« August 2006 | Main | October 2006 »
September 30, 2006
The columnist who mistook his myth for a fact
John Tierney, in his column in today's New York Times, writes about the proposed ban on trans fats in restaurants in New York City. Tierney takes New York's health commissioner, Thomas Frieden, to task for his jihad against restaurants in the Big Apple cooking with trans fats and accuses him of wanting to turn the city into the Big Nanny. As he gets wound up in his argument against Frieden's actions, Tierney posits that forcing restaurants to stop using trans fats could actually cause harm in the long run.
How?
Horror of horrors, by causing restaurants to return to using saturated fats.
For all the rhetoric against trans fats, they're not worse for you than the old-fashioned saturated fats in lard and butter and various cooking oils. As Gina Kolata reported in The Times last year, the scientific consensus from the National Academy of Sciences, the Department of Health and Human Services, the National Heart Lung and Blood Institute, and the Food and Drug Administration is that trans fats are on a par with saturated fats.
Tierney falls into the trap of believing that saturated fats are harmful. He accepts what is at best a frail hypothesis as an absolute fact.
He correctly points out that
Food companies and restaurants voluntarily switched to trans fats to appease consumers and food activists worried about saturated fats. Now that those same activists have made trans fat the new bogeyman, restaurant chains and food companies are again looking to appeal to their customers with healthier alternatives...
But worries that
if New York arbitrarily imposed a deadline, the simplest way to comply would be to go back to using saturated fats. The food wouldn't be any healthier, but it would sound more virtuous after the grandstanding by Bloomberg and his health commissioner about their heroic reduction of trans fats.
Since Tierney, like so many others, has uncritically accepted the notion that saturated fats are dangerous. He believes that anyone truly bent on improving the health of the public shouldn't worry about trans fats, but should instead look to banning saturated fats because
saturated fats are a more logical problem to address than trans fats because we consume a lot more of them.
Although I believe trans fats are far from harmless, I agree with Tierney that the health commissioner is more than a little over reaching on this. Had it not been for the misguided efforts of other food police types, we wouldn't have the trans fat problem today. We would still be using saturated fat and our food would still taste just as good as it always has.
It's almost impossible to rush to action without all the facts in place without getting a real slap in the face from the law of unintended consequences, which is precisely what has happened with the trans fat debacle.
My concern comes from the realization that if a regular columnist for the New York Times uncritically accepts the notion that saturated fats are bad (instead of the unproven hypothesis that it is) and states it as fact, what hope is there that the great unwashed masses will ever see the light?
Posted by mreades at 11:53 AM | Comments (7)
September 29, 2006
Another job for the krill.
In addition to providing probably the most potent source of omega-3 fats (potent because of the phospholipid structure), krill provide another vital service to Mother Nature. According to an article in this weeks Science section of the New York Times, Krill agitate the various strata of the ocean, bringing rich, oxygen-laden water from below up to rejuvenate the oxygen-depleted surface layer.
The upper-most layer of the ocean receives the benefit of sunlight, and, consequently, is where reside the mass of plankton that, as plants, use the sun as their source of energy. This giant biomass of plankton consume the oxygen in this relatively thin upper layer and would ultimately die were there not a way to bring oxygen-rich water up from below.
Enter our friends the krill.
Krill consume plankton, from which they get their omega-3 fats. As the krill move up from below to feed on their plankton banquet, they bring with them oxygenated water.
As the scientist quoted in the Times article puts it
"It's not as if the water is boiling," Dr. Dower said. "It's not like you've put it in a blender." But because it occurs over a large area and the background level is so low, it's a large addition of turbulence. "It may represent a previously unrecognized way to get a pulse of nutrients into the surface layer."
"The novelty here," Dr. Dower added, "is this is biology acting on the physics of the ocean, instead of the other way around."
Please don't write and ask me if I'm worried that consuming krill oil will lead to significant reductions in the agitation of the oceans layers and the depletion of oxygen from the surface layer, the consequent death of the plankton and a major blow to life on earth as we know it, because I don't know. And at this time, given the size of the enormous mass of krill relative to the tiny amounts harvested for their oil, I'm not really worried about it.
Posted by mreades at 8:46 AM | Comments (2)
September 28, 2006
Funny cartoon on the tainted spinach debacle
Published in today's Sacramento Bee
Cartoon by Rex Babin
Posted by mreades at 9:04 AM | Comments (0)
September 27, 2006
More on E. coli O157:H7
Both the Wall Street Journal and the New York Times carried articles today on the recent problems with fresh spinach contaminated with E. coli O157: H7.
The New York Times article by devout low-fatter Marian Burros is full of good information, but completely misses the forest because of all of those trees in the way.
The article starts with a call for more regulation (just what we need) of the produce farming system. It makes a point that I was unaware of (and here I'm assuming the the NY Times fact checkers are accurate).
More outbreaks of disease are now traced to produce than to meat, poultry, fish, eggs and milk combined.
Based on this statement alone, the great unwashed masses might believe that spinich itself is the source of E. coli O157:H7, which is not the case. Since E. coli of all forms, including the virulent O157:H57 strain, are inhabitants of living mammal GI tracts and are not a part of normal plant fauna, it would seem strange that more disease involving E. coli would come from plants. The reason for this, of course, is that meat packing plants and other facilities handling animal products are maintained in a way to reduce the contamination of their products by E. coli. And most products of animal origin are cooked before eating, which kills E. coli. Plant foods, on the other hand, are often eaten raw.
The article goes on to speculate as to how the spinach contamination occured.
The source of the E. coli O157:H7 blamed in the current outbreak is unknown. It may be irrigation water reclaimed from sewage treatment. It may be unsanitary conditions on the farm. But there is increasing suspicion that the cause may be water runoff from the many cattle farms near the fields in the Salinas Valley of California, where produce tainted with the E. coli has caused eight outbreaks of illness since 1995.
Water contaminated with E. coli from cow manure may have been used for irrigation or may have been deposited on the fields by heavy spring rains and flooding.
Dr. Trevor Suslow, a microbiologist at the University of California at Davis, called this case "the catalyst, the tipping point.''
"This is a culmination of incidents that have been going on for 10 years and cattle have become the primary focus,'' Dr. Suslow said. "Data from the last 23 years clearly demonstrate the potential for crop contamination from pathogenic E. coli in the watershed."
So, everyone, it seems, is aware that cattle are the problem, but no one appears to understand that it is the corn feeding of cattle and the subsequent hyper-acidification of their GI tracts that allows this toxic strain to develop. Unless the cattle are corn fed, there isn't a problem.
One of the 'experts' quoted above posits a fairly stupid solution to the problem:
Dr. Suslow asked the question on many critics' minds: "Should cows be raised in close proximity to produce? Ideally you would like to see them well separated."
I say stupid because it's not the raising of cows that causes the problem; it's how they're fed out on corn before slaughter. If he had said that all feed lot operations should be separated from produce farm, I would agree.
