Wednesday, August 31, 2011
"What's Your Weapon?": Billie Jean King, Arthritis Foundation, Ad Council, and USTA Launch Arthritis Campaign
Before Twitter and the U.S. Open was a flutter this afternoon with the news of Venus Williams withdrawing due to the diagnosis of the autoimmune disease- Sjogren's Syndrome, the U.S. Tennis Association was focused on another health related issue. Today the press release went out that tennis legend Billie Jean King was joining the Arthritis Foundation, the Ad Council, and the US Tennis Association (USTA) to launch a public service campaign against arthritis (the leading cause of disability in America).
The ads, launched at the U.S. Open today, feature King (who has osteoarthritis- OA) and highlight the power of movement and exercise as "weapons" in the fight against arthritis. King tells viewers "tennis is my weapon" against arthritis. The ad then asks viewers, "what is your weapon against arthritis?" and directs them to the campaign's website in order to find out: Fight Arthritis Pain. On first view, I was not terribly impressed. The brief ad (33 seconds) does not tell you very much (e.g., King says tennis is her "weapon" but nothing is said about the benefits of movement). The goal of the ad simply appears to be motivating viewers to visit the website for additional information.
The other thing that is not clear in the ad (but clarified in the press release and website) is that this campaign is targeting OA specifically. While OA is the most common type of arthritis, it is not the only type. For example, in contrast to OA which breaks down cartilage, rheumatoid arthritis (RA) (a chronic autoimmune disease) causes inflammation of the lining of the joints. Would the exercise recommendations be the same no matter what type of arthritis? I would say that distinction is unclear for viewers.
However, I did feel better when I read the press release and saw that these ads were tested in focus groups by the Ad Council. Testing your images and messages with your target population is incredibly important. It is reported that participants felt that the concept of "having a weapon" against arthritis was powerful and motivating. That is good news considering formative research by the Ad Council found that only 16% of OA sufferers surveyed felt "very confident" that they could manage their pain. Therefore, if an ad can make viewers feel empowered and confident- that is a good thing.
The press release did not describe the demographics of the focus group participants, but I am assuming they were similar to those originally surveyed (adults age 55+ with OA). If so, it would mean that Billie Jean King was an appropriate "Champion" for the cause and someone that audience admired, having watched her in the 1960s-1970s, her prime competitive years. However, I wonder if she would be the best choice for ads targeting arthritis sufferers in a younger demographic? After all, different types of arthritis can affect people of all ages. Again, this is another reason that I would have wanted to see a clearer definition of the audience for these ads. If we are focused on older adults with OA, then it is a great choice. If we are focused on people of all ages with all types of arthritis, then maybe not.
Overall, I give this campaign a "B". The impetus of the campaign is good in that it is based on research...research that shows that arthritis suffers are too sedentary and do not feel like they have control over their pain management. The campaign aims to address these barriers by empowering viewers with a "champion" who they admire and can model. The campaign also links them to a website with all the information they need about the benefits of exercise for arthritis. However, the execution of this campaign is not as strong as its foundation. It would have benefited from a more clearly defined audience and message.
Labels:
arthritis,
billie jean king,
celebrity,
health communication,
pop culture,
PSA,
tennis
Monday, August 29, 2011
Men who are skinny-fat: There are quite a few of them
The graph below (from Wikipedia) plots body fat percentage (BF) against body mass index (BMI) for men. The data is a bit old: 1994. The top-left quadrant refers to men with BF greater than 25 percent and BMI lower than 25. A man with a BF greater than 25 has crossed into obese territory, even though a BMI lower than 25 would suggest that he is not even overweight. These folks are what we could call skinny-fat men.
The data is from the National Health and Nutrition Examination Survey (NHANES), so it is from the USA only. Interesting that even though this data is from 1994, we already could find quite a few men with more than 25 percent BF and a BMI of around 20. One example of this would be a man who is 5’11’’, weighing 145 lbs, and who would be technically obese!
About 8 percent of the entire sample of men used as a basis for the plot fell into the area defined by the top-left quadrant – the skinny-fat men. (That quadrant is one in which the BMI measure is quite deceiving; another is the bottom-right quadrant.) Most of us would be tempted to conclude that all of these men were sick or on the path to becoming so. But we do not know this for sure. On the standard American diet, I think it is a reasonably good guess that these skinny-fat men would not fare very well.
What is most interesting for me regarding this data, which definitely has some measurement error built in (e.g., zero BF), is that it suggests that the percentage of skinny-fat men in the general population is surprisingly high. (And this seems to be the case for women as well.) Almost too high to characterize being skinny-fat as a disease per se, much less a genetic disease. Genetic diseases tend to be rarer.
In populations under significant natural selection pressure, which does not include modern humans living in developed countries, genetic diseases tend to be wiped out by evolution. (The unfortunate reality is that modern medicine helps these diseases spread, although quite slowly.) Moreover, the prevalence of diabetes in the population was not as high as 8 percent in 1994, and is not that high today either; although it tends to be concentrated in some areas and cluster with obesity as defined based on both BF and BMI.
And again, who knows, maybe these folks (the skinny-fat men) were not even the least healthy in the whole sample, as one may be tempted to conclude.
Maybe being skinny-fat is a trait, passed on across generations, not a disease. Maybe such a trait was useful at some point in the not so distant past to some of our ancestors, but leads to degenerative diseases in the context of a typical Western diet. Long-living Asians with low BMI tend to gravitate more toward the skinny-fat quadrant than many of their non-Asian counterparts. That is, long-living Asians generally tend have higher BF percentage at the same BMI (see a discussion about the Okinawans on this post).
Evolution is a deceptively simple process, which can lead to very odd results.
This “trait-not-disease” idea may sound like semantics, but it has major implications. It would mean that many of the folks who are currently seen as diseased or disease-prone, are in fact simply “different”. At a point in time in our past, under a unique set of circumstances, they might have been the ones who would have survived. The ones who would have been perceived as healthier than average.
The data is from the National Health and Nutrition Examination Survey (NHANES), so it is from the USA only. Interesting that even though this data is from 1994, we already could find quite a few men with more than 25 percent BF and a BMI of around 20. One example of this would be a man who is 5’11’’, weighing 145 lbs, and who would be technically obese!
About 8 percent of the entire sample of men used as a basis for the plot fell into the area defined by the top-left quadrant – the skinny-fat men. (That quadrant is one in which the BMI measure is quite deceiving; another is the bottom-right quadrant.) Most of us would be tempted to conclude that all of these men were sick or on the path to becoming so. But we do not know this for sure. On the standard American diet, I think it is a reasonably good guess that these skinny-fat men would not fare very well.
What is most interesting for me regarding this data, which definitely has some measurement error built in (e.g., zero BF), is that it suggests that the percentage of skinny-fat men in the general population is surprisingly high. (And this seems to be the case for women as well.) Almost too high to characterize being skinny-fat as a disease per se, much less a genetic disease. Genetic diseases tend to be rarer.
