[ed. note: Michael Jorrin, who I like to call Doc Gumshoe, is a longtime medical writer (not a doctor) who writes about non-financial health and medical issues for us a couple times a month. Like all of our authors, he chooses his own topics and his words and opinions are his alone. Enjoy!]

While working on the previous Doc Gumshoe installment about Dr Bereliani and his weapon against the Evil Cardiac Killer, I was struck by the large amount of stuff I ran across about diets of one sort or another. I was going to say “information” rather than “stuff” in that preceding sentence because it sounded more respectful and professional. But “information” implies, somehow, that the material is mostly fact-based, and, while the diet manifestos all included a certain quota of facts, they also all skated a good deal beyond the edges of the fact base and onto the thin ice of fashionable conjecture.

I should not have been surprised at the differences among these many diets – after all, some were pure and simple weight-loss diets, while others seemed to be tailored to avoiding specific diseases or conditions. But it got me to thinking that perhaps those differences are more a matter of marketing than of real, legitimate differences in the objectives of the diet. It struck me that it is more likely than not that the person who wants to lose weight also wants to avoid heart disease, stroke, diabetes, cancer, rheumatoid arthritis – indeed, everything from Alzheimer’s disease to Zollinger-Ellison syndrome. Most diseases and conditions in some way relate to metabolism, and changing our diets is a direct way of tinkering with our metabolism. I also got to wondering what the word “diet” really, fundamentally means.

So I consulted my OED. “Diet” is in Volume 4, Creel – Duzepere, and the etymology is unsurprising – from Latin diæta (Greek δίαιτα) meaning “mode of life.” The OED refrains from stating the obvious, which is that diæta is related to the word for day (die). In mediaeval Latin, diæta meant “a day’s journey,” and “diet” also means a meeting of an official assembly of some sort, like the Diet of Worms that we all jested about in 10th grade.

The OED gives fourteen separate definitions for the noun “diet” as well as six more for the verb. Here are the first three for the noun:

1. Course of life, way of living of thinking
2. Customary course of living as to food; way of feeding
3. Prescribed course of food, restricted in kind or limited in quantity, esp. for medical or penal reasons; regimen

The earliest citation in the OED is from Chaucer, “No deyntee morsel passed thrugh hir throte,… Attempree diete was al hir phisik.”

There we have it. “Attempree” by the way means “tempered” or “moderate,” so back in 1386 it was already thought by some that all that was needed for health was a moderate diet. Have we come much farther than that in 630 years?

Looking at those OED definitions, please notice the fundamental distinction between the first two, which characterize the diet as “customary,” and the third, in which the diet is “prescribed.” The diets that we hear and read about are mostly in the second category, but there’s an expectation among the proponents of these diets that they will shift, over time, from being prescribed to being customary.

The unfortunate reality is that, especially for the multitude of weight-loss diets, this almost never happens. Prescribed diets, whether as an avenue to weight loss or to lowering cholesterol levels or to reducing cardiovascular risk, are, for most people, a severe disappointment. People tend to stick to weight-loss diets for about as long as they keep their New Year’s resolutions. Many famous diets of yesteryear have been consigned to the dustbin of history. Diabetics are supposed to keep away from food and drink that carries a high sugar load, but lots of diabetics – once they have started taking their antidiabetic medications – relapse into their former habits.

Current diet apostles recognize this reality and try to craft their diets in such a way that the transition from “prescribed” to “customary” happens a bit more often, for a few more people. They too would like to be able to present their “tempered” diets as the only medicine most people need. To this end, a common feature of the up-to-date diet is that there is no need, ever, for the dieter to feel hungry. If you Google the phrase “stop counting calories,” you get well over 800,000 hits.

One of the recent best-selling diet books is David Ludwig’s Always Hungry?, which hit number three on the New York Times’ how-to- best seller list. According to Ludwig, we can just say goodbye to counting calories. And among other features of his plan, Ludwig advocates as much full-fat yoghurt and as many nuts as you can stuff into yourself. That’s not his whole plan, of course; there are other, less attention-grabbing parts. Ludwig is on the faculty at the Harvard Medical School and a pediatric endocrinologist. Ped endos are the clan of physicians that study and treat diabetes in children and adolescents, and, as such, they are keenly attuned to the effects of food on our metabolism, which is what the whole dieting thing is about. But Ludwig, like other diet proponents, has to put his recommendations in a context that makes it likely that they will be accepted by the populace.

