Category Uncategorized

Big Fat Liars

Adele Hite, PhD MPH RD 23 Comments

Since 1980, Americans have gotten progressively more lazy and gluttonous. As if this were not bad enough, apparently about 2/3 of the population—the fat 2/3 of the population—have also become unrepentant liars. Although we have no way to explain this precipitous decline in the moral fiber of Americans, we know it must be happening because Americans seem to be getting fatter and fatter even though many of these fat Americans report that they are not eating more calories than their normal-weight, honest, hard-working counterparts.

It seems that when we gave the USDA and HHS the responsibility for determining what food was healthy for each of as individuals, Government Approved Nutrition Experts also developed a magical ability (in Nutrition, we love magic!) to tell the difference between what was Truly True and what was a Big Fat Lie. Here’s a response I got to a food record assignment during an introductory Nutrition course:

Question: What are your barriers to meeting the MyPyramid recommendations? (In other words, what might prevent you from consuming the recommended amount of each food group?)
My answer (after describing the low-carb diet that I used to lose weight and improve my migraines):I have a history of glucose intolerance and overweight/obesity.  Past a certain point of consumption, carbohydrates make me gain weight, raise my blood     pressure, reduce my energy levels, give me migraines, make my blood sugar wonky, and leave me hungry and cranky.  I stick to fiber-rich, nutrient-dense, non-starchy vegetables for my carbohydrates, although I do eat fruit when it is in season locally.
Instructor’s response (I am not making this up):  It is actually the total calories that make you gain weight, not the carbohydrates.  The high fat intake would be more detrimental than the whole grains and fiber rich vegetables.  Refined carbohydrates would cause the symptoms you describe but using whole grains and high fiber fruits and vegetables should not do so.  You need carbohydrate for your brain to function.  It does not function on fat and protein calories.  In fact eating a low carbohydrate diet such as you describe would make you tired, give you migraines, make you hungry and cranky.

Silly me! Of course the Nutrition Expert knows what REALLY caused my weight gain and migraines. Obviously the lack of carbohydrate to my brain prevented me from realizing her innate superiority at understanding and interpreting my own personal experiences. Either that or I’m just a Big Fat Liar.

Let me introduce you to another Nutrition Expert with the magical ability to tell Truth from Fat People Fiction–Michael Pollan:

Consider: When the study began, the average participant weighed in at 170 pounds and claimed to be eating 1,800 calories a day. It would take an unusual metabolism to maintain that weight on so little food. And it would take an even freakier metabolism to drop only one or two pounds after getting down to a diet of 1,400 to 1,500 calories a day — as the women on the “low-fat” regimen claimed to have done. Sorry, ladies, but I just don’t buy it. (Pollan M. Unhappy Meals)

The women in the Women’s Health Initiative (to which Pollan refers) are: Female. Post-menopausal. Overweight. From my experience at the Duke Lifestyle Medicine Clinic (director, Dr. Eric Westman), just about any woman who met those three criteria exhibited this sort of “freaky metabolism.” Not only is it possible for a woman in that hormonal situation to maintain her weight on 1800 kcals/day, it may be absolutely impossible for her to lose weight on 1400-1500 kcals/day—if she’s eating foods that enhance fat storage and prevent fat utilization (carbs, I’m lookin’ at you). In fact, not only did I see many other women like this in clinic, I stopped losing weight myself (at 185 pounds) eating 1200-1500 calories a day—and I wasn’t even postmenopausal. But then, at that point, I wasn’t a Nutrition Expert either. Not like Michael Pollan.

I always wonder why Mr. Investigative Journalist/Nutrition Expert Pollan didn’t go out find a few real live overweight, post-menopausal women and ask them what their personal experiences were with weight loss instead of simply discounting the experiences—and calling into question the humanity and integrity—of the “ladies” in the study. Oh wait, if the ladies he interviews are overweight, they’d all just LIE to him!

Anyway, why ask a real person, when you have Science on your side? Here’s a nutrition textbook explaination just how it is that we KNOW fat people lie:

Another approach to check for underreporting is to compare reported usual energy intake with resting energy expenditure calculated using various equations . . . If a subject’s reported usual energy intake is <1.2 times his or her calculated REE, underreporting of energy, and therefore nutrient, intake is highly likely. (Lee & Nieman, 2007).

In other words, if fat people don’t eat as much as we think they should be eating according to calculations that are known to be notoriously inaccurate, they must be “underreporting” (this is a complicated Scientific Term that means “lying about”) how much they eat. In my current Obesity class at UNC, Dr. Andrew Swick has confirmed—through evaluations done in a metabolic chamber—that some overweight/obese women have energy requirements as low as 1200-1300 calories (hmm, “freaky metabolism” maybe?),  requirements that would be far below “calculated requirements” referred to above. Dr. Swick pointed out to us that some fat people don’t, in fact, eat that much food.

But we should never let reality stand in the way of Government Approved Nutrition Information (code name: GAIN). Our good buddies at the USDA and HHS prepared this helpful chart for the 2010 Dietary Guidelines Advisory Committee Report to show how many calories Americans are consuming compared to the recommended ranges:

The vertical lines are recommended calorie ranges; the pink triangles are the average calorie intake in each group. Caloric intake appears to be within the recommended range for all age levels; adult women in general seem to be consuming at the very low end of their caloric range, about as many calories as a preschool male. That’s right, women over the age of 50 eat, on average, about as much food as 2-5 year old boys.

This must be more of that “freaky metabolism” thing to which Mr. Pollan refers. Or—wait—maybe they are all just LYING (the old ladies, not the little boys): the 2010 Dietary Guidelines for Americans go on to say, “While these estimates do not appear to be excessive, the numbers are difficult to interpret because survey respondents, especially individuals who are overweight or obese, often underreport dietary intake.” And we know what “underreport” means, right?