In populations under significant natural selection pressure, which does not include modern humans living in developed countries, genetic diseases tend to be wiped out by evolution. (The unfortunate reality is that modern medicine helps these diseases spread, although quite slowly.) Moreover, the prevalence of diabetes in the population was not as high as 8 percent in 1994, and is not that high today either; although it tends to be concentrated in some areas and cluster with obesity as defined based on both BF and BMI.
And again, who knows, maybe these folks (the skinny-fat men) were not even the least healthy in the whole sample, as one may be tempted to conclude.
Maybe being skinny-fat is a trait, passed on across generations, not a disease. Maybe such a trait was useful at some point in the not so distant past to some of our ancestors, but leads to degenerative diseases in the context of a typical Western diet. Long-living Asians with low BMI tend to gravitate more toward the skinny-fat quadrant than many of their non-Asian counterparts. That is, long-living Asians generally tend have higher BF percentage at the same BMI (see a discussion about the Okinawans on this post).
Evolution is a deceptively simple process, which can lead to very odd results.
This “trait-not-disease” idea may sound like semantics, but it has major implications. It would mean that many of the folks who are currently seen as diseased or disease-prone, are in fact simply “different”. At a point in time in our past, under a unique set of circumstances, they might have been the ones who would have survived. The ones who would have been perceived as healthier than average.
Tuesday, August 23, 2011
The East Coast Earthquake, Real Time Twitter Chat, and Facebook Applications for Disasters
Well! Today was an interesting day at the office. Up and down the east coast, many of us felt the tremors resulting from an earthquake in Virginia. While I would like to report that we all stayed calm and participated in orderly, safe, and well rehearsed evacuations...that was not the case. It appeared that the shock of experiencing an earthquake (such a rare event on the east coast) caused a little chaos. On my way into my office to grab my bag before hitting the stairs, I experienced a "George Costanza" type moment as a fellow staff person almost knocked me down in her rush to get out. I heard similar stories from my husband who works 4 blocks away. Upon recognition of the earthquake, his co-workers made a beeline for the safest escape route...the elevator?!
After the shaking took us down 13 flights of stairs, I quickly turned to the only reliable source for real time information- Twitter. Since I was the only one in the area who either grabbed my phone or had twitter, I quickly read off what I knew: "It is a 5.9 earthquake in Virginia"; "My colleagues felt it in- Baltimore, DC, Boston, NYC, North Carolina"; "No damage except one broken window is reported in Philadelphia". After being given the go ahead to return to the building and settling back into our work, we received an official text/email from the University reiterating the information Twitter delivered an hour before. According to Twitter's official profile tonight, within one minute of the #earthquake, there were more than 40,000 earthquake-related tweets. They reached 5,500 tweets per second (TPS).
As I discussed in a related post back in March 2011, the question for public health professionals continues to be- "What is the role of social media in emergency preparedness and recovery?"
I believe we are making some strides in answering that question. Just yesterday, the Office of the Assistant Secretary for Preparedness and Response (ASPR)- located within the US Dept of Health and Human Services (HHS)- launched a contest: The ASPR Lifeline Facebook Application Challenge. The goal of the contest is to create applications that prepare individuals for disasters and build resilient communities. Those who opt into the application will be able to identify "lifelines" or Facebook friends that agree to be an individual's emergency contact and act on their behalf in case of an emergency. They will also be able to create a personal preparedness plan and share that plan and the application with others.
Even without the formal application, we have seen social network sites be used for checking in with friends/family and for getting information out quickly. For example, I follow the Philadelphia Office of Emergency Management on Twitter, so I got the message quickly that our 9-1-1 system was being inundated with calls since the earthquake and we should only use it with a real emergency...for infrastructure damage, call 3-1-1 instead.
While the Facebook application sounds like a great addition to emergency preparedness, it is important to also consider implementation issues which will impact its reach and effectiveness:
What were your experiences today during the east coast earthquake? What did you hear/see from your colleagues? How did you get/send information to others? Please share in the comments section below.
After the shaking took us down 13 flights of stairs, I quickly turned to the only reliable source for real time information- Twitter. Since I was the only one in the area who either grabbed my phone or had twitter, I quickly read off what I knew: "It is a 5.9 earthquake in Virginia"; "My colleagues felt it in- Baltimore, DC, Boston, NYC, North Carolina"; "No damage except one broken window is reported in Philadelphia". After being given the go ahead to return to the building and settling back into our work, we received an official text/email from the University reiterating the information Twitter delivered an hour before. According to Twitter's official profile tonight, within one minute of the #earthquake, there were more than 40,000 earthquake-related tweets. They reached 5,500 tweets per second (TPS).
As I discussed in a related post back in March 2011, the question for public health professionals continues to be- "What is the role of social media in emergency preparedness and recovery?"
I believe we are making some strides in answering that question. Just yesterday, the Office of the Assistant Secretary for Preparedness and Response (ASPR)- located within the US Dept of Health and Human Services (HHS)- launched a contest: The ASPR Lifeline Facebook Application Challenge. The goal of the contest is to create applications that prepare individuals for disasters and build resilient communities. Those who opt into the application will be able to identify "lifelines" or Facebook friends that agree to be an individual's emergency contact and act on their behalf in case of an emergency. They will also be able to create a personal preparedness plan and share that plan and the application with others.
Even without the formal application, we have seen social network sites be used for checking in with friends/family and for getting information out quickly. For example, I follow the Philadelphia Office of Emergency Management on Twitter, so I got the message quickly that our 9-1-1 system was being inundated with calls since the earthquake and we should only use it with a real emergency...for infrastructure damage, call 3-1-1 instead.
While the Facebook application sounds like a great addition to emergency preparedness, it is important to also consider implementation issues which will impact its reach and effectiveness:
- Is the application only available to Facebook members who download it ahead of time? Or will it be available to anyone via the mobile web?
- Do these Facebook members typically update their profile via mobile devices in addition to stationary computers (which may not be available during an emergency)?
- During the emergency, are there cell networks/wifi to support the communication? (e.g., many reported that cell networks were jammed immediately following the earthquake)
- Do these "electronic" preparedness plans need to be rehearsed the same way as "in person" plans in order to increase effectiveness?
What were your experiences today during the east coast earthquake? What did you hear/see from your colleagues? How did you get/send information to others? Please share in the comments section below.
Labels:
earthquake,
emergency,
evaluation,
health communication,
HHS,
public health
Monday, August 22, 2011
Refined carbohydrate-rich foods, palatability, glycemic load, and the Paleo movement
A great deal of discussion has been going on recently revolving around the so-called “carbohydrate hypothesis of obesity”. I will use the acronym CHO to refer to this hypothesis. This acronym is often used to refer to carbohydrates in nutrition research; I hope this will not cause confusion.
The CHO could be summarized as this: a person consumes foods with “easily digestible” carbohydrates, those carbohydrates raise insulin levels abnormally, the abnormally high insulin levels drive too much fat into body fat cells and keep it there, this causes hunger as not enough fat is released from fat cells for use as energy, this hunger drives the consumption of more foods with “easily digestible” carbohydrates, and so on.
