With the computer next in line for packing and my internet access limited, my next article will be posted here on May 1, 2006!
Thank you for your patience and I'll be back soon!
Tuesday, April 18, 2006
Monday, April 17, 2006
AHA Must Stop Endorsing Foods with Trans-Fats!
The American Heart Association (AHA) solicits donations on their website with a powerful few sentences: Cardiovascular disease is the No. 1 killer of American men and women. Your secure online gift will support scientific research, education and programs in your community. Consider it an investment in your own future, as well as the health and well-being of your family and friends.
On their website, their mission is stated on their About Us page as "to reduce disability and death from cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question."
Within the organization's Ethics Policy is the statement that "We pursue our mission with honor, fairness and respect for the individual, ever mindful that there is no 'right way' to do the 'wrong thing.' We uphold the values of the AHA in every action and decision. We are committed to act in good faith, to comply with the rule of law and AHA policies and regulations."
How then does the organization reconcile its inclusion of foods rich with health damaging trans-fats in their book, The No-Fad Diet? How exactly do they reconcile the fact that their list of foods bearing the Heart Check Logo include foods using partially hydrogenated oil as an ingredient?
Just this week, yet another medical journal published the deadly effect of industrial trans-fats on health - as reported on MedPage Today, Trans Fats Judged Major Villain in Cardiovascular Disease.
The article above states, quite clearly, "unhealthy trans fats are found in deep-fried foods, bakery products, packaged snack food, margarines, and crackers, and to try to avoid these foods."
Yet, the AHA No-Fad Diet includes these foods in the sample menus and promotes the book to a public as a diet to improve health and reduce health risks. The AHA list of "heart-healthy" foods on their website also includes these foods.
Just how deadly are industrial trans-fats? Findings in the above review are as follows:
On their website, their mission is stated on their About Us page as "to reduce disability and death from cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question."
Within the organization's Ethics Policy is the statement that "We pursue our mission with honor, fairness and respect for the individual, ever mindful that there is no 'right way' to do the 'wrong thing.' We uphold the values of the AHA in every action and decision. We are committed to act in good faith, to comply with the rule of law and AHA policies and regulations."
How then does the organization reconcile its inclusion of foods rich with health damaging trans-fats in their book, The No-Fad Diet? How exactly do they reconcile the fact that their list of foods bearing the Heart Check Logo include foods using partially hydrogenated oil as an ingredient?
Just this week, yet another medical journal published the deadly effect of industrial trans-fats on health - as reported on MedPage Today, Trans Fats Judged Major Villain in Cardiovascular Disease.
The article above states, quite clearly, "unhealthy trans fats are found in deep-fried foods, bakery products, packaged snack food, margarines, and crackers, and to try to avoid these foods."
Yet, the AHA No-Fad Diet includes these foods in the sample menus and promotes the book to a public as a diet to improve health and reduce health risks. The AHA list of "heart-healthy" foods on their website also includes these foods.
Just how deadly are industrial trans-fats? Findings in the above review are as follows:
- Lipid Levels: Trans fatty acids have markedly adverse effects on serum lipids. Their consumption raises levels of low-density lipoprotein (LDL) cholesterol, reduces high-density lipoprotein (HDL) cholesterol, and increases the ratio of total cholesterol to HDL cholesterol, a powerful predictor of coronary heart disease risk. Trans fats also increase triglyceride levels, compared with the intake of other fats.
- Potential Molecular Mechanisms: Fatty acids are powerful modulators of cell function, altering membrane fluidity and responses of membrane receptors. They appear to affect lipid metabolism, although these mechanisms are not well established. Cardiovascular Disease: On a per-calorie basis, trans fats appear to increase coronary heart disease risk more than any other micronutrient, conferring a substantially increased risk at levels as low as 1% to 3% of total energy intake. In a meta-analysis of four prospective cohort studies of nearly 140,000 participants, a 2% increase in energy intake from trans fats was linked to a 23% increase in the incidence of coronary heart disease.
- Sudden Death: A large community-based, case-control study found that levels of trans fats in erythrocyte membranes were associated with an increased risk of sudden cardiac death.
Remember - the AHA claims they are working to "to reduce disability and death from cardiovascular diseases and stroke," while asking for donations to "support scientific research, education and programs in your community." They even state one should "Consider it an investment in your own future, as well as the health and well-being of your family and friends."
Why is the AHA ignoring the evidence in their publication of the No-Fad Diet that industrial trans-fatty acids are contributing to cardiovascular disease?
Why does the AHA promote on their homepage, the link A free, heart-healthy grocery list is just a click away where we find a laundry list of foods containing partially hydrogenated oils?
Within that list we begin to find many foods that use partially hydrogenated oils in the ingredients:
- Kellogg's All-Bran Brown Sugar Cinnamon Bars
- Kellogg's All-Bran Oatmeal Raisin Bars
- Breton Reduced Fat & Sodium Wheat Crackers
- Pepperidge Farm Very Thin Soft 100% Whole Wheat Bread
- Healthy Choice Cheese French Bread Pizza
These are just a sampling from a list online that includes hundreds of products that manufacturers pay the AHA to effectively endorse as healthy with their logo on the box!
The AHA maintains the website HeartCheckMark.org for consumers that states on the homepage "The American Heart Association established its Food Certification Program in 1995 to provide consumers an easy, reliable way to identify heart-healthy foods."
I find it deeply troubling that the foods being promoted as "heart-healthy" are made with heart damaging trans-fats, don't you?
I find it hypocritical that the AHA says they are working to "reduce disability and death from cardiovascular disease and stroke" while at the same time promoting products rich with trans-fats to consumers, don't you?
I think it's downright dishonest for the AHA to promote itself as "trustworthy" and an organization from which one "can count on the information because it comes from America's most reliable source of heart-health information" when the very foods being endorsed contain trans-fats that are known to damage the cardiovascular system!
It's high time the American consumer calls the AHA to task for their contradiction and conflict-of-interest.
As an organization that promotes itself as "trustworthy" it must start to be trustworthy - talk is cheap!
The American Heart Association can redeem itself and earn back the trust it loses each day it promotes foods containing heart-damaging trans-fats if:
- Immediately insist on the removal of its logo from any product containing industrial trans-fats
- Immediately recall the AHA No-Fad Diet book from shelves and re-release only after revisions adequately address the need to eliminate industrial trans-fats from the diet
- Immediately begin a public education campaign to clearly communicate to consumers the heart damaging effects of industrial trans-fats in foods
If you believe the AHA is not doing its part to educate the public about the heart damaging effect of industrial trans-fats and is indeed contributing to their continued use in our food supply and you believe it is time the AHA take responsibility for its endorsement of heart-damaging foods, you can do something about it - stop donating money!
Friday, April 14, 2006
CRP Blocks Action of Leptin in the Obese
Occassionally it happens - I'm stumped by something published in a research paper or from a study. I'm usually stumped because something within the findings or conclusions don't sit right with my understanding of the subject at hand or I don't have enough foundation of the subject at hand to completely "get" the gist of things.
Today, MyDNA's article, What Causes Obesity?, stumped me with the researchers' conslusions. Maybe one or more of my readers will have some insights that will help me better understand why the conclusions are valid - how's that for a teaser? I'm obviously stumped on this one because it's not sitting right with my understanding of the subject at hand!
First though, some background from the article above:
Research data from the University of Pittsburgh suggests that obesity is due — at least in part — to an attraction between leptin, the hormone that signals the brain when to stop eating, and a protein called C-reactive (CRP). The amount of fat regulates the amount of leptin produced by the body: the more fat, the more of the hormone. Obese people produce higher levels of leptin, but somehow they're resistant to its effects. This has led researchers to focus on the interaction between CRP and leptin, which is actually Greek for the word "thin."
Zhao said that the binding of CRP, which is also elevated in obese people, to leptin might help explain why the hormone is not effective.
Zhao said his study suggests researchers should focus their attention on an approach that disrupts the interaction between leptin and CRP, which would allow the hormone to resume its regulatory role.
You may be wondering - why is she stumped?
I'll explain.
Everything above sounds reasonable - someone is obese, they have high levels of leptin being excreted which should be signaling the brain and regulating energy intake well...but CRP is binding the leptin and effectively blocking its path....so, let's block the CRP action and the leptin can get back to doing its job.
