Yesterday in Western Farm Press an angry editorial was published, Last straw – farm programs blamed for obesity, penned by Elton Robinson, a staffer at Editorial Press. He ranted about recent remarks by Dr. Philip James, the British chairman of the International Obesity Task Force at the 10th International Obesity Congress in Sydney, Australia.
In his statement, Dr. James said that existing farm policies, particularly agricultural subsidies in the European Union and the United States, have been damaging people’s health for decades.
“We have concentrated on using taxpayers’ money to featherbed the very parts of the food chain that are causing the obesity epidemic today. The over-production of oil, fat and sugar, largely due to government subsidies to protect farm industry revenues, has contributed over decades to the health crisis we have today.
“People have paid three times over – firstly in taxes to support hundreds of millions of dollars in subsidies in the United States, the EU and elsewhere, secondly in the resulting harm to the health and thirdly in the health insurance taxes and premiums required to cope with a major burden of preventable chronic disease.”
James says there is a fourth cost in terms of jobs in developing countries, saying the trade distortions generated by the use of public funds to prop up domestic sugar production in the United States and the EU has cost more than 1 million jobs among sugar-growing developing countries.
You can read Mr. Robinson's rant in the article, here I want to address one paragraph in particular, found near the end of the editorial:
U.S. farmers are tired of being made the scapegoat for the world’s problems, and this charge by James is the last straw. If the world’s health industries really want to solve the growing world obesity epidemic, start by advocating personal responsibility. Tell people the truth. You are what you eat.
While I totally agree that farmers shouldn't be the target of disdain here, I find Mr. Robinson's remarks disingenous and his finger is pointing in the wrong direction too.
It's really easy to point the finger at the public, insisting the problems of obesity and ill-health start and end with individual responsibility; afterall, it's hard to argue that anyone is forced to eat any particular food or even overeat.
What an individual eats really is a choice.
Or is it?
Like most Americans, I didn't have a clue about where most of my food came from, let alone what farm subsides were, until recently. The world we live in today, in the United States, has created a gap between the farm and table that leaves most people unaware of where their food comes from - how it is grown, produced, refined, value-added, manufacturered, packaged and transported before they ever see it appear in an advertisement or on a supermarket shelf to purchase.
Part of this disconnect is our own fault - we lead busy lives, are more urbanized today than ever before, and don't feel the need to head out to the farm to see how things are done, let alone buy our food at the farm; plenty is available right at the local supermarket. A totally understandable reality - life as we know it in the United States - anything and everything you need is available at the supermarket, so why learn where your food comes from?
Well, for one thing, the other part of the disconnect is the confidence food manufacturers have that we don't care where our food comes from - what's available in the supermarket is simply assumed to be comparable to something we might make at home. Such confidence we have in our food supply - few today question what the long list of ingredients are in the food they're buying, often unaware of what farm crop was processed to create the ingredient in the food in their shopping cart.
Basically, most of us are really naive when it comes to understanding what's called "commodity" foods; these crops are a largely homogeneous product that starts simply as a crop grown by various farmers and upon harvest, the end result is pooled together from different farms where the crop from farm A isn't differentiated from farm B - a uniform standard of quality is assumed and all farmers get the same price for their crop, and this is where subsidies come into play for the farmer.
But, since this isn't about subsidies - how about we talk some truth about what happens next to these crops?
The truth is, it's what happens next - well before any crop reaches the supermarket - that we're painfully lacking in knowledge as a population. It's the next steps in the process from farm to market that Americans must - if they are to be "responsible" consumuers - understand if they're to have any chance of making good decisions about what to eat.
Let's take a look at the largest commodity crop in the United States - corn.
Did you know that the corn you buy in the market, on the cob, in a can or in a bag in the frozen section, isn't the same corn that's in the majority of the food you buy throughout the supermarket?
Commodity corn is hugely profitable - it feeds livestock and is processed into a large number of ingredients used in foods. As the Corn Refiners Association states on it's website page Tapping the Treasure in Corn, "Corn refining is today's leading example of value added agriculture."
"The eight member companies of the Corn Refiners Association, Inc. use over 1.4 billion bushels of U.S.-grown corn to produce a broad array of food, industrial and feed products for Americans and for the world market. Corn refiners use shelled corn which has been stripped from the cob during harvesting. Refiners separate the corn into its components -- starch, oil, protein and fiber -- and convert them into higher value products."