What do the recent crop of diets have in common?

Over time, there has been a shift away from the emphasis on avoiding foods with heavy concentrations of saturated fats and cholesterol. The old-time rogues gallery – especially eggs, butter, and red meat – have been moved out of the cross-hairs. Their places have been taken by added sugars and refined carbohydrates as well as trans-fats.

There are sound reasons for this de-emphasis, although in my view what is logically called for is a moderate change in the course rather than a screeching halt and a reversal of direction. As I wrote in the previous post, severe restrictions on cholesterol intake were based, entirely reasonably at that time, on the discovery that cholesterol was the prime component of the plaque in our arteries. Later discoveries that we ourselves made at least three-quarters of all the cholesterol in our bodies reduced some of the emphasis on dietary cholesterol as the culprit.

Reduced, but not totally exonerated. In spite of the evidence pointing to other things we eat that contribute to the formation of the LDL cholesterol particles that are most implicated in the formation of atherosclerotic plaque, there is some evidence for the participation of dietary cholesterol in the pathology. Specifically, the drug ezetimibe (Zetia, Merck), whose mechanism of action in reducing cholesterol is totally different from either the statins or the PCSK9 inhibitors, needs to be considered. Ezetimibe inhibits the transport of dietary cholesterol from the GI tract into the circulatory system. It does not affect the synthesis of cholesterol at all; its effect is solely on the cholesterol that is in the food we eat – that rogues’ gallery of eggs, butter, and red meat.

In February of this year, we learned that the combination of ezetimibe and simvastatin reduced cardiovascular events such as heart attacks and strokes by about 9% compared with simvastatin alone. We already know that simvastatin, along with other statins, confers a considerable degree of risk reduction. There have been many, many studies, enrolling different types of patients with varying degrees of risk factors, and the results in terms of percentage of risk reduction have varied hugely, but I feel reasonably confident is saying that statin treatment over the long term reduces cardiovascular risk by about 30%. The National Cholesterol Educational Program (NCEP) has, in part, based its treatment guidelines on data showing that a 30 mg/dL reduction in LDL cholesterol reduces the incidence of cardiac events by 30%. So an additional 9% risk reduction, by blocking the absorption of dietary cholesterol, is not negligible.

To put it another way, many current diets are characterized by a huge shift in emphasis: stay away from bread, they preach, but eat as much butter as you want. To which I say, “not so fast.” The tempered diet has room for both.

Does greater emphasis on HDL-cholesterol make sense?

The importance of HDL-cholesterol has been recognized for a long time. The Framingham Risk Calculator subtracts one point from the overall risk score when a person’s HDL level is 60 mg/dL or above, adds one point if it’s between 40 and 49 mg/dL, and adds two points if it’s below 40 mg/dL. The previous Doc Gumshoe piece about the notorious Cardiac Killer explained in some detail the relationship between HDL and cholesterol transport. Let it be enough to say for now that a healthy HDL level – 50 mg/dL or more – is an indication that overall cholesterol transport, in and out, is functioning well.

However, HDL-cholesterol appears to have another beneficial function, namely that it protects the endothelial cells in the vascular system. The endothelial cells form the interior lining of the blood vessels, and one particular component of HDL, apolipoprotein A-1, helps to prevent certain white blood cells called monocytes from attaching to the arterial wall. Those white blood cells are participants in the process of vulnerable plaque formation that results in the release of blood clots and atherosclerotic plaque particles into the blood stream, causing strokes and heart attacks. HDL-cholesterol, it is thought, helps to prevent this process.

Many current popular diet plans include features intended to increase HDL-cholesterol levels. The nuts favored by David Ludwig contain unsaturated fats that favor the increase in HDL cholesterol. Unsaturated fats, both mono- and poly-, are also present in many kinds of fish such as salmon, sardines, herring, mackerel, and sea bass. And they are found in flaxseed, some beans, soy products, and even some green vegetables. Of course, olive oil is the unsaturated fat par excellence and is a featured player in the Mediterranean diet.