It is posited as a feedback-loop process that causes serious problems over a period of years. The term “easily digestible” is within quotes for emphasis. If it is taken to mean “refined”, which is still a bit vague, there is a good amount of epidemiological evidence in support of the CHO. If it is taken to mean simply “easily digestible”, as in potatoes and rice (which is technically a refined food, but a rather benign one), there is a lot of evidence against it. Even from an unbiased (hopefully) look at county-level data in the China Study.
Another hypothesis that has been around for a long time and that has been revived recently, which we could call the “palatability hypothesis”, is a competing hypothesis. It is an interesting and intriguing hypothesis, at least at first glance. There seems to be some truth to this hypothesis. The idea here is that we have not evolved mechanisms to deal with highly palatable foods, and thus end up overeating them. Therefore we should go in the opposite direction, and place emphasis on foods that are not very palatable to reach our optimal weight. You might think that to test this hypothesis it would be enough to find out if this diet works: “Eat something … if it tastes good, spit it out!”
But it is not so simple. To test this palatability hypothesis one could try to measure the palatability of foods, and see if it is correlated with consumption. The problem is that the formulations I have seen of the palatability hypothesis treat the palatability construct as static, when in fact it is dynamic – very dynamic. The perception of the reward associated with a specific food changes depending on a number of factors.
For example, we cannot assign a palatability score to a food without considering the particular state in which the individual who eats the food is. That state is defined by a number of factors, including physiological and psychological ones, which vary a lot across individuals and even across different points in time for the same individual. For someone who is hungry after a 20 h fast, for instance, the perceived reward associated with a food will go up significantly compared to the same person in the fed state.
Regarding the CHO, it seems very clear that refined carbohydrate-rich foods in general, particularly the highly modified ones, disrupt normal biological mechanisms that regulate hunger. Perceived food reward, or palatability, is a function of hunger. Abnormal glucose and insulin responses appear to be at the core of this phenomenon. There are undoubtedly many other factors at play as well. But, as you can see, there is a major overlap between the CHO and the palatability hypothesis. Refined carbohydrate-rich foods generally have higher palatability than natural foods in general. Humans are good engineers.
One meme that seems to be forming recently on the Internetz is that the CHO is incompatible with data from healthy isolated groups that consume a lot of carbohydrates, which are sometimes presented as alternative models of life in the Paleolithic. But in fact among influential proponents of the CHO are the intellectual founders of the Paleolithic dieting movement. Including folks who studied native diets high in carbohydrates, and found their users to be very healthy (e.g., the Kitavans). One thing that these intellectual founders did though was to clearly frame the CHO in terms of refined carbohydrate-rich foods.
Natural carbohydrate-rich foods are clearly distinguished from refined ones based on one key attribute; not the only one, but a very important one nonetheless. That attribute is their glycemic load (GL). I am using the term “natural” here as roughly synonymous with “unrefined” or “whole”. Although they are often confused, the GL is not the same as the glycemic index (GI). The GI is a measure of the effect of carbohydrate intake on blood sugar levels. Glucose is the reference; it has a GI of 100.
The GL provides a better way of predicting total blood sugar response, in terms of “area under the curve”, based on both the type and quantity of carbohydrate in a specific food. Area under the curve is ultimately what really matters; a pointed but brief spike may not have much of a metabolic effect. Insulin response is highly correlated with blood sugar response in terms of area under the curve. The GL is calculated through the following formula:
GL = (GI x the amount of available carbohydrate in grams) / 100
The GL of a food is also dynamic, but its range of variation is small enough in normoglycemic individuals so that it can be treated as a relatively static number. (Still, the reference are normoglycemic individuals.) One of the main differences between refined and natural carbohydrate-rich foods is the much higher GL of industrial carbohydrate-rich foods, and this is not affected by slight variations in GL and GI depending on an individual’s state. The table below illustrates this difference.
Looking back at the environment of our evolutionary adaptation (EEA), which was not static either, this situation becomes analogous to that of vitamin D deficiency today. A few minutes of sun exposure stimulate the production of 10,000 IU of vitamin D, whereas food fortification in the standard American diet normally provides less than 500 IU. The difference is large. So is the difference in GL of natural and refined carbohydrate-rich foods.
And what are the immediate consequences of that difference in GL values? They are abnormally elevated blood sugar and insulin levels after meals containing refined carbohydrate-rich foods. (Incidentally, the GL happens to be relatively low for the rice preparations consumed by Asian populations who seem to do well on rice-based diets.) Abnormal levels of other hormones, in a chronic fashion, come later, after many years consuming those foods. These hormones include adiponectin, leptin, and tumor necrosis factor. The authors of the article from which the table above was taken note that:
Who are the authors of this article? They are Loren Cordain, S. Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, Bruce A. Watkins, James H O’Keefe, and Janette Brand-Miller. The paper is titled “Origins and evolution of the Western diet: Health implications for the 21st century”. A full-text PDF is available here. For most of these authors, this article is their most widely cited publication so far, and it is piling up citations as I write. This means that not only members of the general public have been reading it, but that professional researchers have been reading it as well, and citing it in their own research publications.
In summary, the CHO and the palatability hypothesis overlap, and the overlap is not trivial. But the palatability hypothesis is more difficult to test. As Karl Popper noted, a good hypothesis is a testable hypothesis. Eating natural foods will make an enormous difference for the better in your health if you are coming from the standard American diet, and you can justify this statement based on the CHO, the palatability hypothesis, or even a few others – e.g., a nutrient density hypothesis, which would be closer to Weston Price's views. Even if you eat only plant-based natural foods, which I cannot fully recommend based on data I’ve reviewed on this blog, you will be better off.
The CHO could be summarized as this: a person consumes foods with “easily digestible” carbohydrates, those carbohydrates raise insulin levels abnormally, the abnormally high insulin levels drive too much fat into body fat cells and keep it there, this causes hunger as not enough fat is released from fat cells for use as energy, this hunger drives the consumption of more foods with “easily digestible” carbohydrates, and so on.
It is posited as a feedback-loop process that causes serious problems over a period of years. The term “easily digestible” is within quotes for emphasis. If it is taken to mean “refined”, which is still a bit vague, there is a good amount of epidemiological evidence in support of the CHO. If it is taken to mean simply “easily digestible”, as in potatoes and rice (which is technically a refined food, but a rather benign one), there is a lot of evidence against it. Even from an unbiased (hopefully) look at county-level data in the China Study.
Another hypothesis that has been around for a long time and that has been revived recently, which we could call the “palatability hypothesis”, is a competing hypothesis. It is an interesting and intriguing hypothesis, at least at first glance. There seems to be some truth to this hypothesis. The idea here is that we have not evolved mechanisms to deal with highly palatable foods, and thus end up overeating them. Therefore we should go in the opposite direction, and place emphasis on foods that are not very palatable to reach our optimal weight. You might think that to test this hypothesis it would be enough to find out if this diet works: “Eat something … if it tastes good, spit it out!”
But it is not so simple. To test this palatability hypothesis one could try to measure the palatability of foods, and see if it is correlated with consumption. The problem is that the formulations I have seen of the palatability hypothesis treat the palatability construct as static, when in fact it is dynamic – very dynamic. The perception of the reward associated with a specific food changes depending on a number of factors.