Something with this screams out to me this is the wrong and I base that on my understanding of C-Reactive Protein and its role in what's called "complement biology."
As a simple definition, CRP is a plasma protein - an acute phase protein - produced by the liver. It's a marker in the blood that indicates an inflammatory response to injury - like an overt injury when you sprain your ankle or when something is going on internally in your body - an obscure injury or assault - like when you come in contact with bacteria that can make you ill. Both of these inflammatory responses resolve and the levels of CRP decline again once the potential for permanent harm are no longer an issue.
In both cases, the CRP acted in its complementary role with the immune system to target and destroy or neutralize a potentially harmful situation. In the example of the sprained ankle, the inflammatory response was stimulated to help "clean up" the injured site and limit movement during that process - the pain limits mobility to the body can take care of the injury. In the example of the bacteria, the inflammatory response was stimulated to flag the invading microbes for destruction and elimination from the body.
I hope this detail provides some insight to my understanding of the role of CRP - it works together with the immune system to neutralize something that has the potential to negatively affect well being. The target of inflammatory response is any substance that stimulates an immune response. The substance most often the cause, when the injury is not overt physical injury - proteins or polysaccarides (although any type of molecule that has potential for harm can trigger it).
The reason I'm stumped by the idea we should block the CRP if it's binding the leptin is that leptin is a protein, produced by adipose tissue (fat). The more adipose tissue an individual has, the more leptin they secrete. The findings from the University of Pittsburgh tell us that this leptin is being blocked because it is being bound by CRP and the suggestion is that if we can block the action of the CRP, we can allow the leptin to do its work in regulating appetite again.
Why are the researchers not asking the question "is the leptin levels causing the inflammatory response?"
To me, it seems like the assumption is that the higher levels of leptin are good - what's bad is its not able to do its job because the CRP is inhibiting its action when it binds to it.
But what if the higher levels of leptin are bad - harmful - and that is causing the inflammatory response in an effort to limit damage?
What if the inflammatory response is exactly what we are supposed to see - and the cause of that inflammatory response is what we must resolve for the body to regain equilibrium?
On its face, the issue to be resolved is rightly the obesity. What I don't understand is how blocking the action of the CRP binding the leptin will resolve that. Perhaps a better approach isn't to block the inflammatory response that is limiting the high level of leptin, but to resolve the cause of the weight gain in the first place!
The research conclusion leads one to see:
Leptin => Appetite Control => Weight Regulation
CRP blocks Leptin => Block CRP Action => Leptin Appetite Control => Weight Loss
But....what if the path is this instead:
Poor Diet => Weight Gain => Elevated Leptin => Inflammatory Response to limit damage from high Leptin
Food for thought, isn't it?
Today, MyDNA's article, What Causes Obesity?, stumped me with the researchers' conslusions. Maybe one or more of my readers will have some insights that will help me better understand why the conclusions are valid - how's that for a teaser? I'm obviously stumped on this one because it's not sitting right with my understanding of the subject at hand!
First though, some background from the article above:
Research data from the University of Pittsburgh suggests that obesity is due — at least in part — to an attraction between leptin, the hormone that signals the brain when to stop eating, and a protein called C-reactive (CRP). The amount of fat regulates the amount of leptin produced by the body: the more fat, the more of the hormone. Obese people produce higher levels of leptin, but somehow they're resistant to its effects. This has led researchers to focus on the interaction between CRP and leptin, which is actually Greek for the word "thin."
Zhao said that the binding of CRP, which is also elevated in obese people, to leptin might help explain why the hormone is not effective.
Zhao said his study suggests researchers should focus their attention on an approach that disrupts the interaction between leptin and CRP, which would allow the hormone to resume its regulatory role.
You may be wondering - why is she stumped?
I'll explain.
Everything above sounds reasonable - someone is obese, they have high levels of leptin being excreted which should be signaling the brain and regulating energy intake well...but CRP is binding the leptin and effectively blocking its path....so, let's block the CRP action and the leptin can get back to doing its job.
Something with this screams out to me this is the wrong and I base that on my understanding of C-Reactive Protein and its role in what's called "complement biology."
As a simple definition, CRP is a plasma protein - an acute phase protein - produced by the liver. It's a marker in the blood that indicates an inflammatory response to injury - like an overt injury when you sprain your ankle or when something is going on internally in your body - an obscure injury or assault - like when you come in contact with bacteria that can make you ill. Both of these inflammatory responses resolve and the levels of CRP decline again once the potential for permanent harm are no longer an issue.
In both cases, the CRP acted in its complementary role with the immune system to target and destroy or neutralize a potentially harmful situation. In the example of the sprained ankle, the inflammatory response was stimulated to help "clean up" the injured site and limit movement during that process - the pain limits mobility to the body can take care of the injury. In the example of the bacteria, the inflammatory response was stimulated to flag the invading microbes for destruction and elimination from the body.
I hope this detail provides some insight to my understanding of the role of CRP - it works together with the immune system to neutralize something that has the potential to negatively affect well being. The target of inflammatory response is any substance that stimulates an immune response. The substance most often the cause, when the injury is not overt physical injury - proteins or polysaccarides (although any type of molecule that has potential for harm can trigger it).
The reason I'm stumped by the idea we should block the CRP if it's binding the leptin is that leptin is a protein, produced by adipose tissue (fat). The more adipose tissue an individual has, the more leptin they secrete. The findings from the University of Pittsburgh tell us that this leptin is being blocked because it is being bound by CRP and the suggestion is that if we can block the action of the CRP, we can allow the leptin to do its work in regulating appetite again.
Why are the researchers not asking the question "is the leptin levels causing the inflammatory response?"
To me, it seems like the assumption is that the higher levels of leptin are good - what's bad is its not able to do its job because the CRP is inhibiting its action when it binds to it.
But what if the higher levels of leptin are bad - harmful - and that is causing the inflammatory response in an effort to limit damage?
What if the inflammatory response is exactly what we are supposed to see - and the cause of that inflammatory response is what we must resolve for the body to regain equilibrium?
On its face, the issue to be resolved is rightly the obesity. What I don't understand is how blocking the action of the CRP binding the leptin will resolve that. Perhaps a better approach isn't to block the inflammatory response that is limiting the high level of leptin, but to resolve the cause of the weight gain in the first place!
The research conclusion leads one to see:
Leptin => Appetite Control => Weight Regulation
CRP blocks Leptin => Block CRP Action => Leptin Appetite Control => Weight Loss
But....what if the path is this instead:
Poor Diet => Weight Gain => Elevated Leptin => Inflammatory Response to limit damage from high Leptin
Food for thought, isn't it?
Wednesday, April 12, 2006
Level One Evidence to Treat Metabolic Syndrome Largely Ignored
I read with great interest the recent paper by Dr. Scott M. Grundy, Metabolic Syndrome: Connecting and Reconciling Cardiovascular and Diabetes Worlds, published in the March 21, 2006, Journal of the American College of Cardiology. My writing today is going to be long, but I hope you'll bear with me since this is important information.
In part, the summary is short, concise and on point:
The metabolic syndrome is a constellation of risk factors that carry increased risk for cardiovascular disease and type 2 diabetes. These risk factors are atherogenic dyslipidemia, elevated blood pressure, elevated plasma glucose, a prothrombotic state, and a proinflammatory state. The two major underlying risk factors are obesity and insulin resistance. Primary treatment is lifestyle therapy - weight loss, increased physical activity, and anti-atherogenic diet. As the syndrome worsens, drug therapies directed toward individual risk factors might be required. Ultimately, drugs might be developed that will simultaneously modify all of the risk factors, but such drugs are not currently available.
First let me applaud Dr. Grundy's frank discussion of many of the pressing issues clouding progress to effectively diagnose and treat individuals presenting with features of Metabolic Syndrome - ineffective communication and lack of agreement between the diabetes and cardiology researchers and organizations; pharmaceutical agents that only target individual risk factors and often do not ameliorate the features effectively; pointing to the long-term, geometric increases to risk individuals face as each feature of Metabolic Syndrome presents and/or advances; and the continued neglect in clinical practice of the single best intervention - diet and lifestyle.
