Darwin and the USDA Dietary Guidelines: Nutrient Dense or Just Dense.

Posted: March 24, 2011 in The Nutrition Story, USDA Dietary Guidelines
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Charles Darwin, in his autobiography described

“the oddest case which I have known. A gentleman (who, as I afterwards heard, is a good local botanist) wrote to me from the Eastern counties that the seed or beans of the common field-bean had this year everywhere grown on the wrong side of the pod. I wrote back, asking for further information, as I did not understand what was meant; but I did not receive any answer for a very long time. I then saw in two newspapers, one published in Kent and the other in Yorkshire, paragraphs stating that it was a most remarkable fact that ‘the beans this year had all grown on the wrong side.’ So I thought there must be some foundation for so general a statement.”

I had read this passage a while ago but it suddenly popped up in my mind on reading the new USDA Dietary Guidelines. The Guidlines have a strong recommendation to choose “nutrient dense” food.  Since all the food you ingest contains some kind of macronutrient or micronutrient  and having a food dense in one or another would depend on how much you thought was good I could not really understood what was meant.  I pretty much forgot about it until I saw in a video from a TV broadcast making the same recommendation suggesting that it was intelligible to the general population. I still couldn’t understand what could be meant. The guidelines say, on page 3, “Energy-dense forms of foods, especially foods high in SoFAS, should be replaced with nutrient-dense forms of vegetables…” SoFAs stands for “solid fats and added sugars.” It would be hard to find two more nutrient dense but different substances. So at least nutrient dense is not calorie dense but it is not obvious what it is.  Note added in 2013:when I first posted this, I genuinely did not know that nutrient-dense now means micronutrient-dense but I think the critique of the USDA still stands and for a description of currency of an idea that has no real meaning at all, Darwin’s story is still the best. (And, of course, vitamin deficiencies may be the least of our nutritional problems).

Darwin described how he

“went to my gardener, an old Kentish man, and asked him whether he had heard anything about it, and he answered, ‘Oh, no, sir, it must be a mistake, for the beans grow on the wrong side only on leap-year, and this is not leap-year.’ I then asked him how they grew in common years and how on leap-years, but soon found that he knew absolutely nothing of how they grew at any time, but he stuck to his belief. After a time I heard from my first informant, who, with many apologies, said that he should not have written to me had he not heard the statement from several intelligent farmers; but that he had since spoken again to every one of them, and not one knew in the least what he had himself meant. So that here a belief–if indeed a statement with no definite idea attached to it can be called a belief–had spread over almost the whole of England without any vestige of evidence.”

(In case you think that there is any botanical meaning at all: it is not just the leap-year. It is that there is no right or wrong side of the pod at all).  Is it possible that the USDA guidelines, put together by the famous 13 experts have made a recommendation that was completely devoid of meaning?  Page 11 says that “A nutrient-dense total diet has multiple health benefits and can be implemented in various ways” but what is nutrient-dense?  Although never defined, examples are given on pages 19-20.

• Vegetables, fruits, high-fiber whole grains

• Fat-free or low-fat fluid milk and milk products

• Seafood, lean meat and poultry, eggs, soy products, nuts, seeds, and oils

• Very low in solid fats and added sugars (SoFAS)

• Reduced in sodium

The remarkable thing is that in five out of six, the nutrient density is attained by absence of nutrients: fat-free, low-fat, lean, very-low SoFAS, reduced sodium — and is there anything less dense than skim-milk?  Paraphrasing Darwin, then, here is a dietary recommendation –if indeed a statement with no definite idea attached to it can be called a recommendation — will be spread over almost the whole of the country without any vestige of evidence.

From A Future History of Diabetes:

Posted: January 5, 2011 in American Diabetes Association, Evidence Based Medicine, The Nutrition Story
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I don’t believe in time travel, of course, so when somebody sent me the following article that was supposed to be a chapter from a Study of the History of Diabetes published in 2018, I didn’t think about it much.  Then I read an article about a woman who had been charged with neglect in the death of her son from complications due to diabetes.  It seems she “was trying to live by faith and felt like God would heal him.”

For some reason, that made me think of the Future History, so here is a chapter from the History.