For example, we cannot assign a palatability score to a food without considering the particular state in which the individual who eats the food is. That state is defined by a number of factors, including physiological and psychological ones, which vary a lot across individuals and even across different points in time for the same individual. For someone who is hungry after a 20 h fast, for instance, the perceived reward associated with a food will go up significantly compared to the same person in the fed state.
Regarding the CHO, it seems very clear that refined carbohydrate-rich foods in general, particularly the highly modified ones, disrupt normal biological mechanisms that regulate hunger. Perceived food reward, or palatability, is a function of hunger. Abnormal glucose and insulin responses appear to be at the core of this phenomenon. There are undoubtedly many other factors at play as well. But, as you can see, there is a major overlap between the CHO and the palatability hypothesis. Refined carbohydrate-rich foods generally have higher palatability than natural foods in general. Humans are good engineers.
One meme that seems to be forming recently on the Internetz is that the CHO is incompatible with data from healthy isolated groups that consume a lot of carbohydrates, which are sometimes presented as alternative models of life in the Paleolithic. But in fact among influential proponents of the CHO are the intellectual founders of the Paleolithic dieting movement. Including folks who studied native diets high in carbohydrates, and found their users to be very healthy (e.g., the Kitavans). One thing that these intellectual founders did though was to clearly frame the CHO in terms of refined carbohydrate-rich foods.
Natural carbohydrate-rich foods are clearly distinguished from refined ones based on one key attribute; not the only one, but a very important one nonetheless. That attribute is their glycemic load (GL). I am using the term “natural” here as roughly synonymous with “unrefined” or “whole”. Although they are often confused, the GL is not the same as the glycemic index (GI). The GI is a measure of the effect of carbohydrate intake on blood sugar levels. Glucose is the reference; it has a GI of 100.
The GL provides a better way of predicting total blood sugar response, in terms of “area under the curve”, based on both the type and quantity of carbohydrate in a specific food. Area under the curve is ultimately what really matters; a pointed but brief spike may not have much of a metabolic effect. Insulin response is highly correlated with blood sugar response in terms of area under the curve. The GL is calculated through the following formula:
GL = (GI x the amount of available carbohydrate in grams) / 100
The GL of a food is also dynamic, but its range of variation is small enough in normoglycemic individuals so that it can be treated as a relatively static number. (Still, the reference are normoglycemic individuals.) One of the main differences between refined and natural carbohydrate-rich foods is the much higher GL of industrial carbohydrate-rich foods, and this is not affected by slight variations in GL and GI depending on an individual’s state. The table below illustrates this difference.
Looking back at the environment of our evolutionary adaptation (EEA), which was not static either, this situation becomes analogous to that of vitamin D deficiency today. A few minutes of sun exposure stimulate the production of 10,000 IU of vitamin D, whereas food fortification in the standard American diet normally provides less than 500 IU. The difference is large. So is the difference in GL of natural and refined carbohydrate-rich foods.
And what are the immediate consequences of that difference in GL values? They are abnormally elevated blood sugar and insulin levels after meals containing refined carbohydrate-rich foods. (Incidentally, the GL happens to be relatively low for the rice preparations consumed by Asian populations who seem to do well on rice-based diets.) Abnormal levels of other hormones, in a chronic fashion, come later, after many years consuming those foods. These hormones include adiponectin, leptin, and tumor necrosis factor. The authors of the article from which the table above was taken note that:
Within the past 20 y, substantial evidence has accumulated showing that long term consumption of high glycemic load carbohydrates can adversely affect metabolism and health. Specifically, chronic hyperglycemia and hyperinsulinemia induced by high glycemic load carbohydrates may elicit a number of hormonal and physiologic changes that promote insulin resistance. Chronic hyperinsulinemia represents the primary metabolic defect in the metabolic syndrome.
Who are the authors of this article? They are Loren Cordain, S. Boyd Eaton, Anthony Sebastian, Neil Mann, Staffan Lindeberg, Bruce A. Watkins, James H O’Keefe, and Janette Brand-Miller. The paper is titled “Origins and evolution of the Western diet: Health implications for the 21st century”. A full-text PDF is available here. For most of these authors, this article is their most widely cited publication so far, and it is piling up citations as I write. This means that not only members of the general public have been reading it, but that professional researchers have been reading it as well, and citing it in their own research publications.
In summary, the CHO and the palatability hypothesis overlap, and the overlap is not trivial. But the palatability hypothesis is more difficult to test. As Karl Popper noted, a good hypothesis is a testable hypothesis. Eating natural foods will make an enormous difference for the better in your health if you are coming from the standard American diet, and you can justify this statement based on the CHO, the palatability hypothesis, or even a few others – e.g., a nutrient density hypothesis, which would be closer to Weston Price's views. Even if you eat only plant-based natural foods, which I cannot fully recommend based on data I’ve reviewed on this blog, you will be better off.
Labels:
adiponectin,
glycemic index,
glycemic load,
insulin,
leptin,
paleo diet,
research,
tumor necrosis factor-alpha
Monday, August 15, 2011
Book review: Sugar Nation
Jeff O’Connell is the Editor-in-Chief for Bodybuilding.com, a former executive writer for Men’s Health, and former Editor-in-Chief of Muscle & Fitness. He is also the author of a few bestselling books on fitness.
It is obvious that Jeff is someone who can write, and this comes across very clearly in his new book, Sugar Nation.
Now, with a title like this, Sugar Nation, I was expecting a book discussing trends of sugar consumption in the USA, and the related trends in various degenerative diseases. So when I started reading the book I was slightly put off by what seemed to be a book about a very personal journey, written in the first person by the author.
Yet, after reading it for a while I was hooked, and literally could not put the book down. Jeff has managed to write something of a page-turner, combining a harrowing personal account with carefully researched scientific information, about a relatively rare form of type 2 diabetes.
Jeff has a genetic propensity to insulin resistance, just like his father did. What makes Jeff’s case a little unusual is that Jeff is thin, and apparently has difficulty gaining weight. The most common type of diabetes is type 2, and most of those who develop type 2 diabetes do so via the metabolic syndrome. Typically this involves becoming obese or overweight before getting diagnosed as a diabetic.
In fact, in a thin person who is insulin resistant it seems that body fat cells become resistant to the normal actions of insulin much sooner than in the obese. This essentially means that they start rejecting fat. This is a problem, because fat should either be stored in fat cells (adipocytes) or used for energy; as opposed to being deposited in other tissues or remaining in circulation. Apparently this makes it even more difficult for them to control glucose levels once insulin resistance sets in; there is no “cushion”, so to speak.
Still, Jeff appears to believe that his case was that of a skinny-fat person, where body fat percentage is a lot higher than expected based on a low body mass index, and where excess visceral fat is a main culprit. In fact, Jeff seems to think that most cases of thin folks who developed type 2 diabetes are like this, as they follow the metabolic syndrome progression pattern. Fasting triglycerides go up and HDL cholesterol goes down, among other things, but in a skinny-fat body.
