Gary Taubes has authored an article about why he thinks current anti-obesity campaigns are doomed to fail, and mentions what the alternate strategy should be. This article explains my fundamental opposition to calorie postings, which I've discussed in past blog posts (including the one 5 minutes ago!)
If you have read his work before, you know what he has to say. If you have not, then it is a good summary of his conclusions about the causes of obesity.
Monday, March 28, 2011
Follow up on calorie labeling in restaurants
George Loewenstein, professor of Economic and Psycology at Carnegie Mellon University, authored an editorial in the American Journal of Clinical Nutrition entitled "Confronting reality: pitfalls of calorie posting" (AmJCN, apologies, but you can only read this article if you have a site-license via a library or university).
According to the editorial, mandatory restaurant labeling is more about politics than good science. The goal of the program is to reverse, or at least stop, the obesity epidemic by reducing calorie intake. New York was the first city in the U.S. to implement this policy, and did so based on one study published in 2008. However, this study showed only modest benefit and, by design, was unable to determine causality. This study could only generate a hypothesis. Since then, more rigorous studies have shown a modest benefit, failed to show a benefit, and even caused some harm - people ordered more calories.
A large proportion of people simply ignore the information. However, some people might actually choose to order more calories. Why? Given a limited amount of money to spend, some people appear to order as many calories as they can in order to get a "better deal." I would have to consult with my economist-in-training girlfriend to see if this is a sound explanation. But perhaps it fails because the premise is wrong - obesity is not simply the result of oblivious gluttony (see next blog post).
Regardless of the fundamental problem, namely that obesity is driven by the poor quality of the food and not merely the quantity, mandatory calorie postings in restaurants began with poor footing and they have not gained any since. The author remarks (with cynicism) that this policy may continue because it is better than the alternatives, such as taxing specific food items or reducing particular subsidies. This industry-favoring approach is echoed in the campaign sponsored by the Hershey (yes, the chocolate) Center for Health & Nutrition in collaboration with the American Dietetic Association named Moderation Nation. Hopefully the science will overcome the politics in this food fight.
According to the editorial, mandatory restaurant labeling is more about politics than good science. The goal of the program is to reverse, or at least stop, the obesity epidemic by reducing calorie intake. New York was the first city in the U.S. to implement this policy, and did so based on one study published in 2008. However, this study showed only modest benefit and, by design, was unable to determine causality. This study could only generate a hypothesis. Since then, more rigorous studies have shown a modest benefit, failed to show a benefit, and even caused some harm - people ordered more calories.
A large proportion of people simply ignore the information. However, some people might actually choose to order more calories. Why? Given a limited amount of money to spend, some people appear to order as many calories as they can in order to get a "better deal." I would have to consult with my economist-in-training girlfriend to see if this is a sound explanation. But perhaps it fails because the premise is wrong - obesity is not simply the result of oblivious gluttony (see next blog post).
Regardless of the fundamental problem, namely that obesity is driven by the poor quality of the food and not merely the quantity, mandatory calorie postings in restaurants began with poor footing and they have not gained any since. The author remarks (with cynicism) that this policy may continue because it is better than the alternatives, such as taxing specific food items or reducing particular subsidies. This industry-favoring approach is echoed in the campaign sponsored by the Hershey (yes, the chocolate) Center for Health & Nutrition in collaboration with the American Dietetic Association named Moderation Nation. Hopefully the science will overcome the politics in this food fight.
Tuesday, March 22, 2011
Chipotle beef salads
Just wanted to share this week's dinners. I bought a pot roast cut of beef at Costco this weekend. Half of it went into the slow cooker with ground chipotle (also bought this weekend), soy sauce (I now only have gluten free in the fridge), and some other seasonings; the other half went into the freezer. I cooked the meat on low all day while I was working in the lab.
For the sake of cost and convenience, the Costco pot roast was an easy choice. Definitely conventionally raised. However, my mom bought me some grass-fed beef neck bones at the farmer's market this weekend (thanks mom!). The "bison guy" wasn't able to make it this week, so there was a red meat alternate there. I'm looking forward to combining those bones with some left over bison marrow bones to make a batch of bone broth. And of course, I'll cook it in the slow cooker while I'm working.