According the USDA and HHS, Americans aren’t fat because they are told to eat foods they don’t need to eat, Americans are fat because they eat too much–and then lie about it.

So, let me sum this up for the folks at home:

Fat people say that they don’t eat more calories than their normal weight (and apparently morally superior) counterparts.  But we know they are lying because Nutrition Experts—like Michael Pollan—KNOW how much fat people eat should be eating (i.e. A LOT of food—otherwise, golly, they wouldn’t be so darn fat).  ).  He KNOWS this because he’s a Nutrition Expert and because we have scientists who have calculations that tell us how much fat people are supposed to eat (i.e. A LOT) so when fat people say they don’t each as much as scientists think they eat (i.e. A LOT), well then, the only possible explanation for that is that the fat people are LYING!  And if that’s not enough evidence for you (and really, it should be), you can absolutely believe that that fat people LIE about how much they eat because the Government says they do.

And the government never lies.

References:

Lee RD and Nieman DC. Nutritional Assessment, 4th ed. Boston: McGraw Hill, 2007.

Pollan M. Unhappy Meals. The New York Times Magazine, January 28, 2007

U.S. Department of Agriculture and U.S. Department of Health and Human Services. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010. June 15, 2010.

U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2010. http://www.cnpp.usda.gov/DGAs2010-PolicyDocument.htm Accessed January 31, 2010.

How to Choose Foods Wisely?

Adele Hite, PhD MPH RD 4 Comments

I don’t have the answer; I’m just askin’ the question.

I’m not much for food rules. I’m not much for rules in general (ask my mother). Still, I feel an obligation to provide some guidance that counterbalances the Government-Approved Information on Nutrition (code name: “GAIN”) that screams at us from every shelf in the supermarket.

There are a lot of “how to” guides on choosing foods wisely, from Michael Pollan’s 7 rules to the How to Find Real Food at the Supermarket from Darya Pino to a grass-fed, organic approach from Healthy Eating Politics to a more academic approach from Carlos Monteiro (scroll down to his discussion on meat and bread).

I like all of these.  At the same time, I want something I could give to patients and clients that will help them make reasonable choices—yes, even if they are buying food at a gas station. Most importantly, I want to make this something everyone can do regardless of income level. We have to acknowledge that, at least for now, many “cleanly produced” foods (grassfed beef, farmers’ market eggs, organically-raised produce, etc.) are WAY more expensive than their grocery store counterparts.  Still, I think I would recommend grocery store pork chops over organic “convenience” foods like this

even though all 25 ingredients are “organic”!! even the tofu!

Here’s my initial stab at a “choose wisely” approach. However, I think my own brain capacity is quite limited (especially when I’m trying to wrap it around biostatistics). I’d love some feedback and suggestions for improvement from the community of folks who are doing their best to “choose wisely” on a daily basis. This is not geared toward any particular “dietary approach,” although—as it happens—reducing processing tends to reduce unnecessary carbohydrates. Hmmm. How truly convenient.

If Nutrition Experts Built Bridges–

Adele Hite, PhD MPH RD 10 Comments

If you are an engineer, your plan—bottom line, no fudging about—has to WORK. All. The. Time. It’s what we expect from engineers.

On the other hand, if you are a Government-Approved Nutrition Expert, your plan doesn’t have to work AT ALL.

Which may be why we don’t let Nutrition Experts build bridges.

To ensure a more impressive rate of success, engineers tend to build their bridges and elevators based on a few mysterious but fundamental concepts like physics (or as we say around here, fweezix). Now, to paraphrase Barbie, I understand that physics is TOUGH. But it is also, well, insurmountably the real deal, and anything that defies the laws of physics is generally—for lack of a better word—considered to be magic.

Now, from my biochemistry classes, it looks like the principles of nutrition are built on chemistry, and the principles of chemistry are built on—you guessed it!—politics physics But when I step across the hall to my public health classes, then the principles of nutrition are based on the Dietary Guidelines, which—as they tend to be in defiance of the laws of physics—I guess must be magic!

Despite the rockin’ groove, I’m not sure that I believe in magic.

But Calories In = Calories out is not magic, it’s physics, right? It seems indisputable—a veritable law of thermodynamics—that if you consume fewer calories than you expend, you will lose weight. Conversely, if you consume more calories than you expend, you will gain weight. Duh.

Sometimes when things aren’t working (i.e. major bridge oopie ), we get a glimpse of the realities of the physics behind the system. Let’s take a look at a category of individuals that do lose weight easily—too easily: Type 1 diabetics. A type 1 diabetic could eat 5000 calories a day, never move a muscle, and still lose weight (for the record: this is not a good thing). What happens to those calories? Why don’t they get stored as fat (hello? calories IN?) A type 1 diabetic can’t store them as fat. Why not? No insulin. Without insulin, the body cannot store energy at all. Type I diabetics must be given insulin or they literally waste away. It’s not because they try harder; it’s because of physics.

What this means is that it can’t just be the amount of calories that we are consuming, but also the source. And in the case of unnecessary carbohydrates in the diet, it’s likely to be both. The increase in caloric intake we’ve seen in the past 30 years has come almost entirely from industrialized carbohydrate food products—subsidized and endorsed by the USDA.