If you look back at all the years of family farming in this country (and the world over) where the family cow grazed and was fed hay or other silage, you could probably count the number of cases of E. coli O157:H7 borne disease on the fingers of one foot. Since the focus seems to be cattle waste in general and not just that from corn-fed cattle, I can see a real problem brewing up for the cattle industry. If they were smart, the folks running PR for grass fed beef would be all over this situation.
Right now, though, the entities taking virtually all the fire are the spinach growers and packagers. Whenever any kind of widespread problem such as this recent outbreak of E. coli contaminated spinach occurs, the lawyers can't be far behind.
The Wall Street Journal in an article titled 'How a Tiny Law Firm Made Hay Out of Tainted Spinach' tells of lawyers going after the deep pockets of Dole Food Co. and other larger produce handling firms. What's amazing is how quickly these law firms can spring into action.
Before health officials warned the public about bad spinach, before grocers yanked fresh spinach off their shelves, before consumers cleaned out their refrigerators, the Seattle law firm Marler Clark had filed its first bad-spinach lawsuit.
Then, as word of the bacteria outbreak began to spread this month, lawyers at the firm posted messages on the firm's E. coli blog, www.ecoliblog.com. They reached out to reporters and waited for the calls and emails to stream in. Now Marler Clark is representing 76 clients. Bill Marler, a 49-year-old partner in the firm, tracks them with Post-it Notes on a U.S. map hanging in his office.
If you're considering filing suit because you've eaten tainted spinach, what kind of settlement can you expect?
Less-severe E. coli cases, with symptoms such as diarrhea, vomiting and dehydration, are usually worth between $25,000 and $500,000 when they are settled, Mr. Marler says. Those involving hemolytic uremic syndrome, or HUS, a potentially life-threatening disease that affects the kidneys and occurs in about 5% to 15% of E. coli patients, can run from $1 million to his highest HUS settlement of $15.6 million.
The problem is, as I see it, that these lawyers are going after the wrong people. As Bill Marler says when accused of being an ambulance chaser, look to the
industry reforms he says came about after he locked horns with companies. Jack in the Box Inc. raised its minimum burger-cooking temperatures to 155° from 140°; the company says the change was unrelated to the legal action. The Centers for Disease Control and Prevention requires hospitals to report HUS cases. Odwalla, another defendant in a Marler Clark suit, began pasteurizing its juices following a 1996 E. coli outbreak.
If Mr. Marler and others went after the real culprits here, the corn-fed cattle business, not just the innocent bystanders, the spinach growers and packagers, they could accomplish some real good.
There is an old legal theory that goes something like this. Let's say someone brings a lion in a cage into a community. He has the steel cage made with 2 inch diameter bars, and all the joints in the cage welded. He then has the whole affair wrapped with heavy chain, locked with multiple locks. Now let's say (we don't know how) that the lion escapes and mauls or maybe even kills someone in the community. Common law has it that the guy who brought the lion into the town in the first place is liable. Granted, he did everything possible to prevent the lion from escaping, but he still is the person who brought the lion and put people at risk.
In the case of the E. coli O157:H7 it would seem to me that the folks who corn feed the cattle are in the same position as the guy who brought the lion to town. The spinach growers and packagers would be more like the people who maybe welded the lion's cage together. They're sloppy job was complicate in allowing the lion to escape, but the real fault lies with the guy who exposed everyone to the lion in the first place.
You could take the whole thing a step further and ask who provides the information to those feeding cattle on corn. It's none other than the good folks at the U.S. Department of Agriculture. If you don't believe it, look in their manuals for cattle feeding. So, at it's foundation, it's our own government that has brought the lion to town.
Posted by mreades at 1:23 PM | Comments (5)
September 26, 2006
Framingham follies
Have you ever watched a movie that had a surprise ending, say, The Sixth Sense, for example, then watched it again? Once you know the ending, you see all kinds of things that make the ending obvious that you didn't see the first time through. When you have a movie (or a novelistic) experience like this, it makes you appreciate the talent of the creative people who make the movie (or write the novel). If these folks had just sprung the surprise ending on you without cleverly concealing all the clues, you would feel cheated.
It's kind of the same with scientific research. Researchers uncover scientific knowledge bit by painstaking bit--sometimes over years--until a piece of the scientific puzzle is clarified. Once this piece is known, you can roam back through the scientific literature and find all the papers that lead to its clarification. Just as you would feel cheated if you watched The Sixth Sense a second time and didn't see all the evidence of what was going on (which is really obvious once you know the ending) and were just slapped in the face with the surprise ending, you should find something amiss if practically the entire scientific establishment touts something as a fact and you can't go back and find the evidence that leads to this conclusion.
I've been making this quest back through scientific time to look for the clues that lead to the conclusion (the surprise ending) that diet causes cholesterol to go up and that diet causes heart disease. So far, I haven't found the clues. In fact, I've found clues that deny the conclusion.
Let's start early on with some of the first evidence that came before even Ancel Keys published his discredited Seven Countries Study that kicked off the whole low-fat debacle. Let's look at data from the venerable Framingham study that was so inconclusive that it wasn't even published in a peer-reviewed journal.
For those who don't know the Framingham Heart Study was kicked off back in the late 1940s in Framingham, MA. under the direction of the National Heart Institute (now known as the National Heart, Lung, and Blood Institute) According to their website
The objective of the Framingham Heart Study was to identify the common factors or characteristics that contribute to CVD by following its development over a long period of time in a large group of participants who had not yet developed overt symptoms of CVD or suffered a heart attack or stroke.
A large number of residents of Framingham were recruited into this longitudinal study that is still going on today. There are children (and probably grandchildren) of the original Framingham participants enrolled in the study currently. Researchers are monitoring diet, medication history, and a host of other parameters, and have generated God only knows how many papers using this data that has been collected over the past almost 60 years.
One of the first ideas that the researchers had was to look at how diet related to cholesterol levels and how diet related to the development of heart disease. I'll give you the surprise ending right up front: there wasn't any correlation. What's interesting about this part of the study, however, is that the researchers didn't publish it at the conclusion of the study, so it never really saw the light of day. You've probably heard the old saying that doctors bury their mistakes. Well, researchers often bury outcomes they don't expect and don't welcome.
In the case of this part of the Framingham study, ten years after the work was completed a statistician gathered the data and put it into typewritten form with a blue binding and disseminated it to the academic community under the name of the then director of the project Dr. Willam Kannel. As the statistician, Tavia Gordan, put it in the editorial note at the beginning
This report is based on a selection from a large body of tabular material prepared since the completion of data collection for the Framingham Diet Study. Unfortunately, these data were never incorporated into a definitive report by the original investigators and a large amount of very careful and thoughtful work has lain unused in the Framingham files. [my italics]
Once I learned of the existence of this report, I got hot on its trail.
I found the beaten up copy shown on the left through the Internet. It set me back a little over $80. When I got my hands on it, I was at first a little disappointed because I had expected a lot more information for my 80+ bucks than it looked like I was holding in my hands. Then I flipped through it and struck gold inside the back cover. Before we get to that, however, let's look at what this report shows.