Almost all the corn grown in the United States is sold to the eight companies who "refine" it for use as something else. The CRA includes a flow chart on their website to highlight the refining process and the many end-products that come from the crop.
Corn is refined to become an ingredient - a food sweetener - and supplies more than 56% of the added sugars in our diet today. Yes - corn; not as food, but as sweetener, with no nutritional value whatsoever, simply calories as corn syrup, dextrose and high fructose corn syrup.
Then there is the starch - as the CRA highlights on their starch page, "Literally thousands of supermarket staples are produced using both regular and specially modified starches. Many of today's instant and ready-to-eat foods are produced using starches which enable them to maintain the proper textural characteristics during freezing, thawing and heating. Other starches are the backbone of instant pie and pudding fillings which require little or no cooking compared to traditional formulations."
There are also the bioproducts too, citric acid, lactic acid, food gums, vitamin c, vitamin e, monosodium glutamate (MSG) and xanthan gum. Oh, and let's not forget - corn oil, with the majority produced in the United States used in cooking and salad oils, margarines and shortenings.
All this from a cob of corn that none of us would willingly eat if given an ear to chomp on - it's a different corn, definitely not the sweet corn we think of as corn on the cob!
Not only is this corn refined beyond any point of recognition as corn, the entire step-by-step process from farm to market is highly inefficient and wastes energy; and I'm not just talking calories. I was shocked to learn just how much oil and electricity is required in the growing, refining and transportation of this one crop.
On the farm - synthetic nitrogen fertilizer, made from natural gas and the use of electricity; fuel to drive the tractors, combines and other farm equipement; fuel to take harvested crop to central grain elevator.
At the grain elevator - electricity to run elevator; fuel to drive crops in trucks to processing plants.
Processing plant - electricity to run plant; fuels required to intensively process crops; fuel to drive ingredients to manufacturers.
Manufacturers - electricity & fuel to run operations; fuel to transport refined products to distribution centers by truck, planes and trains; plastics (petroleum based) to package foods.
The we drive the products all around the country to various supermarkets, convenience stores, restaurants and fast food establishments.
Again, all this from a cob of corn that none of us would willingly eat if given an ear to chomp on - it's a different corn, definitely not the sweet corn we think of as corn on the cob!
Hardly anyone in the US ever sees this intensive use of energy to make foods that are highly processed, complicated food products that no longer resemble the food crop they started as.
As Michael Pollan said in We Are What We Eat, in an edited excerpt of a plenary speech delivered at the Ecological Farming Conference in Asilomar, CA, in January 2005, "Take a typical fast food meal. Corn is the sweetener in the soda. It's in the corn-fed beef Big Mac patty, and in the high-fructose syrup in the bun, and in the secret sauce. Slim Jims are full of corn syrup, dextrose, cornstarch, and a great many additives. The “four different fuels” in a Lunchables meal, are all essentially corn-based. The chicken nugget—including feed for the chicken, fillers, binders, coating, and dipping sauce—is all corn. The french fries are made from potatoes, but odds are they're fried in corn oil, the source of 50 percent of their calories. Even the salads at McDonald's are full of high-fructose corn syrup and thickeners made from corn."
Why do we process corn? According to Pollan, "There is a powerful industrial logic at work here, the logic of processing. We discovered that corn is this big, fat packet of starch that can be broken down into almost any basic organic molecules and reassembled as sweeteners and many other food additives. Of the 37 ingredients in chicken nuggets, something like 30 are made, directly or indirectly, from corn."
I don't want anyone to think I'm picking on corn - other commodity crops include wheat and soybeans. Those crops are also highly processed into a large number of ingredients that make their way into thousands of foods sold in the supermarket - again, often not even close to resembling what the original crop started as, and always dependent on our naivate of the process, energy cost and nutritionally inferior end product.
So, if Mr. Robinson wants some truth - here's a start - get to know what's in your food, where it came from, why it's used to enhance profits. Then think about just how much it really costs in terms of energy wasted (electricity and oil), excess energy provided (calories consumed) and long term health effects.
Friday, September 29, 2006
Thursday, September 28, 2006
Omega-3 Information
A number of people have emailed and posted comments asking for more information about omega-3 fatty acids - what foods and/or supplements contain omega-3; how much is in each; how do you calculate the ratio; etc.