He makes it a point to state that the long-term risk for antherosclerotic cardiovascular disease is greater than the sum of the risk factors associated with Metabolic Syndrome individually. As Dr. Grundy also points out clearly, "primary treatment is lifestyle therapy - weight loss, increased physical activity, and anti-atherogenic diet."
When Dr. Grundy included a section dedicated to the evidence for lifestyle intervention, I was hopeful he would include evidence that provides a comprehensive presentation of the most effective lifestyle interventions supported by hard data. To sum up my expectations - level one evidence, randomly controlled studies, investigation that includes the primary risk factors (BMI and/or waist circumference; total cholesterol, HDL, LDL, triglycerides, TC/HDL ratio, fasting glucose, insulin levels, and blood pressure) or included individuals with Metabolic Syndrome specifically; studies at least six months in length with good compliance rates and overall statistically significant results.
So, which studies did he include to support his statement that "Beyond reducing risk for cardiovascular disease, weight reduction and increased physical activity slows progression to type 2 diabetes in individuals with the metabolic syndrome."
J. Tuomilehto, J. Lindstrom, J.G. Eriksson et al. and Finnish Diabetes Prevention Study Group, Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, N Engl J Med 344 (2001), pp. 1343–1350.
W.C. Knowler, E. Barrett-Connor, S.E. Fowler et al. and Diabetes Prevention Program Research Group, Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin, N Engl J Med 346 (2002), pp. 393–403.
To say I was disappointed by the two studies he included is an understatement. To be clear, both were indeed level one studies - randomly controlled, long-term and with controls to compare the intervention group results. Neither, however, is clear and convincing that the lifestyle interventions were effective for the features of Metabolic Syndrome.
Let me explain why. In the first, Tuomilehto et al, indeed had two groups with multiple features of Metabolic Syndrome. While the findings support that the intervention group did better than the control, they continued to have Metabolic Syndrome as evidenced by their waist circumferance, cholesterol levels, fasting glucose and blood pressure. This particular study also did not provide enough key data for cholesterol since it did not evaluate impacts on LDL cholesterol.
In the second, Knowler et al investigate how lifestyle intervention compares with a pharmaceutical intervention to delay diabetes and conclude that lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. But, the lifestyle intervention was more effective than metformin. Unfortunately this study, again, did not look at enough risk markers to effectively communicate its value as an intervention for Metabolic Syndrome. The investigators did not look at total cholesterol, LDL, HDL, triglycerides, blood pressure or insulin values. Without a complete investigation of these risk markers, this data lacks and is inappropriate to use in support of lifestyle intervention because it leaves too many questions unanswered.
So, neither of these studies supports the idea that lifestyle intervention can reverse the features of Metabolic Syndrome effectively. The fact that Dr. Grundy didn't include evidence, from trials specifically looking at those with features of Metabolic Syndrome or studies that evaluated enough risk markers to reach conclusions about the features of Metabolic Syndrome begs the question - is there a lack of evidence?
The answer is clearly no!
We have dozens of studies that point to the efficacy of lifestyle interventions that not only delay progression of the features, but that can reverse the features! I am very disappointed that Dr. Grundy failed to include any of them. In fact, I would say, without hesitation, that his omission borders on negligence to his colleagues and those individuals seeking methods to improve their condition!
I know that's a very strong statement. But, it must be said if we are going to start to see evidence-based medicine in practice. Anything other than the use of strong evidence is mere speculation or wishful thinking and is nothing more than lip-service. Dr. Grundy has an obligation to his colleagues, clinicians and the public to fully explore the literature and present those studies that clearly indicate which lifestyle interventions work! He failed to do that. And he didn't just fail to find one study - he failed to find or include dozens of studies.
Case in point: Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. A randomized trial of a low-carbohydrate diet for obesity N Engl J Med. 2003;348:2082–2090
Key aspects of the above study - one year, randomly controlled trial; measured cholesterol, insulin, blood pressure, weight, insulin response and glucose levels. The results are best summed up in a graphic:
Golay A, Eigenheer C, Morel Y, Kujawski P, Lehmann T, de Tonnac N. Weight-loss with low or high carbohydrate diet? Int J Obes Relat Metab Disord. 1996;20:1067–1072
Key aspects of the above study - one year, randomly controlled trial; compared low carbohydrate with a low fat diet; measured cholesterol, BMI, glucose, cholesterol, insulin and blood pressure. Again, the results are best summed up in a graphic:
Late last year, Volek & Feinman published a comprehensive review of the literature and found that the degree of carbohydrate restriction directly parallels improvement in the features of metabolic syndrome. As part of their paper, Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction, they included a table of one dozen studies of varying time lengths:
Notice in the above graphic the stunning improvements, across the board, when carbohydrate restriction is used as the dietary intervention.
They also review fourteen studies of ad libitum consumption of carbohydrate restricted diets compared with low-fat diets. The results again strongly support the use of carbohydrate restricted diets to specifically reduce or reverse the features of Metabolic Syndrome:
Now you may be thinking this is all fine and dandy, but surely the conventional wisdom and recommendation to follow a low-fat diet must have merit, otherwise the leading health organizations would stop recommending them since we're told things now are strictly evidence-based?
Unfortunately, the dogma that supports the low-fat paradigm finds little support in the evidence for the features of Metabolic Syndrome. And, sadly, the negative effect of low-fat diets on the risks have been long-known and ignored.
Our first key date in the history of understanding the negative effects of low-fat diets on the features of Metabolic Syndrome comes from data from none other than the "Father of Metabolic Syndrome," Gerald Reaven's work. In 1986, Dr. Reaven published Effect of dietary carbohydrate on the metabolism of patients with non-insulin dependent diabetes mellitus. (Nutr Rev. 1986;44:65–73) and found reducing carbohydrate to 40% of the calories improved individuals to a greater degree than when they consumed 55% of their diet as carbohydrate.
Little research was done to replicate the results or to explore if further reductions of carbohydrate would result in even greater improvements. The biggest reason for the stall in the research was, and remains, the fear of dietary fat. Yet, in 2004, Gannon and Nuttall published, Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. (Diabetes. 2004;53:2375–2382) and found that when carbohydrate is reduced to 20% of calories, the improvements exceed those seen in Reavens' work where carbohydrate was restricted to just 40% of calories! Numerous other studies - from Gannon, Nutall, Westman, Volek, Noakes, Phinney, Yancy, Stern, Brehm and others resulted in similar findings. Yet, these studies continue to be omitted from reviews and analysis of effective lifestyle interventions! This is not only neglectful, it's shameful.
In the United States, we have a real crisis today - 25% of all adults are estimated to already have Metabolic Syndrome; another 20-30% are at risk for developing Metabolic Syndrome; and some 4% of all adolescents and 30% of overweight adolescents meet the criteria for Metabolic Syndrome. If we do not do something now to educate those already affected or at risk for the disorder - and do it quickly - these numbers will continue to grow with pre-mature death the end result of our failure to act from an evidence-based approach.
When compared side-by-side - carbohydrate-rich, low-fat diets and carbohydrate restricted diets - we see dramatically different results. The low-fat diets often raise LDL and triglycerides, lower HDL, have little impact on glycemic control, and minimal effect on blood pressure. These effects are negative impacts that increase the risk of progression of Metabolic Syndrome. While the low-fat diet can and often will result in weight loss, the long-term the benefit of weight loss is negated as weight is re-gained and completely offset by the negative effect on the risk markers for Metabolic Syndrome.
On the other hand, a carbohydrate restricted diet - whether fat or protein or a combination of both is substituted for calorie requirements - has a profound effect on triglycerides, significantly lowering them, raising HDL, improving TC/HDL ratios, increasing insulin sensitivity and glycemic control, reducing blood pressure and reducing weight. Again, in the long-term, it is not certain if the weight loss can be sustained as we have few studies to date that meet the standard of level one evidence. However, the positive impacts on the risk markers of Metabolic Syndrome are promising, especially given the fact that recent data suggests that even without weight loss, such improvements to the various risk factors are seen when carbohydrate restriction is followed.
