less shock to the constitution, than that by sweat, or stools. But that diuretics may be employed to the best advantage, it is requisite to chuse such as, besides increasing the quantity of urine, may at the same time render the animal oil more miscible with the watery vehicle of the blood, than otherwise it would be.
Now soap hath that quality in a singularly eminent degree; and is withal so safe, that it may be taken in large quantities every day for years together; in a word, it is the true remedy for corpulency where it is curable.
It is no small additional recommendation of this remedy, that it is highly proper for relieving complaints, and curing diseases arising from corpulency, even independently on diminishing it; such as, amongst the chronic tribe, short-windedness; lethargy, &cc. of the acute kind, bastard peripneumonies, which are more difficult to cure in very fat persons than others: And, in general, whatever disorders may be owing to viscidity of juices, a never failing attendant on plenitude and defect of motion.
The fittest soap for this purpose is that from Alicant in Spain, as being not only more cleanly and less disagreeable, but much more easily dissolved in water, than the home-made Castile soap.
As to the manner of exhibiting it, the properest time is at night when going to bed. A drachm [1/8 of a fluid ounce]may be tried for the first four or five days; and if that create no remarkable disorder, the quantity should be increased to two , three, and, in very stubborn cases, to four drachms; which last dose, needs not in any case to be exceeded. It may be taken either in the form of a bolus, with any palatable syrup; or in the shape of pills; or dissolved in a gill [5 fluid ounces] or more of soft water.
To explain and illustrate what he had advanced, the author subjoins the following case.
"A judicious and experienced physician, in his younger days had been very active, and used much exercise, both on foot and on horseback; and for many years seemed as little liable to extreme corpulency as most people. By insensible degrees, as he diminished his daily labours, fatness stole upon him, and kept increasing; insomuch that, when I met with him about six years ago, I found him in the greatest distress through mere corpulency, of any person not exceeding middle age, I ever knew. He was then about forty-five. He was obliged to ride from house to house to visit his patients in the town where he practiced, being quite unable to walk an hundred yards at a stretch; and was in no small degree lethargic. In other respects, he seemed pretty clear of any remarkable disease, except gout, of which he had fest some, not very violent, attacks. I warmly recommended the inward use of soap, in order to reduce his corpulency, as the only safe and effectual remedy in his case, and a remedy which he might continue to use the longest; I enforced my advice by the reasonings above urged, of which he was too good a judge not to perceive their full cogency. Accordingly, he weighted twenty stone and eleven pounds [291 pounds], jockey weight [fully dressed], a vast load for him to bear, who is little above middle figure, and withal small boned. He took every night at bed-time, a quarter of an ounce of common home-made Castille soap, dissolved in a quarter of a pint of soft water. In about two or three months time, he began to feel more freedom, and an increase of activity, which encouraged him to persevere. And that he did with such success, that in August, 1756, (as he informs me in a letter now lying before me) his bulk was reduced two whole stone weight [28 pounds]; and he could walk a mile with pleasure. He had continued the use of the soap all the time between June, 1754, and August, 1756, with very short interruptions, in the manner and quantity above-mentioned; it operated remarkably by urine, without ever producing the least troublesome effect. And now, while I am sending these pages to the press (April, 1760) I am certainly informed that he is hearty and well. He used no other method or medicine all the while, to which the extraordinary change in his favour, can with any colour of reason be imputed."
There you have it straight from the weight-loss guru of the mid 1700s. Reduce your fat intake and drink soap, and you’ll be on your way to a cleaner, slimmer, fitter you.
Posted by mreades at 10:30 PM | Comments (0)
January 11, 2006
It's the real ...HFCS?
The front page of today's Wall Street Journal carried an article discussing a sticky problem for Coke. (See related article in the San Diego Union Tribune) It seems that our burgeoning population of friends from south of the border prefer their Coke the old Mexico way. Not only do they prefer it, they're willing to pay a lot more for it (up to $1.25 per 8 ounce bottle) while the less expensive one dollar per 20 ounce American stuff languishes on the shelf.
Why? Not because the Hispanic population is nostalgic for the dinged up, blue, old-fashioned bottle stamped "Hecho en Mexico," but because they think it tastes better.
Fans insist the Mexican cola, made with cane sugar, has a better "mouth feel" than the U.S. formula.
One connoisseur of soft drinks observes that
Cane sugar gives it [Mexican Coke] a cleaner taste.
Why is this a problem for Coke? Because sales of Mexican Coke are on the rise while sales of the U.S. bottled variety are on the decline. And, since the profit margin of Coke made in Mexico is much, much less than on that made in this country, Coke's bottom line is feeling the pinch.
Why doesn't Coke just make it here in the good ol' US of A using cane sugar? Ah, but there's the rub.
As the Wall Street Journal article points out:
U.S. bottlers switched from cane sugar to high-fructose corn syrup in the 1980s to cut costs.
Coke and Pepsi have been toe-to-toe competitors for ages, and Coke had always come out on top. Until the early 1980s. Until that time both companies were sweetening their drinks with cane sugar (sucrose). Then Pepsi reformulated their drinks and began using high fructose corn syrup (HFCS). The marketing geniuses at Pepsi initiated the "Pepsi Challenge," in which Pepsi challenged Coke to a blind taste test. If you were around at that time, you would have encountered people offering you a taste of two unlabeled cola beverages. You were supposed to taste, then select the one you thought was tastier. According to Pepsi, the vast majority of people picked Pepsi as their favorite. I took the "Pepsi Challenge" myself at least a dozen times, and each and every time I picked Coke as the better tasting of the two. However, by Pepsi's accounting, I was in the minority. But I can attest to - at least in my mouth - the "cleaner" taste and better "mouth feel" of the cane sugar sweetened drink.
After this bit of Pepsi bravado the executives at Coke realized that they had a problem. Not only were Pepsi sales soaring at their product's expense, but their product cost more to make, putting a double hickey on their bottom line. Consequently, the decision was quickly made to change the sweetener in Coke from sucrose to HFCS.
Thus was born New Coke.