The project was undertaken between the years 1957-1960 and involved a sample of around 1000 participants who were to be studied over the following 36 months to
test the hypothesis that "The regulation of the level of serum cholesterol and the development of coronary heart disease are related to
1. The caloric balance
2. Level of animal fat intake
3. Level of vegetable fat intake
4. Level of protein intake
5. Level of cholesterol intake..."
The dietary studies were performed using a couple of techniques described here and here (both are large PDF files). Basically, researchers interviewed the subjects multiple times over the study period using a fairly complex Food Frequency Questionnaire (FFQ). (From a previous post you should know that I'm not a big fan of FFQs, but in this case with the kind of attention to detail the interviewers used, the FFQ has some value.
What did they find?
In terms of caloric balance vis a vis serum cholesterol they discovered that
calories per day showed a slight negative association with serum cholesterol (over all age groups) in men but no association in women.
In other words the more calories the men consumed, the lower were their serum cholesterol levels. Obviously, this wasn't what the researchers expected to find.
This finding is somewhat puzzling and it is reasonable to inquire if this is related in some way to the level of physical activity.
Typical research thinking: if we don't get the data that is consistent with our hypothesis, we must have overlooked something. It seems that the idea that maybe the hypothesis is wrong never crosses their minds.
In this case, they were banking on the idea that perhaps those subjects who ate more may have been more physically active and thus have lower cholesterol levels than those who ate less but were sedentary. After fiddling around with the different levels of activity of the subjects, the data fesses up:
Men in the same physical activity class tend to have higher serum cholesterol levels at lower caloric intake. This finding is contrary to expectation. [I'll bet it was.]
In other words, even after correcting for differing levels of physical activity, the correlation remains the same: those subjects with lower caloric intake tended to have higher levels of cholesterol and vice versa.
What about fat intake?
Paralleling the findings for total calories there is a slight negative association between daily intake of total fat (and also of animal fat) with serum cholesterol level, in men but not in women. This parallel is not surprising given the high correlation between fat intake and total caloric intake. No association between percent of calories from fat and serum cholesterol level was shown; nor between ratio of plant fat to animal fat intake and serum cholesterol level.
How about protein?
There was a trivial negative correlation between daily protein intake (in grams) and serum cholesterol level.
Dietary cholesterol?
There is no indication of a relationship between dietary cholesterol and serum cholesterol level. If the intake on animal fat is held constant there is still no relation of cholesterol intake to serum cholesterol level. If (further) a multiple regression is calculated [using animal fat and dietary cholesterol] there is also little suggestion of an association between this pair of variables and serum cholesterol level.
The researchers weren't going to give up easily.
The failure to turn up any positive association between food intake and serum cholesterol level in the Framingham Diet Study led to the exploration of a large number of variant analyses. [In other words, maybe if we torture the data unmercifully, it will confess to anything. Alas, for them, this wasn't the case.] These were uniformly unsuccessful in finding expected relationships. Only a fraction of these explorations are included in this report.
When it comes to diet and coronary heart disease, nothing changes.
In undertaking the diet study at Framingham the primary interest was, of course, in the relation of diet to the development of coronary heart disease (CHD). It was felt, however, that any such relationship would be an indirect one, diet influencing serum cholesterol level and serum cholesterol level influencing the risk of CHD. However, no relationship could be discerned within the study cohort between food intake and serum cholesterol level.
In the period between the taking of the diet interviews and the end of the 16-year follow-up, 47 cases of de novo CHD developed in the Diet Study group. The means for all the diet variables measured were practically the same for these cases as for the original cohort at risk. There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group...
The study conclusions:
With one exception there was no discernible association between reported diet intake and serum cholesterol level in the Framingham Diet Study Group. The one exception was a weak negative association between caloric intake and serum cholesterol level in men. [As to] coronary heart disease--was it related prospectively to diet. No relationship was found.
So, I would say that the results of this study were pretty clear. These guys tried as hard as they could to show a correlation between diet and serum cholesterol and between diet and the incidence of coronary heart disease, but failed. The data conclusively demonstrated no such correlations.
Imagine my surprise when I discovered the yellowed news clipping shown below taped into the back of my $80 booklet. This clipping, from the Framingham newspaper dated October 30, 1970, is worth the $80 all by itself. Apparently, despite all the supporting evidence, Dr. Kannel, the director of the study and the guy listed as lead author, wasn't buying into all this nonsense about there being no correlation. He felt the need to 'clarify' the already crystal clear findings.
The clipping begins:
Although there is no discernible relationship between reported diet intake and serum cholesterol levels in the Framingham Diet Study group, "it is incorrect to interpret this finding to mean that diet has no connection with blood cholesterol," Dr. William B. Kannel, director of the Framingham Heart Study has stated.
Clarification, indeed.
Hmmm, I guess Dr. Kannel didn't enjoy the surprise ending of that movie, so decided to change it on the fly. I think the rest of this remarkable clipping is legible, so read it and laugh. It's a grand example of what I've written about before: scientists who present their conclusions one way in a scientific paper that other scientists will look at and call them on if they are incorrect and a totally different way to the press that reports to the population at large.
Note: I've already gotten a couple of comments from people who can't read the clipping. I'm traveling right now and don't have the original in hand. When I get back in a couple of days, I'll do something to make the entire thing legible, even if I have to type it out (God forbid) by hand.
Several people have written in with a method to view this file. Right click on the image, then transfer to somewhere accessible. Open and enlarge with whatever picture viewing software you have.
Posted by mreades at 4:36 PM | Comments (12)
September 21, 2006
Corn-eating-cow crap chuckin' up your insides blues
You are no doubt aware of the recent outbreak of food poisoning coming from fresh spinach. At least 100 people have become infected and at least one has died. The culprit in this infectious disease is a type of E. coli, a common bacteria found in our own GI tracts as well as in GI tracts throughout the animal kingdom. The particular bacteria causing this recent nasty outbreak is a strain called E. coli O157:H7.
Health officials nationwide are hot on the trail of this E. coli strain, trying to track down which spinach growers, shippers, and/or packagers are responsible for foisting this plague off on the rest of us. As an editorial in today's New York Times points out, however, they are totally on the wrong trail.
We all have our own strains of E. coli in our own GI tracts that we live with in peaceful co-existance. When we get a dose of someone else's E. coli, as long as they are a friendly strain, we do okay. When we get a dose of a foreign E. coli such as the strain found commonly in Mexico, for example, we often end up with a case of Montezuma's Revenge that makes us miserable for the first few days after we get home.
The acidity of our own stomachs can usually wipe out a dose of normal E. coli that we pick up eating food that has been handled with (I got this from a medical school microbiology lecture, and it has stuck with me since) the freshly fecaled fingers of food servers or fruit and vegetable pickers. (That's why your mother always told you to wash that apple before you ate it.) But the O157:H7 strain is a little different.
Your stomach juices are not strong enough to kill this acid-loving bacterium, which is why it's more likely than other members of the E. coli family to produce abdominal cramps, diarrhea, fever and, in rare cases, fatal kidney failure.