The bottom line is that a large number of researchers have invested years of time studying diet and nutrition to learn how different macronutrient ratios affect the risk markers associated with Metabolic Syndrome. We have level one evidence that points clearly to carbohydrate restriction as an effective lifestyle intervention.
We have millions of people in the United States today who are being denied this evidence each time a review is published and the author omits the data from these gold standard studies because they counter the established dogma.
I've said it before and I'll say it again - DOGMA IS NOT EVIDENCE!
I implore you to take the time to read the paper published by Dr. Jeff Volek and Dr. Richard Feinman - Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction - and review the 112 references included in their extensive review of the literature.
If you do that - take the time - I think you'll find yourself asking the same question I do - When will the leading medical organizations and experts finally take an evidence-based approach to making recommendations for those at risk for or already presenting features of Metabolic Syndrome?
In part, the summary is short, concise and on point:
The metabolic syndrome is a constellation of risk factors that carry increased risk for cardiovascular disease and type 2 diabetes. These risk factors are atherogenic dyslipidemia, elevated blood pressure, elevated plasma glucose, a prothrombotic state, and a proinflammatory state. The two major underlying risk factors are obesity and insulin resistance. Primary treatment is lifestyle therapy - weight loss, increased physical activity, and anti-atherogenic diet. As the syndrome worsens, drug therapies directed toward individual risk factors might be required. Ultimately, drugs might be developed that will simultaneously modify all of the risk factors, but such drugs are not currently available.
First let me applaud Dr. Grundy's frank discussion of many of the pressing issues clouding progress to effectively diagnose and treat individuals presenting with features of Metabolic Syndrome - ineffective communication and lack of agreement between the diabetes and cardiology researchers and organizations; pharmaceutical agents that only target individual risk factors and often do not ameliorate the features effectively; pointing to the long-term, geometric increases to risk individuals face as each feature of Metabolic Syndrome presents and/or advances; and the continued neglect in clinical practice of the single best intervention - diet and lifestyle.
He makes it a point to state that the long-term risk for antherosclerotic cardiovascular disease is greater than the sum of the risk factors associated with Metabolic Syndrome individually. As Dr. Grundy also points out clearly, "primary treatment is lifestyle therapy - weight loss, increased physical activity, and anti-atherogenic diet."
When Dr. Grundy included a section dedicated to the evidence for lifestyle intervention, I was hopeful he would include evidence that provides a comprehensive presentation of the most effective lifestyle interventions supported by hard data. To sum up my expectations - level one evidence, randomly controlled studies, investigation that includes the primary risk factors (BMI and/or waist circumference; total cholesterol, HDL, LDL, triglycerides, TC/HDL ratio, fasting glucose, insulin levels, and blood pressure) or included individuals with Metabolic Syndrome specifically; studies at least six months in length with good compliance rates and overall statistically significant results.
So, which studies did he include to support his statement that "Beyond reducing risk for cardiovascular disease, weight reduction and increased physical activity slows progression to type 2 diabetes in individuals with the metabolic syndrome."
J. Tuomilehto, J. Lindstrom, J.G. Eriksson et al. and Finnish Diabetes Prevention Study Group, Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, N Engl J Med 344 (2001), pp. 1343–1350.
W.C. Knowler, E. Barrett-Connor, S.E. Fowler et al. and Diabetes Prevention Program Research Group, Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin, N Engl J Med 346 (2002), pp. 393–403.
To say I was disappointed by the two studies he included is an understatement. To be clear, both were indeed level one studies - randomly controlled, long-term and with controls to compare the intervention group results. Neither, however, is clear and convincing that the lifestyle interventions were effective for the features of Metabolic Syndrome.
Let me explain why. In the first, Tuomilehto et al, indeed had two groups with multiple features of Metabolic Syndrome. While the findings support that the intervention group did better than the control, they continued to have Metabolic Syndrome as evidenced by their waist circumferance, cholesterol levels, fasting glucose and blood pressure. This particular study also did not provide enough key data for cholesterol since it did not evaluate impacts on LDL cholesterol.
In the second, Knowler et al investigate how lifestyle intervention compares with a pharmaceutical intervention to delay diabetes and conclude that lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. But, the lifestyle intervention was more effective than metformin. Unfortunately this study, again, did not look at enough risk markers to effectively communicate its value as an intervention for Metabolic Syndrome. The investigators did not look at total cholesterol, LDL, HDL, triglycerides, blood pressure or insulin values. Without a complete investigation of these risk markers, this data lacks and is inappropriate to use in support of lifestyle intervention because it leaves too many questions unanswered.
So, neither of these studies supports the idea that lifestyle intervention can reverse the features of Metabolic Syndrome effectively. The fact that Dr. Grundy didn't include evidence, from trials specifically looking at those with features of Metabolic Syndrome or studies that evaluated enough risk markers to reach conclusions about the features of Metabolic Syndrome begs the question - is there a lack of evidence?
The answer is clearly no!
We have dozens of studies that point to the efficacy of lifestyle interventions that not only delay progression of the features, but that can reverse the features! I am very disappointed that Dr. Grundy failed to include any of them. In fact, I would say, without hesitation, that his omission borders on negligence to his colleagues and those individuals seeking methods to improve their condition!
I know that's a very strong statement. But, it must be said if we are going to start to see evidence-based medicine in practice. Anything other than the use of strong evidence is mere speculation or wishful thinking and is nothing more than lip-service. Dr. Grundy has an obligation to his colleagues, clinicians and the public to fully explore the literature and present those studies that clearly indicate which lifestyle interventions work! He failed to do that. And he didn't just fail to find one study - he failed to find or include dozens of studies.
Case in point: Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. A randomized trial of a low-carbohydrate diet for obesity N Engl J Med. 2003;348:2082–2090
Key aspects of the above study - one year, randomly controlled trial; measured cholesterol, insulin, blood pressure, weight, insulin response and glucose levels. The results are best summed up in a graphic:
Golay A, Eigenheer C, Morel Y, Kujawski P, Lehmann T, de Tonnac N. Weight-loss with low or high carbohydrate diet? Int J Obes Relat Metab Disord. 1996;20:1067–1072
Key aspects of the above study - one year, randomly controlled trial; compared low carbohydrate with a low fat diet; measured cholesterol, BMI, glucose, cholesterol, insulin and blood pressure. Again, the results are best summed up in a graphic:
Late last year, Volek & Feinman published a comprehensive review of the literature and found that the degree of carbohydrate restriction directly parallels improvement in the features of metabolic syndrome. As part of their paper, Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction, they included a table of one dozen studies of varying time lengths:
Notice in the above graphic the stunning improvements, across the board, when carbohydrate restriction is used as the dietary intervention.
They also review fourteen studies of ad libitum consumption of carbohydrate restricted diets compared with low-fat diets. The results again strongly support the use of carbohydrate restricted diets to specifically reduce or reverse the features of Metabolic Syndrome:
Now you may be thinking this is all fine and dandy, but surely the conventional wisdom and recommendation to follow a low-fat diet must have merit, otherwise the leading health organizations would stop recommending them since we're told things now are strictly evidence-based?
Unfortunately, the dogma that supports the low-fat paradigm finds little support in the evidence for the features of Metabolic Syndrome. And, sadly, the negative effect of low-fat diets on the risks have been long-known and ignored.
Our first key date in the history of understanding the negative effects of low-fat diets on the features of Metabolic Syndrome comes from data from none other than the "Father of Metabolic Syndrome," Gerald Reaven's work. In 1986, Dr. Reaven published Effect of dietary carbohydrate on the metabolism of patients with non-insulin dependent diabetes mellitus. (Nutr Rev. 1986;44:65–73) and found reducing carbohydrate to 40% of the calories improved individuals to a greater degree than when they consumed 55% of their diet as carbohydrate.
Little research was done to replicate the results or to explore if further reductions of carbohydrate would result in even greater improvements. The biggest reason for the stall in the research was, and remains, the fear of dietary fat. Yet, in 2004, Gannon and Nuttall published, Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. (Diabetes. 2004;53:2375–2382) and found that when carbohydrate is reduced to 20% of calories, the improvements exceed those seen in Reavens' work where carbohydrate was restricted to just 40% of calories! Numerous other studies - from Gannon, Nutall, Westman, Volek, Noakes, Phinney, Yancy, Stern, Brehm and others resulted in similar findings. Yet, these studies continue to be omitted from reviews and analysis of effective lifestyle interventions! This is not only neglectful, it's shameful.