What a marketing gimmick! People still argue over whether the resulting hoorah was plotted by the marketing folks at Coke or if they just serendipitously blundered into it. Suddenly no one was thinking about Pepsi any longer; instead they were caught up in the debate over the taste merits of New Coke verses 'old' Coke.
Old Coke, made with sucrose, became Classic Coke. But then a funny thing happened over the years. Classic Coke began to morph into New Coke, at least in the ingredients section of their labels. First, the ingredients in Classic Coke changed from: Carbonated water, sucrose, caramel...to Carbonated water, sucrose and high fructose corn syrup, caramel...to Carbonated water, sucrose and/or high fructose corn syrup, caramel...to Carbonated water, high fructose corn syrup and/or sucrose, caramel...to finally Carbonated water, high fructose corn syrup, caramel... And, New Coke went the way of the Dodo bird.
In my local supermarket there is only Classic Coke and in the large bottles it is labeled: Carbonated water, high fructose corn syrup, caramel... In the smaller bottles and cans it is still labeled Carbonated water, high fructose corn syrup and/or sucrose, caramel...
So, the big question is: who cares? What difference does it make that Coke has finally accomplished what it set out to do in the early 1980s, which is to have its product made with the less expensive HFCS?
It matters because of the difference between fructose and sucrose and what they do to us metabolically.
Plain table sugar, sucrose, is a disaccharide, which is a sugar made of two sugar molecules. Sucrose is made of equal amounts of glucose and fructose. Fructose is a monosaccharide (one sugar). So, if you eat two teaspoons of table sugar you get one teaspoon of glucose and one teaspoon of fructose. If you eat two teaspoons of fructose you get two teaspoons of fructose.
High fructose corn syrup is, like table sugar, made up of both fructose and glucose, but with more fructose than glucose. There are multiple HFCS formulas with the fructose component ranging from 55 percent to 90 percent of the content. If you consume a product containing HFCS you are going to get more fructose than if you consume the same amount of sucrose. Since everything anymore is made with HFCS fructose consumption has increased dramatically since the 1970s when HFCS began to be made in large quantities.
Fructose is not a benign sugar. In fact, many people (yours truly included) believe that the enormous increase in the consumption of fructose is driving much of the increase in obesity, diabetes, and the rest of the disorders making up the metabolic syndrome.
Most nutritionally savvy people (the readers of this blog, for example) know that fructose is a bad actor metabolically; for those who don't, I'll lay out the case for why in another post. What I want to stress now is that we've all switched from sucrose to HFCS thanks to our fearless leaders in Washington. These are the guys (and gals) who keep the sugar price supports so high that manufacturers in this country have all turned to the much less expensive HFCS to the detriment of our national health.
Let's let the ABC investigative reporter John Stossel tell it in an
excerpt from his book Give Me a Break
When public interest groups compile lists of corporate welfare recipients, a company named Archer Daniels Midland is usually at the top of the list. You may never have heard of ADM, because it's name rarely appears on consumer products, but it's huge. It's products are in most processed foods.
ADM collects welfare because of two cleverly designed special deals. The first is the government's mandated minimum price for sugar. Because of the price supports, if the Coca-Cola Company or Pepsi wants to buy sugar for its soda, it has to pay 22 cents a pound - more than twice the world price. So Coke (and most everyone else) buys corn sweetener instead. Guess who makes corn sweetener? ADM, of course. Now guess who finances the groups that lobby to keep sugar prices high?
Why does ADM get these special deals? Bribery. Okay, it's not bribery - that would be illegal. ADM just makes "contributions." Through his business and family, former ADM chairman Dwayne Andreas gave millions in campaign funds to both Mondale and Reagan, Dukakis and Bush, Dole and Clinton. President Nixon's secretary Rosemary Woods, says Andreas himself brought $100,000 in cash to the White House. He even paid the tuition for Vice President Hubert Humphrey's son. Republicans, Democrats, it doesnt matter. ADM just gives.
It also flies people around on its corporate jets. When we contacted Andreas to ask for an interview, he arranged to fly us to ADM's Decatur, Illinois, headquarters in one of ADM's jets. I've seen private jets before, but ADM's was a step above. A flight attendant served us excellent food on gold-plated china. The camera crew and I loved it. Bet the politicians like it, too.
A limo took us to Dwayne Andreas's office. Once the cameras were rolling, I brought our the questions about "corporate welfare." I foolishly thought I could get him to admit he was a rich guy milking the system. I thought he'd at least act embarrassed about it. Fuggeddaboutit. He was unfazed.
John Stossel: Mother Jones [magazine] pictured you as a pig. You're a pig feeding at the welfare trough.
Dwayne Andreas: Why should I care?
John Stossel: It doesn't bother you?
Dwayne Andreas: Not a bit.
Give me a break, indeed.
The next time you see a report on how the obesity statistics are climbing or how many more people are coming down with diabetes or how the high blood pressure and stroke figures just won't go down, don't blame the manufacturers. Write your congressman instead.
Posted by mreades at 09:18 PM | Comments (11)
January 10, 2006
Lileks on Steyn
A shorter argument by James Lileks ispired by the Steyn piece. Lileks writes one of the blogs I never miss. He is a terrific writer and usually muses on many different issues. He includes a cornucopia of wonderful material in his blog. One of my favorites is his reproduction of the 1949 Sunbeam comic book on the story of bread with his commentary. Flip through it for a blast from the past.
Unlike most of his stuff, this particular piece is in his Screed Section and is atypical for him. Steyn must have struck a chord.
Posted by mreades at 02:41 PM | Comments (4)
Steyn on the multicultural front
A thought-provoking, lengthy piece by Mark Steyn that was originally published in the New Criterion but picked up by the Wall Street Journal. It's a little over the top in a couple of places but he makes his point, and it's one I tend to agree with. The entire piece is well worth reading.
According to Steyn all our hand wringing over most of our political sacred cows is much like worrying over just what to wear to dinner on the Titanic. All of our seemingly important cultural quarrels are in danger of running up against the monster iceberg of spreading Islamic fundamentalism brought about by, if nothing else, the disparity in birthrates between the cultural West and cultural Islam.