Chapter IV.  ACCORD to The Court

We have seen how, early in the history of medicine, diabetes was recognized as a disease of carbohydrate intolerance and how, until the discovery of insulin, removing carbohydrate from the diet became the major treatment (Chapters I and II).  We chronicled the shift away from this medical practice under the influence of low fat recommendations and the ascendancy of pharmacology that followed the discovery of insulin.  Nonetheless, it persisted in the popular mind that you don’t give candy to people with diabetes, even as health agencies seemed to encourage sucrose (sugar) consumption.

The rather sudden reappearance of carbohydrate restriction, the so-called modern era in diabetes treatment, is usually dated to 2008, the precipitating event, publication of the ACCORD study in which a group undergoing  “intensive treatment” to lower blood glucose showed unexpected deaths [1].  ACCORD concluded that “These findings identify a previously unrecognized harm of intensive glucose lowering in high-risk patients with type 2 diabetes.” The intensive treatment turned out to be intensive pharmacologic therapy and this flawed logic lead to a popular uprising of sorts, a growing number of patients claiming that they had been hurt by intensive drug treatment and typically that they had only been able to get control of their diabetes by adherence to low carbohydrate diets. Blogs compared the ACCORD conclusion to an idea that alleviating headaches with intensive aspirin led to bleeding and we should therefore not treat headaches.

The conflict culminated in the large judgment for the plaintiff in Banting v. American Diabetes Association (ADA) in 2017, affirmed by the Supreme Court in 2018.  Dalton Banting, coincidentally a distant relative of the discoverer of insulin, was an adolescent with diabetes who took prescribed medications and followed a diet consistent with ADA recommendations.  He experienced worsening of his symptoms and ultimately had a foot amputated. At this point his parents found a physician who recommended a low carbohydrate diet which led to rapid and sustained improvement.  The parents claimed their son should have been offered carbohydrate-restriction as an option.  The case was unusual in that Banting had a mild obsessive-compulsive condition, expressed as a tendency to follow exactly any instructions from his parents or other authority figures.  Banting’s lawyers insisted that, as a consequence, one could rely on his having complied with the ADA’s recommendations.  Disputed by the defense, this was one of several issues that made Banting famous for vituperative courtroom interactions between academics.

Banting was a person with type 2 diabetes.  Unlike people with type 1 diabetes, he was able to produce insulin in response to dietary (or systemic) glucose but his pancreas was progressively dysfunctional and his body did not respond normally, that is, he was insulin-resistant.  Although most people with type 2 diabetes are at least slightly overweight, Banting was not, although he began gaining weight when treated with insulin.

The phrase “covered with insulin…” rocked the court: the president of the ADA, H. Himsworth, Jr., was asked to  read from the 2008 guidelines [2], never rescinded: “Sucrose-containing foods can be substituted for other carbohydrates in the meal plan or, if added to the meal plan, covered with insulin or other glucose lowering medications.”

Jaggers (attorney for Banting): “Are there other diseases where patients are counseled to make things worse so that they can take more drugs.”

Himsworth: “We only say ‘can be.’  We don’t necessarily recommend it.  We do say that ‘Care should be taken to avoid excess energy intake.’”

It soon became apparent that Himsworth was in trouble.  He was asked to read from the passage explaining the ADA’s opposition to low carbohydrate diets:

“Low-carbohydrate diets might seem to be a logical approach to lowering postprandial glucose. However, foods that contain carbohydrate are important sources of energy, fiber, vitamins, and minerals and are important in dietary palatability.”

Jaggers: “Important sources of energy?  I thought we wanted to avoid excess energy,” and “would you say that taking a vitamin pill is in the same category as injecting insulin?”

Finally,

Jaggers: “Dr. Himsworth, as an expert on palatability, could you explain the difference between Bordelaise sauce and Béarnaise sauce?” [laughter]

Damaging as this testimony was, the tipping point in the trial is generally considered to have been the glucometer demonstration.  Banting consumed a meal typical of that recommended by the ADA  and glucometer readings were projected on a screen for the jury, showing, on this day, so-called “spikes” in blood glucose.  The following day, Banting consumed a low carbohydrate meal and the improved glucometer readings were again projected for the jury.  Defense argued that one meal did not prove anything and that one had to look at the whole history of the lifestyle intervention but was unable to show any evidence of harm from continued maintenance of low blood sugar despite testimony of several expert witnesses.  In the end, the jury agreed that common sense overrides expert testimony and that Banting should have been offered the choice of a carbohydrate-restricted diet.