Somewhat predictably, what Jeff found out is that, in his case, adopting a low carbohydrate diet made an enormous difference. In fact, it made the difference between having a fairly normal life versus constantly suffering through hypoglycemic episodes. And, at the stage in which Jeff caught the problem, he did not have to avoid all natural carbohydrate-rich foods, not even things like apples. (He had to control portions though.) It is the refined carbohydrate-rich foods that were the problem for him.
I must say that I disagree with a few of the statements in the book. For example, the author seems to believe that excess saturated fat and salt may be quite unhealthy. I think that foods rich in refined carbohydrates and sugars are much more of a problem; cut them out and often excess saturated fat and salt either cease to be a problem, or become healthy. Jeff doesn’t seem to think that excess omega-6 fats can also cause diabetes; I believe the opposite to be true, via a pro-inflammatory path.
Still, this is a great book on so many levels. Jeff meticulously records his experience dealing with doctors, most of whom seem to be clueless as to what to do to prevent the damage that is caused by abnormally high glucose levels. This happens even though diabetes is those doctors’ main area of expertise. He talks about himself with complete abandon, and manages to mix that up with quite a lot of relevant research on diabetes. He gives us an insider’s view of the professional bodybuilding culture, including its use of insulin injections. His description of the Amish is very interesting and somewhat surprising.
For these reasons and a few others, I think this is a great book, and highly recommend it!
(Source: Bodybuilding.com)
It is obvious that Jeff is someone who can write, and this comes across very clearly in his new book, Sugar Nation.
Now, with a title like this, Sugar Nation, I was expecting a book discussing trends of sugar consumption in the USA, and the related trends in various degenerative diseases. So when I started reading the book I was slightly put off by what seemed to be a book about a very personal journey, written in the first person by the author.
Yet, after reading it for a while I was hooked, and literally could not put the book down. Jeff has managed to write something of a page-turner, combining a harrowing personal account with carefully researched scientific information, about a relatively rare form of type 2 diabetes.
Jeff has a genetic propensity to insulin resistance, just like his father did. What makes Jeff’s case a little unusual is that Jeff is thin, and apparently has difficulty gaining weight. The most common type of diabetes is type 2, and most of those who develop type 2 diabetes do so via the metabolic syndrome. Typically this involves becoming obese or overweight before getting diagnosed as a diabetic.
In fact, in a thin person who is insulin resistant it seems that body fat cells become resistant to the normal actions of insulin much sooner than in the obese. This essentially means that they start rejecting fat. This is a problem, because fat should either be stored in fat cells (adipocytes) or used for energy; as opposed to being deposited in other tissues or remaining in circulation. Apparently this makes it even more difficult for them to control glucose levels once insulin resistance sets in; there is no “cushion”, so to speak.
Still, Jeff appears to believe that his case was that of a skinny-fat person, where body fat percentage is a lot higher than expected based on a low body mass index, and where excess visceral fat is a main culprit. In fact, Jeff seems to think that most cases of thin folks who developed type 2 diabetes are like this, as they follow the metabolic syndrome progression pattern. Fasting triglycerides go up and HDL cholesterol goes down, among other things, but in a skinny-fat body.
Somewhat predictably, what Jeff found out is that, in his case, adopting a low carbohydrate diet made an enormous difference. In fact, it made the difference between having a fairly normal life versus constantly suffering through hypoglycemic episodes. And, at the stage in which Jeff caught the problem, he did not have to avoid all natural carbohydrate-rich foods, not even things like apples. (He had to control portions though.) It is the refined carbohydrate-rich foods that were the problem for him.
I must say that I disagree with a few of the statements in the book. For example, the author seems to believe that excess saturated fat and salt may be quite unhealthy. I think that foods rich in refined carbohydrates and sugars are much more of a problem; cut them out and often excess saturated fat and salt either cease to be a problem, or become healthy. Jeff doesn’t seem to think that excess omega-6 fats can also cause diabetes; I believe the opposite to be true, via a pro-inflammatory path.
Still, this is a great book on so many levels. Jeff meticulously records his experience dealing with doctors, most of whom seem to be clueless as to what to do to prevent the damage that is caused by abnormally high glucose levels. This happens even though diabetes is those doctors’ main area of expertise. He talks about himself with complete abandon, and manages to mix that up with quite a lot of relevant research on diabetes. He gives us an insider’s view of the professional bodybuilding culture, including its use of insulin injections. His description of the Amish is very interesting and somewhat surprising.
For these reasons and a few others, I think this is a great book, and highly recommend it!
Wednesday, August 10, 2011
Should Public Health Professionals "Give A Shit" About MTV's New Campaign?
Has anyone else seen #giveashit on Twitter in the past few days? MTV has launched the "Give a Shit" campaign to increase civic engagement and encourage people to voice their concerns for any issue about which they are passionate. Many are voicing concerns about important public health issues like access to clean water. Great way to engage young people, right? Using a play on words. Using foul language. But the question remains- what are the goals of the campaign? Will the campaign actually improve public health?
The primary strategy for messaging about the campaign is a YouTube video featuring Nikki Reed (of Twilight fame). The tone of the two-minute video is hard to classify. In some ways it appears to be a parody of a real PSA (e.g., it simulates Nikki on the toilet so she can use that time to "give a shit"). But then it seems to have genuine moments when it motivates people to join a movement- any movement. Nikki tells viewers that all they have to do is "give a shit". It doesn't matter if they don't actually DO anything...if they CARE, then the world's problems will cease to exist.
As you can imagine, I take issue with this premise. So much of what we know in public health is based on evaluation data that has shown us that "knowledge" does not equal behavior change. "Increasing awareness" about pregnancy does not eliminate unprotected sex. Having the "intention" to stop smoking does not help when someone is addicted to nicotine. Therefore, it is unclear to me how just caring about an issue like access to clean water will result in positive change.
Next, the video goes on to say that once you care about the issue, you should alert your social networks. It shows images of posts to Twitter like, "I just gave a shit about global warming". So I went into Twitter to see if it is actually happening, and it is. The #giveashit hash tag is alive and well and users are reporting that they care about children with special needs, animal cruelty, etc. But again, I'm still at a loss as to how this "caring" and "twitter posting" actually leads to an increase in positive civic engagement. I tried to look for additional information on their website: www.give-a-shit.org but the site is not currently functioning. That is a problem as well. If the goals of the campaign are already unclear, it does not help that users cannot access information beyond the YouTube video. Several advocacy websites offer a brief overview of the campaign that may be helpful in the absence of a functioning website.
So while the play on words is "cute" and I appreciate a campaign that aims to combat the apathy that can be rampant regarding serious public health issues...I don't understand how this campaign will actually change behavior. And no- I don't agree that just caring about an issue will make all problems go away. If it did, we in public health would be out of a job.
The primary strategy for messaging about the campaign is a YouTube video featuring Nikki Reed (of Twilight fame). The tone of the two-minute video is hard to classify. In some ways it appears to be a parody of a real PSA (e.g., it simulates Nikki on the toilet so she can use that time to "give a shit"). But then it seems to have genuine moments when it motivates people to join a movement- any movement. Nikki tells viewers that all they have to do is "give a shit". It doesn't matter if they don't actually DO anything...if they CARE, then the world's problems will cease to exist.