This particularly virulent strain of E. coli comes from the GI tracts of cattle that have been fattened with grain--particularly corn--instead of grass or other silage. Grains and corn are not the natural foods of cattle, and when cattle are fed nothing but in an effort to fatten them, they develop highly acidic GI tracts. The E. coli O157:H7 is a strain that has evolved to live in this highly acidic environment, and, consequently, is immune to the acid in our own stomachs that is typically potent enough to knock out the regular garden-variety E. coli we most often encounter.
Beef cattle are not the only carriers of the O157 strain.
In 2003, The Journal of Dairy Science noted that up to 80 percent of dairy cattle carry O157. (Fortunately, food safety measures prevent contaminated fecal matter from getting into most of our food most of the time.)
As anyone who has been around cows of any variety knows, they defecate prodigiously. In the case of beef cattle and dairy cattle that have been corn fed, these patties are teeming with O157:H7, which can contaminate all kinds of things it comes into contact with, including the groundwater. As long as cattle continue to be corn fed, we continue to produce massive amounts of this virultent strain that will continue to find its way into water and other foods. In the case of the spinach, who knows? It could have been irrigated with water infected with O157:H7 from run off from a nearby feedlot.
How do we know that the next time we buy celery or lettuce that we won't get a dose of O157:H7? We don't, and unless we do something about the source of the problem, we run this risk more and more.
According to the above mentioned Journal of Dairy Science there is a solution.
When cows were switched from a grain diet to hay for only five days, O157 declined 1,000-fold.
And as the Times points out
In a week, we could choke O157 from its favorite home -- even if beef cattle were switched to a forage diet just seven days before slaughter, it would greatly reduce cross-contamination by manure of, say, hamburger in meat-packing plants. Such a measure might have prevented the E. coli outbreak that plagued the Jack in the Box fast food chain in 1993.
Because of the growing demand for grass-fed beef, more and more ranchers are opting to let their cattle graze, but we are a long way from the demise of the feedlot. As consumers we can do our part by voting with our dollars. Buy grass-fed beef everychance you get. If enough people insist, it will be better for us, the cows and the environment. The only losers as far as I can see would be the E. coli O157:H7.
Here is a great website telling you everything you need to know about grass-fed beef, including where to find it in your neck of the woods. Take your dollars and get out there and vote.
Posted by mreades at 3:44 PM | Comments (11)
September 19, 2006
Protein Power verses Intermittent Fasting
Anyone who is a regular reader of this blog will have noticed that the last post on intermittent fasting generated an enormous number of comments, just about all of which I tried to answer. Most of these comments were questions about intermittent fasting or people giving their dietary histories or people informing us that they were starting an intermittent fast. Other comments asked for answers to specific medical questions while others wanted to know if MD and I had abandoned the low-carb diet in favor of intermittent fasting. I figured that this would be a good time to set the record straight.
MD and I feel strongly that we as a species have a genome that was molded by the forces of natural selection over the past few million years to operate optimally on the food that was at hand during those few million years. What was available? Mainly fairly high-protein, high-fat fare. There weren't a lot of carbohydrates readily available until the advent of agriculture a few thousand years ago. For the time that we developed our ancestors ate meat, fish, insects, clams, reptiles and pretty much anything live they could get their hands on. This primarily protein and fat diet was supplemented with whatever fruits, nuts, berries, roots, shoots and tubers were in season. Work done by Loren Cordain shows that, based on the Ethnographic Atlas, modern day hunter gatherers get about 65 percent of their calories from animals and the other 35 percent from plants. Most researchers believe that Paleolithic man got more than that from animals because during Paleolithic times many more large animals roamed the earth than do today. In fact, Paleolithic man hunted many of these large animals to extinction.
It is pretty safe to say that the macronutrients that set our genome were fat and protein. Many unenlightened people seem to believe that early man lived in land of carbohydrate abundance, and, consequently, thrived on a high-carbohydrate diet. It can easily be seen that this wasn't the case simply by calculating how much food would have to be consumed to get enough calories from the available plant sources.
Taking 3000 kcal as being the average (it's probably on the low side) daily energy intake of our Paleolithic ancestors and looking at how much plant food would be required to obtain those kcal is an eye-opening experience. I ran just a few foods through the USDA nutritional calculator and found that it would take 48 cups of blackberries--that's 3 gallons of blackberries--to provide 3000 kcal. I don't know how many readers have ever picked blackberries, but I have, and I can tell you that picking 3 gallons takes a lot of time. And, much though I love blackberries, I couldn't come anywhere near eating 3 gallons of them in a day. How about blueberries? 36 cups; over 2 gallons. Spinach? 103 cups. Celery? 111 stalks. Apples? 42.
It was only after the advent of agriculture that calorically dense carbohydrate foods came into existence and became the common fare for man. Until then, our ancestors, if they were to subsist on plant foods only, would have had a pretty rough time of it getting enough without eating all the time. Which is exactly what the mountain gorillas do. Although mountain gorillas have the same carnivore GI tract that we do, early in their evolution (probably lead by the gorilla version of Dean Ornish) they opted for vegetarianism. These animals eat constantly to get enough plant food to meet their energy needs. They take food to bed with them so it will be available when they first awaken. They roam through the jungle throughout the day eating non-stop except for brief rest periods.
Given the above facts, it's pretty clear that early man ate a fair amount of meat. After all, it takes only a couple of 16 ounce fatty steaks to provide 3000 kcal, which is a whole lot easier to down than 3 gallons of blackberries. It would then stand to reason that as a species we would perform better on a meat, or at the very least, a higher protein, lower carb diet since that's what we had to eat for a few million years. In one of my favorite quotes, Dr. Blake F. Donaldson, a crusty old physician from New York who wrote a book called Strong Medicine, says:
During the millions of years that our ancestors lived by hunting, every weakling who could not maintain perfect health on fresh fat meat and water was bred out.
When we saw patients in our clinic for obesity and the other so-called diseases of civilization, MD and I successfully treated them with diets that approximated what we--based on the anthropological evidence--believed early man ate. We basically gave them the food they were designed by nature to eat. Obviously we couldn't have them eating fresh mastodon steaks or cave bear fillets, so we had them eat the modern day equivalent (or as equivalent as it could get in the modern day) that could be found at the grocery store or in restaurants. We had to develop a diet that was palatable, not overly difficult to obtain and prepare, and that would allow them to live their regular lives and go about their business. After refining and tweaking, the diet we came up with is what we described in the book Protein Power. We diddled with it a little more and added a few supplements and made some more lifestyle recommendation such as getting more sunshine and getting rid of excess iron that went along with our Paleolithic origins and published the Protein Power LifePlan.
Since that time we've continued to think about the optimal diet and experiment with different permutations of the Paleolithic diet. We still believe that a low-carbohydrate, higher-protein, higher-diet is the optimal one for humans. In thinking about how to make a low-carb diet better, it dawned on us that there is another factor besides the actual food eaten in any particular diet: the timing of the eating. We began to think about how often Paleolithic man ate. We looked at data from modern day hunters and found that most of them didn't eat all that often, and that when they did eat, they gorged.