Banting was held in New York State which adheres to the Frye standard: in essence, the idea that scientific evidence is determined by “general acceptance.” The explicit inclusion of common sense was, in fact, a legal precedent [3].   The Supreme Court ultimately concurred and held that the more comprehensive standards derived from Daubert v. Merrill-Dow, could sensibly be seen to encompass common sense.

The final decision in Banting lead to numerous law suits.  The ADA and other agencies changed their tactics claiming that they never were opposed to low carbohydrate diets and, in fact, had been recommending them all along [4].  This is discussed in the next chapter.

References

1. Gerstein, H. C. et al., Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med 358 (24), 2545 (2008).

2. American Diabetes Association, Nutrition Recommendations and Interventions for Diabetes–2008. Diabetes Care 31 (Suppl 1), S61 (2008).

3. Berger, M, Expert Testimony: The Supreme Court’s Rules Issues in Science and Technology (2000).

4. American Diabetes Association, Nutrition Recommendations and Interventions for Diabetes–2018. Diabetes Care 40 (Suppl 1), S12 (2018).

Damned statistics and the nutrition literature

Posted: January 3, 2011 in Uncategorized
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A guide for consumers and the media

For Mark Twain’s hierarchy of lies, damned lies and statistics, we should really add epidemiological lies, those reports showing that brown rice or trans-palmitoleic acid will prevent diabetes and diet soda will make you fat, which appear every week or so in ABCNews.  (I mean the generic media, but ABCNews and I have a close relationship: sometimes they even print what I tell them).  If you’ve been eating white rice instead of brown rice and you develop diabetes ten years later, it is the fault of your choice of rice. Everybody knows that this is ridiculous but the data are there showing an almost 4-fold increased risk, so how can you argue with the numbers.

These kinds of studies are always based on associations and the authors are usually quick to tell you that association doesn’t mean causality even as they interpret the data as a clear guide to action (“Substitution of whole grains, including brown rice, for white rice may lower risk of type 2 diabetes.”)   In fact, to most scientists, association can be a strong argument for causality.  That is not what’s wrong with them. Philosophically speaking, there are only associations.  All we really know is that there is a stream of particles and there is an association between the presence of a magnet and the appearance of a spot on a piece of photographic paper (anybody remember photographic paper?).  God does not whisper in your ear that the particle has a magnetic moment.  It is the strength of the idea behind the association and the presentation of the idea that determines whether the association implies causality.  What most people really mean is that “association does not necessarily imply causality.  You may need more information.” What’s wrong with the rice story is that the idea is lacking in common sense.  The idea that the type of rice you eat has any meaningful impact by itself, or even whether one can guess whether it has a positive or negative impact on a general lifestyle, is absurd.  But what about the statistics? Here the problem is really presentation of the data.  The number of papers in the literature pointing out the errors in interpretation of statistics is very large although it is still less than the number of papers making those errors.  There are numerous problems and many examples but let’s look at the simplest case: limitations of reporting relative risk and alternatives.

images-1Here’s a good example cited in a highly recommended popular statistics books, Gerd Gigerenzer’s “Calculated Risks.” He discusses a real case, the West of Scotland Coronary Prevention Study (WOSCOPS) comparing the statin drug, pravastatin to placebo in people with high cholesterol.  The study was started in 1989 and went on for about 5 years.  (These days, I think you can only compare different statins; everybody is so convinced that they are good that a placebo would be considered unethical):

1. First, the press release: “People with high cholesterol can rapidly reduce… their risk of death by 22 per cent by taking…pravastatin.”

2. Now, ask yourself what this means? If 1000 people with high cholesterol take pravastatin, how many people will be saved from a heart attack that might have otherwise killed them?  Think about this, then look at the data, the data that should have  been reported in the media.

3. The data:

Treatment        deaths during 5 years (per 1000 people with high cholesterol)

pravastatin             32

placebo                  41

Right off, it doesn’t look as good as you might have thought.  Overall, death from a heart attack is a major killer, but if you take a thousand people and watch them for five years, not that many people die from a heart attack. Now there are three standard ways of representing the data.

4. Data presentation – Relative risk reduction.

Risk is the number of cases divided by total number of people in the trial (or risk per total number). So you calculate a risk for 1000 people on the drug = 32/1000 = 03.2 % and similarly for people on the statin. Risk reduction for comparing treatments is\ the difference between the two risks.  The relative risk reduction here  is just the reduction in risk divided by the risk for the placebo:

Risk reduction (number of people saved per thousand)  = 41-32 = 9. Saving 9 lives doesn’t sound that great but lets get the per cent as reported.