As you can imagine, I take issue with this premise. So much of what we know in public health is based on evaluation data that has shown us that "knowledge" does not equal behavior change. "Increasing awareness" about pregnancy does not eliminate unprotected sex. Having the "intention" to stop smoking does not help when someone is addicted to nicotine. Therefore, it is unclear to me how just caring about an issue like access to clean water will result in positive change.
Next, the video goes on to say that once you care about the issue, you should alert your social networks. It shows images of posts to Twitter like, "I just gave a shit about global warming". So I went into Twitter to see if it is actually happening, and it is. The #giveashit hash tag is alive and well and users are reporting that they care about children with special needs, animal cruelty, etc. But again, I'm still at a loss as to how this "caring" and "twitter posting" actually leads to an increase in positive civic engagement. I tried to look for additional information on their website: www.give-a-shit.org but the site is not currently functioning. That is a problem as well. If the goals of the campaign are already unclear, it does not help that users cannot access information beyond the YouTube video. Several advocacy websites offer a brief overview of the campaign that may be helpful in the absence of a functioning website.
So while the play on words is "cute" and I appreciate a campaign that aims to combat the apathy that can be rampant regarding serious public health issues...I don't understand how this campaign will actually change behavior. And no- I don't agree that just caring about an issue will make all problems go away. If it did, we in public health would be out of a job.
Labels:
celebrity,
give a shit,
health communication,
MTV,
PSA,
public health
Media Must Cover Suicides Cautiously- In Today's Philadelphia Inquirer
An editorial that I co-authored ran in today's Philadelphia Inquirer. The piece is in response to media coverage of the suicide of a Philadelphia Firefighter. In a previous blog post following a celebrity suicide, I discussed the public health implications of the media coverage that follows. It can either encourage negative behavior in the audience by including unsafe and unnecessary details like detailing suicide methods...or it can encourage positive help-seeking behavior by including resources like the National Suicide Prevention Lifeline. I encourage all bloggers, communication professionals, and journalists to review the expert recommendations on how to safely report on suicides.
I look forward to hearing your comments!
Labels:
celebrity,
health communication,
public health,
suicide
Monday, August 8, 2011
Potassium deficiency in low carbohydrate dieting: High protein and fat alternatives that do not involve supplementation
It is often pointed out, at least anecdotally, that potassium deficiency is common among low carbohydrate dieters. Potassium deficiency can lead to a number of unpleasant symptoms and health problems. This micronutrient is present in small quantities in meat and seafood; main sources are plant foods.
A while ago this has gotten me thinking and asking myself: what about isolated hunter-gatherers that seem to have thrived consuming mostly carnivorous diets with little potassium, such as various Native American tribes?
Another thought came to mind, which is that animal protein seems to be associated with increased bone mineralization, even when calcium intake is low. That seems to be due to animal protein being associated with increased absorption of calcium and other minerals that make up bone tissue.
Maybe animal protein intake is also associated with increased potassium absorption. If this is true, what could be the possible mechanism?
As it turns out, there is one possible and somewhat surprising connection, insulin seems to promote cell uptake of potassium. This is an argument made many years ago by Clausen and Kohn, and further discussed more recently by Benziane and Chibalin. See also this recent commentary by Clausen.
Protein is the only macronutrient that normally causes transient insulin elevation without any glucose response. And the insulin response to protein is nowhere near that associated with refined carbohydrate-rich foods. It is much lower, analogous to the response to natural carbohydrate-rich foods.
A very low carbohydrate diet with more animal protein, and less fat, would induce insulin responses after meals, possibly helping with the absorption of potassium, even if potassium intake were rather limited. Primarily carnivorous diets, like those of some traditional Native American groups, would fit the bill.
Also, a low carbohydrate diet with emphasis on fat, but that was not so low in carbohydrates from certain sources, would probably achieve the same effect. This latter sounds like Kwaśniewski’s Optimal Diet, where people are encouraged to eat a lot more fat than protein, but also a small amount of carbohydrates (e.g., 50-100 g/d) from things like potatoes.
Kwaśniewski’s suggestions may sound counterintuitive sometimes. But, as it turns out, potatoes are good sources of potassium. One potato may not be a lot, but that potato will also increase insulin levels, bringing potassium intake up at the cell level.
A while ago this has gotten me thinking and asking myself: what about isolated hunter-gatherers that seem to have thrived consuming mostly carnivorous diets with little potassium, such as various Native American tribes?
Another thought came to mind, which is that animal protein seems to be associated with increased bone mineralization, even when calcium intake is low. That seems to be due to animal protein being associated with increased absorption of calcium and other minerals that make up bone tissue.
Maybe animal protein intake is also associated with increased potassium absorption. If this is true, what could be the possible mechanism?
As it turns out, there is one possible and somewhat surprising connection, insulin seems to promote cell uptake of potassium. This is an argument made many years ago by Clausen and Kohn, and further discussed more recently by Benziane and Chibalin. See also this recent commentary by Clausen.
Protein is the only macronutrient that normally causes transient insulin elevation without any glucose response. And the insulin response to protein is nowhere near that associated with refined carbohydrate-rich foods. It is much lower, analogous to the response to natural carbohydrate-rich foods.
A very low carbohydrate diet with more animal protein, and less fat, would induce insulin responses after meals, possibly helping with the absorption of potassium, even if potassium intake were rather limited. Primarily carnivorous diets, like those of some traditional Native American groups, would fit the bill.
Also, a low carbohydrate diet with emphasis on fat, but that was not so low in carbohydrates from certain sources, would probably achieve the same effect. This latter sounds like Kwaśniewski’s Optimal Diet, where people are encouraged to eat a lot more fat than protein, but also a small amount of carbohydrates (e.g., 50-100 g/d) from things like potatoes.
Kwaśniewski’s suggestions may sound counterintuitive sometimes. But, as it turns out, potatoes are good sources of potassium. One potato may not be a lot, but that potato will also increase insulin levels, bringing potassium intake up at the cell level.
Wednesday, August 3, 2011
Let's Talk Safety Climate and the Airlines: "Welcome Aboard"
I spent the past few weeks out on vacation in the beautiful Pacific Northwest (which explains my brief absence from Pop Health). While the trip was wonderful, it is quite nice to be back on the blog. And in fact, my trip provided me with the inspiration for this post. On my return flight home, I encountered an array of travel nightmares (delays, mechanical problems, cancelled flights, lost luggage). While many people may just consider these as an inconvenience, they also got me thinking about my safety. As we sat at the gate and waited for test after test, my husband assured me that they wouldn't put us on the plane if it wasn't safe. However, I wondered aloud if that was true. With the pressure for the airlines to have better on-time statistics and less angry customers, can we be put on a plane that is unsafe? My experience with USAirways, the similar experiences that I read about on Twitter, and the information I found regarding their dysfunctional relationship with their Pilots Association got me interested in the safety climate of the airline industry.