An excerpt on multiculturalism:
That's what the war's about: our lack of civilizational confidence. As a famous Arnold Toynbee quote puts it: "Civilizations die from suicide, not murder"--as can be seen throughout much of "the Western world" right now. The progressive agenda--lavish social welfare, abortion, secularism, multiculturalism--is collectively the real suicide bomb. Take multiculturalism. The great thing about multiculturalism is that it doesn't involve knowing anything about other cultures--the capital of Bhutan, the principal exports of Malawi, who cares? All it requires is feeling good about other cultures. It's fundamentally a fraud, and I would argue was subliminally accepted on that basis. Most adherents to the idea that all cultures are equal don't want to live in anything but an advanced Western society. Multiculturalism means your kid has to learn some wretched native dirge for the school holiday concert instead of getting to sing "Rudolph the Red-Nosed Reindeer" or that your holistic masseuse uses techniques developed from Native American spirituality, but not that you or anyone you care about should have to live in an African or Native American society. It's a quintessential piece of progressive humbug.
And on the birthrate disparity and the unwillingness for people anywhere to give up benefits they view as rights:
What's the better bet? A globalization that exports cheeseburgers and pop songs or a globalization that exports the fiercest aspects of its culture? When it comes to forecasting the future, the birthrate is the nearest thing to hard numbers. If only a million babies are born in 2006, it's hard to have two million adults enter the workforce in 2026 (or 2033, or 2037, or whenever they get around to finishing their Anger Management and Queer Studies degrees). And the hard data on babies around the Western world is that they're running out a lot faster than the oil is. "Replacement" fertility rate--i.e., the number you need for merely a stable population, not getting any bigger, not getting any smaller--is 2.1 babies per woman. Some countries are well above that: the global fertility leader, Somalia, is 6.91, Niger 6.83, Afghanistan 6.78, Yemen 6.75. Notice what those nations have in common?
Scroll way down to the bottom of the Hot One Hundred top breeders and you'll eventually find the United States, hovering just at replacement rate with 2.07 births per woman. Ireland is 1.87, New Zealand 1.79, Australia 1.76. But Canada's fertility rate is down to 1.5, well below replacement rate; Germany and Austria are at 1.3, the brink of the death spiral; Russia and Italy are at 1.2; Spain 1.1, about half replacement rate. That's to say, Spain's population is halving every generation. By 2050, Italy's population will have fallen by 22%, Bulgaria's by 36%, Estonia's by 52%. In America, demographic trends suggest that the blue states ought to apply for honorary membership of the EU: In the 2004 election, John Kerry won the 16 with the lowest birthrates; George W. Bush took 25 of the 26 states with the highest. By 2050, there will be 100 million fewer Europeans, 100 million more Americans--and mostly red-state Americans.
As fertility shrivels, societies get older--and Japan and much of Europe are set to get older than any functioning societies have ever been. And we know what comes after old age. These countries are going out of business--unless they can find the will to change their ways. Is that likely? I don't think so. If you look at European election results--most recently in Germany--it's hard not to conclude that, while voters are unhappy with their political establishments, they're unhappy mainly because they resent being asked to reconsider their government benefits and, no matter how unaffordable they may be a generation down the road, they have no intention of seriously reconsidering them. The Scottish executive recently backed down from a proposal to raise the retirement age of Scottish public workers. It's presently 60, which is nice but unaffordable. But the reaction of the average Scots worker is that that's somebody else's problem. The average German worker now puts in 22% fewer hours per year than his American counterpart, and no politician who wishes to remain electorally viable will propose closing the gap in any meaningful way.
Posted by mreades at 02:20 PM | Comments (7)
January 09, 2006
It's lame
A couple of weeks ago I posted on the large JAMA study showing that, contrary to what we've heard ad nauseum over the past decade, fiber consumption produced no protective effect against colon cancer. Now comes one of the more bizarre studies that I've ever read.
The British journal Colorectal Disease published a paper a few months ago with the promising title "Diet and colorectal cancer: implications for the obese and devotees of the Atkins diet." Hey, now were getting somewhere thinks I when this little baby fell into my hands through the agency of the university inter-library loan department. Then I began to read it.
I don't know if medical journals have the equivalent of slow news days or if this particular journal, which I hadn't previously seen, is a lower tier journal, but I can't figure how this paper got published. I'm glad it did because most people will only get to read the abstract (my university didn't have a subscription to the journal, thus my reliance on inter-library loan), and the abstract implies much that isn't developed in the paper. I'm sure many people writing articles on low-carb diets will in the future reference this paper as one that shows low-carb diets to reduce the risk of colorectal cancer. The paper, however, doesn't really do that. In fact, it doesn't do much of anything.
When we take a look at the abstract, we - as low-carb devotees - see some exciting stuff:
Colorectal cancer (CRC) is the second most common cause of cancer-related death in the Western world and its prevalence is increasing. Potential causes of this increase are changes in diet and the increases in obesity seen. This paper looks at the literature surrounding diet and obesity and the links to this increase in CRC. Heralded as a weight loss miracle we investigate whether the literature suggests the Atkins diet may actually do more harm than good by acting to increase an individual's risk of CRC. Obesity has been demonstrated to be a major factor in the increase in CRC although links to changes in diet are more tenuous. Published studies on diet suggest the Atkins diet may help reduce rather than increase the risk of CRC.
As we go through the paper, however, excitement wanes.
Basically, the paper can be summarized pretty quickly. Here is the Cliff Notes version.