Relative risk reduction = 9/41 = 22 % as indicated, and it does sound like a big deal but there are other ways to look at the data.

5.  Data presentation – Absolute risk reduction.  Again, you start with risk, the number of cases divided by total number but you calculate the actual fraction.  The absolute risk reduction is the difference between these two fractions.

For pravastatin, risk = 32/1000

For placebo, risk = 41/1000

Absolute risk reduction = (41/1000) – (32/1000) = 9/1000 = 0.9 % (less than 1 %)

6.  Data presentation – Number needed to treat (NNT): This is a good indicator of outcomes.  If you treat 1000 people, 9 will survive who might have otherwise died. So,

number that you have to treat  to save one life = NNT  =  1000/9 = 111 people .

7. Conclusion: 22 % risk reduction is true enough but it seems like it didn’t really tell you what you want to know.  Cutting to the chase, would you take a statin if you had high cholesterol (more than about 250 mg/dl) and, as in WOSCOPS, no history of heart attacks. On the basis of this study alone, it’s not clear.  First, the risk is low.  There is clearly a benefit but how predictable is that benefit?  In the study, 99 % of the people had no benefit.  Of course, if you are the one out of a hundred, the drug would be a good thing.  The question is not easy to answer but the point of what’s written here is that the statistics as reported in the media might have led you to jump to conclusions.  Before you jump, though, you might ask about side-effects.  This is a complicated subject because although the side-effects are rare, their incidence is not zero and they can be severe but this post is only about the statistics.


The Seventh Egg.

Posted: October 22, 2010 in Uncategorized
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Stepping back and looking at the recent scientific literature, I am struck with how life is a miracle.  How could humans have evolved in the face of threats from red meat, from eggs, even from the dangers of shaving?  (If you write about nutrition you have to create a macro that types out “I’m not making this up:” the Caerphilly Study [1] shows you the dangers of shaving… or is it the dangers of not shaving?).  With 28% greater risk of diabetes here, 57 % greater risk of heart disease there how could our ancestors have ever come of child-bearing age?  With daily revelations from the Harvard School of Public Health showing the Scylla of saturated fat and the Carybdis of sugar between which our forefathers sailed, it is amazing that we are here.

These studies that the media writes about, are they real?  They are certainly based on scientific papers.  If the media is not always able to decipher them, reporters do generally talk to the researchers. And the papers must have gone through peer review and yet many actually defy common sense.   Can the medical literature have such a high degree of error?  Could there be a significant number of medical researchers who are not doing credible science?  How can the consumer decide?  I am going to try to answer these questions.  When people ask questions like “could the literature be wrong?,” the answer is usually “yes” and I will try to explain what’s wrong and how to read the nutritional literature in a practical way. I am going to try to make it simple.  It is science, but it is pretty simple science.  I am going to illustrate the problem with the example of a paper by Djoussé [2].  But first, a joke.

It was a dumb joke. In my childhood, there was the idea, probably politically incorrect, that Indians, that is, Native Americans, always said “how” as a greeting.  The joke was about an Indian with a great memory who is asked what he had for breakfast on New Years day the previous year.  He says “eggs.”  They are then interrupted by an earthquake or some natural disaster and the interviewer and the Indian don’t meet again for ten years.  When they meet, the interviewer says “how.”  The Indian answers “scrambled.”

If the interviewer had been an epidemiologist he might have asked if he had developed diabetes.   Djoussé, et al. [2] asked participants about how many eggs they ate and then ten years later, if they developed diabetes it was assumed to be because of the eggs.  Is this for real?  Do eggs cause changes in your body that accumulate until you develop a disease, a disease that is, after all, primarily one of carbohydrate intolerance?  The condition is due either to the inability of the pancreas to produce insulin in response to carbohydrate (type 1) or to impaired response of the body to the insulin produced and a deterioration of the insulin-producing cells of the pancreas (type 2).  Common sense says that there is something suspicious about the idea that eggs would play a major role.  It is worth trying to understand the methodology and see if there is a something beyond common sense, and whether this is a problem in other studies besides   Djoussé’s.