The meat was tender and crumbled apart by the time I came home. I served it over a large bed of spinach with bell pepper, carrots, black beans, and gorgonzola. Dressed it with balsamic vinaigrette. Doesn't get much lower in carbs, higher in vegetables, and easier than this. I have to say though, that much gorgonzola isn't for the faint of heart.
For the sake of cost and convenience, the Costco pot roast was an easy choice. Definitely conventionally raised. However, my mom bought me some grass-fed beef neck bones at the farmer's market this weekend (thanks mom!). The "bison guy" wasn't able to make it this week, so there was a red meat alternate there. I'm looking forward to combining those bones with some left over bison marrow bones to make a batch of bone broth. And of course, I'll cook it in the slow cooker while I'm working.
Monday, March 21, 2011
Symposium on reducing dietary saturated fat
The latest issue of the American Journal of Clinical Nutrition has a perspective article highlighting topics discussed at an international nutritional symposium (Nutrition Symposium). The goal of the symposium was to reach an expert consensus on the current state of research regarding the evidence for the reduction of dietary saturated fat for the prevention of cardiovascular disease (CVD). There were several notable researchers. This included Walter Willett, the nutrition research juggernaut who leads the ongoing Nurse's Health Study, and Ronald Krauss, whose research describes the deleterious effects of high carbohydrate diets on LDL particle and subsequent atherogenicity.
The article seemed oddly cold and ambiguous. While this may seem like an odd criticism of a scientific article, I usually characterize scientific writing as calculated and skeptical. Perhaps it was just strange to see how little confidence the experts had on the available data which have been used to establish a very specific and rigorous public health message; that is, "reduce your saturated fat intake. I don't care how you do it. Good God! Why aren't you reducing your saturated fat intake?!"
Regardless, there were some interesting and important topics discussed:
1. Given that some evidence, but certainly not all (my words), indicates that it is beneficial to reduce saturated fat intake, there is insufficient research examining what nutrients should replace it. Thus, replacing saturated fat with transfats or carbohydrates, especially refined carbohydrates, likely offers no benefit and may increase the risk of CVD.
2. There is actually little to no direct human evidence that monounsaturated fats (think olive oil) offer a beneficial replacement for saturated fats to reduce the risk of CVD. The recommendations given are based on animal studies, epidemiological studies, and risk factors (cholesterol) and not intervention studies with hard CVD outcomes.
3. There is no consistent epidemiological evidence that dairy products adversely effect CVD risk and no intervention research indicating that it actually does. Although I would not have this perception given the nutritional Zeitgeist.
4. Research needs to address the role of individual saturated fats in the diet (although whole foods never contain them in isolation). Single biomarkers for CVD risk, such as LDL, HDL, triglycerides, LDL particle size, and many more, may be insufficient to judge the effects of diet on actual CVD risk (although by my count, most of these markers are adversely affected by refined carbohydrates and unaffected or improved by fat). Also, genetics appear to play an important role, but there isn't enough data to clarify this role.
I'm not sure what the impetus was to have all of these researchers convene and address this issue. I can only imagine (hope?) that it has been the mounting skepticism for the current dietary recommendations given by numerous organizations; and thus, an opportunity to reevaluate the evidence. I'm happy to see that refined carbohydrates are being put under the microscope not only for obesity, but now also for heart disease.
(Side note: I'm doing my best to avoid becoming a sarcastic or overtly critical blogger who constantly points out perceived flaws in what I share. But I have to say that I'm concerned that eight of the eleven organizations that provided (unrestricted) grants were industrial food groups, most of which were dairy groups.)
The article seemed oddly cold and ambiguous. While this may seem like an odd criticism of a scientific article, I usually characterize scientific writing as calculated and skeptical. Perhaps it was just strange to see how little confidence the experts had on the available data which have been used to establish a very specific and rigorous public health message; that is, "reduce your saturated fat intake. I don't care how you do it. Good God! Why aren't you reducing your saturated fat intake?!"