The Mediterranean diet tends to be a “customary” diet rather than a “prescribed” diet, and study in Spain confirmed that people who followed the Mediterranean diet as a usual daily practice had a lower incidence of cardiac events than people who were on a prescribed diet emphasizing fruits, vegetables, and minimizing fats of any kind – more like the “food pyramid” diets and diets put forward by the American Heart Association. Also, a study conducted under the Nurses’ Study program found that the Mediterranean diet was associated with longer telomeres. Telomeres protect our DNA, and longer telomeres should lead to increased longevity; therefore the Mediterranean diet might favor increased longevity.

An eminent spokesman for the Mediterranean diet is Dariush Mozaffarian of the Harvard School of Public Health. In a lengthy paper in Circulation (2011;123:2870-2891), he spells out the Mediterranean diet in some detail. For example, his classification of grains is shown in the figure below. The green area at the top is good for us, but as we go down to the dark pink area, the foods on it are on the “be careful” list, and the deep red at the bottom is to be shunned at all costs. However, what Mozaffarian is putting together is a prescribed diet meant to guard against cardiovascular risk. I don’t see Mozaffarian’s presentation of the cardioprotective diet as a customary diet. It’s a bit difficult to imagine that most people who are not specifically concerned with cardiovascular risk would adhere to a customary diet that omitted foods like white bread, pasta, potatoes, corn, and virtually all deserts, as in the figure below.

Another diet guru, Gary Taubes, author of Good Calories, Bad Calories, objects to some of the items in the light green area in the table above, namely milled whole grains, which includes those supposedly healthful whole grain breads, breakfast cereals, and pastas. According to Taubes, and to another diet authority, Robert Lustig (not to be confused with David Ludwig!), when those whole grains are milled they get so pulverized that they’re just as bad as refined grains. They claim that this leads to the overproduction of insulin, which in turn instructs the liver to store glucose as fat.

So, if we omit milled whole grains, what’s left? And also, how is it that insulin could be bad for us? Isn’t diabetes a disease of insulin deficiency?

Training the dietary cross-hairs on foods with a high glycemic load

The glycemic index quantifies the glucose content of a food or beverage on a scale of 1 to 100, while glycemic load assesses the amount of glucose per serving of that food or beverage. Those data are crucial for constructing a diet, whether a weight-loss diet or a diet aimed at controlling diabetes or reducing cardiovascular risk. At the risk of being tediously repetitive, here’s why:

1. Glucose that is not converted to energy tends to be stored as fat.
2. Glucose in the bloodstream signals our pancreatic beta cells to secrete insulin, but excessive amounts of insulin can effectively exhaust insulin receptors throughout the body, leading to diabetes.
3. Diabetes itself contributes to acute cardiovascular events. Atherosclerotic plaques in persons with diabetes are more unstable and likely to rupture; they contain a richer lipid core and are more susceptible to inflammation.

The shift in emphasis from avoiding high-fat foods to minimizing those that carry a high glycemic load appears to be reasonable. Here’s a short selection from a list of more than 100 food and drink items from the Harvard Medical School:

Food / beverage	Glycemic index (glucose = 100)	Glycemic load per serving
Vanilla cake from Betty Crocker mix	42	24
Bagel, plain white	72	25
Baguette, white	95	15
Coca Cola	63	16
Unsweetened orange juice	50	12
Cornflakes	93	23
Instant oat meal	83	30
Corn on the cob	60	20
Couscous	65	9
White rice	89	43
Milk, full fat	41	5
Milk, skim	32	4
Apple	39	6
Raisins	64	28
Kraft mac & cheese	64	32
Baked russet potato	111	33
Carrots	35	2
Hummus (chick pea dip)	6	0

Something that the table makes clear is that it doesn’t matter a whole lot whether the glycemic load is in the form of sugar or refined carbohydrates.   That’s because we convert the carbohydrate to glucose really, really quickly.   A lot of the difference in glycemic load is, of course, the serving size.   For example, the Coca Cola serving is 250 ml, which is about a cup; people who buy those supersized soda pops that Mayor Mike Bloomberg excoriated take in a multiple of that glycemic load.   But it’s eye-opening that for equivalent quantities, Coke has three times the glycemic load as whole milk.   A quart of Coke carries a glycemic load equivalent to two large baked potatoes.   