Would obesity rates have skyrocketed without the Guidelines prompting Americans to eat fewer animal products—especially meat and eggs which contain Very Scary saturated fat and cholesterol—and more whole grain cereal products? We’ll never know. But physics does tell us that carbohydrate foods have particular qualities that affect fat storage and metabolism, specifically: “A high carbohydrate meal stimulates the production of insulin. Insulin inhibits the body’s ability to use fat for energy and stimulates the uptake of fat and its storage as triacylglycerol” (Campbell & Farrell, 2009). That’s straight from my biochemistry textbook.

Now I don’t care if you eat carbs or not. Some of my best friends are carbs. But can we stop pretending that somehow—magically—there’s no relationship between the two figures above?

Apparently we can’t. According to many Nutrition Experts, including Marion Nestle, our low-fat Dietary Guidelines can be blamed only in that they do not do more to “address caloric intake, portion size, inactivity, and other contributors to obesity” (Woolf & Nestle, 2008). Notice that “caloric intake,” “portion size” and “inactivity” are all things that are our fault—in contrast to a diet recommendation of mostly carbohydrates, something the USDA and HHS are responsible for. In other words, if chubby little Americans can’t “achieve energy balance” by eating less and exercising more, it’s not because the Guidelines aren’t helping us, it’s because we are simply not trying hard enough.

(True Confession: I mostly just wanted to draw that cartoon.)

Should we reduce our calories? Maybe not a bad idea for some folks.

What kind of calories should we reduce? Ask an engineer. Unless you believe in magic . . .

References:

Campbell MK, Farrell SO. Biochemistry, 6th ed. United States: Thomson, 2009. p. 730.

Centers for Disease Control and Prevention (CDC). Trends in intake of energy and macronutrients–United States, 1971-2000. Morbidity and Mortality Weekly Report. 2004 Feb 6;53(4):80-2.

Woolf SH, Nestle M. Do dietary guidelines explain the obesity epidemic? American Journal of Preventive Medicine. 2008 Mar;34(3):263-5.

Public Health Nutrition’s Epic Fail

Adele Hite, PhD MPH RD 8 Comments

Mostly I just wanted to say “epic fail” because it embarrasses my kids, but then, they are always harshing on my mellow.

The stated goals of the US Dietary Guidelines are to promote health, reduce risk of chronic disease, and reduce the prevalence of overweight and obesity.

How’s that working for us?

First the good news. Cholesterol levels and hypertension have trended downwards since the creation of our first Dietary Guidelines.

It is possible that the changes in these risk factors reflect a trend that was already well underway when the Dietary Guidelines were written . . .

. . . although some folks like to attribute the changes to improvements in our eating habits (Hu et al 2000; Fung et al 2008). And btw, yes, they actually have improved with regards to the dietary recommendations set for in our Guidelines. Don’t believe me? You’re not alone. Here’s the data.

Soooooo . . . if our diets really have improved, and if those improvements have led to related improvements in some disease risk factors (because cholesterol levels and even blood pressure levels are not diseases in and of themselves, but markers—or risk factors—for other disease outcomes, like heart disease and stroke), let’s see how the Guidelines fared with regards to actual disease.

This trend is a little ironic in that cancer was, at first, one of the primary targets for nutrition reform. It was Senator George McGovern’s ire at the Department of Health, Education, and Welfare’s (now the Department of Health and Human Services) failure to aggressively pursue nutritional links to cancer that was at least part of the motivation behind giving the “lead” in nutrition to the USDA in 1977 (Eskridge 1978; Blackburn, Interview with Mark Hegsted). In fact the relationship between dietary fat and cancer had so little solid evidence behind it, the 2000 Dietary Guidelines Advisory Committee had this to say: “Because relationships between fat intake and cancer are inconclusive and currently under investigation, they are deleted.”

I guess we can then feel assured that the reason that the restrictions against fat and saturated fat are still in the Dietary Guidelines is because their relationship to heart disease isn’t inconclusive or “currently under investigation”? If that’s the case, somebody better tell these folks. So what did happen to heart disease as we lowered our red meat consumption and our egg intake, while we increase our intake of “heart-healthy” grains and vegetable oils?

Well, you’d think with all of that reduction in fat and saturated fat, plus the decrease in smoking, we’d be doing better here, but at least—well, at least for white people—the overall trend is down; for black folks, the overall trend is up.

Oops. Not so good.

Hmmm.

Oh. Well. This can’t be good. And of course, my favoritest graph of all:

I’m not sure, but it sorta kinda looks like the Dietary Guidelines haven’t really prevented much, if any, disease. Maybe we could get those guys at Harvard to take a closer look? I mean, looking at these trends—and using the language allowed with associations—you might say that the development and implementation of Dietary Guidelines for Americans is associated with a population-wide increase in the development of cancer, heart failure, stroke, diabetes, and overweight/obesity. Anyway, you might say that. I would never say that. I’m an RD.

Are there other explanations for these trends? Maybe. Maybe not.

It’s always a good idea to blame food manufacturers, but we have to remember that they pretty much supply what we demand. And in the past 30 years, what we’ve demanded is more “heart-healthy” grains, less saturated fat, and more Poofas. Yes, food manufacturers do help shape demand through advertising, but the Dietary Guidelines don’t have anything to do with that.

Oh yeah. That‘s so whack, it’s dope.

References:

Blackburn H. Interview with Mark Hegsted. “Washington—Dietary Guidelines.” Accessed January 24, 2011. http://www.foodpolitics.com/wp-content/uploads/Hegsted.pdf

Centers for Disease Control and Prevention (CDC). National Center for Health Statistics, Division of Health Interview Statistics, data from the National Health Interview Survey. http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm. Accessed 15 August 2010.