Regardless, there were some interesting and important topics discussed:
1. Given that some evidence, but certainly not all (my words), indicates that it is beneficial to reduce saturated fat intake, there is insufficient research examining what nutrients should replace it. Thus, replacing saturated fat with transfats or carbohydrates, especially refined carbohydrates, likely offers no benefit and may increase the risk of CVD.
2. There is actually little to no direct human evidence that monounsaturated fats (think olive oil) offer a beneficial replacement for saturated fats to reduce the risk of CVD. The recommendations given are based on animal studies, epidemiological studies, and risk factors (cholesterol) and not intervention studies with hard CVD outcomes.
3. There is no consistent epidemiological evidence that dairy products adversely effect CVD risk and no intervention research indicating that it actually does. Although I would not have this perception given the nutritional Zeitgeist.
4. Research needs to address the role of individual saturated fats in the diet (although whole foods never contain them in isolation). Single biomarkers for CVD risk, such as LDL, HDL, triglycerides, LDL particle size, and many more, may be insufficient to judge the effects of diet on actual CVD risk (although by my count, most of these markers are adversely affected by refined carbohydrates and unaffected or improved by fat). Also, genetics appear to play an important role, but there isn't enough data to clarify this role.
I'm not sure what the impetus was to have all of these researchers convene and address this issue. I can only imagine (hope?) that it has been the mounting skepticism for the current dietary recommendations given by numerous organizations; and thus, an opportunity to reevaluate the evidence. I'm happy to see that refined carbohydrates are being put under the microscope not only for obesity, but now also for heart disease.
(Side note: I'm doing my best to avoid becoming a sarcastic or overtly critical blogger who constantly points out perceived flaws in what I share. But I have to say that I'm concerned that eight of the eleven organizations that provided (unrestricted) grants were industrial food groups, most of which were dairy groups.)
Wednesday, March 16, 2011
Roast Chicken and Salad
My girlfriend and I had a wonderful homemade dinner this past Saturday. Not only was it wonderful because it was with her (*wink*), but also because it was lowish-carb and fairly sustainable.
We followed a recipe from Cook's Illustrated for a Peruvian Style roast chicken. We bought an organic free-range bird from Trader Joe's. The two meals we got out of it made it absolutely worth the $12 (versus $7 conventionally raised).
The chicken was dressed with a homemade spicy mayo. It consisted of blended spices, herbs, egg (I try to make free range my staple), and olive oil. Rocky may have used raw eggs to build muscle, I use them for emulsions.
The chicken was accompanied by a large spinach salad. Beets, red bell pepper, cucumber, and feta, with a balsamic vinaigrette.
For dessert, we made vanilla-bourbon pudding (not pictured to hide the evidence). I'd been meaning to use vanilla beans gifted to me a couple of Christmases ago, and this seemed like an ideal recipe. Despite the long time, they were still manufacture-sealed and remained fresh. There's no denying that the pudding had plenty of sugar and ensured this wasn't a truly low carb supper. But hey, it was the weekend.
We followed a recipe from Cook's Illustrated for a Peruvian Style roast chicken. We bought an organic free-range bird from Trader Joe's. The two meals we got out of it made it absolutely worth the $12 (versus $7 conventionally raised).
The chicken was dressed with a homemade spicy mayo. It consisted of blended spices, herbs, egg (I try to make free range my staple), and olive oil. Rocky may have used raw eggs to build muscle, I use them for emulsions.
The chicken was accompanied by a large spinach salad. Beets, red bell pepper, cucumber, and feta, with a balsamic vinaigrette.
For dessert, we made vanilla-bourbon pudding (not pictured to hide the evidence). I'd been meaning to use vanilla beans gifted to me a couple of Christmases ago, and this seemed like an ideal recipe. Despite the long time, they were still manufacture-sealed and remained fresh. There's no denying that the pudding had plenty of sugar and ensured this wasn't a truly low carb supper. But hey, it was the weekend.