Everyday we encounter airline advertising that hopes to recruit our business by highlighting a company's high standards for safety, comfort, reasonable prices, and customer service. The ads also try to capitalize on things that we value, for example- freedom. Some memorable slogans include, "You are now free to move about the country" (Southwest); "We love to fly and it shows" (Delta); "Come fly the friendly skies" (United). While these slogans are catchy and convincing, they represent the "espoused values" of the airlines. Espoused values are values and norms stated by the organization. They can often be found in companies' strategic plans, goals, and/or taglines. For example, USAirways has an initiative called "Customers First" which strives to address key service elements that affect their customers.
In addition to espoused values, we also find "enacted values"; these are the norms that are actually exhibited by employees. These values may or may not be in line with the espoused values. That is why even though "Customers First" can be an espoused value, you can still end up bumped off a flight and sleeping in the airport because the rude gate agent told you there was no flight availability. In order to hear about other customers experiences with enacted values, I turned to Twitter and was amazed by what I saw. There were hundreds of comments to or about @usairways that were identical to mine- lots of mechanical failures ending in flight cancellations and luggage that was lost for days. I understand Twitter may be skewed towards the negative because people are less likely to tweet about the on-time departures...however, if you look at another airline (e.g., @southwestair) you see almost nothing about mechanical problems.
A less biased way to learn about employees' values and their level of congruence with the organization executives, is to hear from them directly. Just a few weeks ago, the US Airline Pilot Association- USAPA (the union that represents USAirways pilots), posted on their website to alert customers to the pressure they are receiving from USAirways executives to fly under unsafe conditions. On June 16, 2011, a pilot with 30-years of experience was escorted from the airport after she refused to fly a plane overseas after it failed multiple safety checks. A second group of pilots refused to fly the plane as well. This is not the first time that USAPA has spoken out against the executives. In 2008, they posted a customer alert in USA Today because they were being pressured to fly with less fuel in order to save money.
The examination and measurement of espoused/enacted values and their connection to safety outcomes (e.g., occupational injuries) is the exciting field of safety climate research. The term "safety climate" was coined in 1980 by Dr. Dov Zohar and has been prevalent in the Industrial and Organizational Psychology literature before making its way into the public health literature. For those interested, the journal Accident Analysis & Prevention recently dedicated an issue to safety climate and occupational health.
Safety climate research has been used to assess the climate of a variety of industries (e.g., healthcare). I propose that it is essential for examining the values within individual airlines and their connection to safety outcomes (e.g., worker injuries, passenger injuries, mechanical failures, near-misses, etc). The discrepancy discussed above between employee and company values can become a very dangerous combination.
Everyday we encounter airline advertising that hopes to recruit our business by highlighting a company's high standards for safety, comfort, reasonable prices, and customer service. The ads also try to capitalize on things that we value, for example- freedom. Some memorable slogans include, "You are now free to move about the country" (Southwest); "We love to fly and it shows" (Delta); "Come fly the friendly skies" (United). While these slogans are catchy and convincing, they represent the "espoused values" of the airlines. Espoused values are values and norms stated by the organization. They can often be found in companies' strategic plans, goals, and/or taglines. For example, USAirways has an initiative called "Customers First" which strives to address key service elements that affect their customers.
In addition to espoused values, we also find "enacted values"; these are the norms that are actually exhibited by employees. These values may or may not be in line with the espoused values. That is why even though "Customers First" can be an espoused value, you can still end up bumped off a flight and sleeping in the airport because the rude gate agent told you there was no flight availability. In order to hear about other customers experiences with enacted values, I turned to Twitter and was amazed by what I saw. There were hundreds of comments to or about @usairways that were identical to mine- lots of mechanical failures ending in flight cancellations and luggage that was lost for days. I understand Twitter may be skewed towards the negative because people are less likely to tweet about the on-time departures...however, if you look at another airline (e.g., @southwestair) you see almost nothing about mechanical problems.
A less biased way to learn about employees' values and their level of congruence with the organization executives, is to hear from them directly. Just a few weeks ago, the US Airline Pilot Association- USAPA (the union that represents USAirways pilots), posted on their website to alert customers to the pressure they are receiving from USAirways executives to fly under unsafe conditions. On June 16, 2011, a pilot with 30-years of experience was escorted from the airport after she refused to fly a plane overseas after it failed multiple safety checks. A second group of pilots refused to fly the plane as well. This is not the first time that USAPA has spoken out against the executives. In 2008, they posted a customer alert in USA Today because they were being pressured to fly with less fuel in order to save money.
The examination and measurement of espoused/enacted values and their connection to safety outcomes (e.g., occupational injuries) is the exciting field of safety climate research. The term "safety climate" was coined in 1980 by Dr. Dov Zohar and has been prevalent in the Industrial and Organizational Psychology literature before making its way into the public health literature. For those interested, the journal Accident Analysis & Prevention recently dedicated an issue to safety climate and occupational health.
Safety climate research has been used to assess the climate of a variety of industries (e.g., healthcare). I propose that it is essential for examining the values within individual airlines and their connection to safety outcomes (e.g., worker injuries, passenger injuries, mechanical failures, near-misses, etc). The discrepancy discussed above between employee and company values can become a very dangerous combination.
Labels:
air travel,
airlines,
health communication,
injuries,
occupational health,
public health,
safety,
southwest,
usairways
Monday, August 1, 2011
There is no doubt that abnormally elevated insulin is associated with body fat accumulation
For as long as diets existed there have been influential proponents, or believers, who at some point had what they thought were epiphanies. From that point forward, they disavowed the diets that they formally endorsed. Low carbohydrate dieting seems to be in this situation now. Among other things, it has been recently “discovered” that the idea that insulin drives fat into body fat cells is “wrong”.
Based on some of the comments I have been receiving lately, apparently a few readers think that I am one of those “enlightened”. If you are interested in what I have been eating, for quite some time now, just click on the link at the top of this blog that refers to my transformation. It is essentially high in all macronutrients on days that I exercise, and low in carbohydrates and calories on days that I don’t. It is a cyclic approach that works for me; calorie surpluses on some days and calorie deficits on other days.
But let me set the record straight regarding what I think: there is no doubt that insulin is associated with body fat accumulation. I was told that an influential health blogger (whom I respect a lot) denied this recently, going to the extreme of saying that no professional metabolism or endocrinology researcher believes in it, but I couldn’t find any evidence of that statement. It is not hard at all to find professional metabolism and endocrinology researchers who have asserted that insulin is associated with body fat accumulation, based on very reliable evidence. Actually, this is Biochemistry 101.
What I think is truly unclear is whether insulin spikes associated with carbohydrate-rich foods in general are the cause of obesity. This idea is, indeed, probably wrong given the evidence we have from various human populations whose members consume plenty of non-industrialized carbohydrate-rich foods. On a related note, I particularly disagree with the notion that the pancreas gets tired over time due to having to secrete insulin in bursts, which seems to also be one of the foundations on which many low carbohydrate diet varieties rest.
As with almost everything related to health, the role of insulin in body fat gain is complex, and part of that complexity is due to the nonlinear relationship between body fat gain and postprandial insulin release. Industrial carbohydrate-rich foods have a much higher glycemic load than natural carbohydrate-rich foods, even though their glycemic index may be the same in some cases. In other words, the quantity of easily digestible carbohydrates per gram is much higher in industrial carbohydrate-rich foods.