Centers for Disease Control and Prevention (CDC). National Center for Health Statistics, Division of National Health and Nutrition Examination Surveys. Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1976–1980 Through 2007–2008. http://www.cdc.gov/NCHS/data/hestat/obesity_adult_07_08/obesity_adult_07_08.pdf

Accessed February 1, 2011.

Eskridge NK. McGovern Chides NIH: Reordering Priorities: Emphasis on Nutrition. BioScience, Vol. 28, No. 8 (August 1978), pp. 489-491.

Fast Stats: An interactive tool for access to SEER cancer statistics. Surveillance Research Program, National Cancer Institute. http://seer.cancer.gov/faststats. Accessed on 11-1-2011.

Fung TT, Chiuve SE, McCullough ML, Rexrode KM, Logroscino G, Hu FB. Adherence to a DASH-style diet and risk of coronary heart disease and stroke in women. Arch Intern Med. 2008 Apr 14;168(7):713-20. Erratum in: Arch Intern Med. 2008 Jun 23;168(12):1276.

Hu FB, Stampfer MJ, Manson JE, Grodstein F, Colditz GA, Speizer FE, Willett WC. Trends in the incidence of coronary heart disease and changes in diet and lifestyle in women. N Engl J Med. 2000 Aug 24;343(8):530-7.

Morbidity and Mortality: 2009 Chart Book on Cardiovascular, Lung, and Blood Diseases. Bethesda, Md: National Institutes of Health: National Heart, Lung, and Blood Institute; 2009.

Kinky Stuff about Fatty Acids

Adele Hite, PhD MPH RD Leave a comment

That’s fatty ACIDS. It’s not that kind of site.

I was a young adult in the 1980s, just after the first Dietary Guidelines rocked our world. Yes, I remember the bacon-and-eggs frowny face on the cover of Times. It was in the checkout lane as I was buying my low-fat, fruit-and-sugar filled yogurt. Of course, I would soon come to my senses and switch to fat-FREE yogurt. Why? Because animal fat, including whatever remaining milkfat was in my yogurt, has Very Scary saturated fat in it. Did I know what that meant? Of course not. But I do now.

At my house, we like to joke that fats suffer from a serious PR problem (that’s what passes for humor around here). It’s so easy to think FAT=FAT. And “saturated” fat sounds even more ominous and creepy, saturating our blood with icky gooey . . . um . . . somethingy. Surely those loverly ladies Mona Unsaturated Fatty Acid (MUFA) and Polly Unsaturated Fatty Acid (PUFA)—Moofa and Poofa to friends—are better company to keep.  That seems to be what the folks at Harvard think, anyway.

Enter actual biochemistry.

In biochem class, I found out that “saturated” simply meant that the carbon chain of a fatty acid was fully “saturated” with hydrogen and therefore, there are no double bonds.  That’s not very scary.

Yeah, but my BFF, Polly Unsaturated, as it turns out, was more of a frenemy than I thought.


Kinda cute. Check out those double bonds. That’s what makes Poofa unsaturated.

Turns out, miss Poofa is into some radically kinky stuff.

Just about everyone has heard of antioxidants. They are why we are supposed to eat fruitsandvegetables. The point of antioxidants is to deal with “free radicals,” which sound like some kind of hippie flashback, but is simply a term to describe a molecule with one or more unpaired electrons that reacts easily with other molecules. In cell membranes, they can really cause problems because the long, straight profile of a fatty acid chain can get oxidized by reacting with a free radical, causing it to bend, which weakens the integrity and functionality of the membrane.

Prime targets of free radicals are unsaturated bonds, specifically: Poofas.

Even a middle-schooler can see (I know, I asked one) that this just doesn’t look good for the cell membrane.   It gets worse. The reaction that occurs not only damages that particular fatty acid, but is a self-propagating reaction. It starts and then it doesn’t stop—until an antioxidant comes along. The results: lotsa crooked Poofas.

The academic-industrial complex has recited to us the story that we should increase the consumption of corn and soybean oils—which contain about 60% of these fatty acids—because they are so good for us. They have the population studies to prove it. But this tale is as twisted as an oxidized Poofa. Ever since 1980, when we told people to start eating more Poofas, folks who are concerned about their health have eaten more Poofas. While we don’t really know if consuming corn and soybean oil will make you a healthier person, we do know that caring about your health will.  And even though people who care about their health are generally more healthy than people who aren’t, as a population we are all less healthy.  Could it be the Poofas that have saturated our food supply?

By sheer coinkydink, corn and soybean oils happen to be big moneymakers for food processors. That’s why I really get bent out of shape when we’re told that we grow soy and corn so we can feed it to cows. That’s like saying we drill for oil so we can make lipstick.

We may find out in the long run that it isn’t just our increase in carbohydrates, but our increase in Poofa–and the corresponding decrease in not-so-scary saturated fat–that is truly at the root of our current health crises. In which case, miss Poofa can kiss my butter.

Americans don’t follow Guidelines—or do they?

Adele Hite, PhD MPH RD 2 Comments

One of the enduring myths of our current nutrition culture is that Americans don’t follow recommendations–have never followed them–because if we had, this obesity thing wouldn’t have happened. According to the 2010 Dietary Guidelines Advisory Committee Report, “average American food patterns currently bear little resemblance to the diet recommended in the 2005 Dietary Guidelines for Americans.”

As proof, the following figure is provided:

FIGURE 1: Americans don’t follow dietary recommendations!

It seems pretty obvious that Americans are woefully off-base when it comes to eating anything close to what the USDA and HHS have been recommending for the past thirty years. I would bet my RD certification that this figure will be shown in PowerPoints across the land to demonstrate—to the accompaniment of much hand-wringing—how we must “make the healthy choice the easy choice” for those poor, dumb Americans who will otherwise just eat themselves into obesity and ruin airplane trips for the rest of us.