Tuesday, October 3rd, I will post a comprehensive list of foods, fats/oils and supplements for readers, along with recommended reading, resources and additional information.
I want to thank everyone who's inquired for their patience - such a post requires time to compile and reference properly!
Tuesday, October 3rd, I will post a comprehensive list of foods, fats/oils and supplements for readers, along with recommended reading, resources and additional information.
I want to thank everyone who's inquired for their patience - such a post requires time to compile and reference properly!
Wednesday, September 27, 2006
Diabetes Disconnect
Sometimes I have to wonder how some experts in the diabetes community can sleep at night.
From an outsider perspective (that would be me) it seems many held as "expert" in the diagnosis and management of diabetes, who say they believe in the goal of improving the lives of those with diabetes, remain apathetic to their own findings, and the conclusions of numerous studies, that find alarming numbers of people are walking around with undiagnosed diabetes who are experiencing major complications because they are unaware they have diabetes!
Case in point - the recent publication of Evidence of Nephropathy and Peripheral Neuropathy in US Adults With Undiagnosed Diabetes in the September/October issue of Annals of Family Medicine. This was a study funded by a grant from the National Institute for Diabetes & Digestive & Kidney Diseases (NIDDK), an agency within the National Institutes of Health (NIH). Your tax dollars at work.
In this study, the researchers "sampled adults 40 years of age and older for this analysis because this population in the NHANES had both monofilament and urine testing. We also used the subsample of participants who had fasting plasma glucose measurements, resulting in an unweighted sample size of 2,571."
The findings in the cohort, "24.9% of adults 40 years and older with undiagnosed diabetes had signs of nephropathy and 21.5% had signs of peripheral neuropathy adds to the accumulating literature which documents undiagnosed diabetes is not a benign condition but represents a serious public health concern."
The researchers continued "These findings, along with estimates of the prevalence of complications at the time of diagnosis, suggest the time before diagnosis of diabetes is neither benign nor quiescent. The time from disease onset to clinical diagnosis has been estimated to be at least 9 to 12 years. Furthermore, onset of type 2 diabetes is often insidious, with a prodrome of subclinical disease that may last more than 10 years and involves insulin resistance and other metabolic abnormalities. Insulin resistance in the absence of diabetes has been shown to be a risk factor for cardiovascular disease, prolonging the period of potential risk for complications. In fact, increased prevalence of microalbuminuria and sensory neuropathy is found in those with impaired glucose tolerance."
Now, their conclusion: "Mass population screening for diabetes is not recommended at this time despite evidence that early treatment can prevent complications."
Now you can see why I wonder why some can sleep at night.
People who have any type of diabetes are subject to long-term complications.
These complications are broken down into two groups: microvascular (small blood vessels) and macrovascular (large blood vessels).
The microvascular complications include
From an outsider perspective (that would be me) it seems many held as "expert" in the diagnosis and management of diabetes, who say they believe in the goal of improving the lives of those with diabetes, remain apathetic to their own findings, and the conclusions of numerous studies, that find alarming numbers of people are walking around with undiagnosed diabetes who are experiencing major complications because they are unaware they have diabetes!
Case in point - the recent publication of Evidence of Nephropathy and Peripheral Neuropathy in US Adults With Undiagnosed Diabetes in the September/October issue of Annals of Family Medicine. This was a study funded by a grant from the National Institute for Diabetes & Digestive & Kidney Diseases (NIDDK), an agency within the National Institutes of Health (NIH). Your tax dollars at work.
In this study, the researchers "sampled adults 40 years of age and older for this analysis because this population in the NHANES had both monofilament and urine testing. We also used the subsample of participants who had fasting plasma glucose measurements, resulting in an unweighted sample size of 2,571."
The findings in the cohort, "24.9% of adults 40 years and older with undiagnosed diabetes had signs of nephropathy and 21.5% had signs of peripheral neuropathy adds to the accumulating literature which documents undiagnosed diabetes is not a benign condition but represents a serious public health concern."