Once we decided that meal timing was probably important in the development of our genome just as was the kinds of foods consumed, we started looking for evidence in the medical literature. There we came upon the studies on intermittent fasting (IF).
I covered intermittent fasting at length in the previous post. I was amazed that whatever goes on during the fasting process is potent enough to overcome the health negating effects of ad lib feeding because the animals that were underwent the IF had the same health benefits as did those that were calorically restricted yet the IF animals ate the same as the (ultimately sickly) ad libitum fed animals. And the IF animals lived as long as the calorically restricted animals despite eating as much as the much less long-lived ad lib fed animals.
Clearly something powerful takes place during a fast. What is the mechanism? Who knows at this point. But it's something that should inspire a battalion of researchers to get busy looking into.
Now, based on the IF research data, MD and I are of the opinion that a Protein Power style diet interspersed with a little fasting is probably the optimal diet. We ourselves follow this diet. We eat one meal a day sometimes, a couple of meals others, and sometimes three squares. If we're not hungry we don't eat. We try to fight off the culturally induced feelings of, Oh, it's lunchtime, so I must we must be hungry: let's eat.
We tried the IF as written up in the post because we wanted to see if there was a particular regimen we could give people wanting to try it out. We know from many years of taking care of people on diets, that dieters want rules. The more we would write our material in such a way as to give patients (and readers) a lot of lee way in how they could prepare their low-carb diets, the more calls we got from these patients asking for us just to give them a set of meal plans. We found that the IF was easiest for us with a 6 PM cutoff; that's why I described it that way.
There is probably no magic in the 24 hours; who knows, maybe it's 15 hours. It just isn't known at this point. I'm firmly convinced, however, that there is an advantage to going without food for periods here and there. I'm convinced for a couple of reasons. First, all the data on IF is pretty persuasive. Second, all the Ornishes, Barnards, Grundys and the other AOE (Architects of the Obesity Epidemic) recommend that we all eat a lot of small meals throughout the day. Given the track records of these people alone, it militates that we should eat large meals separated by long periods of time.
We still fully believe in Protein Power. We haven't abandoned it in favor of IF. We have added IF to our own lives from time to time, especially if we go off the Protein Power wagon. But, we also IF using strict Protein Power, too, In short, IF is just an adjunct to the Protein Power diet that makes it work better by making it even more like the Paleolithic diet we cut our collective teeth on.
Once again I have to reiterate that I can't answer specific medical questions over the Internet. Unless you're my patient (and by that I mean someone who I have examined) I can't tell you why you're having this reaction or that. If your ankles are swelling, I don't know why unless I can take a medical history and examine you. If you're exhausted on the IF or any other regimen, it could be that you need a little potassium, or it could be something else. Whatever it is, I can't give you an answer unless I take a medical history and do an exam.
One final note:
One of the commenters on the IF post is Robb Wolf who has worked with Loren Cordain and is himself well read on the literature of IF. He sent me an interview with Dr. Thomas Seyfried on ketosis and cancer that he said I could share with my readers. (click Download file to download the PDF) In the interview Dr, Seyfried discussed IF and some of its therapeutic uses. (You can also click here to read Dr. Seyfried's paper on ketosis and brain cancer published this year in Nutrition & Metabolism)
Robb is the Editor-in-chief of the publication Performance Menu: Journal of Nutrition and Athletic Excellence, which contains articles on IF. (Click here to take a look)
Posted by mreades at 10:45 PM | Comments (24)
September 13, 2006
Fast way to better health
How would you like it if I told you there was a way to eat pretty much anything and everything you wanted to eat and still maintain your health? Or better yet, what if I told you that you could eat pretty much anything and everything you wanted and even improve your health? Would you be interested? I figured as much.
There is a way to reduce blood sugar, improve insulin sensitivity, reduce blood pressure, increase HDL levels, get rid of diabetes, live a lot longer, and still be able to lose a little weight. All without giving up the foods you love. And without having to eat those foods in tiny amounts. Sounds like a late-night infomercial gimmick, but it isn't.
Before I get to the real nitty gritty of how such a thing can be done, let's look at a method that has been proven in countless research institutions to bring about all the above-mentioned good things. It's called caloric restriction.
When researchers restrict the caloric intake of a group of lab animals to about 30 to 40 percent of that of their ad libitum (all they want to eat) fed counterparts, they find that the calorically restricted animals live 30 percent or so longer, don't develop cancers, diabetes, heart disease, or obesity. These calorically restricted (CR) animals have low blood sugar levels, low insulin levels, good insulin sensitivity, low blood pressure and are, in general, much healthier than the ad lib fed animals.
Most of the work in caloric restriction has been done on rodents, but there is a long term study on Rhesus monkeys (17 years at this point) that appears to confirm the rodent data on longevity and health with CR in primates. There are no human longevity studies, but there are a number of human studies on CR and health that show that human subjects under CR conditions reduce blood sugar, improve insulin sensitivity, reduce blood pressure, etc., so it stands to reason that if humans reduced their caloric intake by 30-40 percent for their entire lives, they would also live longer.
Caloric restriction is a terrific way to lose weight and get healthy; problem is, it's not much fun. When rats live out their little ratty lives calorically restricted in their cages they seem to show signs of depression and irritability. Primates do for sure. If primates don't get enough cholesterol, they can actually become violent. But, if you're willing to put up with a little irritability, hostility and depression, it might be worth cutting your calories by 30 percent for the rest of your long, healthy miserable life.
Doesn't sound so cheery? You're not ready to sign up yet?
Well, there is a better way.
A number of different research teams have studied a method by which rodents can get all the health and longevity benefits of caloric restriction without calorically restricting. And the method has been studied in humans and seems to achieve the same health benefits and, if an old Spanish study can be believed, maybe even an increase in lifespan.
What is this magic method?
Intermittent fasting.
In regular fasting one goes entirely without food, which is caloric restriction carried to the extreme. Going entirely without food in the short term leads to improvement in health, but also leads to an extremely short life unless the fast is aborted.
Intermittent fasting (IF) is just as its name implies: a period of fasting alternated with a period of eating.
But isn't that what we do anyway? We eat breakfast, then fast until lunch. Then, after lunch, we fast until supper. Then we fast all night. Uh, not exactly.
In research settings animals that are intermittently fasted are fed every other day, so they eat whatever they want for a day, then they are denied food for a day. Interestingly, on feeding days most of the animals eat a almost double the amount that their ad lib fed mates do. Thus the IF animals eat about the same number of calories overall that the ad lib fed animals eat, but, and this is a huge 'but,' the IF animals enjoy all the health advantages that the CR animals do, and, in fact, are even healthier than the CR animals.