Aside from the fact that Americans are being evaluated on whether or not they follow the Guidelines, rather than whether or not the Guidelines are actually appropriate, there are some serious “truth in advertising” issues going on with this figure.

First, note the data collection time points: National Health and Nutrition Examination Surveys from 2001-2004, and 2005-2006. And the fun begins . . .

1) The figure shows that we eat too many calories from SoFAS. But this concept was not part of the Guidelines until the 2010 Dietary Report, the report that contains this figure. In other words, Americans are being held to standards that hadn’t even been created yet.

2) The saturated fat “cut-off” is based on a 7% of calories. The recommended limit for saturated fat at the time the data were collected and at the time this document was written is 10% of calories, not 7%.

3) The standards for whole grain consumption given in the Guidelines that the public would be familiar with when the data were collected were pretty vague: “Choose a variety of grains daily, especially whole grains” (from the 2000 Dietary Guidelines). I don’t know how this translates into an absolute amount of whole grains that Americans don’t consume.

4) The report that contains this figure (the 2010 Dietary Guidelines Advisory Committee Report) indicates that added sugars should be less than 25% of calories. Current research indicates that added sugar consumption by Americans is around 16% of total calories (Welsh et al, 2010, JAMA). According to this figure, Americans consume 242% more added sugars than recommended. Another mystery.

5) In the fine print, it says that the sodium cut-off is based on the recommended Adequate Intake (AI) amount. The AI amount is a “goal for adequate intake,” and, as such, is more of a floor than a ceiling. The AI amount is currently set at 1500 mg of sodium for adults. On the other hand, the Dietary Guidelines that were in effect at the time the data were collected set sodium recommendations at 2400 mg (2000 DGs) and 2300 mg (2005 DGs) per day.

Americans don’t follow the Guidelines–but the standards being used in a number of cases aren’t even part of the Guidelines?

Here’s a different perspective on whether or not Americans are following dietary recommendations:

FIGURE 2: Or do they? Black lines represent lower limits of Acceptable Macronutrient Distribution Range (AMDR) given in the Dietary Guidelines; red lines designate upper limits of AMDR.

Since 1980, Americans have been told to increase their carbohydrate consumption and reduce their fat intake. Since 1980, we’ve done just that. American’s consumption patterns fall within the recommended AMDR levels, with the exception of saturated fat, which—at 11% of total calories—is just slightly more than the recommended limit of 10% of calories. (If you are interested in just exactly how well Americans have complied with the dietary recommendations of the past 30 years, you can find the gory details here.)  Far from being careless and casual consumers of anything and everything, Americans have radically shifted their eating patterns to match recommendations.

So why don’t Americans get any credit for actually lowering their fat intake and raising their carbohydrate intake, as we were told to do? I think there are a couple of things behind that.

First, I think one of the purposes of information like that presented in Figure 1 is to make sure the responsibility for overweight and obesity continues to rest squarely on the chubby little shoulders of Americans themselves and in no way reflects a possible lack of appropriateness of (or—gasp!—good scientific basis for) the Guidelines themselves. This is an attitude that pervades the Dietary Guidelines.

Second, the USDA’s Center for Nutrition Policy and Promotion would really like another $9 million to “help Americans develop eating behaviors that are more consistent with the Dietary Guidelines for Americans.” It would be a little awkward to ask for a funding increase to convince Americans to follow current dietary recommendations if we were already doing that—and they still weren’t working.

This is where recommendations become fanaticism.  According to Neil Postman, “the key to all fanatical beliefs is that they are self-confirming.”  The USDA and HHS seem unwilling to even acknowledge that the dietary shift that has occurred during the past thirty years has actually been in the direction of compliance with recommendations; in fact–according to Figure 1–they are willing to fudge the numbers to prove otherwise.  That’s not nice, and it’s sure not science.

References:

Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric sweetener consumption and dyslipidemia among US adults. JAMA. 2010 Apr 21;303(15):1490-7

It’s not the Guidelines

Adele Hite, PhD MPH RD 14 Comments

One of the enduring mysteries to me about the whole Dietary Guidelines issue is the extent to which my concerns regarding their effectiveness causes some folks to question my intelligence, knowledge, professionalism, and—I think—prescription drug use.

Take the graphic above, which appears to show a relationship in time between one event (the installation of a plastics factory) and another trend (rise in cancer rates). This does not demonstrate cause-and-effect, of course, but I think that most public health officials would be concerned enough about the clear inflection point and the following steep upward trend in disease to want to investigate the potential for a cause-effect relationship, or at least begin to ask some questions.

But when the graph looks like this, it’s a different story:


Every time I show someone the above relationship, I get remarks like, but what about physical activity levels? television? women in the work force? desk jobs? automobiles? anything, anything but the Guidelines!

Keeping in mind that the obesity graph above only shows the temporal relationship between when the Dietary Guidelines were implemented and when the rapid rise in obesity took place, I thought I would look at some of the other possible causes that are invoked in the name of avoiding the possibility that we’ve been wrong about public health nutrition for the past thirty years.

It’s not the Guidelines #1: For some reason, Americans got much lazier in the past 30 years than they have ever been before.

I will say right off the bat that we don’t have a lot of clear data about physical activity levels because we didn’t really start paying attention to it until Americans started getting fat. However, the 1983 Public Health Objectives for Americans offer some insight: “The American lifestyle is still relatively sedentary. The proportion of adults aged 18-65 regularly exercising has been estimated at just over 35% . . .” [From: Promoting Health/Preventing Disease. Public Health Service Implementation Plans for Attaining the Objectives for the Nation (Sep. – Oct., 1983), p. 155].