Tuesday, March 15, 2011
Vitamin (C)an't help you much
I was looking through Facebook this morning and came upon a picture posted by a friend. It was her breakfast; and it was intended to fight off her cold. It consisted of:
fast food oatmeal
orange juice
Airborne
two other random supplements
fast food oatmeal
orange juice
Airborne
two other random supplements
If you think the supplement industry has developed a successful model for monetizing the placebo effect, then the cold-remedy arm of this industry should be the flagship. The common (viral) cold is an elusive malady. It has a weak seasonal trend, a wide range of signs and symptoms that vary person to person, and has always been particularly difficult to prevent or treat. As the saying goes, "if you don't treat your cold, it could last as long as 7-10 days. If you do treat it, you'll get over it in as little as 7-10 days." Despite the paucity of evidence that any treatment (let alone a supplement) can prevent or reduce the severity of a cold, most people seek a remedy.
Vitamin C is probably best known for ostensibly treating the common cold, and perhaps the most widely used. However, according to a 1998 Cochrane Collaboration analysis (and as of 2011, still considered up to date by the group), numerous trials have failed to show that vitamin C can reduce the severity or duration of the common cold when taken at the onset of a cold compared to a placebo. However, the report did indicate modest reductions in cold duration and severity if vitamin C supplements were taken preventatively or taken by intensely training athletes (Cochrane Vitamin C). While simply having no benefit would be a waste of money, it is a bigger problem when the supplement (or food) is detrimental.
When we are sick, we look for easily prepared and comforting foods. Sometimes this means chicken noodle soup. We also try to get some therapeutic benefit from our food. Again, sometimes this means chicken noodle soup. However, many times it simply means foods that naturally contain or are fortified with high amounts of vitamin C. So if we are short on time and want some food-therapy, we end up with something resembling my friend's breakfast. And please know that I've fallen victim to this for the entirety of the past decade, so I pass no judgement in this post. But what else are we getting besides vitamin C?
This meal likely has between 65 and 80 grams of sugar, depending if the oatmeal included the complementary brown sugar, and tens of grams of starch. The irony is that glucose and vitamin C are taken up by cells in the body via the same mechanism. Thus, vitamin C and glucose may compete to gain entry into the cells, so that high concentrations of glucose can prevent cellular uptake of vitamin C. Provisional data suggest that lower tissue concentrations of vitamin C in diabetics is due directly to hyperglycemia, and that a large bolus of glucose can deplete tissue concentrations of normal individuals to that of diabetic's (see Cunningham 1988 for details). And while it is pure speculation, it would be interesting to see if the benefits of preventative vitamin C supplementation reported in the Cochrane study were at least partially attributable to normalizing low vitamin C secondary to high glucose consumption. But alas, maybe another post.
So while it is always tempting to find a quick fix to our ailments, even ones as benign as a cold, there doesn't appear to be one available. And our attempts can likely put us in nutritional disarray at some of our most vulnerable times.
This meal likely has between 65 and 80 grams of sugar, depending if the oatmeal included the complementary brown sugar, and tens of grams of starch. The irony is that glucose and vitamin C are taken up by cells in the body via the same mechanism. Thus, vitamin C and glucose may compete to gain entry into the cells, so that high concentrations of glucose can prevent cellular uptake of vitamin C. Provisional data suggest that lower tissue concentrations of vitamin C in diabetics is due directly to hyperglycemia, and that a large bolus of glucose can deplete tissue concentrations of normal individuals to that of diabetic's (see Cunningham 1988 for details). And while it is pure speculation, it would be interesting to see if the benefits of preventative vitamin C supplementation reported in the Cochrane study were at least partially attributable to normalizing low vitamin C secondary to high glucose consumption. But alas, maybe another post.
So while it is always tempting to find a quick fix to our ailments, even ones as benign as a cold, there doesn't appear to be one available. And our attempts can likely put us in nutritional disarray at some of our most vulnerable times.
Friday, March 11, 2011
HDL and colon cancer: HDL particle, dietary carbohydrate, who knows?!
HealthDay has published a news article about a recent study that demonstrated an inverse association between high-density lipoprotein (HDL) and colon cancer. The brief article can be found here:
HDL/Colon Cancer article
The study used data from the EPIC trial, which is a European trial investigating the relationship between cancer and lifestyle, environment, and nutrition. The current study is known as a nested case-control study, which means previously collected cohort data (the EPIC trial) is used to generate a cohort-of-interest (certain blood levels of HDL, insulin, etc) and a matched cohort (control group). A relationship between the variable of interest and cancer is determined by an incidence rate ratio (RR). The RR is the ratio of the rate of developing the disease (colon cancer) in the experimental group (elevated HDL) to the rate in the control group (normal HDL); an RR greater than 1 indicates an increased rate of disease, less than 1 indicates a decreased rate, and 0 indicates no change in rate. Statistics are then used to quantify the relationship between the variables and ensure that the RRs are not simply an artifact of random chance.