Obesity is a huge problem worldwide. Many people looking for a solution have tried the Atkins and other low-carbohydrate diets. These low-carbohydrate diets recommend meat accompanied by non-starchy vegetables. Studies have shown a correlation between meat consumption and colorectal cancer (CRC). Other studies have shown no correlation between meat consumption and CRC. Studies have shown that consumption of non-starchy vegetables and fruits are protective against CRC. Some studies have shown a correlation between fat consumption and CRC; others have shown no such correlation. some studies show that carbohydrate intake, especially of sugars and refined starches, increase the risk for CRC; these findings have not been confirmed in other studies. The paper then makes a strange comment:
The reduction in carbohydrate on this diet (Atkins) may result in less fruit and vegetables ingested and for this reason the Atkins diet may actually increase the risk of CRC. This should not be the case for the phases where more carbohydrate is permitted; the problem is that as with many diets, there tends to be high rates of noncompliance and the initial induction phase may deter people from eating fresh fruit and vegetable, despite some public health measures of encouragement to do otherwise. Of additional concern is that dieters may solely utilize the 'induction' phase of the Atkins diet plan as an effective weight loss strategy before reverting back to an unhealthy regime of sugary foods.
More Cliff Notes:
Once again studies have shown dietary fat to cause increased risk for CRC; others don't. Most studies have shown that obesity is a risk factor for CRC. In fact, obesity is probably the most significant risk factor. Low-carbohydrate diets are lower in calories than non-diets. Consuming fewer calories brings about weight-loss. Weight-loss reduces risk for CRC. And, therefore, the Atkins and other low-carb diets are a go. As the authors conclude:
Until there is more conclusive evidence, it does not appear that the Atkins diet plan should be rejected. Indeed, from the current evidence it may actually be beneficial by reducing the risk of developing CRC; total energy intake may be a more significant risk factor and any diet conferring a decreased calorie intake would presumably decrease this risk.
There is so much data out there showing that low-carb diets reduce the risk of CRC in so many ways that it's really a shame that this kind of wishy washy crapola uses up valuable ink.
Reading this paper makes me recall the one and only time I ever listened to Howard Stern when I heard him say the following to a Star Trek fanatic who had spent God only knows how much time trying to derive the language of Klingons:
It's lame, Dude. It's really lame.
Posted by mreades at 07:54 PM | Comments (7)
January 08, 2006
A new way to scramble eggs
Within a day after my previous post on the virtues of egg consumption for breakfast the New York Times Magazine (free registration) ran an article on a different way to scramble/poach eggs. I haven't tried it yet because I had already had my eggs poached the traditional way before I read the article.
I'm sure the distaff half of the Eades team will try this method soon. When she does, I'll let you know how it went.
Posted by mreades at 11:01 PM | Comments (5)
January 06, 2006
Better than cornflakes
Wanna have good breakfast that keeps you from eating so much at lunch? Wanna have a healthy breakfast that cuts 400 plus Calories out of your diet over the next 36 hours. Wanna have a breakfast food that markedly reduces your hunger throughout the day? Well, you can. Does this sound like the latest infomercial for some kind of weight-loss gimmick? It isn't.
New research published in the current issue of the Journal of the American College of Nutrition (JACN) shows that you can do all of the above by adding a couple of eggs to your breakfast.
The authors of this paper cleverly designed and implemented a study that cleaned up the fuzzy research done over the past several years on the topic of what kind of breakfast provides the greatest satiety throughout the rest of the day. An example: a study was published in 1999 that compared breakfasts consisting of All-bran, bananas and milk, bacon and eggs, corn flakes or a croissant. In terms of producing the greatest satiety, the All-bran breakfast came in first with the bacon and eggs a distant third. Problem was that the weight of the All-bran consumed in the study was almost twice that of the bacon and eggs, which suggests that instead of the All-bran it may have been the weight and volume of the larger breakfast that caused the increased satiety.
The researchers in the JACN study used the same group of overweight subjects and two different breakfasts on two different days separated by a couple of weeks. Each subject acted as her (all subjects were overweight females) own control.
The two breakfasts were designed to be roughly the same size, the same weight, and the same caloric content. The only thing different were the amounts of fat, protein, and carbohydrate.
The egg breakfast was comprised of 2 eggs-scrambled, 2 slices of toast, and 1 tablespoon of reduced calorie fruit spread. The bagel-based breakfast was comprised of a 3.5 inch diameter bagel, 2 tablespoons of cream cheese, and 3 oz of non-fat yogurt. The weight and energy content of the "egg breakfast" and the "bagel breakfast" were similar. Leftover breakfast was weighed to determine the intake.
After consuming one of the two breakfasts, the subjects completed a standardized questionnaires designed to determine their feelings of fullness and cravings. They completed the same questionnaires twice more at 90 minute intervals. Along with filling out the questionnaires the subjects
spent about 195 min reading, listening to music or watching movies that did not have references to food/eating. Lunch, comprised of pasta with marinara sauce and sliced apples, was offered 3.5 hours after completion of the breakfasts. Subjects were encouraged to eat as much food they wanted. Food intake was monitored discretely to determine the weight and caloric content of the food consumed. Weight of food offered was noted and each remaining food component was separately weighed after the breakfast and lunch. Subjects were urged to not drink water during lunch. Water was offered ad-libitum after lunch. Participants were allowed to leave at this time, but were asked to keep a food-intake and activity diary for the next 24 hours. Detailed instructions on keeping the food diary were provided.
As a part of the clever design of this study implemented to prevent bias in filling out the questionnaires and in the actual lunchtime and later food intake (it's a well known fact that experimental subjects want to "please" the researchers) the researchers told the subjects
that the purported aim of the study was to monitor the effect of breakfast on blood pressure and alertness. Alertness assessment questionnaires were given and blood pressure was measured along with the fullness and food craving questionnaires.
Two weeks later the subjects returned to the lab and repeated the exercises with the opposite breakfast.
When the results were tallied it turned out that after the subjects breakfasted on eggs they reported a greater feeling of fullness and less hunger at the next meal and over the next day as well. And not only did they report less hunger, they actually ate less. After eating the eggs for breakfast the subjects consumed 164 fewer Calories at lunch than when they ate the bagel. More amazing, they took in 420 fewer calories over the next 36 hours after eating the eggs.
As we all know, eggs are a great low-carb food containing virtually zero carbohydrates while being chocked full of great quality protein. But what about cholesterol? Even the authors of this study, all of whom are from mainstream medical research institutions, weren't worried about the cholesterol issue.