What did the experimenters actually do.  First, people were specifically asked “to report how often, on average, they had eaten one egg during the past year,” and “classified each subject into one the following categories of egg consumption: 0, < 1 per week, 1 per week, 2-4 per week, 5-6 per week, and 7+ eggs per week.”  They collected this data every two years for ten years.  With this baseline data in hand they then followed subjects “from baseline until the first occurrence of a) type 2 diabetes, b) death, or c) censoring date, the date of receipt of the last follow-up questionnaire” which for men was up to 20 years.  Thinking back over a year: is there any likelihood that you might not be able to remember whether you had 1 vs. 2 eggs on average during the year?  Is there any possibility that some of the men who were diagnosed with diabetes ten years after their report on eggs changed their eating pattern in the course of ten years?  Are you eating the same food you ate ten years ago?  Quick, how many eggs/week did you eat last year?

Reading a scientific paper: the Golden Rule.

Right off, there is a problem in people reporting what they ate but this is a limitation of many nutritional studies and, while a source of error, it is depends on how you interpret the data.  All scientific measurements have error.  It is not a matter of ignoring the data but rather not interpreting results beyond measurement.  So, here’s how I read a scientific paper.   First, I look for the pictures.  What? A professor of biochemistry looks for the pictures first?  In a scientific paper, of course, they are called figures but it’s not just saving a thousand words.  (I get a thousand emails every couple of weeks). It’s about presentation of the data.

The principle is that a scientific paper is supposed to explain. The principle is laid out in what I call the golden rule of scientific papers.  It comes from the Book PDQ Statistics by Geoffrery Norman and David Streiner.  PDQ stands for Pretty Darned Quick and some of the humor is pretty sophomoric (e.g. it has Convoluted Reasoning or Anti-intellectual Pomposity detectors) but it is an excellent introductory statistics book.  Here’s the Golden Rule:

“The important point…is that the onus is on the author to convey to the reader an accurate impression of what the data look like, using graphs or standard measures, before beginning the statistical shenanigans.  Any paper that doesn’t do this should be viewed from the outset with considerable suspicion.”

— Norman & Streiner, PDQ Statistics [3]

In other words: teach.  Make it clear.  Eye-balling Djoussé, et al., we see that there are no figures.     A graph of number of eggs consumed vs number of cases of diabetes is what would be expected of the golden rule.  The results, instead are stated in the Abstract of the paper as the following mind-numbing statistics. (You don’t really have to read this)::

“Compared with no egg consumption, multivariable adjusted hazard ratios (95% CI) for type 2 diabetes were 1.09 (0.87-1.37), 1.09 (0.88-1.34), 1.18 (0.95-1.45), 1.46 (1.14-1.86), and 1.58 (1.25-2.01) for consumption of <1, 1, 2-4, 5-6, and 7+ eggs/week, respectively, in men (p for trend <0.0001). Corresponding multivariable hazard ratios (95% CI) for women were 1.06 (0.92-1.22), 0.97 (0.83-1.12), 1.19 (1.03-1.38), 1.18 (0.88-1.58), and 1.77 (1.28-2.43), respectively (p for trend <0.0001).”

What does all this mean? I will just state what the statistics mean because it is worth considering the conclusion as stated by the authors.

The meaning of the statistics is that there was no risk of consuming 1 egg/week compared to eating none.  Similarly, there was no risk in eating 2-4 eggs/week or 5-6 eggs/week.  But when you up your intake to 7 eggs or more per week, that’s it.  Now, you are at risk for diabetes.  The relative risk is small but there it is. You are now at greater risk.

Since I like pictures, I will try to illustrate this with a modified still from the movie, The Seventh Seal directed by Ingemar Bergman.  Very popular in the fifties and sixties, these movies had a captivating if pretentious style: they sometimes seemed to be designed for Woody Allen’s parodies.  One of the famous scenes in The Seventh Seal is the protagonist’s chess game with Death.  A little PhotoShop and we have a good feel for what happens if you go beyond 5-6 eggs/week.

 

1. Ebrahim S, Smith GD, May M, Yarnell J: Shaving, coronary heart disease, and stroke: the Caerphilly Study. Am J Epidemiol 2003, 157(3):234-238.

2. Djoussé L, Gaziano JM, Buring JE, Lee IM: Egg consumption and risk of type 2 diabetes in men and women. Diabetes Care 2009, 32(2):295-300.