In the United States, we have a real crisis today - 25% of all adults are estimated to already have Metabolic Syndrome; another 20-30% are at risk for developing Metabolic Syndrome; and some 4% of all adolescents and 30% of overweight adolescents meet the criteria for Metabolic Syndrome. If we do not do something now to educate those already affected or at risk for the disorder - and do it quickly - these numbers will continue to grow with pre-mature death the end result of our failure to act from an evidence-based approach.
When compared side-by-side - carbohydrate-rich, low-fat diets and carbohydrate restricted diets - we see dramatically different results. The low-fat diets often raise LDL and triglycerides, lower HDL, have little impact on glycemic control, and minimal effect on blood pressure. These effects are negative impacts that increase the risk of progression of Metabolic Syndrome. While the low-fat diet can and often will result in weight loss, the long-term the benefit of weight loss is negated as weight is re-gained and completely offset by the negative effect on the risk markers for Metabolic Syndrome.
On the other hand, a carbohydrate restricted diet - whether fat or protein or a combination of both is substituted for calorie requirements - has a profound effect on triglycerides, significantly lowering them, raising HDL, improving TC/HDL ratios, increasing insulin sensitivity and glycemic control, reducing blood pressure and reducing weight. Again, in the long-term, it is not certain if the weight loss can be sustained as we have few studies to date that meet the standard of level one evidence. However, the positive impacts on the risk markers of Metabolic Syndrome are promising, especially given the fact that recent data suggests that even without weight loss, such improvements to the various risk factors are seen when carbohydrate restriction is followed.
The bottom line is that a large number of researchers have invested years of time studying diet and nutrition to learn how different macronutrient ratios affect the risk markers associated with Metabolic Syndrome. We have level one evidence that points clearly to carbohydrate restriction as an effective lifestyle intervention.
We have millions of people in the United States today who are being denied this evidence each time a review is published and the author omits the data from these gold standard studies because they counter the established dogma.
I've said it before and I'll say it again - DOGMA IS NOT EVIDENCE!
I implore you to take the time to read the paper published by Dr. Jeff Volek and Dr. Richard Feinman - Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction - and review the 112 references included in their extensive review of the literature.
If you do that - take the time - I think you'll find yourself asking the same question I do - When will the leading medical organizations and experts finally take an evidence-based approach to making recommendations for those at risk for or already presenting features of Metabolic Syndrome?
Monday, April 10, 2006
AHA Gets a Pass on Health Damaging Trans-fats
In July 2005 I wrote a scathing review of the American Heart Association's "No-Fad Diet," a book promoted as "weight-loss strategies...based on reliable scientific research and are backed by respected medical professionals. The American Heart Association has the information you can trust."
The main thrust of my criticism was that here we have the AHA including foods rich with trans-fats in their sample menus and advice, yet the scientific evidence is clear that trans-fats are a detriment to health. The sample menus in the book included things like fast food bacon biscuits, donuts, animal crackers, fast food sub sandwiches, and microwave popcorn. All foods notorious for high levels of trans-fats.
Recently two publications have mentioned my review in their own review of the book. Souix Valley Hospital & Health System Newsletter, Winter 2006 and the March 16, 2006 edition of The Mountain Times.
The Souix Valley Health Newletter
The book relies heavily on the credibility of the AHA, and one internet blogger, Regina Wilshire, criticizes Dr. Eckels for including some sample menus that contain unhealthy trans-fats. What the book proposes, more than anything else, however, is a practical approach to diet that may involve compromises. While there may be no safe level of trans fats, a low level is better than a high one.
The Mountain Times
The No-Fad Diet book gains a great deal of credibility from its explicit association with the American Heart Association, which is highlighted in large type on the back cover. However, Regina Wilshire, an internet blogger who says she has lost weight successfully through the low-carbohydrate Atkins approach, takes the AHA to task for using sample menus that encourage the eating of foods containing trans-fats.
“On page 35 they provide a bullet point with ‘Avoid trans fats’ and then include foods notorious for their trans-fat content in their sample menus, giving a greenlight to eating them,” Wilshire writes. Wilshire’s examples, taken from the book, include: low-fat graham crackers, light microwave popcorn, whole wheat English muffins, reduced fat vanilla wafers, a six-inch fast food ham submarine sandwich and a glazed doughnut.
Dr. Eckel and the AHA are certainly not endorsing trans-fats, and they might well be embarrassed by such criticisms. What the book proposes, more than anything else, is that any effort to lose weight is bound to involve some compromises between the ideal and the practical. While there may be no safe level of trans fats, a low level is better than a high one.
These excuses mix just enough fact with fiction to sound halfway credible! Sure trans-fats are unhealthy they say. But instead of stating the hard truth - one should not eat any man-made trans-fats, they give consumers a false sense of security, give the manufactuers of this poison a free pass, and excuse the AHA from responsibility for promoting the junk food! This sets the lay public up for poor health as many will not be able to distinguish these few facts from the unsubstantiated bunk.
And the bunk here is that "a little" trans-fat is better than a lot.
The long-term health effects are disregarded and the science that concludes man-made trans-fats are detrimental to health are dismissed.
The reviews state that including foods with trans-fats is not an endorsement. Double-speak. The idea that the AHA and the author, Dr. Eckel, aren't "endorsing" trans-fats is without merit - if they're in the book, specifically included in a sample menu for one to follow if they can't make a menu themself or want a simple easy exmple to follow - that's an endorsement no matter how you slice it. It's myopic to think it's not.
Let's not forget, the long-term health effects are specficially negative to the cardiovascular system - the very thing the AHA purports to be providing evidence-based information about in an effort to reduce the risk of cardiovascular disease! The data clearly shows that man-made trans-fats (partially hydrogenated oils) elevate LDL and lower HDL - two things everyone, even the general public, understands increases the risk of cardiovascular disease!
Yet, the AHA gets a free pass for including foods with trans-fats from almost every reviewer of the book. I find this unacceptable and will continue to maintain that the book is not based on evidence, is not healthy, is certainly not going to reduce one's risk for cardiovascular disease, and is a hazaard to follow in umpteen ways. More distrubing is that it is nothing more than lip-service to an unwitting public - the public trusts the AHA and the AHA is promoting a diet that includes a class of fats that the Institutes of Medicine (IOM) concluded have "no safe level" of consumption for humans.
The idea that the public simply won't accept a diet that isn't littered with foods that are unhealthy is not a reason to lie to them, pacify them and tell them they can have their cake and eat it too. Instead of attempting to engage in a meaningful dialogue where facts based on facts are exchanged, the AHA pushes emotional buttons in an attempt to sway readers from the task at hand - eliminating man-made trans-fats from the diet. It's a pitiful and pathetic act and not worthy of any attention by those who are looking to engage in that meaningful dialogue in pursuit of truth about diet and health.
In fact, what we need is a scientific community dedicated to neutralizing harmful ingredients we have inflicted on ourselves; not endorsing and recommending ones we know are harmful. If America is craving healthy snack foods let them eat organic fruit and nuts. Is that such a difficult idea or what?
If we are going to make a difference we must start by taking the path of truth and stop lying to the American public that junk food is acceptable in moderation.
The hawked book promises “don’t give up your favorites." Instead of evoking integrity, the book is schizophrenic - promoting a "no fad" approach to diet while also promoting foods known to be damaging to health.
By refusing to support industry that is detrimental to our health we can send a message to the puppets we have sitting in many of the leading health organizations: health does not come out of a can, a bottle, or any other man made disposable. Health does not come from chemistry. Health comes from the soil - from real whole foods that served us well for millenia that too many today wouldn't even recognize if itwere on their plate.
We have all heard the saying, "Think globally, Act locally." Well, your own body is as local as you can get. Everything you consume is a personal statement of how you view your body and health.
This is a personal challenge to any and all of my friends and readers who see the irony of the AHA encouraging donuts, fast food bacon biscuits and other assorted junk food - Let's all take a stand for ourselves, our health and say "enough is enough." Put down the soda, the chips, and donuts and declare your body a toxin-free zone. If you're not up to this challenge, ignore me and belly up to the bar. It was the wise bartender who said "name your poison."