The glycemic index/load data don’t take into account another bit of data that can have an important impact

on how diet affects our metabolism.   Mozaffarian points out an interesting difference between glucose and fructose, fructose being the naturally-occurring form of sugar in most fruits.   Fructose produces a somewhat smaller glycemic response, but seems to trigger more lipogenesis – i.e., conversion to fat – than glucose.   It has also been suggested that we humans respond somewhat differently to the taste of fructose than to that of sucrose (i.e., sugar).   The taste of sugar strikes us as just a bit sweeter.   Therefore, to get the equivalent sensation of sweetness, the quantity of fructose (as in high fructose corn syrup, used to sweeten most soda pop) would have to be boosted.   But the soda pop makers are reluctant to do that; they probably don’t want to be accused of super-sweetening their products.   Therefore, I suspect, many people are simply not satisfied with the old-time 8 ounce soda; thus the supersized containers – and the soda pop makers are okay with that.

Another factor that needs to be considered when thinking about diets is the how they affect our sense of satiety.   Which is to say, after a meal that adheres to those dietary recommendations, do we feel full and satisfied, or are we still hungry?   If the former, we’re apt to go along with the diet, but if we’re supposed to push our chairs back while our tummies are still asking for more, we’re apt to misbehave.   A lot of it is subjective, of course, but experience tells us that some foods give rise to the sense of satiety while other foods make us want more.   There are reasons why the appetizers tend to be savory, while deserts are sweet.   Those tiny anchovies wrapped around capers raise the curtain on the feast to come and the butterscotch sundae brings it down.   There’s some evidence that familiar foods induce the sense of satiety more quickly than novelties; the novelties – if we like them – cry out to us, “keep tasting!”    

And it’s very clear that adherence is just about the most important consideration in evaluating the effectiveness of a diet.   You can lead the horse to water, etc.   A diet emphasizing a lot of soy-based meals has a very low glycemic load, and is also pretty cheap; whether many people will voluntarily stick with it is another matter.   About five years ago there was a lawsuit in Illinois charging that the compulsory soy-based diet in Illinois prisons constituted cruel and unusual punishment; this diet was instituted in Illinois when that fellow Rod Blagojevitch was governor.   Florida prison inmates have made similar claims.   The soy prison diet exactly fits the third OED definition – a prescribed diet restricted in kind or limited in quantity, especially for penal reasons.   Happily, for the majority of us not in Illinois or Florida prisons, diets are a matter of choice.   But those factors apply nonetheless.

No condition or treatment area is more affected by these various factors than diabetes.  

Diet and the current diabetes treatment landscape

Earlier in this piece, I noted that some diet experts had raised red flags in relation to milled whole grains, because they trigger the secretion of insulin which instructs the liver to store glucose as fat. This seems more than a bit contradictory in the context of diabetes, which (as the disease progresses) is characterized by insulin deficiency, so how could it be bad to trigger the release of insulin?

There is indeed something to it, however. The usual course of diabetes – we ‘re talking here about type 2 diabetes, usually abbreviated as T2DM – is that the individual’s pancreatic beta cells secrete more and more insulin in response to increasing glycemic load. The insulin receptors, which are in every cell in the body, get overloaded and are unable to respond to the insulin and convert the glucose to energy. The glucose cannot be converted to glycogen in the liver, which requires the action of insulin. Instead, it spills into the urinary tract. Lipids in the diet are stored as adipose tissue. The individual gains weight – a lot of weight. Eventually the whole mechanism of glucose metabolism crashes. And the individual, now diabetic, begins literally to starve. In the absence of a working insulin system, all that stored fat cannot easily be employed as energy. The prognosis for advanced untreated T2DM is not good.

Treatment for T2DM employs several strategies, which were discussed in previous Doc Gumshoe posts, 19 and 26 June 2014. (You can check all the old posts at http://www.stockgumshoe.com/author/mjorrin/.) But a common event in the course of treatment is that eventually, the oral antidiabetic agents, regardless of mechanism, stop working as effectively as they did initially, and patients need exogenous insulin.