3. Norman GR, Streiner DL: PDQ statistics. 3rd edition. Hamilton, Ont.: B.C. Decker; 2003.

The benefit in replacing dietary carbohydrate with protein

Posted: September 12, 2010 in Uncategorized
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The study of metabolic pathways provides an insight into chemical reactions and the way they function in living systems but, in the end, even a biochemistry professor still has to answer the question  “What should I eat.”  Adam Cambell, an editor at Men’s Health magazine once asked me: “You’ve just had a meal that conforms to your idea of good nutrition and satisfying portions of food but you’re still hungry.  What should you do?”

“Think of a perfectly-cooked juicy steak or perfectly-prepared fish, or some similar high protein food that you usually like,” I suggested.  “If that sounds good, you’re hungry and you should eat something.  If it doesn’t sound good, you’re not hungry.  You may want desert.  You may want something feeling good in your mouth, but you’re not hungry.” What I meant, of course, is that foods that are high in protein, and lower in carbohydrate, tend to be more filling. This satiating effect of protein is well-known in the biochemical literature and is one of the advantages of diets that restrict carbohydrates and keep protein high.  The fact that protein is satisfying also means that it provides its own control over intake and, for that reason, “concerns” about high protein intake that you hear from nutritional expert are not usually a real problem.  In the obesity epidemic where there was a large increase in carbohydrate consumption and a general decline in fat consumption, protein stayed about the same.  When nutritionists carry out experiments in which people can eat freely, they generally do not change their protein consumption.  In fact, it now seems likely that most people are not getting enough protein.  Recent studies show that people benefit from replacing carbohydrate in their diet with protein, the benefit is in better weight control, in an improved ratio to lean body mass compared to fat and in better control of blood insulin and glucose.  I will describe some of the features of this problem with references to papers in the scientific literature that are either open access or have been made publicly available and public and do not require a subscription.

Nutritionists who study protein think that we need modification of official recommendations for protein consumption.  Donald Layman at the University of Illinois has reviewed some of the important research on this question and he came up with several important points:

•    Protein is a critical part of the adult diet. Beyond physical growth which is only important for a brief period in your life, there is a continuing need to repair and remodel muscle and bone

•    Protein needs for adults relate to body weight not, as you sometimes see, as a per cent of total calories. So, if you are reducing calories, protein needs to stay high and may be a higher percentage of total calories. In choosing a diet, you should establish the grams of protein first.

•    The amount of protein at each meal can be important.  Research indicates that an ideal is 30 g of protein per meal although this may not be practical for everybody. It is recommended that breakfast be high in protein.

•    Most adults benefit from protein intakes above the minimum RDA (recommended daily allotment) and this is especially true for an aging population with increased risks of poor health.  The RDA represents a minimum daily intake for active healthy adults but most people will benefit from replacing at lest some carbohydrate in the diet with protein.

The full story on protein recommendations can be found at Nutrition & Metabolism (no subscription required.

A look at the science

Proteins are generally more complicated molecules than fat or carbohydrate.  Like starch, they are polymers (think chain of beads).  Most starches are homopolymers (all the beads are the same, glucose in this case), but protein molecules are made of 20 different kinds of beads (amino acids).  About half are interchangeable or can be made from other nutrients and are said to be non-essential.  The other half are required in the diet and are said to be essential amino acids, or, for some reason, the more modern term is indispensable.  Now your body is continually breaking down and re-synthesizing its own proteins, the most obvious function of dietary protein is supplying amino acids to replenish body proteins so high quality dietary proteins will be those that supply all the essential amino acids.  Meat, fish and eggs are high quality proteins but combinations of vegetables can also supply the full complement of amino acids.  Many web sites and other sources will give you information about how vegetables can be combined to supply amino acids, but there is another aspect of protein nutrition that should be considered.  Amino acids, like carbohydrate are not just sources of cell material but may have a signaling function.  Remember that it is not just that glucose supplies energy but that it stimulates the release of insulin which further controls metabolism.  Amino acids also perform this function and stimulate insulin release and trigger other physiologic processes, in particular, synthesis of new body protein and provide control over blood glucose.  One essential amino acid in particular, leucine, is of greatest importance in this role.  In comparative studies, diets that are high in leucine improve the ratio of lean body mass to fat. Whey and other milk proteins are particularly high in leucine; red meat is also a good source.