Aren't we lucky to have so many to poisons to choose from?
The main thrust of my criticism was that here we have the AHA including foods rich with trans-fats in their sample menus and advice, yet the scientific evidence is clear that trans-fats are a detriment to health. The sample menus in the book included things like fast food bacon biscuits, donuts, animal crackers, fast food sub sandwiches, and microwave popcorn. All foods notorious for high levels of trans-fats.
Recently two publications have mentioned my review in their own review of the book. Souix Valley Hospital & Health System Newsletter, Winter 2006 and the March 16, 2006 edition of The Mountain Times.
The Souix Valley Health Newletter
The book relies heavily on the credibility of the AHA, and one internet blogger, Regina Wilshire, criticizes Dr. Eckels for including some sample menus that contain unhealthy trans-fats. What the book proposes, more than anything else, however, is a practical approach to diet that may involve compromises. While there may be no safe level of trans fats, a low level is better than a high one.
The Mountain Times
The No-Fad Diet book gains a great deal of credibility from its explicit association with the American Heart Association, which is highlighted in large type on the back cover. However, Regina Wilshire, an internet blogger who says she has lost weight successfully through the low-carbohydrate Atkins approach, takes the AHA to task for using sample menus that encourage the eating of foods containing trans-fats.
“On page 35 they provide a bullet point with ‘Avoid trans fats’ and then include foods notorious for their trans-fat content in their sample menus, giving a greenlight to eating them,” Wilshire writes. Wilshire’s examples, taken from the book, include: low-fat graham crackers, light microwave popcorn, whole wheat English muffins, reduced fat vanilla wafers, a six-inch fast food ham submarine sandwich and a glazed doughnut.
Dr. Eckel and the AHA are certainly not endorsing trans-fats, and they might well be embarrassed by such criticisms. What the book proposes, more than anything else, is that any effort to lose weight is bound to involve some compromises between the ideal and the practical. While there may be no safe level of trans fats, a low level is better than a high one.
These excuses mix just enough fact with fiction to sound halfway credible! Sure trans-fats are unhealthy they say. But instead of stating the hard truth - one should not eat any man-made trans-fats, they give consumers a false sense of security, give the manufactuers of this poison a free pass, and excuse the AHA from responsibility for promoting the junk food! This sets the lay public up for poor health as many will not be able to distinguish these few facts from the unsubstantiated bunk.
And the bunk here is that "a little" trans-fat is better than a lot.
The long-term health effects are disregarded and the science that concludes man-made trans-fats are detrimental to health are dismissed.
The reviews state that including foods with trans-fats is not an endorsement. Double-speak. The idea that the AHA and the author, Dr. Eckel, aren't "endorsing" trans-fats is without merit - if they're in the book, specifically included in a sample menu for one to follow if they can't make a menu themself or want a simple easy exmple to follow - that's an endorsement no matter how you slice it. It's myopic to think it's not.
Let's not forget, the long-term health effects are specficially negative to the cardiovascular system - the very thing the AHA purports to be providing evidence-based information about in an effort to reduce the risk of cardiovascular disease! The data clearly shows that man-made trans-fats (partially hydrogenated oils) elevate LDL and lower HDL - two things everyone, even the general public, understands increases the risk of cardiovascular disease!
Yet, the AHA gets a free pass for including foods with trans-fats from almost every reviewer of the book. I find this unacceptable and will continue to maintain that the book is not based on evidence, is not healthy, is certainly not going to reduce one's risk for cardiovascular disease, and is a hazaard to follow in umpteen ways. More distrubing is that it is nothing more than lip-service to an unwitting public - the public trusts the AHA and the AHA is promoting a diet that includes a class of fats that the Institutes of Medicine (IOM) concluded have "no safe level" of consumption for humans.
The idea that the public simply won't accept a diet that isn't littered with foods that are unhealthy is not a reason to lie to them, pacify them and tell them they can have their cake and eat it too. Instead of attempting to engage in a meaningful dialogue where facts based on facts are exchanged, the AHA pushes emotional buttons in an attempt to sway readers from the task at hand - eliminating man-made trans-fats from the diet. It's a pitiful and pathetic act and not worthy of any attention by those who are looking to engage in that meaningful dialogue in pursuit of truth about diet and health.
In fact, what we need is a scientific community dedicated to neutralizing harmful ingredients we have inflicted on ourselves; not endorsing and recommending ones we know are harmful. If America is craving healthy snack foods let them eat organic fruit and nuts. Is that such a difficult idea or what?
If we are going to make a difference we must start by taking the path of truth and stop lying to the American public that junk food is acceptable in moderation.
The hawked book promises “don’t give up your favorites." Instead of evoking integrity, the book is schizophrenic - promoting a "no fad" approach to diet while also promoting foods known to be damaging to health.
By refusing to support industry that is detrimental to our health we can send a message to the puppets we have sitting in many of the leading health organizations: health does not come out of a can, a bottle, or any other man made disposable. Health does not come from chemistry. Health comes from the soil - from real whole foods that served us well for millenia that too many today wouldn't even recognize if itwere on their plate.
We have all heard the saying, "Think globally, Act locally." Well, your own body is as local as you can get. Everything you consume is a personal statement of how you view your body and health.
This is a personal challenge to any and all of my friends and readers who see the irony of the AHA encouraging donuts, fast food bacon biscuits and other assorted junk food - Let's all take a stand for ourselves, our health and say "enough is enough." Put down the soda, the chips, and donuts and declare your body a toxin-free zone. If you're not up to this challenge, ignore me and belly up to the bar. It was the wise bartender who said "name your poison."
Aren't we lucky to have so many to poisons to choose from?
Friday, April 07, 2006
Fools Folly
Shame on Dr. John G. Sotos, a cardiologist whose Op/Ed "A Modest -- and Slimming! -- Proposal" appeared in today's Washington Post.
In it, he suggests we adopt a public policy for the food industry modeled on our current encironmental policy, better known as "Tradable Emission Allowances" that allow companies who pollute less to credit companies that pollute more. He thinks basing such a credit system on calories per ounce would solve our growing obesity problem.
A program for tradable emission allowances could target foods with a high caloric density, that is, foods with a high number of calories per ounce. These foods are more likely to produce weight gain than foods with a low density of calories. It's easier to eat 1,000 calories in dessert than in vegetables, because the calories in dessert are concentrated.A food's caloric density generally depends on its water and fat content. Dry, fatty foods have the highest caloric density, because water has weight but no calories and because fat has more calories per ounce than proteins and carbohydrates. For example, butter, which is fatty and dry, has 195 calories per ounce. Frozen spinach has seven calories per ounce.
A specific example illustrates how tradable emission allowances could work. Suppose the calorie-emission allowance is set to 100 calories for each ounce of food emitted into the environment (i.e., sold). A four-ounce food item having more than 400 calories could not, therefore, be sold unless "calorie credits" were purchased to cover the excess calories. So a standard four-ounce stick of butter, containing 780 calories, could not enter the marketplace until the butter producer acquired 380 additional calorie-credits from someone having credits to sell.
On the other hand, the producer of a four-ounce block of frozen spinach would emit only 28 calories into the environment and could sell the unused 372 calorie-credits to the butter producer.With such a program, high-density foods would become more expensive and low-density foods would become cheaper. Unlike a tax, the program could be designed so the net cost change to consumers was zero. Thus, consumers who alter their eating habits need pay no more to eat the same number of calories. The hope, which should be tested, is that the number of calories eaten would drop, owing to the difficulty of consuming large numbers of calories from low-density foods. This would then reduce food costs and, ultimately, health-care costs.
As a cardiologist, Dr. Soto should know it's not just about calories. While his idea is certainly novel, it fails at the very core of our nutrient requirements - actual micronutrients - vitamins, minerals, trace elements, amino acids, and fatty acids - in a food per ounce!
Some examples of foods that would fall under those with too many calories per ounce:
In it, he suggests we adopt a public policy for the food industry modeled on our current encironmental policy, better known as "Tradable Emission Allowances" that allow companies who pollute less to credit companies that pollute more. He thinks basing such a credit system on calories per ounce would solve our growing obesity problem.