The researchers continued "These findings, along with estimates of the prevalence of complications at the time of diagnosis, suggest the time before diagnosis of diabetes is neither benign nor quiescent. The time from disease onset to clinical diagnosis has been estimated to be at least 9 to 12 years. Furthermore, onset of type 2 diabetes is often insidious, with a prodrome of subclinical disease that may last more than 10 years and involves insulin resistance and other metabolic abnormalities. Insulin resistance in the absence of diabetes has been shown to be a risk factor for cardiovascular disease, prolonging the period of potential risk for complications. In fact, increased prevalence of microalbuminuria and sensory neuropathy is found in those with impaired glucose tolerance."
Now, their conclusion: "Mass population screening for diabetes is not recommended at this time despite evidence that early treatment can prevent complications."
Now you can see why I wonder why some can sleep at night.
People who have any type of diabetes are subject to long-term complications.
These complications are broken down into two groups: microvascular (small blood vessels) and macrovascular (large blood vessels).
The microvascular complications include
- Diabetic retinopathy: Eye damage that can lead to blindness if untreated.
- Diabetic nephropathy: Kidney damage that can lead to kidney failure if not treated.
- Diabetic neuropathy: Nerve damage resulting in many different symptoms, the most common of which is loss of sensation, tingling, and numbness in the feet and hands.
The macrovascular complications include
- Arteriosclerotic heart disease: The blood vessels that supply blood to heart tissue are blocked. This is the most common cause of death in people with diabetes, just as it is in people who do not have diabetes.
- Arteriosclerotic cerebrovascular disease: The arteries to the brain are blocked, leading to stroke or sometimes loss of intellectual function.
- Arteriosclerotic peripheral vascular disease (PVD): The arteries that carry blood to the legs become narrowed or clogged. If blood flow ceases completely, amputation may be necessary.
Here we have a study pointing to the damage and complications ravaging those who haven't been diagnosed - and the researchers conclude there is no reason to recommend more aggressive screening for diabetes. Basically they're saying it's okay to allow the ticking timebomb within to keep ticking away to the point of no return, "DESPITE THE EVIDENCE THAT EARLY TREATMENT CAN PREVENT COMPLICATIONS!"
Nibbles & Bites
You may notice some changes in my sidebar today - I've updated links to include more websites, blogs and online support forums and removed many who do not include regular updates.
Some notable articles to take time to read:
Adam Campbell, Men's Fitness Insider
How To Change Your Life For The Better
What they Don't Tell you about Diabetes
Healthy Blood Sugar Targets
Dr. Jonny Bowden
Hats off to Michael Eades- read this blog!
Dr. Mike Eades
Framingham follies
Recent Headlines I Don't Have Time to Write About:
The Economist
Bitter consequences
Food Navigator USA
Nutrition labels may confuse public
International Herald Tribune
WHO: Fight against chronic diseases, obesity can use anti-smoking campaigns as models
Enjoy!
Some notable articles to take time to read:
Adam Campbell, Men's Fitness Insider
How To Change Your Life For The Better
What they Don't Tell you about Diabetes
Healthy Blood Sugar Targets
Dr. Jonny Bowden
Hats off to Michael Eades- read this blog!
Dr. Mike Eades
Framingham follies
Recent Headlines I Don't Have Time to Write About:
The Economist
Bitter consequences
Food Navigator USA
Nutrition labels may confuse public
International Herald Tribune
WHO: Fight against chronic diseases, obesity can use anti-smoking campaigns as models
Enjoy!
Learning More than you Want to Know
The October 2006 issue of National Geographic has a story that is an eye-opening read of one journalist's lesson about living in the world we do - sometimes you don't want to know just how many chemicals are resident in your body.
Worth reading - Chemicals Within Us
Worth reading - Chemicals Within Us
Eating an Eye-Popping 6,000 Calories a Day - No Effect on Cholesterol
This morning I found it necessary to change the tie-in to the article I planned to write about, Only another 5,500 calories to go ..., that appeared in the Guardian earlier this month. Originally I planned to tie-in to the movie that inspired the as-yet unpulished study featured in the article - Super Size Me.
But then, this morning, Dr. Mike Eades wrote an article in his blog with an even better tie-in - data published from the original Framingham Study! As Dr. Eades notes, the original data was massaged to death and "These guys tried as hard as they could to show a correlation between diet and serum cholesterol and between diet and the incidence of coronary heart disease, but failed. The data conclusively demonstrated no such correlations."
How does this relate to the Guardian story?