The benefit in substituting protein for carbohydrate is greatest for people with diabetes.  The studies from the laboratories of Mary Gannon and Frank Nuttall are pretty remarkable and I show you a picture of the actual results from their experiments.  They studied the effect of reducing dietary carbohydrate on responses of people with diabetes.  The figure shows that after 5 weeks on a diet with 20 % available glucose (circles in the figure), the response to meals is drastically improved compared to the response if the traditional diet is continued (triangles).  As the diet proceeded, hemoglobin A1c was also reduced.  Gannon and Nuttall have also showed that diets with slightly higher glucose may be effective but the response depends on how much glucose is in the diet.  A very important feature of the studies of this study is that the diets were designed so that patients maintained their weight, in other words, benefit accrued even though no weight was lost.  Given how hard it is to lose weight, this has to be considered a real plus for the higher protein, lower carbohydrate diet.  You can see the whole study, again, without subscription here.

Is there a danger of too much protein?

How many times have you read an article in the media, or even in the medical literature, warning you about the dangers of high protein diets for your kidneys, or for kidney stones, or whatever.   Probably quite a few.  Are they for real?  To answer that question, think of how often you have read an article in the media describing somebody who actually had kidney problems or stones due to a high protein diet? That number is zero or close (there’s always a case study someplace with an isolated patient).

To understand the danger in a high protein diet for people with normal kidneys, consider the following conversation I had with an expert on kidney disease when I was the editor of Nutrition & Metabolism.

RF: I received a manuscript today that rather strongly and categorically says that there is no danger in high protein diets for people with normal kidneys.

Nephrologist: That’s right.

RF: It is?  Can we document that?

N: How do you document that there are no people with three eyes.  We have looked very hard for it and we never found it.

So, what’s wrong.  Mostly what’s wrong is that we never got around to agreeing on what high protein is.  Diets that encourage you to replace carbohydrate with protein are only trying to counteract the high carbohydrate message. Few people actually eat huge amounts of protein.  As discussed above, protein tends to be more satisfying than carbohydrate and what might be considered high protein is pretty average.

In other words, there is common sense.  A healthy high protein diet is currently estimated to have a daily intake of about 1 to 4 g of protein for every kg (2.2 lbs) of body weight while the USDA recommendation is only 0.8 g/kg).  So, if you weigh 175 lbs., an optimal level of protein will be at least 80.  The diet shown below is actually quite a bit higher. Is this really unusual?  In fact, if you ate 3 eggs or even bigger portion of  brisket, do you think something terrible will happen.  Is this dangerous?  To say that normal eating, even with occasional over-indulgence, is dangerous requires real proof and that’s what’s always been missing.

Finally, it is likely that for people with diabetes, there is great danger to kidneys from continued high blood sugar and most physicians would say that this risk is real while any risk from high protein is conjecture.

The bottom line: Substituting protein for carbohydrate in the diet improves blood glucose and insulin control.  As part of a weight loss diet, higher protein preserves lean mass compared to higher carbohydrate diets but the benefits of higher protein, lower carbohydrate diets provide benefit even in the absence of weight loss.

Atkins-bashing and the spirit of Bill Buckley

Posted: September 2, 2010 in Lipophobes, The Nutrition Story
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The headline read “Vascular effects of a low-carbohydrate high-protein diet.”   The article, as anticipated, was trying to trash low carb diets. This is not uncommon. Those of us who work in the field are used to it.  Low carbohydrate diets are the thing that doctors and nutritionists love to hate.  Every junior faculty in a medicine department feels obligated to write a review showing how bad such diets are, frequently by saying that they don’t conform to the recommendations of the USDA, an example of what was the original meaning of “begging the question”, namely assuming the question in deducing the answer, that is: The USDA guidelines defines healthy diets. The Atkins diet says that the USDA guidelines are bad.  The Atkins diet does not conform to the USDA guidelines. The Atkins diet is unhealthy. QED.

The paper in question, however, turned out to be especially infuriating, claiming that a low-carbohydrate  diet will cause the build-up of plaque that is characterized as atherosclerosis but the experiment was absurd.   It reminded me of the kind of articles that William F. Buckley, Jr. used to write, the kind that made you wonder: does he really not see how illogical this stuff is.  By coincidence the low carb-atherosclerosis paper appeared about the same time as Gary Wills’s portrait of Buckley appeared in the Atlantic.  It was a very sympathetic review although Wills was not blind to Buckley’s faults.  I saw in Buckley’s personality this same kind of thing that was in the atherosclerosis paper. I understood pleasure in being infuriating but you can always do that while trying to get it right. I suddenly had some perspective on it all. I could see a mindset where the truth was not the main reinforcer as we say in behavioral psychology.  Buckley was simply motivated by something else. So first, I’ll tell you about the low carbohydrate diet paper.