The most recent research—2010—on physical activity levels in America paints a much different picture:


From: Adabonyan I, Loustalot F, Kruger J, Carlson SA, Fulton JE. Prevalence of highly active adults–Behavioral Risk Factor Surveillance System, 2007.

This may not be the complete story, but there is little evidence to suggest that we have become radically more sedentary since 1980. And if we have, one would have to ask just why that would occur?

It’s not the Guidelines #2: Moms went to work, leaving the kids in front of TV sets!


Labor force participation rate of women by age of youngest child, March 1975-2007

Women began entering the workforce, even with small children at home, long before obesity rates began to climb.


Labor Force Participation of Women, Married with children under age 6. From: The first measured century

It’s not the Guidelines #3: Blame television! Television came along and we all turned into couch potatoes.



Television was in over 85% of American homes in 1960, 20 years before obesity rates began to climb. (However, it is possible that MTV, which debuted in 1980 along with the Dietary Guidelines, is at the root of our obesity crisis—anything, anything but the Guidelines!)

It’s not the Guidelines #4: We used to work at physically demanding jobs!


With these wonderful graphs from the book The first measured century: an illustrated guide to trends in America, 1900-2000, by Theodore Caplow, Louis Hicks, Ben J. Wattenberg, I looked for a similar pattern to that of the obesity trend, a parallel trend that might be a primary factor in the rise in obesity in America. The dashed lines represent the beginning of the obesity measurements above (beginning in 1960), while the solid lines shows when the first Dietary Guidelines were released (in 1980). To find some sort of correlated trend, we would want to find a flat-ish sort of line between the dashed line and the solid one, followed by a steep incline after the solid line, showing a concurrent trend.   Alternately, we might look for a curve similar to the obesity one, but shifted to the left, showing a trend that preceded the obesity one.  I didn’t find either in the transition from manual labor to more sedentary jobs.

It’s not the Guidelines #5: In the past, we used to walk everywhere–or ride our scooters, or our ponies!


I grew up in the 70s.  We rolled around in great big cars without our seat belts on.  Not such a great idea, but cars were an integral part of Americans lives long before obesity rates took off.

It’s not the Guidelines #6: Some seismic shift in our eating habits made many of us gain weight at an alarming rate.


From:  Gross et al, 2004, Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment.  AJCN

Wait a minute—this looks familiar. Hmmm. Dramatic rise in carbohydrate intake? Dramatic rise in obesity! Who’da thunk? And why did we start eating all those carbs? Not because we were sitting in front of the TV while our moms went to work (we were, but that’s not why). We started filling our plates with cereals and starches because the Dietary Guidelines told us to.

References:

Adabonyan I, Loustalot F, Kruger J, Carlson SA, Fulton JE. Prevalence of highly active adults–Behavioral Risk Factor Surveillance System, 2007. Prev Med. 2010 Aug;51(2):139-43.

Gross L, Li L, Ford ES, Liu S.  Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment.  American Journal of Clinical Nutrition, Vol. 79, No. 5, 774-779, May 2004

Public Health Reports (1974-) , Vol. 98, Supplement: Promoting Health/Preventing Disease. Public Health Service Implementation Plans for Attaining the Objectives for the Nation (Sep. – Oct., 1983), pp. 1-177

Fat? Blame Mom

Adele Hite, PhD MPH RD Leave a comment

“Adverse factors encountered during fetal life have the dual effect of perturbing prenatal growth patterns and establishing a pre-susceptibility to major disease states in adult life”

Langley Evans: Proc Nutr Soc. 2001;60(4):505-13.

Jimmy Moore of Livin’ La Vida Low Carb wrote a great post recently entitled “When Does Being Fat Become Your Fault?”  In it he states that his weight is 295 pounds. I would guess that’s accurate.  I have had the pleasure of meeting Jimmy many times & he’s a big guy. From what I understand, so was Dr. Atkins of the Atkins Diet fame. So is my 18-year old son.

In the past, when people meet some of the vocal and active members of the low-carb community who don’t necessarily match expectations of what a socially-acceptable “healthy” weight would be, I’ve been asked if the whole low-carb thing is a farce. Maybe people feel comfortable posing this question to me because I’m not heavy (anymore). And I think I can say that my weight loss journey was probably a little easier for me than for others, but not because I have more willpower or I just don’t eat that much (I love food!!). It may be because my mother insisted that I eat an egg for breakfast every morning as a child. I wasn’t there to check this out, but I assume that’s how she ate when she was pregnant with me. We were a meat-at-every-meal family. Why am I telling you this? Because it matters.

Epigenetics is a new term that gets used a lot without people know just exactly what it means. Simply put, epigenetics is the study of how the environment (especially the prenatal environment) can effect gene expression, as opposed to changing the genetic material itself. This means that certain metabolic features that are controlled by our genetic material—for instance, hormones, enzymes, appetite regulation signaling factors—may be upregulated or downregulated due to influences from our environment.

The effect of prenatal environment—including diet—on how genes are expressed can then in turn effect how we end up interacting with our current environment. Some folks get a “triple whammy”—genes that code for obesity, a prenatal environment that affects the expression of those and other genes, and an obesogenic environment. Can we honestly say that these folks have some character flaw that makes being fat their fault?


There are many things beyond our control, especially intrauterine environment, which have a primary impact on how much we weight as adults–perhaps even more impact than our current dietary habits.  I know this personally because my son, who was born when I was in my most strict vegetarian phase, has had much more trouble with his weight than my son whose pregnancy was one in which the doctor insisted that I eat high quality protein–at every single meal (unheard of for me).  My “vegetarian phase” pregnancy was a difficult one. I was on bed rest or in the hospital most of my last trimester; my son was born 6 weeks early anyway. He was a skinny little kid, but as soon as adolescence kicked in (a hyperinsulinemic phase in general), he began gaining weight.