Well, a Swedish researcher, Dr. Fredrik Nyström, wanted to have some fun with excess research funds, and since watching Super Size Me he had been thinking of how, in all the studies of obesity and metabolism, hardly anyone has studied what happens when you force healthy people to put on weight. The few studies there have been took place in the 60s and 70s.
So he decided to conduct a 30-day trial with volunteers consuming fast food morning, day and night. Any fast foods they wanted as long as they consumed 6,000 eye-popping calories a day and agreed not to engage in physicial activity.
It wasn't difficult to find volunteers.
Late last year, after delivering a lecture on the ills of overeating, he casually asked if any of the students would be prepared to gorge themselves for the sake of science. He was deluged with applications, but mostly from men (he thinks that women are too wary of gaining weight). They all had to be in good health, but as he says: "Young med students usually are." Nyström then simply chose the ones who seemed "the most highly motivated".
In February, seven healthy medical students in their early 20s spent weeks stuffing themselves with hamburgers, pizzas, milk shakes and 200g bacon breakfasts - all on the university's tab. A second group of subjects are just now hitting the junk food. Physical exercise is to be avoided. Bikes are out. To discourage walking even the shortest distance, free bus passes have been issued.
Those participating found out how hard it was to eat that many calories each day - breakfast at home was allowed, provided it was bacon-and-eggs based. And the fast food didn't have to come exclusively from McDonald's: hamburgers could be exchanged for pizzas, as long as most of the calories still came from saturated fats, those having the most effect on levels of cholesterol. Still, it wasn't unusual for students to be about to go to bed only to discover that they were some 600 calories short of their daily target, and forced to face a large calorific milk shake rather than a mug of hot milk.
While the data itself is not yet published, the researchers have already noted that the while the students did gain between 5% and 15% extra weight and initially (in the first week) felt tired, none experienced the mood swings reported by Morgan Spurlock in the movie Super Size Me.
Interestingly, in the Swedish experiment, while the liver readings got steadily worse until the third week, they then took a turn for the better. The liver, it would seem, adapts. Cholesterol, meanwhile, was hardly affected.
The full findings are due for publication early next year, but the information we have at this point from the study is that, as Dr. Eades pointed out from the Framingham Study, serum cholesterol isn't really affected by our diet. At least not as much as we're led to believe!
As Dr. Nyström pointed out, "If you only look at the already overweight, you'll only do research on those with least resistance to calories, so to speak."
I'm going to be watching for the data when it's finally released and will write more about it once it's published. In the meantime, I don't think it wise for anyone to go out and follow such a diet as described above - but I do think this type of study is important in our understanding of nutrition & metabolism.
But then, this morning, Dr. Mike Eades wrote an article in his blog with an even better tie-in - data published from the original Framingham Study! As Dr. Eades notes, the original data was massaged to death and "These guys tried as hard as they could to show a correlation between diet and serum cholesterol and between diet and the incidence of coronary heart disease, but failed. The data conclusively demonstrated no such correlations."
How does this relate to the Guardian story?
Well, a Swedish researcher, Dr. Fredrik Nyström, wanted to have some fun with excess research funds, and since watching Super Size Me he had been thinking of how, in all the studies of obesity and metabolism, hardly anyone has studied what happens when you force healthy people to put on weight. The few studies there have been took place in the 60s and 70s.
So he decided to conduct a 30-day trial with volunteers consuming fast food morning, day and night. Any fast foods they wanted as long as they consumed 6,000 eye-popping calories a day and agreed not to engage in physicial activity.
It wasn't difficult to find volunteers.
Late last year, after delivering a lecture on the ills of overeating, he casually asked if any of the students would be prepared to gorge themselves for the sake of science. He was deluged with applications, but mostly from men (he thinks that women are too wary of gaining weight). They all had to be in good health, but as he says: "Young med students usually are." Nyström then simply chose the ones who seemed "the most highly motivated".
In February, seven healthy medical students in their early 20s spent weeks stuffing themselves with hamburgers, pizzas, milk shakes and 200g bacon breakfasts - all on the university's tab. A second group of subjects are just now hitting the junk food. Physical exercise is to be avoided. Bikes are out. To discourage walking even the shortest distance, free bus passes have been issued.