Eggs are a convenient, affordable and nutritious source of key macro and micronutrients. They are an integral and established part of breakfast in numerous cultures and may be eaten safely on a regular basis. Discretionary use of eggs has been traditionally advised due to their cholesterol content and the earlier implications in coronary heart disease risk. However, recent data from the Nurses Health Study showed that egg consumption did not contribute to the risk of coronary heart disease or stroke.
So, there you have it. Don't worry about the cholesterol. Eat a couple of eggs for breakfast instead of a pop tart or some other nasty, carb-laden processed breakfast food, keep your hunger suppressed, and your weight loss chugging along.
Posted by mreades at 10:04 PM | Comments (3)
January 05, 2006
The sugar hypothesis
I’m always amazed at how the lipid hypothesis of heart disease has wormed its way deep into souls of physicians, scientists, and medical/nutritional writers the world over. The most flimsy piece of research that seems to confirm this entrenched bias is not only accepted uncritically (not by yours truly, of course), but shouted from the rooftops by the likes of USA Today, the New York Times, Reuters, and other general publications.
Then along comes a study with some true value that, although published in a prestigious journal, is vigorously ignored. Such seems to be the fate of a tremendous piece of research appearing in the current issue of Diabetes Care. Since this journal, like JAMA, makes available to the public the full text of articles its editors deem of significant public health importance, you can get the article in its entirety here.
Researchers at University College in London looked at the mortality data generated over the past 33 years from the Whitehall Study, which, like the Women’s Health Initiative, is a large, government funded study. In the Whitehall Study
18,403 nonindustrial London-based male civil servants aged 40—64 years were examined between September 1967 and January 1970. In brief, measurements included height, weight, blood pressure, six-lead electrocardiogram, lung function (forced expiratory volume in 1 s and forced vital capacity), plasma cholesterol concentration, and a glucose tolerance test. A self-administered questionnaire was completed regarding employment grade, smoking habits, health status, and physical activity.
After an overnight fast the participants of this study underwent a glucose tolerance test in which they drank a preparation containing 50 grams of glucose. Two hours later they had their blood sugars measured. In a normal glucose tolerance test blood sugars typically return to normal within two hours after having consumed a glucose drink. The researchers wanted to record these 2-hr post glucose load figures and see how they correlated with mortality over the ensuing years.
The researchers divided the study participants according to their 2-hr blood glucose values into three groups. Those with 2-hr glucose levels below 95 mg/dl were considered normal; those who measured 96-199 mg/dl were deemed glucose intolerant; and those with 2-hr blood glucose levels at 200 mg/dl or greater were classified as diabetic.
As might be expected, after 33 years the diabetic group fared poorly compared to the normal and even the glucose intolerant group. Having a diabetic 2-hr post load glucose profile increased the odds off all-cause mortality by 2.37 and of death from coronary heart disease by 3.70. Clearly having an abnormal glucose tolerance test is bad news for prospects of a long life, more so, in fact, than a "bad" cholesterol test.
But, the most interesting aspect of this study is what the researchers found in the normal group first at 10 years then at 33 years down the road. Everyone knows that a markedly elevated blood sugar level or a diabetic glucose tolerance test bodes poorly for long term mortality, but what about the lower end of the curve? Is there a difference there? Is there a difference in long term mortality between a blood glucose level of, say, 95 mg/dl and one of 85 mg/dl, both of which are considered normal.
At the 10 year followup of the 18, 403 men the researchers found that heart disease mortality started to increase at blood sugar levels above 95 mg/dl, but that those subjects with blood sugar levels below 95 mg/dl showed no increased risk for death from heart disease.
After 33 years, however, the picture changes. The cutoff level drops to 83 mg/dl. In other words, in terms of cardiovascular mortality, the risk starts to rise as 2-hr post load blood sugars reach 83 mg/dl and that there is a linear increase in risk between 83 mg/dl and 95 mg/dl. I’m sure that after 40 years, the minimum level will drop a few points further.
Why this increase in risk? According to the authors:
Several mechanisms may account for the link between elevated glucose level and CHD risk. A raised glucose level at baseline may indicate emerging insulin resistance and a downward trajectory in glycemic control, with increased risk of glucose intolerance, diabetes, and CHD in subsequent years. Related risk factors, particularly hypertension and an atherogenic lipoprotein profile [even these folks are in the grip of the lipid hypothesis], tend to develop in parallel with insulin resistance. Other pathways include oxidative stress and formation of advanced glycation end products that accelerate atherosclerosis when blood glucose is only slightly raised. A further indirect mechanism involves common antecedents of hyperglycemia and CHD such as poor early growth. Adjusting for conventional risk factors, existing baseline CHD and socioeconomic position in the present study reduced the size of the glucose-CHD association by 45%. This is evidence of a causal role for glycemia in CHD etiology. It is also consistent with an element of confounding and with risk-factor clustering of the metabolic syndrome type.
What needs to be grasped about this study is that there is no comparable study showing mortality related to cholesterol levels, despite all the ignorant hoorah to the contrary. In fact, in this very Whitehall Study researchers measured cholesterol levels and found no significant differences between them in those subjects with normal blood sugar, those who were glucose intolerant, and those with outright diabetes (see Table 1 in the study).
This is all important stuff. It’s much more important for your long term health to work on keeping your blood sugar down than it is to work to keep your cholesterol down. It’s especially important when you realize that most people try to keep their cholesterol levels at bay be consuming a low-fat, high-carbohydrate diet, which is a diet containing, in many cases, a cup and a half to two cups of sugar equivalents per day. Now, remember, a normal blood sugar equates to only a teaspoon of glucose dissolved in the blood. So, it shouldn’t take a rocket scientist to realize that a couple of cups of sugar added to this teaspoon will rapidly run blood sugar levels up, up, up. This misguided effort to focus on cholesterol levels can only end up increasing the risk for early mortality from heart disease, the very thing reducing cholesterol is supposed to prevent.