When this happens, many patients gain weight. In fact, many patients whose diabetes is under good control, as assessed by their hemoglobin A1c levels, are overweight or obese. That’s because all it takes to keep HbA1c at a desirable level is enough insulin. Persons with diabetes monitor their direct blood glucose at fairly short intervals and base their insulin dosage on those immediate readings, not on the HbA1c reading, which provides an indication of what blood glucose levels have been over a period of several weeks. So it’s relatively easy for a person with diabetes to increase the insulin dose to compensate for what we might uncharitably call dietary excesses, and still keep their blood glucose at acceptable levels. But this can, and does, lead to considerable weight gain.

What kind of diet might prevent this? Perhaps not a prescribed diet, “as for penal reasons,” that doesn’t take into account factors like satiety and the likelihood of adherence, but a diet that might approximate a “customary course of living as to food,” tempered and moderate – a diet that most people could stick to for a long time. Persons with diabetes – along with persons desiring to shed some excess avoirdupois and persons wishing to avoid any of the ailments in the cardiovascular spectrum – i.e., nearly everybody … such persons are not prisoners, subsisting only on what’s in the tin dish shoved through the little opening in their cell doors. Such persons – that’s most of us – do not want to be Always Hungry and denied the pleasures of eating food that tastes good and makes us feel good.

Most nutritionists and, in fact, most of the clinical community, agree that what’s fundamentally wrong with the American diet is that way too much of what we eat is not really food, but food products, jazzed up with extra sugar, salt, transfats, and other stuff that’s no good for us. We’re too busy to buy real food and cook it, so we take short cuts, and those short cuts are a big part of the problem. There are certainly people out there calling attention to the situation – see Michael Pollan’s many books.

The diet gurus certainly recognize this, but with the best intentions, they prescribe diets that are hard to stick to. They need to put forward a provocative hypothesis to attract attention to their books or videos or whatever it is they’re using to promote their diet plan. Some of the ones who single out sugar as the villain of villains go so far as to warn against something as innocent as eating an apple, because an apple is nothing but a conduit for a lot of fructose. So much for “an apple a day keeps the doctor away.”

It’s easy to forget, when harkening to the preaching against sugar, that sugar – glucose – is the fuel that our bodies subsist on. Too much glycemic load certainly is a problem, for the reasons we’ve talked about. But let us not elevate tempered warnings into an absolute proscription. The simple-minded proclamations of some diets – “here’s the one fruit you should never never eat” – attract attention and maybe sell diet books, but they are not a pathway to a sustainable life plan.

Something that a lot of these diet gurus favor is dark chocolate, because is furnishes the right kind of fat – not transfats – and, we all hope, delivers the kind of metabolic benefits we’ve talked about here. David Ludwig says he eats low-sugar dark chocolate every day because of those benefits. But I suspect that daily dark chocolate is part of the provocative hypothesis – what was once forbidden is now mandatory.

However, the forbidden vs. mandatory axis is, in my opinion, a big part of what’s ineffective about prescribed diets. We want what’s forbidden, we shun what’s mandatory. A few of us may remember the famous New Yorker cartoon about broccoli: the kid, sitting at the dinner table, says “I say it’s spinach, and I say the hell with it.” If it becomes mandatory, there will be people saying the same thing about dark chocolate.

The diabetes treatment community, including the clinicians and the pharmaceutical companies, is keenly aware of the predicament posed by increasing rates of both obesity and diabetes, the increasing cardiovascular risks that these trends bring, and the discouraging results of diet plans as well as of many anti-obesity drugs. An encouraging development is that some diabetes agents now also have properties that keep the patient’s weight under control as well as his/her HbA1c. And the most recent and potentially best news is that a couple of newer agents have been demonstrated not only to control blood glucose and weight, but to confer significant cardiovascular benefits. The details of the studies confirming that bit of news won’t be made public until the American Diabetes Association has its annual meeting in June, at which time Doc Gumshoe will provide a full-scale review. The drugs in question are liraglutide (Victoza), from Novo-Nordisk, and empagliflozin (Jardiance), from Eli Lilly and Boehringer Ingleheim.

In the meantime, permit me to circle back to my point of departure: what we all need is a tempered and moderate course of living as to food. We should eat real food, experience pleasure at the dining table, and we should not have to push back our chairs feeling hungry.