Those participating found out how hard it was to eat that many calories each day - breakfast at home was allowed, provided it was bacon-and-eggs based. And the fast food didn't have to come exclusively from McDonald's: hamburgers could be exchanged for pizzas, as long as most of the calories still came from saturated fats, those having the most effect on levels of cholesterol. Still, it wasn't unusual for students to be about to go to bed only to discover that they were some 600 calories short of their daily target, and forced to face a large calorific milk shake rather than a mug of hot milk.
While the data itself is not yet published, the researchers have already noted that the while the students did gain between 5% and 15% extra weight and initially (in the first week) felt tired, none experienced the mood swings reported by Morgan Spurlock in the movie Super Size Me.
Interestingly, in the Swedish experiment, while the liver readings got steadily worse until the third week, they then took a turn for the better. The liver, it would seem, adapts. Cholesterol, meanwhile, was hardly affected.
The full findings are due for publication early next year, but the information we have at this point from the study is that, as Dr. Eades pointed out from the Framingham Study, serum cholesterol isn't really affected by our diet. At least not as much as we're led to believe!
As Dr. Nyström pointed out, "If you only look at the already overweight, you'll only do research on those with least resistance to calories, so to speak."
I'm going to be watching for the data when it's finally released and will write more about it once it's published. In the meantime, I don't think it wise for anyone to go out and follow such a diet as described above - but I do think this type of study is important in our understanding of nutrition & metabolism.
Tuesday, September 26, 2006
Of Death and Diabetes
The September 25 issue of Critical Care published a study, The role of body mass index and diabetes in the development of acute organ failure and subsequent mortality in an observational cohort, that found "obesity by itself is not a significant predictor of either acute organ failure or death during or after acute organ failure in this cohort. However, the presence of DM, which is related to obesity, is a strong predictor of both acute organ failure and death after acute organ failure."
Yesterday afternoon I started reading through some of the articles published in the media about the study. Most were short items that included the basics found in the original press release issued to alert the media about the study publication.
One in particular stood out however, the article at Fox News, Diabetes May Be Cause of Deaths Linked to Obesity, a reprint of the WebMD article. It opened simply, "Another wrinkle has been added to the debate over whether obesity is a major cause of early death. New research suggests that it is, but only in people who also have diabetes."
Such drama makes a good teaser to capture your attention to read further, but unless you read the full-text, you won't know the full context of the findings. That's because the media is spinning this as a controversy because the findings are contrary to our assumptions; when in fact the data is alarming and needs a bit more attention to the details.
For example, the WebMD article included, "The new findings are not likely to end the medical debate about whether obesity is a direct or indirect cause of early death. The issue made headlines a year ago last spring, when CDC researchers reported that the risk of obesity-related death was much lower than had been previously believed. Researchers also reported no increase in death risk among people who were overweight but not obese. The report was widely criticized, and a reanalysis of the same data by researchers from the Harvard School of Public Health showed a strong association between obesity and early mortality."
So, what is the data really?
What the researchers did was analyze data from 15,408 participants in the Atherosclerosis Risk in Communities (ARIC) study to assess outcomes in the cohort regarding the development of acute organ failure within three years of the baseline examination, in-hospital death while ill with acute organ failure, and death within three years from baseline in all subject and those who developed acute organ failure. At the baseline examination both BMI and the presence of diabetes were defined; so was acute organ failure.
This particular population included adults aged 44 to 66, and they were diverse:
Yesterday afternoon I started reading through some of the articles published in the media about the study. Most were short items that included the basics found in the original press release issued to alert the media about the study publication.
One in particular stood out however, the article at Fox News, Diabetes May Be Cause of Deaths Linked to Obesity, a reprint of the WebMD article. It opened simply, "Another wrinkle has been added to the debate over whether obesity is a major cause of early death. New research suggests that it is, but only in people who also have diabetes."
Such drama makes a good teaser to capture your attention to read further, but unless you read the full-text, you won't know the full context of the findings. That's because the media is spinning this as a controversy because the findings are contrary to our assumptions; when in fact the data is alarming and needs a bit more attention to the details.
For example, the WebMD article included, "The new findings are not likely to end the medical debate about whether obesity is a direct or indirect cause of early death. The issue made headlines a year ago last spring, when CDC researchers reported that the risk of obesity-related death was much lower than had been previously believed. Researchers also reported no increase in death risk among people who were overweight but not obese. The report was widely criticized, and a reanalysis of the same data by researchers from the Harvard School of Public Health showed a strong association between obesity and early mortality."