The maddening thing about all this is that you will probably never read about this tremendously important study in your local paper. But the next time some boob publishes anything that points a finger at cholesterol or, God forbid, fat in the diet, you will read all about it.
Oh, by the way, what’s the best way to keep your blood sugar low? How about by not eating a lot of it and letting the body make the sugar as it needs it. In my clinical experience, most patients on low-carbohydrate diets reduce their blood sugar levels into the 75-85 mg/dl range.
Posted by mreades at 11:10 PM | Comments (5)
January 04, 2006
"I have vision, and the rest of the world wears bifocals."*
A study appeared in the journal Cell last week that the authors are touting as a revelation of the "widely recognized" link between consumption of a high-fat diet and development of type II diabetes. (Click here to see the scientific paper).
A quick glance at just the abstract of this article is all it takes to realize that it is an extremely technical paper dealing with basically the reduced lifespan of a certain glucose transporter on the mouse pancreatic beta cell membrane as a function of a high-fat diet:
Pancreatic β cell-surface expression of glucose transporter 2 (Glut-2) is essential for glucose-stimulated insulin secretion, thereby controlling blood glucose homeostasis in response to dietary intake. We show that the murine GlcNAcT-IVa glycosyltransferase is required for Glut-2 residency on the β cell surface by constructing a cell-type- and glycoprotein-specific N-glycan ligand for pancreatic lectin receptors. Loss of GlcNAcT-IVa, or the addition of glycan-ligand mimetics, attenuates Glut-2 cell-surface half-life, provoking endocytosis with redistribution into endosomes and lysosomes. The ensuing impairment of glucose-stimulated insulin secretion leads to metabolic dysfunction diagnostic of type 2 diabetes. Remarkably, the induction of diabetes by chronic ingestion of a high-fat diet is associated with reduced GlcNAcT-IV expression and attenuated Glut-2 glycosylation coincident with Glut-2 endocytosis. We infer that β cell glucose-transporter glycosylation mediates a link between diet and insulin production that typically suppresses the pathogenesis of type 2 diabetes.
I have known a lot of medical reporters, and none of them in their daily scans of the medical literature would have picked up this article to report on. In fact, I’m quite sure that their eyes would have quickly glazed over had any even tried to read it. So how did it get picked up?
Either the journal or the authors themselves issued a press release proclaiming this great discovery. Few, if any, medical reporters could understand this article or its supposed significance, so they relied on the authors to tell them what it meant. These reporters then parroted the authors claims to the world without really having a clue themselves as to what it was all about.
So, it’s the authors here who are at fault for all this blather; not the poor medical reporters.
And the authors are quite excited about their work:
"Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency," said Dr Jamey Marth, UCSD professor of cellular and molecular medicine.
"The GnT-4a enzyme is required to synthesize a glycan structure that holds the glucose transporter in place at the beta cell surface. The loss of this key transporter is directly linked to reduced GnT-4a protein glycosylation, a high-fat diet, and type 2 diabetes," he added.He then gushes:
"If you could somehow stimulate production of this enzyme, you might be able to render animals, and perhaps humans, resistant to high-fat diet-induced diabetes."
Discounting the fact that mice aren’t simply fuzzy miniature people and don’t respond the same to diet or much of anything else as we do (which means this study has little, if any, human relevance), I’m reminded by that last statement of one of my favorite scenes in one of my favorite movies.
About two third of the way through Butch Cassidy and the Sundance Kid
Morons. I’ve got morons on my team. Nobody is going to rob us going down the mountain. We have got no money going down the mountain. When we have got the money, on the way back, then you can sweat.
I feel kind of the same way about the idea that this is some kind of exciting study showing definitively how high-fat diets lead to type II diabetes.
I want to say,
Morons. I’ve got morons on my team. Nobody gets diabetes from eating fat when no one eats fat anymore. Diabetes is skyrocketing while people are eating less fat than they ever have in history. If and when the fat consumption curve mirrors the diabetes curve instead of going in the opposite direction, well, then you can sweat.
* Butch to Sundance.
Posted by mreades at 10:37 PM | Comments (3)
January 03, 2006
Brace yourselves for more low-fat buncombe
A study appeared in the current issue of the Journal of the American Medical Association (JAMA) slated to land on doctors’ desks tomorrow that will, I’m sure, make all the major news services. This study purports to show that a long term low-fat diet doesn’t cause weight gain, and that it actually brings about a weight loss.
You will be able to witness the bias in the reports on this study by how enthusiastically the writers embrace the supposed findings.
It’s all pretty much nonsense, however, as the study didn’t really show anything much at all.
The researchers randomized almost 50,000 women between the ages of 50 to 79 into a study group, the members of which consumed a lower-fat, higher-carbohydrate diet, and a control group, the members of which continued on with their regular diets. These two groups were followed for almost nine years, and were evaluated for dietary compliance and weight loss along the way.
During the first year the members of the study group (the low-fat group received constant attention from the research staff whereas the control group were basically given a pat on the back and sent on their way.
Women assigned to the control group received a copy of the Dietary Guidelines for Americans as well as other diet- and health-related educational materials, but otherwise had no contact with study dietitians.
In contrast, women randomized to dietary intervention were assigned to groups of 8 to 15 participants for a series of sessions structured to promote dietary and behavioral changes that would result in reducing total dietary fat to 20% and increasing intake of vegetables and fruit to 5 or more servings and grains (whole grains encouraged) to 6 or more servings daily. Participants were informed that the diet was not intended to promote weight loss and were encouraged to maintain usual energy intake by replacing fat calories with calories from other sources, mainly carbohydrate. Eighteen group sessions were scheduled during the first 12 months, after which the session frequency was reduced to 4 per year for the duration of the trial. Individual contacts were completed in person or by telephone or mail for women who could not attend the sessions. Group activities were supplemented throughout the course of the study by an intervention protocol consisting of 3 individual interviews that used reflective listening techniques that were validated in a pilot study at 3 centers, targeted message campaigns, and personalized feedback.