In normoglycemic folks, this leads to an abnormally elevated insulin response, among other hormonal responses. For example, circulating growth hormone, which promotes body fat loss, is inversely correlated with circulating insulin. Insulin drives fat, typically from dietary sources of fat, into adipocytes. That fat may also come from excess carbohydrates, packaged into VLDL particles.
Under normal circumstances, that would be fine, since our body is designed to store fat and release it as needed. But the abnormal insulin response elicited by industrial carbohydrate-rich foods, together with other hormonal responses, leads to a little more body fat accumulation, and for longer, than it should. And I’m talking here about people without any metabolic damage. Saturated and monounsaturated fats are healthy when eaten, but when they are stored as excess body fat, they become pro-inflammatory.
Body fat is like an organ, secreting many hormones into the bloodstream, several of which are pro-inflammatory. One of those pro-inflammatory hormones, which I believe is closely linked with many diseases of civilization, is tumor necrosis factor. (The acronym is now TNF. Apparently the “-alpha” after its name and acronym has been dropped recently.) Dietary fat, particularly saturated fat, seems to be anti-inflammatory. In other words, body fat accumulation is the problem. You only need 30 g/d of excess body fat accumulation to gain around 24 lbs of fat per year. Over three years, that will add up to over 70 lbs of body fat.
In my view, ultimately it is excess inflammation (which is, in essence, a vascular response) that is at the source of most of the diseases of civilization.
That is where the nonlinearity comes in. Insulin is healthy up to a point. Beyond that, it starts causing health problems, over time. And one of the main mechanisms by which it does so is via excessive body fat accumulation, with different damage threshold levels for different people. Insulin may decrease appetite as it goes up, but it increases it if goes down too much. If it goes up abnormally, typically it will go down too much. As it reaches a trough it induces hypoglycemia, even if mildly.
Take a look at the graph below, from this post showing the glucose variations in normoglycemic individuals. There is a lot of variation among different individuals, but it is clear that the magnitude of the hypoglycemic dips is inversely correlated with the magnitude of the glucose spikes. That inverse correlation is due primarily to the effect of insulin. Under normal circumstances, a decrease in circulating insulin would promote an increase in free fatty acids in circulation, which would normally have a suppressing effect on hunger in the hours after a meal. But industrial carbohydrate-rich foods lead to increases and decreases in glucose and insulin that are too steep, causing the opposite effect.
You may ask: why do you keep talking about industrial carbohydrate-rich foods? Why not talk about industrial protein- or fat-rich foods as well? The reason is that the food industry has not been very successful at producing industrial protein- or fat-rich foods that are palatable without adding a lot of carbohydrate to them.
More often than not they need enough carbohydrate added in the form of sugar to become truly addictive.
Based on some of the comments I have been receiving lately, apparently a few readers think that I am one of those “enlightened”. If you are interested in what I have been eating, for quite some time now, just click on the link at the top of this blog that refers to my transformation. It is essentially high in all macronutrients on days that I exercise, and low in carbohydrates and calories on days that I don’t. It is a cyclic approach that works for me; calorie surpluses on some days and calorie deficits on other days.
But let me set the record straight regarding what I think: there is no doubt that insulin is associated with body fat accumulation. I was told that an influential health blogger (whom I respect a lot) denied this recently, going to the extreme of saying that no professional metabolism or endocrinology researcher believes in it, but I couldn’t find any evidence of that statement. It is not hard at all to find professional metabolism and endocrinology researchers who have asserted that insulin is associated with body fat accumulation, based on very reliable evidence. Actually, this is Biochemistry 101.
What I think is truly unclear is whether insulin spikes associated with carbohydrate-rich foods in general are the cause of obesity. This idea is, indeed, probably wrong given the evidence we have from various human populations whose members consume plenty of non-industrialized carbohydrate-rich foods. On a related note, I particularly disagree with the notion that the pancreas gets tired over time due to having to secrete insulin in bursts, which seems to also be one of the foundations on which many low carbohydrate diet varieties rest.
As with almost everything related to health, the role of insulin in body fat gain is complex, and part of that complexity is due to the nonlinear relationship between body fat gain and postprandial insulin release. Industrial carbohydrate-rich foods have a much higher glycemic load than natural carbohydrate-rich foods, even though their glycemic index may be the same in some cases. In other words, the quantity of easily digestible carbohydrates per gram is much higher in industrial carbohydrate-rich foods.
In normoglycemic folks, this leads to an abnormally elevated insulin response, among other hormonal responses. For example, circulating growth hormone, which promotes body fat loss, is inversely correlated with circulating insulin. Insulin drives fat, typically from dietary sources of fat, into adipocytes. That fat may also come from excess carbohydrates, packaged into VLDL particles.
Under normal circumstances, that would be fine, since our body is designed to store fat and release it as needed. But the abnormal insulin response elicited by industrial carbohydrate-rich foods, together with other hormonal responses, leads to a little more body fat accumulation, and for longer, than it should. And I’m talking here about people without any metabolic damage. Saturated and monounsaturated fats are healthy when eaten, but when they are stored as excess body fat, they become pro-inflammatory.
Body fat is like an organ, secreting many hormones into the bloodstream, several of which are pro-inflammatory. One of those pro-inflammatory hormones, which I believe is closely linked with many diseases of civilization, is tumor necrosis factor. (The acronym is now TNF. Apparently the “-alpha” after its name and acronym has been dropped recently.) Dietary fat, particularly saturated fat, seems to be anti-inflammatory. In other words, body fat accumulation is the problem. You only need 30 g/d of excess body fat accumulation to gain around 24 lbs of fat per year. Over three years, that will add up to over 70 lbs of body fat.
In my view, ultimately it is excess inflammation (which is, in essence, a vascular response) that is at the source of most of the diseases of civilization.
That is where the nonlinearity comes in. Insulin is healthy up to a point. Beyond that, it starts causing health problems, over time. And one of the main mechanisms by which it does so is via excessive body fat accumulation, with different damage threshold levels for different people. Insulin may decrease appetite as it goes up, but it increases it if goes down too much. If it goes up abnormally, typically it will go down too much. As it reaches a trough it induces hypoglycemia, even if mildly.
Take a look at the graph below, from this post showing the glucose variations in normoglycemic individuals. There is a lot of variation among different individuals, but it is clear that the magnitude of the hypoglycemic dips is inversely correlated with the magnitude of the glucose spikes. That inverse correlation is due primarily to the effect of insulin. Under normal circumstances, a decrease in circulating insulin would promote an increase in free fatty acids in circulation, which would normally have a suppressing effect on hunger in the hours after a meal. But industrial carbohydrate-rich foods lead to increases and decreases in glucose and insulin that are too steep, causing the opposite effect.
You may ask: why do you keep talking about industrial carbohydrate-rich foods? Why not talk about industrial protein- or fat-rich foods as well? The reason is that the food industry has not been very successful at producing industrial protein- or fat-rich foods that are palatable without adding a lot of carbohydrate to them.
More often than not they need enough carbohydrate added in the form of sugar to become truly addictive.
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