A program for tradable emission allowances could target foods with a high caloric density, that is, foods with a high number of calories per ounce. These foods are more likely to produce weight gain than foods with a low density of calories. It's easier to eat 1,000 calories in dessert than in vegetables, because the calories in dessert are concentrated.A food's caloric density generally depends on its water and fat content. Dry, fatty foods have the highest caloric density, because water has weight but no calories and because fat has more calories per ounce than proteins and carbohydrates. For example, butter, which is fatty and dry, has 195 calories per ounce. Frozen spinach has seven calories per ounce.
A specific example illustrates how tradable emission allowances could work. Suppose the calorie-emission allowance is set to 100 calories for each ounce of food emitted into the environment (i.e., sold). A four-ounce food item having more than 400 calories could not, therefore, be sold unless "calorie credits" were purchased to cover the excess calories. So a standard four-ounce stick of butter, containing 780 calories, could not enter the marketplace until the butter producer acquired 380 additional calorie-credits from someone having credits to sell.
On the other hand, the producer of a four-ounce block of frozen spinach would emit only 28 calories into the environment and could sell the unused 372 calorie-credits to the butter producer.With such a program, high-density foods would become more expensive and low-density foods would become cheaper. Unlike a tax, the program could be designed so the net cost change to consumers was zero. Thus, consumers who alter their eating habits need pay no more to eat the same number of calories. The hope, which should be tested, is that the number of calories eaten would drop, owing to the difficulty of consuming large numbers of calories from low-density foods. This would then reduce food costs and, ultimately, health-care costs.
As a cardiologist, Dr. Soto should know it's not just about calories. While his idea is certainly novel, it fails at the very core of our nutrient requirements - actual micronutrients - vitamins, minerals, trace elements, amino acids, and fatty acids - in a food per ounce!
Some examples of foods that would fall under those with too many calories per ounce:
- almonds, walnuts, peacans, sunflower seeds - basically all nuts and seeds
- nut & seeds butters
- natural cheese
- any natural oil or fat, including those that are essential
- fatty fish
- some fruits, like avocados and coconut
- poultry, like duck
- natural sweeteners, like honey
The list is by no means inclusive of all the natural, whole foods that would fall into the "over 100 calories per ounce" folly. I don't know about you, but I see such a system as harmful to farmers and growers who are producing these very foods - foods that are healthy and good in our diet. While Dr. Soto may think he's on to something here - I think it's an unworkable idea that isn't going to make a dent in our eating habits or obesity epidemic.
What will work is for the American population to be told the truth about what the evidence tells us about diet, health and weight gain or loss; and provide them with usable tools - including a variety of dietary options that are scientifically supported - to get their weight down and improve their health.
The message "eat less and move more" doesn't work, isn't going to work and the evidence shows there are alternatives to the carbohydrate-rich, low-fat diet repeated day-in-day-out to the public, that work better, faster and with greater improvements in health risks!
Thursday, April 06, 2006
Diabetes: Are we Angry Yet?
The National Health and Nutrition Examination Survey (1988–1994 and 1999–2002) and the Behavioral Risk Factor Surveillance System (1995 and 2002) reveal that not much has improved for diabetics in the United States in the last decade. On some measurements of diabetic control, things have actually gotten worse. But, you wouldn't know that from the conclusions found in the abstract of Improvements in Diabetes Processes of Care and Intermediate Outcomes: United States, 1988–2002 that states: "Diabetes processes of care and intermediate outcomes have improved nationally in the past decade. But 2 in 5 persons with diabetes still have poor LDL cholesterol control, 1 in 3 persons still has poor blood pressure control, and 1 in 5 persons still has poor glycemic control."
The American Diabetes Association (ADA) and the National Diabetes Eduction Program both are clear - an HbA1c higher than 7 indicates "poor control" of diabetes. Yet the data in the above full-text article shows that poor glycemic control is prevalent not in 20% of those with diabetes, but 58.7% of diabetics!
What's more, some organizations like the International Diabetes Federation (IDF) actually set the bar lower - to 6.5 or less as the target for controlled blood sugar. But for now let's not bicker about which is a more accurate measure over the long-term for health complications - something more troubling is found in the data - the number able to maintain an HbA1c of 6 or less has fallen considerably - from 23.4% of those with diabetes in the 1990's to just 16.4% in the most recent survey.
Add to that, the overall average HbA1c didn't change at all - it remained steady at 7.7% - poor control.
That, my friends, is not an improvement by any stretch of the imagination!
So while some are patting themselves on the back for "improvements" over the last decade, I implore you to look beyond the headlines and read the data and the tables in the full article. It is only with this full information can you begin the task of asking "why, with all of our advances in medicine, do we still have those with diabetes unable to adequately control their blood sugar?"
"Why do so many still have very high LDL levels (37% greater than 130), low HDL levels (68% less than 50) and often alarming levels of triglycerides (53% higher than 150)?"
"Why do one in three have high blood pressure?"
Many will challenge these questions with "well, that's the path of complications with diabetes - all we can hope to do is slow it down."
My retort - poppycock!
I'm going to state this very clearly - the ADA diet, the carbohydrate-rich, low-fat diet preached to every type II diabetic in this country - is a death sentence!
Over time it leads to less and less ability to control blood sugar adequately, leading to increased reliance on medications, increased complications and side-effects from both the poor glycemic control and medications, which in turn leads to further worsening of the condition. It's a vicious cycle and it starts with the insane recommendation to eat a low-fat, carbohydrate rich diet upon diagnosis of type II diabetes.
Back in January I wrote that Diabetics Must Demand Accountability from the ADA because "The ADA survives because we, as a nation, are not demanding they be accountable to every diabetic out there who has followed their recommendations and still are declining each day. The ADA continuing to promote the idea of managing the disease symptoms and progressive complications is NOT good enough anymore."
"Only an aggressive campaign that openly and honestly reviews every last piece of scientific data available and comprehensively details exactly what metabolic and/or endocrine improvement is seen with each option will be an acceptable start."
In the above survey data, evey last item reviewed points to problems with the recommended diet, yet there is no mention of this in the paper - the discussion is limited to medical interventions and slowing the progression of the disease rather than asking the hard question - why with all of our medical advancements, interventions and intensive education programs are we getting nowhere with glycemic control?
It's easy to blame the person with diabetes as the culprit here - if only they'd follow the guidelines - instead of asking if the guidelines are contributing to the problem. When the assumption is that the guidelines are accurate it's difficult to ask the question and even harder to persue an answer which could throw everything you think you know out the window.
I'll close here with the same challenge I wrote in Janaury:
Type II Diabetics, ask yourself, do you want to have to take medication every day for the rest of your life and progressively add more and more as the years go by?
No? Well...Demand the ADA begin to tell you the truth about restricting carbohydrate in your diet!
Demand the ADA begin to give you actual IMPROVEMENT in, not just medical management of, your metabolism, endocrine system and thus, your diabetes!
The American Diabetes Association (ADA) and the National Diabetes Eduction Program both are clear - an HbA1c higher than 7 indicates "poor control" of diabetes. Yet the data in the above full-text article shows that poor glycemic control is prevalent not in 20% of those with diabetes, but 58.7% of diabetics!
What's more, some organizations like the International Diabetes Federation (IDF) actually set the bar lower - to 6.5 or less as the target for controlled blood sugar. But for now let's not bicker about which is a more accurate measure over the long-term for health complications - something more troubling is found in the data - the number able to maintain an HbA1c of 6 or less has fallen considerably - from 23.4% of those with diabetes in the 1990's to just 16.4% in the most recent survey.
Add to that, the overall average HbA1c didn't change at all - it remained steady at 7.7% - poor control.
That, my friends, is not an improvement by any stretch of the imagination!
So while some are patting themselves on the back for "improvements" over the last decade, I implore you to look beyond the headlines and read the data and the tables in the full article. It is only with this full information can you begin the task of asking "why, with all of our advances in medicine, do we still have those with diabetes unable to adequately control their blood sugar?"
"Why do so many still have very high LDL levels (37% greater than 130), low HDL levels (68% less than 50) and often alarming levels of triglycerides (53% higher than 150)?"
"Why do one in three have high blood pressure?"