The thing that drives the nutritional establishment crazy is not that low carbohydrate are effective for weight loss. Everybody knows that. The earliest writers on food, Brillat-Savarin for example, made the observation that the principles of fattening your pig for market by feeding her grains applied to humans as well. What gets people nuts is that the cardiovascular risk that was supposed to follow from the increase in fat did not materialize.  In fact, when actually studied, low carbohydrate diets reduced cardiovascular risk, dramatically lowering triglycerides (fat in the blood), increasing HDL (the so-called “good cholesterol”)  and improving other risk factors.  In fact, the paper by Foo, et al. in PNAS admitted “randomized trials suggest low-carbohydrate diets may accelerate weight loss with surprisingly little negative effect on serum markers of cardiac risk such as cholesterol,” but that didn’t stop the authors who were able to come up with new warnings about atherosclerosis from low-carbohydrate diets.

It wasn’t people, that developed atherosclerosis. It turns out that the low-carbohydrate diet was administered to mice.  Now this could be news since mice are not particularly susceptible to atherosclerosis possibly because they have high HDL (again, the “good cholesterol”). But this was not your ordinary mouse.  This was a mouse that was genetically engineered to be susceptible to cardiovascular disease.  This was an apoE-knockout mouse, a mouse  from which the genes for apolipoprotein E had been deleted ((ApoE-/-).  Apolipoprotein E (apoE) is one of the protein components of the cholesterol and fat-carrying particles known as lipoproteins (LP) that circulate in the blood. It is required for efficient clearance of some of these particles. One wit on the internet suggested that giving an apoE knock-out mouse atherosclerosis was the behavioral equivalent of teaching a cat to go to sleep.  Did the authors not know this was nonsense?  Did they really believe that a low carbohydrate diet had more biological importance than a difference in species and a mutation that predisposed to atherosclerosis? What were they thinking? At stake is the corruption of science and the the corruption of medicine. The coincidental appearance of Wills’s picture of Buckley was helpful:

“Bill was considered an elitist because he loved to use big words. But he did it not from hauteur but from impishness. This was part of his playfulness. He liked to play games in general, and word games were especially appealing to him. He used the big words for their own sake, even when he was not secure in their meaning. One of his most famous usages poisoned the general currency, especially among young conservatives trying to imitate him. They took oxymoron in the sense he gave it, though that was the opposite of its true meaning. He thought it was a fancier word for “contradiction,” so young imitators would say that “an intelligent liberal” was an oxymoron. But the Greek word means “something that is surprisingly true, a paradox,” as in a shrewd dumbness.”

That was it.  The Beth Israel doctors were just having fun.  But cardiology is a serious business and this couldn’t be a pattern but this was a context where getting it right counted.  Atkins was a threat and the truth wasn’t really part of the game.  Wills said that  Buckley “never considered himself an intellectual” as he was always a risk taker.  His debate-team style was not really about the truth.  He certainly gave the impression that he thought he was an intellectual but it turns out that, in the end, he was just screwing around.

So what do Dr. Foo and Dr. Rosenzweig actually believe?  The press release from Beth Israel said that Rosenzweig went off his Atkins diet because his resident Dr. Foo kvetched at him in the hospital cafeteria.  You have to wonder why he went on the diet in the first place.  A recent survey showed that physicians were more likely to recommend low fat diets to their patients while using low carbohydrate diets themselves, although maybe it is easy to talk them out of it. A survey of physicians’ knowledge was also informative. In fact most physicians did not know that low-fat diets increased triglycerides or that carbohydrates are most likely to increase them.  The exception was cardiologists who were aware of these facts.  So maybe it wasn’t surprising that Rosenzweig would have been on the low carbohydrate diet.  That he went off it does suggest that he is as cavalier with his own health as with that of his patients and the readers of PNAS.  In the end, though, this does real harm.  At least for people with diabetes, control of carbohydrates can be life-saving. Buckley at least functioned in the area of journalistic politics whose standards are ambiguous at best.  In the comparison to the Beth Israel doctors, William F. Buckley comes off as rather likable, surely an oxymoron.

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