So, we’ve got two groups of women, one of which has intense attention and counseling on dietary and behavioral changes while the other didn’t really get squat in terms of attention or care. What happened?
Hold on to your seat for this one.
During the first year the women in the group that got the constant attention lost a little over 4 pounds more than the women in the group that were ignored. By the end of the study the weight loss difference had narrowed to less than a pound.
All I can say is that if I conducted a study that showed these puny differences given all the time, effort, and instruction I had put into the control group, I certainly wouldn’t be crowing about it.
When the study results are probed a little, some interesting findings bubble to the surface, the most important of which is that the difference in caloric intake between the women in the two groups is about 120 kcal per day. If we multiply this 120 kcal per day times 365 days per year times 9 years, we find that over the course of the study the women in the control group consumed almost 400,000 (394,200 to be exact) fewer calories than did the women who ate what they wanted. If we take those calories and divide them by 3500 (roughly the number of calories in one pound of body fat) we find that, based on the reduction in calories alone, the women on the lower-fat, higher-carb study diet should have each lost over 112 pounds more than the women on the control diet. Yet they lost less than one pound more. Doesn’t sound much like a recommendation for the diet to me.
It’s interesting to see how the editors of JAMA have played this situation. Most medical journals make their full-text content available only to subscribers or to those who have university affiliations. Anyone can get the abstract, but the full test can be had only by a few. Occasionally a few of these journals - JAMA is one of these few - will release the full text of certain papers to the public that the editors feel are of considerable public health importance. This paper is one of those papers and can be had in full by clicking here.
What’s interesting is that this same issue of JAMA contains an editorial about this paper that is less than flattering. But, strangely, this editorial paper is not available to the public. What’s more, the editorial can’t even be had in abstract form.
What does this editorial say? Let’s hit the high spots.
It starts out thus:
The article by Howard and colleagues in this issue of JAMA, which reports on the largest, most ambitious randomized dietary intervention trial conducted to date, has concluded that a low-fat diet program does not produce weight gain. Despite the impressive features of this landmark study, the findings on long-term weight change are somewhat underwhelming.
It goes on to note:
The article by Howard et al is quick to focus attention on popular diets such as Atkins, the Zone, and Sugar Busters!, whose authors have blamed the current obesity epidemic in large part on the low-fat (high-carbohydrate) eating pattern advocated by most authorities during much of the past quarter century. Does the recent study refute allegations that the low-fat dietary approach caused weight gain on a national scale? Perhaps it does to some extent. On the other hand, despite some successes, overall the low-fat dietary approach has been a failure with the US public, [my italics] which is in desperate need of effective obesity treatment and prevention strategies.
The authors of the editorial point out, as I did in my post yesterday, that what is required for serious weight-loss is commitment and adherence to a program.
This is a general truth for virtually all aspects of medical treatment, especially for the most potent disease cures. Great results usually are predicated on great adherence levels. Modern medicine has much more work to do in the area of facilitating high long-term adherence levels. Focusing collective efforts on addressing this challenging aspect of obesity treatment and prevention would no doubt serve society well.
Unfortunately, the public has become so entrenched in current obesity prevalence and treatment trends that many have come to view lifestyle modification as a mediocre means of preventing and reversing obesity, but this could not be further from the truth. Many have accepted the belief that living in today’s society is incompatible with what is required to apply lifestyle changes, or even worse—that they barely work. Inadequate lifestyle counseling by physicians might contribute to this perception. However, most able-bodied persons who can find a way to overcome the monumental logistical and psychological barriers that prevent the full application of lifestyle change can reverse obesity within months. It seems simplistic, but a potential solution for the obesity crisis depends directly on finding a means of properly dosing lifestyle change recommendations. The medical profession and society in general have underdosed this potent cure by a long shot.
And the authors end by finding the above study a little less than stupendous and recommending more work on self discipline.
Even though the WHI Dietary Modification Trial was not a weight-loss study, the modest weight-loss findings somehow still seem dissatisfying. Much more work needs to be done on the obesity front, including a concerted collective effort focused on developing reliable methods of facilitating high long-term adherence levels to substantial lifestyle efforts...
I wonder why the editors of JAMA saw fit NOT to make this editorial available for your reading pleasure when they were so fre with the actual article?
Remember all this as you read the press reports tomorrow rabbiting on about how the low-fat diet really does work.
Posted by mreades at 11:04 PM | Comments (7)
January 02, 2006
If wishes were horses, beggars would ride.
When you wish upon a star, makes no difference who you are. Anything your heart desires will come to youIf your heart is in your dreams, no request is too extreme
When you wish upon a star as dreamers do
Ah, would that it were so. If ol' Jiminy Cricket had it right and all it took was wishing...
MD and I get a lot of mail from viewers of our cooking show on PBS, most of which are from folks wondering where we get certain ingredients, or telling us that the recipes on our website are missing an ingredient, or requesting - as many people are wont to do - our advice on specific medical issues. Some letter writers make comments on specific shows or give advice on how to make future shows better. Some are enthusiastic supporters; some are critical. Take for example an excerpt from the following letter:
I think your show is very informative for us diabetics, however, you should really talk more to the camera (AKA the viewers) instead of each other when doing the recipes.
Also, Dr. Michael needs to either help more or just let Dr. Mary do the show herself. I don't think it looks nice that he stands there and drinks his coffee. He always seems to be in the way and he doesn't like to get his hands dirty.
Perhaps if I follow through on Resolution #4, letters like this one will be a thing of the past.
Other letters just make me shake my head. For example, we received the letter excerpted below:
I am diabetic with heart problems. My main problem is that I like carbohydrates even though the consequences are often elevated blood sugar levels above 225.
I have been looking for a diet which could do the following:
Allow me to maintain blood sugar levels of 125 or less. Is not a diet of punishment or denial of foods I like. Result in weight loss. (note: I weigh 252 lbs and I am 5 feet seven inches tall) Increase my longevity and resurrect my sex life which has gone south due to diabetes. I am looking for a simple diet which would be highly repetitious which would deal with my problems.