Many will challenge these questions with "well, that's the path of complications with diabetes - all we can hope to do is slow it down."
My retort - poppycock!
I'm going to state this very clearly - the ADA diet, the carbohydrate-rich, low-fat diet preached to every type II diabetic in this country - is a death sentence!
Over time it leads to less and less ability to control blood sugar adequately, leading to increased reliance on medications, increased complications and side-effects from both the poor glycemic control and medications, which in turn leads to further worsening of the condition. It's a vicious cycle and it starts with the insane recommendation to eat a low-fat, carbohydrate rich diet upon diagnosis of type II diabetes.
Back in January I wrote that Diabetics Must Demand Accountability from the ADA because "The ADA survives because we, as a nation, are not demanding they be accountable to every diabetic out there who has followed their recommendations and still are declining each day. The ADA continuing to promote the idea of managing the disease symptoms and progressive complications is NOT good enough anymore."
"Only an aggressive campaign that openly and honestly reviews every last piece of scientific data available and comprehensively details exactly what metabolic and/or endocrine improvement is seen with each option will be an acceptable start."
In the above survey data, evey last item reviewed points to problems with the recommended diet, yet there is no mention of this in the paper - the discussion is limited to medical interventions and slowing the progression of the disease rather than asking the hard question - why with all of our medical advancements, interventions and intensive education programs are we getting nowhere with glycemic control?
It's easy to blame the person with diabetes as the culprit here - if only they'd follow the guidelines - instead of asking if the guidelines are contributing to the problem. When the assumption is that the guidelines are accurate it's difficult to ask the question and even harder to persue an answer which could throw everything you think you know out the window.
I'll close here with the same challenge I wrote in Janaury:
Type II Diabetics, ask yourself, do you want to have to take medication every day for the rest of your life and progressively add more and more as the years go by?
No? Well...Demand the ADA begin to tell you the truth about restricting carbohydrate in your diet!
Demand the ADA begin to give you actual IMPROVEMENT in, not just medical management of, your metabolism, endocrine system and thus, your diabetes!
Alarming Rates of Childhood Obesity & Related Diseases
The other day, WebMD reported newly released CDC statistics in "Obesity Epidemic Balloons to New Girth," that show 70% of adults are overweight or obese in the United States. Of that, 32% obese with a BMI greater than 30 and 5% super-obese with a BMI greater than 40. As stunning as those statistics are for the adult population - the statistics regarding the rates of obesity amongst our children are downright frightening!
Children:
Children:
- aged 2-5 years, 26% currently have a body weight in the 85th percentile or higher, with 14% of all children of this age group in the 95th percentile or higher
- children aged 6-11 years, 37% have a body weight in the 85th percentile or higher, with 19% of all children of this age group in the 95th percentil or higher
- children aged 12-19 years, 34% have a body weight in the 85th percentile or higher, with 17% of all children of this age group in the 95th percentile or higher
Add to this, a study, Worldwide trends in childhood overweight and obesity, published in the premier issue of the International Journal of Pediatric Obesity this month - it paints a bleak picture of where we are and where we're headed with our children and their growing girth.
From the 1970s to the end of the 1990s, the prevalence of overweight or obesity in school-age children doubled or tripled in several large countries in most regions, such as Canada and the United States in North America; Brazil and Chile in South America; Australia and Japan in the Western Pacific region, and Finland, Germany, Greece, Spain and the UK in Europe.
Based on the secular trends reported here, and assuming they continue on a linear basis, we estimate that over 46% of school-age children will be overweight...in the Americas by 2010; ...[b]y 2010, one in seven children in the Americas is predicted to be obese. The implications for local health services as these children develop obesity-related chronic diseases in later adolescence and early adulthood, are difficult to estimate, but planning for this disease burden needs to be undertaken urgently. For some countries the costs may not be easily absorbed into the domestic economy, and health outcomes may be correspondingly poor.
Folks, within the next four years, if we continue on the current path, 50% of our children will be overweight with one in seven obese! I don't even want to imagine what these statistics translate to in terms of type II diabetes, metabolic syndrome and other obesity related disorders for our children in the future.
To me, this is appalling and a clear indication we are failing our children.
We're quick to blame the marketers, manufacturers, television, fast food restaurants, childrens' characters, not having enough time, lack of safe play space outside and more - but the hard truth is, as parents, we control every last thing our children eat, do and see each day! Ultimately it is the parent who is responsible when their child has learned out-of-control eating habits and sits idle each day.
Am I being too hard on parents?
I don't think so - I speak from experience as a mom and understand the difficulty we parents face in maintaining healthy eating habits and levels of activity in an environment that encourages the exact opposite. But it is my responsibility as a parent to be up to the challenge and do the hard work necessary for my childs health and well-being.
If I don't step up and take that responsibility seriously, why would anyone else? Think about it - if marketers and manufaturers are working hard to convince my child to eat junk food and I buy it for him, are the marketers and manufacturers responsibile when he eats it, or am I when I buy it and subsequently feed it to him?
In my mind, the only person responsible in such a scenario is me - I bought the junk food and I fed it to my child...no one made me do it, no one forced my hand and, conversely, no one can make me buy or feed it to my child.
So while many are quick to blame everyone and anyone to absolve themself - the hard truth is that we parents make the final choice of how and what to feed our kids, how often they get outside to play, and how often they're allowed to sit around doing nothing more than watching television or playing video games.
The statistics cited in the above two articles are frightening for our future. We are raising a generation of children who are getting fatter by the day - not only does the excess weight present a challenge for our children today, it is setting the stage for ill-health in the long-term! The Kansas City Star reported today "Study: More children using drugs that treat Type 2 diabetes" that researchers reviewing prescriptions dispensed in the last four years showed that drugs used to treat and prevent Type II Diabetes IN CHILDREN doubled in the last four years. Four years! Doubled!
Sadly, I'm not surprised. I am however concerned that many parents are ignoring the obvious - the lifelong complications they are imposing on their children because they aren't paying attention to the details and making their childrens' short and long-term health priority number one.
Yes, it's often easier to believe you don't have time, you are doing all you can and that somehow your child will be insulated from harm - obesity and type II diabetes only happens to other kids. The numbers tell us that we're in trouble in the United States - not impending, soon-to-happen if we do nothing trouble - but deep trouble today.
We're pretty good at wringing our hands and hoping someone will do something to reverse the trend. The truth is that only you - the parent - can do the hard work necessary to ensure your child is eating a healthy diet and is active every day!
Waiting for the government, schools, daycare, health organizations, politicians, doctors, the food industry or others to fix the problem for you is no longer an option any parent should consider viable for the long-term health of their child. It's time we parents step up to the plate and take responsibility for what we're feeding our kids, what messages we allow marketers to ingrain in their minds, and what activities we encourage them to engage in each day.
More importantly, it's time we parents stepped up to be the role model our kids need to learn from and want to emulate. It's time to put down the big gulp and bag of chips, grab a bottle of water and a bag of blueberries and go take a walk with you child, run with your child at the park and laugh together as you decide what the clouds look like today as you kick back, enjoy your snack and rest from all that fun together!
Trust me - your kids are worth the effort!
Wednesday, April 05, 2006
What's Up?
For all of my readers who emailed to inquiry why I hadn't written anything in over a week - I was traveling and didn't have access to a computer. Now that I'm home again, I will resume adding to my blog as time permits in the coming weeks as I now have to pack up the house and prepare for a long distance move.
And, just where am I and my family moving? The lovely state of Missouri!
My husband, son and I had a great trip out there to close on our new home and are excited about the upcoming move. The time crunch to prepare for the move and then settle in at the new house may leave my blog without a new entry some days.
For now - I'll write as often as I can, but can make no promises about frequency! I appreciate your patience in the coming weeks and look forward to resuming daily posts once we're settled in.
Thanks!
And, just where am I and my family moving? The lovely state of Missouri!
My husband, son and I had a great trip out there to close on our new home and are excited about the upcoming move. The time crunch to prepare for the move and then settle in at the new house may leave my blog without a new entry some days.
For now - I'll write as often as I can, but can make no promises about frequency! I appreciate your patience in the coming weeks and look forward to resuming daily posts once we're settled in.
Thanks!
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