Like caloric restriction, intermittent fasting reduces oxidative stress, makes the animals more resistant to acute stress in general, reduces blood pressure, reduces blood sugar, improves insulin sensitivity, reduces the incidence of cancer, diabetes, and heart disease, and improves cognitive ability. But IF does even more. Animals that are intermittently fasted greatly increase the amount of brain-derived neurotrophic factor (BDNF) relative to CR animals. CR animals don't produce much more BDNF than do ad libitum fed animals.
What's BDNF? (The Wikipedia definition is actually pretty good)
BDNF, as its name implies, is a substance that increases the growth of new nerve cells in the brain, but it does much more than that. BDNF is neuroprotective against stress and toxic insults to the brain and is somehow--no one yet knows how, exactly--involved in the insulin sensitivity/glucose regulating mechanism. Infusing BDNF into animals increases their insulin sensitivity and makes them lose weight. Humans with greater levels of BDNF have lower levels of depression. BDNF given to depressed humans reduces their depression. And Increased levels of BDNF improves cognitive ability. In short, you want as much BDNF as you can get., and with IF you can get a lot.
But, who wants to go all day every other day without food?
Well, you don't have to. MD and I, using ourselves (selflessly, I might add) as subjects have worked it out.
Most rodents feed throughout the day and night, so restricting them for 24 hours does just that: it restricts them for 24 hours. In humans, however, the situation is different. We humans, for the most part, eat only during our waking hours. So if we fast for a day, we end up fasting for about 34 hours and eating for 14, which isn't the same as 24 on, 24 off.
Let me show you what I mean.
Let's say you pick a day to start. You eat all day, then go to bed, wake up in the morning and fast all day, then go to bed. You wake up the next morning and eat all day, then go to bed and start again. So, assuming you eat until 10 PM on your eat day, once you quit eating you don't eat again until 8 AM 34 hours later. If you eat from 8 AM that day until 10 PM, you've eaten for 14 hours. so, you're on (eating) for 14 hours and off (fasting) for 34. MD and I spent a couple of weeks doing it that way, and I'm here to tell you, it's no fun. At least not on the fast days. The eating days were a different story; they were great, but we would spend the entire day dreading the fast day coming up.
We fooled around with a number of different eat-fast-eat regimens and came up with something that works pretty well. We set up our cutoff time as 6 PM. On the day we started, we ate until 6 PM, then fasted until 6 PM the next day. On the next day we ate supper right after 6 PM and ate breakfast and lunch (and a few snacks) the next day until 6 PM when we started fasting again.
The advantage of this regimen is that we were able to eat every day. One day we would get supper--the next day we would get breakfast and lunch. On no days would we go entirely without food. This schedule worked the best for us.
On the times during the day that we ate, we didn't stick with our normal low-carb fare; we ate pretty much whatever we wanted, including a fare amount of higher carb stuff. We stuck with the regimen for a few weeks just to see if we could tolerated it, which we did just fine. We ultimately drifted back to our normal low-carb diet, however, just because it seemed to work better with our schedules. We could have been happy on the intermittent fasting regimen for the long term.
I would think that the optimal way to go would be to follow an intermittent fast using low-carb foods during the eating periods. One would get the best of all worlds healthwise this way.
Over the period that we followed the various IF regimens we lost a little weight because, unlike the rodents, we couldn't eat twice as much during the eating days as we would have eaten were we not fasting. We didn't check any lab work to see if any values had changed. We weren't doing a hard core study; we were simply evaluating IF as a practical means for humans to use to improve their health.
In thinking about the process I came to the conclusion that IF was probably the way Paleolithic man ate. We modern humans have become acculturated to the three square meals per day regimen. Animals in the wild, particularly carnivorous animals, don't eat thrice per day; they eat when they make a kill. I would imagine that Paleolithic man did the same. If I had to make an intelligent guess, I would say that Paleolithic man probably ate once per day or maybe even twice every three days. In data gathered from humans still living in non-Westernized cultures in the last century, it appears that they would gorge after a kill and sleep and lay around doing not much of anything for the next day or so. When these folks got hungry, they went out and hunted and started the cycle again.
If you buy into the idea that the Paleolithic diet is the optimal diet for us today because it is the diet we were molded by the forces of natural selection to perform best on, then you should probably also buy into the idea that a meal timing schedule more like that of Paleolithic mean would provide benefit as well.
One of the things MD and I took away from our IF experience is the idea that we don't have to eat three meals per day. We now often skip lunch and don't seem any the worse for it. Sometimes we get up and get going with all our projects and don't eat breakfast. We try to skip a meal here and there because figure it's probably good for us. When you get used to it, you don't really even think about it. And it's good for you. Don't take my word for it--look at the medical literature.
There have been a few human studies on IF, and all have shown a marked improvement in virtually every parameter tested. None of the subjects in any of these studies has done the full 24 on-24 off that MD and I did. Most fasted until 5 or 6 PM on the fast days, then ate, then ate regularly on the eat days. Even with this wimpy IF schedule the subjects did better.
One of the recent papers published on the less rigid IF schedules caught my eye because one of the authors was Don Laub, who used to be the chairman of the plastic surgery department at Stanford. When I was in medical school I thought I wanted to be a plastic surgeon so I went to Stanford during a part of my senior year and worked with Dr. Laub as my mentor.
In this study, published in the journal Medical Hypothesis in March of this year, Dr. Laub along with two other physicians (neither of whom I know) underwent their version of and intermittent fast. The three of them have since May 2003 been on a version of the IF in which they consume about 20-50 percent of their estimated daily energy requirements on the fast day and eat whatever they want on the non-fast days.
Since starting their regimen they have
observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette's, Meniere's) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes.
In their paper these researchers discuss a 1957 paper from the Spanish medical literature.
...the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH.
There is much more to the IF story that I will continue in another post. I would do it in this one, but I (actually my web guy) upgraded my blogging software and somehow the little buttons that let me link to other sites are AWOL. I can't italicize or set off quotes or do any of the things I normally do in the course of posting. I'm hoping that I will get this straightened out soon. When I do, I'll go into the subject in a little more detail and show a chart that demonstrates the difference between CR and IF. (Note: the problem is solved; all links are working.)
In the meantime, if any of the readers of this blog would like to undertake an intermittent fast, I would love to hear the results of the experience. Please send a comment.
Posted by mreades at 2:08 PM | Comments (123)
September 7, 2006
Jane Brody: Mistress of unshakable stupidity
In going through the Science section of the New York Times I came upon the Personal Health article by Jane Brody on the next to last page. When writing on most medical subjects Ms. Brody is typically fairly reasonable and usually covers most of the pros and cons of whatever medical procedure or subject she's writing about. Unless, of course, that subject is nutrition. When Ms. Brody writes on nutrition, especially if the subject involves fats, she becomes a foaming-at-the-mouth imbecile.
This week's article is a case in point. Ms. Brody decided to tackle the issue of the health dangers of trans fatty acids in the diet, but instead of sticking to the case in point--trans fats--she decided to mount a jihad against saturated fat in the process.