This letter writer goes on to detail the diet he is currently following, which, although it contains a fair amount of protein, is not remotely a low-carb diet, though he seems to think it is. In addition to his semi-sort-of-pseudo low-carb diet he mentions that:
Sometimes I have two pieces of cake and two or three scoops of ice cream but not at the same time.
He then cuts to the chase:
If possible, I require two things from you.
1. An uncomplicated, tasty, low carbohydrate diet which would result in significantly lowered blood sugars, reduction of insulin intake and weight loss.
2. I would need the name of a physician in [name of city withheld], familiar with your diet, with whom I could consult and monitor my progress.
So, to boil it down to its essence, here is what this reader wants. A diet that lets him eat what he wants, lose weight like crazy, rid him of his diabetes, and cure his heart disease. People who think like this inspire the allusion to the Disney When You Wish Upon a Star song. If only wishing would make it so.
But it doesn't.
Anyone who has lost weight following any kind of a diet, including a low-carb diet, has worked at it. Let me put this in capital letters. LOSING WEIGHT IS NOT EASY. KEEPING IT OFF IS LESS EASY YET.
I believe that following a low-carb diet is the easiest, most effective, most healthful way for a person to lose weight, but it still isn't easy. It's hard work requiring effort, planning, and diligence. The only truly easy diet is to eat whatever you want whenever you want and to hell with the consequences. That's a snap. So, if it's easy you want, there is your plan.
Losing weight is a difficult proposition at best. But so is getting a college education, getting up and going to work everyday, maintaining a household, nurturing relationships, rearing children, keeping your yard looking nice, and doing most of the things we all do to keep the bills paid and our lives moving along. No one thinks these things are easy. You don't find books on the Professor's Quick Guide to a College Degree in Three Days. Or The Gardener's Guide to a Perfect Lawn in 10 Minutes per Week. Or Rearing Perfect Children Effortlessly. Or Get and Keep the Job of your Dreams in One Easy Lesson. These things are all absurd and we know they are all absurd, but somehow we all keep thinking that weight-loss should be easy if we could but find the perfect diet that allows us to eat the all foods we love and never be hungry again.
When you wish upon a star...
If you have lost a significant amount of weight, give yourself a pat on the back because you have accomplished one of the most difficult feats imaginable. If you've lost weight and kept it off for at least five years, you deserve thunderous applause.
In the coming year MD and I will share our knowledge and experience with you to give you the tools you need to lose weight and improve your health as easily as possible, but don't think it's going to be a cake walk. It will take perseverance and effort on your part, but the rewards will be worthwhile.
And although MD and I will help, it's up to you to do the work. As I tell patients that I counsel with one on one: I'm like the Auto Club. When you go to the Auto Club for directions, the people there give you a detailed map showing explicitly how to get from point A to point B, but they don't get in the car and drive you.
You've got to drive this weight-loss car yourself.
Make this the year that you buckle yourself in and do it.
Posted by mreades at 10:36 PM | Comments (7)
January 01, 2006
Happy New Year
I would like to wish each of you a happy, prosperous, and healthy new year.
I've read (probably from some pop psychology source) that one is more likely to keep one's resolutions if said resolutions are declared publicly. Valid or not, I'm going to give it a try to see if it works better than my usual method, which is to think about the changes I would like to make and the various things I would like to accomplish, write them down on Jan. 1, then immediately forget about them. What's worse, despite writing them down, I can never seem to find them at year's end to see how well I did.
With the above in mind, I'm going to list my 2006 resolutions on this post so that maybe I'll be inspired to do a little better since you all will be watching. I'll do a revisit at the end of the year to see how well I did.
Here goes.
In 2006 I hereby resolve to:
1. Be more organized.
This is a perennial favorite of mine, which, sadly, always goes unfollowed. My wife is a neat freak; I'm a slob. We have adjacent work areas, and hers is neat as a pin. Mine is a disaster. She calls my method of organizing my stacks of scientific papers, books, and journals the GAP method (GAP stands for great amorphous pile; she calls my briefcase the GAP with handles) We're like the odd couple, except, unlike Oscar, I hate living in a disorganized mess. Maybe this is the year I'll do something about it.
2.Follow my own diet more closely.
This one is also a perennial favorite, but one that is pursued much more closely than the previous one. I pretty much stick to the program most of the time, but it seems as if I always give in to all the Christmas junk in between Christmas and Jan. 1, which is probably why it's always a resolution.
3.Become more digitally adept.
You will be able to see if I follow through on this one by how quickly (and if) I get this blog looking like a blog. I need to link to other blogs, put some color in to make it look more snappy, figure out how to add pictures, charts, photos, etc. I want to do all this, but I hate working my way up the learning curve to figure out how to do it.
4.Spend more time in my own kitchen.
If you've ever seen our TV it's pretty apparent that MD is the cook and I'm the color commentator. Over the past couple of months I've gotten a little more into the cooking end of things, but I need to make an effort to spend even more time.
5.Learn about a culture I know nothing about.
I'm going to make a study of the Etruscans. I love Etruscan art, but I know absolutely nothing about the Etruscans, so this year all that will change.
6.Work on my French and Spanish.
I can speak both (French better than Spanish) well enough to get by, but I'm far from fluent in either. Before I shuffle off to my reward I would love to become fluent in another language, and the best opportunity I have is with one of these two.
7.Read more.
Anyone who knows me will think this a bizarre resolution for me because I read voraciously. But for some reason my reading volume has fallen off the past couple of years, and I need to get it back up to snuff.
8.I want to try my hand at fiction this year. After authoring or co-authoring a dozen or so non-fiction books, I'm ready to try something a little different. Pray for me.
9.Get our website up and functional.
It's close. I hope to have it going within the next couple of weeks. I'll keep you posted.
I guess that's enough to keep me busy for the next year. Now that I've made these public maybe the idea that others are watching will keep my feet to the fire. I hope so.
Once again. Happy New Year to all!
Posted by mreades at 01:47 PM | Comments (4)