The HealthDay article cites that "for each 16.6 milligrams per deciliter (mg/dL) increase in HDL and 32 mg/dL increase in apoA, the risk of colon cancer was cut by 22 percent and 18 percent, respectively." And this risk reduction was independent of other risk factors for colon cancer.
The authors of the study propose that the HDL particle itself may directly reduce the risk of colon cancer, possibly through an anti-inflammatory mechanism. However, this is speculation. It could be that high HDL is simply an indicator of an anti-colon cancer lifestyle or metabolic profile outside of what was controlled for.
HDL concentration is generally elevated in healthier people, and is manipulated by obesity, smoking, exercise, and other factors, including diet. The authors controlled for meat, fruit, vegetables, calories, and fiber. However, they didn't control for carbohydrate consumption, nor the most offensive carbohydrate - sugar. This is particularly interesting because HDL has been described as a marker for dietary carbohydrate (Sacks 2009), that is, the less carbohydrate that is consumed, the higher the concentration of HDL. Therefore, this data could suggest that decreased dietary carbohydrate, and therefore replacement by more protein, fat, or both, could have decreased the rate of colon cancer.
However, suggesting that carbohydrate reduction would reduce the risk of colon cancer is as speculative as suggesting that the HDL per se reduces the risk of colon cancer. This is just a good exercise to demonstrate how observational data can easily be used to speculate or support a theory. And since there is essentially no end to what one can speculate, perhaps observational data should be reported sans speculation.
HDL/Colon Cancer article
The study used data from the EPIC trial, which is a European trial investigating the relationship between cancer and lifestyle, environment, and nutrition. The current study is known as a nested case-control study, which means previously collected cohort data (the EPIC trial) is used to generate a cohort-of-interest (certain blood levels of HDL, insulin, etc) and a matched cohort (control group). A relationship between the variable of interest and cancer is determined by an incidence rate ratio (RR). The RR is the ratio of the rate of developing the disease (colon cancer) in the experimental group (elevated HDL) to the rate in the control group (normal HDL); an RR greater than 1 indicates an increased rate of disease, less than 1 indicates a decreased rate, and 0 indicates no change in rate. Statistics are then used to quantify the relationship between the variables and ensure that the RRs are not simply an artifact of random chance.
The HealthDay article cites that "for each 16.6 milligrams per deciliter (mg/dL) increase in HDL and 32 mg/dL increase in apoA, the risk of colon cancer was cut by 22 percent and 18 percent, respectively." And this risk reduction was independent of other risk factors for colon cancer.
The authors of the study propose that the HDL particle itself may directly reduce the risk of colon cancer, possibly through an anti-inflammatory mechanism. However, this is speculation. It could be that high HDL is simply an indicator of an anti-colon cancer lifestyle or metabolic profile outside of what was controlled for.
HDL concentration is generally elevated in healthier people, and is manipulated by obesity, smoking, exercise, and other factors, including diet. The authors controlled for meat, fruit, vegetables, calories, and fiber. However, they didn't control for carbohydrate consumption, nor the most offensive carbohydrate - sugar. This is particularly interesting because HDL has been described as a marker for dietary carbohydrate (Sacks 2009), that is, the less carbohydrate that is consumed, the higher the concentration of HDL. Therefore, this data could suggest that decreased dietary carbohydrate, and therefore replacement by more protein, fat, or both, could have decreased the rate of colon cancer.
However, suggesting that carbohydrate reduction would reduce the risk of colon cancer is as speculative as suggesting that the HDL per se reduces the risk of colon cancer. This is just a good exercise to demonstrate how observational data can easily be used to speculate or support a theory. And since there is essentially no end to what one can speculate, perhaps observational data should be reported sans speculation.
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