She starts out mildly enough:
The culinary battle between butter and margarine has raged for decades, but, it turns out, for the wrong reason. We now know that the partly hydrogenated fatty acids in margarine and many processed foods are harmful to health -- more harmful, in fact, than the saturated fat in butter. [my italics]
The clause I italicized implies that saturated fats are harmful, which hasn't really been shown in the scientific literature.
She goes on to report that
Gram for gram, trans fats, as they are commonly called, are more hazardous to the heart than the saturated fats that damage arteries. Like saturated fats, they raise the "bad," or L.D.L., cholesterol that can become glued to arteries; but unlike saturated fats, they also lower the "good" H.D.L. cholesterol that clears away these harmful deposits.
More of the same. She's saying that trans fats are more dangerous than saturated fats in oh so many ways, which, of course, implies that saturated fats are dangerous as well. She, strangely, for her, gives saturated fats a left-handed compliment by implying, at least, that they do raise HDL. Of course, she doesn't say this directly--our Jane would never do such a thing.
She charges on with her anti-saturated fat zealotry
Butter is not a heart-healthy choice because its saturated fat far outweighs the trans fat in traditional stick margarines.
And finally in describing the substitutions available for trans fats she takes a swipe at saturated fats of non-animal origin:
The bad news is that some substitutions -- to tropical oils like palm, palm kernel and coconut -- are reintroducing more heart-damaging saturated fats [my italics] to American diets and causing environmental devastation in several countries where palm and coconut trees grow.
Two statements that have no substantiation. To paraphrase Tom Cruise's client in the movie Jerry McGuire, SHOW ME THE PAPERS! If Jane Brody (or anyone else) can show me well done medical studies showing that saturated fat causes heart disease, I'll eat my words and quit eating and promoting saturated fat. But they can't do it. You would think with as many people--both medical and non-medical--spouting the anti-saturated fat line out there as there are, that the scientific literature would be crawling with studies demonstrating how saturated fat causes heart disease. But the scientific literature isn't crawling with such papers. In fact, there really aren't any. If you think there are, well, SHOW ME THE PAPERS.
I'll admit that there are a lot of scientific papers out there that mention saturated fat as a risk factor in the same way that Jane Brody does in her article. The authors of these papers assume that everyone 'knows' that saturated fats have been proven beyond a shadow of a doubt to be a major cause of heart disease. Whereas such non-scientific dolts as Jane Brody describe saturated fats as being 'artery clogging' (in fact, most of them think of the term saturated fats as being incomplete unless written as artery-clogging saturated fats), the scientific dolts talk of the 'putative risk for heart disease' concerns about saturated fats. Most authors of medical literature have so been taken in by the anti-saturated fat bias that they don't even bother referencing another article when making such pronouncements, and if they do reference another article, it's always an article that itself doesn't really make the case against saturated fats but instead parrots the idea that these fats are bad without showing data as to why.
After her anti-saturated fat diatribe in the early parts of her article Ms. Brody goes on to write a pretty decent piece on the trans fats, discussing the health problems they cause, their sources, and how to avoid them by asking the right questions and reading labels. I have a different take than she does on the amount of trans fats eaten by the average person, but that's a small quibble.
After multiple paragraphs of fairly sane writing, she returns to her anti-saturated fat ways as she winds her article down.
To protect heart health, you would be wise, as well, to avoid foods made with tropical oils (palm, palm kernel and coconut), which contain saturated fatty acids.
And she finishes off with a bizarre ending. Her penultimate paragraph ends with
Soft and liquid margarines have little or no trans fats. And American producers are working hard to develop alternative methods of producing shelf-stable vegetable oils, which should be on the shelf in the next year or so.
Earth to Jane, Earth to Jane. How do you think we got trans fats in the first place? American producers working hard to find a substitute for saturated fats came up with trans fats. Which, of course, Jane Brody now savages. How do you know, Ms. Brody, that what the American producers come up with to replace trans fats won't be worse?
How about just returning to the perfectly acceptable saturated fats that humans have consumed for millennia?
I can imagine her whiny response: But those fats are artery clogging.
SHOW ME THE PAPERS!
Posted by mreades at 4:47 PM | Comments (18)
September 5, 2006
A tax on soft drinks?
There is a giant conference taking place in Sydney, Australia right now where all the usual mainstream nutritional suspects are conferring, confabbing, and otherwise hobnobbing about the worldwide obesity epidemic. Any time this many self-important academic nabobs get together in an effort to solve important problems, you can bet that at least one, if not a dozen, moronic recommendations will be in the offing. The Sydney conference did not disappoint. (Click here and here and here for news reports.)
One of the presenters, Barry Popkin, from the University of North Carolina has made the recommendation that countries facing an obesity crisis should add a tax to sugary soft drinks to make them much more expensive. Much more expensive soft drinks would shift consumption to less sugary products. As Dr. Popkin put it
If you doubled the price ... of a regular Coke, people would drink Diet Coke or water, or milk or juice or something.
Ignoring the fact that Dr. Popkin has himself castigated fruit juices as being no better than soft drinks in terms of sugar content, will taxing soft drinks mean people will consume less sugar?
It sounds reasonable, at least from an economic perspective, but will it really work? If it would reduce consumption of high-fructose corn syrup, I would be all for it, but I fear that it really isn't that simple.
I think Dr. Popkin has run afoul of the philosopher George Santayana's famous saying:
Those who cannot remember the past are condemned to repeat it.
Or, in Dr. Popkin's case, those who never knew the past are condemned to figure it out the next time around.
I posted a few weeks ago on some old nutritional research I had come across published in 1970 by researchers at the University of London. Said little book, which set me back about $30, is a report on the dietary studies of Dr. Edward Smith done in the early 1860s in various areas of England. These studies were the first comprehensive nutritional surveys ever done and are extremely revealing. At some point I plan to post on the entire survey, but today I want to look at the portion that is germane to a discussion of a soft drink tax.
One of the many groups of people surveyed were cotton workers, who, of all the so-called indoor workers (Dr. Smith compared the diets of indoor workers to those of outdoor workers, and compared the diets of the various indoor workers), made the most money and had the highest standard of living.
When he first surveyed the various groups in 1861 the diets of the cotton workers reflected their higher levels of income. Their diets contained more calories and pretty much more of all the components surveyed. A depression swept through the area where all the cotton workers were employed in 1862, cutting their incomes by about half. The depression didn't affect the other indoor workers nearly as much as it did the higher paid cotton workers.
You can see from the chart above the impact the depression of 1862 had on the diets of the cotton workers. The first column is the diet that the cotton workers consumed in 1861 while they were earning a substantial income. The second column shows the change in diet as a consequence of reduced earnings during the depression of 1862. The third column shows the diet of other indoor workers in 1863 while the depression was still present. (I haven't shown the other charts in the book showing that the diet of the other indoor workers prior to the depression was virtually the same as that shown in the third column.)
What does all this tell us that is relevant to the idea of a soft drink tax?