  • In terms of genetics, he got flat feet and a large build (his father’s side)
  • In terms of epigenetics, he got a vegetarian mother who ate little fat and protein while he was swimming about in utero.
  • In terms of environment, he got a vegetarian mother through his first 6 years of life; now he has a college dining hall to contend with.


His fasting insulin is higher than “normal,” (a likely result of my eating habits, not his), so he has an uphill battle even though he lifts weights, is active, and eats a low-carb diet.  He does pretty well, but imagine if he’d first spent years trying to control his weight with a high-carb, low-fat diet?

That’s just my n=1 perspective. But if what he experienced is a real effect, imagine the population-size effect. It might look a lot like the obesity and diabetes rates we are experiencing now. So what does the science tell us about that possibility? Here’s a brief glance, much of it courtesy of a lecture by Dr. Linda Adair in Fall 2009.

If the mother’s supply of nutrients does not meet the demands of the fetus, there are a few adaptive measures that take place:

  • The fetus will grow less, but maintain head & brain circumference at the expense of skeletal muscle and some other organs.
  • The fetus will become more metabolically efficient as endocrine function is altered to enhance survival.

From animal studies, scientists have seen that, even with normal nutrition after birth, adult offspring of prenatally malnourished mothers have:

  • Increased blood pressure
  • Abnormal glucose tolerance
  • Impaired inflammatory response
  • More body fat
  • Eat more
  • Move less

Hmmm. Should we assume that these mice have some sort of lack of willpower or other character flaw?


Vickers, M. H. et al. Am J Physiol Regul Integr Comp Physiol 285: R271-R273 2003;

From epidemiology studies, especially the Dutch Hunger Winter, we’ve seen that exposure to famine during pregnancy results in higher rates of markers of insulin resistance and higher rates of obesity in adults. Note the type of nutrients that were most restricted during the “Hunger Winter” were protein and fat.  In fact, the protein-to-carbohydrate ratio has been shown to be the most predictive marker with regards to some of the negative health outcomes in adulthood.


Calories derived from carbohydrate, protein, and fat in the official daily rations provided between April 1941 and April 1947.  

Follow-up studies for the Dutch Hunger Winter and other famine or near-famine situations show that babies conceived during nutrient-restricted periods grow up to have increased risk of impaired glucose tolerance, obesity, high blood pressure, and other negative health outcomes in adulthood.

Other population studies have shown a consistent association between low weight for length at birth (a possible sign that the body is selectively nourishing the brain rather than the body, see above) and impaired glucose tolerance, insulin resistance, and type 2 diabetes.


In the Nurses’ Health Study, smaller babies grew up to have an increased risk of type 2 diabetes.

Other factors, such as environmental toxins may pre-dispose kids to obesity, either as children or later in life.

People who may be affected by these epigenetic mechanisms may be metabolically—not psychologically—inclined to eat more and move less. It’s not a character flaw; it’s a biological imperative. It is what their bodies are telling them to do. At what point do we stop blaming these people (who may now make up a majority of our population) and start trying to figure out how to assist them with their efforts to be healthy?

I don’t want to go all mama grizzly on people, but my blood pressure goes through the roof when I hear my classmates make comments like:

“Well, any diet intervention is going to show an improvement in obese people. They’ve been stuffing their faces with tons of calories before this.”

and

“People are fat because they eat too much. Period.”

I think of all the wonderful people I met at the clinic. Of myself. Of Jimmy. And my son. I can count on one hand the number of overweight/obese people I’ve met whom I think actually fit these generalizations.

The thing about the low-carb approach is that it attracts people who have been unsuccessful any other way–for a good reason.  A highly dysregulated system needs a stronger intervention.  It isn’t going to turn someone with a dysregulated system into a model-thin person, but it will often allow them to lower insulin levels to the point where good health is an achievable goal, even if it doesn’t come with a socially-approved weight. Let me emphasize: I do not think low-carb is the only way to do this, but it certainly should be considered as an option.

Until we can move past our “calories-in, calories out,” preconceived notions about what constitutes “healthy” food and what makes people fat, we are doing much of the population a tremendous injustice. Our refusal to entertain any other theories besides the current high carb/low fat dietary regime (which is still, after all, a theory although it is treated as a fact) is possibly the worst failure in public health since the rejection of germ theory in the 19th century. My son is the funniest person I know, and he doesn’t hate me for my very-likely part in mucking up his metabolism. He deserves better.

References:

de Rooij SR, Painter RC, Holleman F, Bossuyt PM, Roseboom TJ. The metabolic syndrome in adults prenatally exposed to the Dutch famine. Am J Clin Nutr. 2007 Oct;86(4):1219-24.

Heijmans BT, Tobi EW, Stein AD, Putter H, Blauw GJ, Susser ES, Slagboom PE, Lumey LH.Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17046-9. Epub 2008 Oct 27

Langley-Evans SC. Fetal programming of cardiovascular function through exposure to maternal undernutrition. Proc Nutr Soc. 2001 Nov;60(4):505-13. Review

Painter RC, de Rooij SR, Bossuyt PM, de Groot E, Stok WJ, Osmond C, Barker DJ, Bleker OP, Roseboom TJ. Maternal nutrition during gestation and carotid arterial compliance in the adult offspring: the Dutch famine birth cohort. J Hypertens. 2007 Mar;25(3):533-40.