If you'll look at the chart and compare the first column with the second, you will notice a substantial decrease in the amounts consumed in almost every category except for sugar (there is not much decrease in milk, but there wasn't much to start with). Relative to every other category, sugar consumption decreased less with falling income. All the categories fell to the point that they were similar to that of the other lesser-paid indoor workers. Except for sugar and meat. What this tells us is that once people started making more money and developed the taste for sugar (which was relatively expensive back then) they didn't want to let it go. When times got hard, they continued to spend on sugar and got rid of the meat, bread and potatoes.
As the authors of this report put it
Whilst the previously higher levels of bread and potatoes of the cotton workers fell to about the same levels as those of other indoor workers, sugar remained appreciable higher, and the meat and fats became much lower. The effect of these and other changes was to reduce the amount of calories and nutrients in the diet to a level that was now quite close to the average of the indoor workers. The sugar consumed during the depression consisted in a significantly higher proportion of treacle than that consumed before the depression--about 40 percent of the total compared with less than 25 percent. It was mostly spread on bread, so it was used as a substitute for butter rather than for solid sugar in drinks and cooking.
In nutritional terms, it would have been better if some of the money spent on sugar had been diverted to buy bread and potatoes, since this would have given them very many more calories for the same money, as well as providing some protein, vitamins and minerals, which sugar lacks entirely. In fact, however, we find that a taste for the sweetness of sugar tends to become fixed. The choice to eat almost as much sugar as they used to do, whilst substantially reducing the amount of meat, reinforces our belief that people develop a liking for sugar that becomes difficult to resist or overcome.
Indeed.
So, based on the experiences of the cotton workers, I suspect the same thing would happen were we to levy a huge tax on sugary drinks. The sugar junkies of today would simply continue to feed their habits at the expense of more nutritious foods as did the sugar junkies in 1862.
I suspect that the outcome of this tax, were it ever to be initiated, would be another example of the law of unintended consequences at work.
In my opinion, a much better way to attack the problem is with education.
Posted by mreades at 11:06 PM | Comments (8)
September 1, 2006
Antibiotics and medical economics
In going through my daily readings this morning I came upon a couple of articles that show how medicine and economics sometimes combine to produce a less than optimal outcome. The first article was in Healthday entitled Steer Clear of Antibiotics for Colds; the second from WebMD entitled Drug-Resistant Staph May Get Nastier.
The first article is basically a reminder that colds (and flus, for that matter) are viral infections that don't respond to antibiotic treatment. The second discusses a dangerous type of drug-resistant staphylococcal infection that is spreading in epidemic proportions. What do these two articles have in common?
The real take-home message from both is that antibiotics are over prescribed and that the more antibiotics are prescribed unnecessarily (and necessarily, too) the greater the likelihood that resistant strains of bacteria will select out and emerge in numbers that threaten us all. We're in an escalating race already, with new antibiotics being developed all the time to counteract the bacteria that have become resistant to the old antibiotics. Soon, the bacteria will become resistant to the new antibiotic and the cycle repeats. In the old days, penicillin treated almost everything; now it treats almost nothing.
How does this cycle intersect with medical economics?
Simple.
A medical practice is a business just like any other. And for any business to remain successful (unless it's the only game in town) that business has to keep its customers happy.
Despite the white coats, the stethoscopes, otoscopes, scalpels, and all the other medical equipment they ply (not to mention the God like attitude), doctors are in business to make money. They have house payments, car payments, kids that need braces, money for vacations, vet bills, and all the other expenses that non-doctors have. Crass though it sounds, they are all concerned about the bottom lines of their practices. Since patients are the lifeblood of a medical practice, no doctor wants to lose patients. The best way not to lose patients is to keep them happy, which doctors do by treating them successfully. Conversely, the way doctors lose patients is by not making them well.
When a patient comes into a doctor's office with a bad cold, the doctor has a couple of options. He (I'm going to use 'he' because, well, because I'm a he and I could easily be talking about myself here. I hate the cumbersome construction of he or she. I live with an extremely competent 'she' physician to whom I daily turn for all kinds of medical advice, so I can be exempted from accusations of sexism.) can counsel the patient on the fact that the infection is viral and that rest, fluids, Tylenol, etc. are the treatments of choice. Or he could say something along the lines of, 'Well, looks like you've got a little infection going on. It's probably just a cold, but I'm going to put you on an antibiotic just in case.'
The first scenario I described is the correct way to treat the patient, but often ends up costing the doctor the patient. As a result, the second script is the one most often followed because it keeps the patient happy. Let me explain.
Going to the doctor costs money. No one likes to spend money and get nothing in return. If, during a heat wave, you've called the air conditioner guy to look at your air conditioner that isn't working well and he comes out, checks it with all his paraphernalia, then tells you, "Yeah, it's working fine, it just can't keep up with this heat. That'll be $75 please. You feel ripped off. You don't want to be told it's working okay; you want it to cool your bloody house. It's the same with doctors. People pay money to doctors to get them well, not to be told to rest and increase their fluids--even though that is the proper treatment for a cold.
When MD and I ran a huge primary care medical practice in Arkansas, the number one complaint about some of the doctors who worked with us was: he (or she) didn't do anything. From the patient's perspective, he (or she) came into the clinic to purchase wellness--instead, these people got told to go home, rest, drink a lot of fluid, and take Tylenol, which they had probably been doing in the first place.
These dissatisfied patients would often go to another doctor a day or two later who would give them a prescription for an antibiotic.. The patient would take the antibiotic and get well almost immediately. And never go back to the first doctor. It doesn't take many of these experiences to ensure that doctors hand out antibiotic prescriptions right and left, even though they know they don't do any good.
Why did the patients get well when they started taking the antibiotics if antibiotics don't work for colds? Because these patients were almost over their colds when they started taking the antibiotics. Their own immune systems had defeated the viral infection just about the same time they started taking the drug. (Usually a cold or other viral upper respiratory infection runs its course in 5 to 10 days. Most people wait a few days before going to the doctor in the first place. If the doctor tells them to rest and drink fluids, it takes them a couple of more days to get an appointment with someone else. So, by the time the second doctor visit comes around, the virus is almost beaten down.) One of the hallmarks of a viral infection is that when the immune system finally knocks it out, recovery is almost immediate. So, if someone starts taking a drug right before this immediate improvement takes place, it's difficult to convince that person that the drug didn't really do it.
Sometimes a viral infection beats down the immune system a little, allowing an actual bacterial infection to set up shop. At that point, antibiotics are required to knock out the infection. Many doctors, myself included, use that excuse to give antibiotics on the first appointment.
The absolute best way to treat a cold or other viral upper respiratory infection is to rest, drink fluids, take Tylenol for the discomfort. If the problem doesn't get better in a few days, see a physician. If the doc tells you it's just a virus, go home and continue you rest and fluid regimen. If you're not better in a few days, or if you start coughing up yellowish sputum or blowing nasty yellowish, green snot out of your nose, it's likely that you may have developed a bacterial infection. Go back to your same doc or call the office. You'll probably get a prescription for an antibiotic then.
Help your doctor practice good medicine and prevent the spread of drug-resistant bacteria.
Posted by mreades at 2:02 PM | Comments (9)