Rich-Edwards JW, Colditz GA, Stampfer MJ, Willett WC, Gillman MW, Hennekens CH, Speizer FE, Manson JE.Birthweight and the risk for type 2 diabetes mellitus in adult women. Ann Intern Med. 1999 Feb 16;130(4 Pt 1):278-84.

Vickers MH, Breier BH, McCarthy D, Gluckman PD. Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition. Am J Physiol Regul Integr Comp Physiol. 2003 Jul;285(1):R271-3

Healthy Food? No Such Thing

Adele Hite, PhD MPH RD 4 Comments

A word about “healthy” food. I have no idea what that means. To be honest, I’d love for that term to disappear altogether. The World Health Organization describes health as “a state of complete physical, mental, and social well-being, and not merely the absence of disease or infirmity.” If “being healthy” is the equivalent of “being well,” then it is easy to see that the phrase “healthy food” makes little sense. It’s hard to be “well” and be “food” at the same time!

Think about it for a minute from your own perspective in the food chain. Becoming food is not a healthy thing to have happen to you. This is why the antelope runs away from the lion and why many plants, which can’t run away, have developed a number of biochemical toxins to defend themselves.

This looks like healthy kale:

This looks like yummy kale:

But this is not “healthy” kale; it’s dead kale. It might be delicious, and it might help make you a healthy person, but it definitely not “healthy” kale. It isn’t going to grow or propagate. It is—I hope–going to get eaten.

The term “healthy” is appropriately applied to things that live and grow: people, plants, animals, environments, communities, economies. Food—i.e. something about to be eaten—isn’t living and growing. The things we consume as food may or may not allow us to become healthy (well) people in a healthy community with a healthy economy and environment.

Why am I splitting hairs over an over-used term like “healthy food”? Why does it even matter whether or not we refer to food as “healthy” or not? And aren’t some foods always “healthy”—for everyone? Y’know, like spinach, and chocolate?

To answer the first two questions: How we speak reflects how we think. When we use the phrase “healthy foods” there is an underlying assumption that

1) we know and are in agreement about how to define “healthy” foods

2) there exists a specific set of foods that fit this definition, while the rest do not.

Which brings me to the last question, aren’t some foods always “healthy/unhealthy”? Hmm. For someone whose current health status requires a low-fiber diet, kale is not “healthy.” For a kid surviving on a subsistence diet who needs the calories and the 8 essential vitamins and minerals in a bowl of Lucky Charms (not to mention the marshmallow surprises!) cereal is “healthy” (not optimal, not perfect—but better than nothing).

Note that I am not saying “Everything in moderation.” I am saying “Everything in context.”

I can tell you what foods contain the nourishment that humans require; I can tell you what foods frequently create health problems for many people. I can look back on our recent history and tell you what has happened in our food system that has not worked to create a healthy environment, economy, or society. But I cannot determine what foods or what lifestyle will create a state of health or wellness for you right now and certainly not 30 years down the road—no one can but you, and you can really only do that through educated guesswork and listening to the expert within. Nutrition experts can (if properly trained) help you with both of those things, but they can’t if they’ve already determined that they “know” what “healthy” food—for you and everyone else—is.

Just what the world needs – another blog

Adele Hite, PhD MPH RD Leave a comment

My blog reflects my own efforts to begin to translate what I learn about science into meaningful information, policy input, and dinner. This is science put into practice, in the kitchen and in my advocacy work.

Here’s the problem as I see it, plain and simple:

Really, though, there’s nothing simple about it. As a student of epidemiology I must claim that this only shows an association, not cause-effect. Whether the Guidelines “caused” the rapid rise in obesity has yet to be determined, but it’s clear that they certainly did not prevent it. To me, what is more interesting is why nutrition epidemiologists aren’t all over this particular—and remarkably obvious– association trying to figure it out. Instead, I read study after study on the arcuate nucleus and the “built” environment and circadian rhythms and the health belief model and how these things contribute to obesity—and virtually no one says “Um, excuse me, but what about the one public policy piece that since 1980 has influenced every single aspect of our food environment from our cultural norms to how nutrition research gets funded and everything in between?  You know, the Dietary Guidelines?”

As Dr. Su from Carbohydrates Can Kill said, it is like there is an invisible electric fence when it comes to questioning our national dietary policy. Scientists just don’t go there.

So of course, I want to go there.

Although I love nothing more than a romantic evening for one at PubMed, don’t expect a lot of article-jousting here. Frequently those arguments (leptin insulin ghrelin, oh my!) boil down to a collection of snapshots from experimental data that may or may not create a physiologically significant or practically useful collage.  I spent a few years at the Duke Lifestyle Medicine Clinic working with patients who were overweight/obese and frequently struggling with diabetes. This experience has focused my interests on the interactions between biology, culture, and the individual and how these influences become manifest in individual differences and population-wide similarities with regards to nutritional needs, food choices, and consumption patterns (a framework borrowed from anthropology and applied to eating, hence the name of the blog).

In addition, my experiences so far in graduate school—including an interning stint at the American Dietetic Association’s Washington, DC office—have made it very clear that when it comes to the science of nutrition, the playing field is far from level. In fact, I’m not sure our current crisis can be solved by science, or certainly not by science alone. Since the advent of the Dietary Guidelines for Americans in 1980, all aspects of nutrition research have become warped by industry and politics. And–as any grad student can tell you—the most political industry of all is the scientific/academic one.

At the same time, I’m not here to wring my hands in anguish. I’m actively trying to figure out what to do about this mess we’re in. I’d love all the feedback and help and ideas I can get from anyone with enough time on their hands to wade through my musings. Let’s save the world & have fun doing it.