So, what is the data really?
What the researchers did was analyze data from 15,408 participants in the Atherosclerosis Risk in Communities (ARIC) study to assess outcomes in the cohort regarding the development of acute organ failure within three years of the baseline examination, in-hospital death while ill with acute organ failure, and death within three years from baseline in all subject and those who developed acute organ failure. At the baseline examination both BMI and the presence of diabetes were defined; so was acute organ failure.
This particular population included adults aged 44 to 66, and they were diverse:
- 29.9% had normal BMI (21 to 24);
- 39% had an overweight BMI (25 to 29); and
- 27.5% had an obese BMI (30+)
What the researchers learned was, at baseline those with a BMI of 30 or higher were more likely than those with a lower BMI to also have diabetes (22.4% versus 7.9%; p = greater than 0.01).
Where the data is very interesting, even alarming, is the incidence of diabetes.
Overall 11.9% (1,890 subjects) had diabetes. Those with diabetes were more likely to have a BMI of 30 or higher, with 52% of those diagnosed with diabetes also at a BMI of 30 or higher.
The distribution of diagnosed diabetes was:
- BMI less than 20 = 4.4% had diabetes
- BMI 20 - 24 = 4.9% had diabetes
- BMI 25 - 29 = 10% had diabetes
- BMI 30 or higher = 22.4% had diabetes
When we see the incidence of diabetes as related to BMI, it is much easier to understand why the results were what they were. Those with higher BMI also had a higher incidence of diabetes. In the cohort, almost one in four with a BMI greater than 30 had diabetes!
In the three years of follow-up, the risk of developing acute organ failure was similar across BMI - 0.9% of subjects with normal BMI, 0.8% of subjects with overweight BMI and 0.9% of subjects with obese BMI. This one piece of data is probably the most important in the findings - regardless of BMI, the risk of developing acute organ failure was virtually identical across the cohort. But, at the same time, again regardless of BMI, the strongest independent predictor of development of acute organ failure was the presence of diabetes - as a risk factor, it carried a three-fold risk (odds ratio 3.2; 95% CI 2.1 to 4.7). It didn't matter what a person weighed - what mattered was the presence of diabetes.
The numbers here speak for themselves, quite loudly I might add, that the risk of developing acute organ failure is very high in those who have diabetes.
In addition, the data speaks volumes about the risk of death.
All cause mortality was also significantly higher in those with diabetes (again, regardless of BMI) - with almost a three-fold risk compared with those who did not have diabetes (odds ratio 2.7; 95% CI 2.1 to 3.5) Over the course of three years, 5.4% of subject with diabetes died compared with 1.6% of subjects without diabetes.
This is the kind of finding where the reaction "any questions?" is rhetorical - the finding is so statistically significant and strongly points to the problem - diabetes; not simply body weight.
As the researchers noted in their discussion "the development of acute organ failure and death after acute organ failure is more related to the presence of [diabetes] DM than to an increased BMI...Our results do not support the contention that obesity itself is a risk factor for increased mortality in patients with acute organ failure...In addition, our findings did not confirm an increased mortality in overweight or obese critically ill patients without [diabetes] DM...Our findings suggest that [diabetes] DM and associated hyperglycemia with insulin resistance, rather than obesity itself, is responsible for the development of acute organ failure and subsequent adverse outcomes in this middle-aged US population...Results of this study indicate that the presence of [diabetes] DM, rather than an increased BMI, accounts for a higher risk of acute organ failure and associated mortality."
But these findings are not going to stop those firmly of the belief that body weight alone is most important. It doesn't matter than numerous studies keep finding that diabetes, hyperglycemia and elevated blood sugars (even at levels some consider "normal") are statistically significant predictors of chronic illness and premature death.
The bottom line from this study is clear in my view - diabetes is a killer in those who are normal weight, overweight and obese.
To simply assume and continue to perpetuate the myth that someone who is overweight or obese is at a higher risk for developing chronic illness or dying prematurely simply because they are overweight or obese is engaging in scare tactics to motivate change in diet and lifestyle in the population - noble cause, but for the wrong reason.
It's pretty clear that the risk of diabetes is significantly higher as weight increases, but weight alone, in this study, was not a predictor of developing acute organ failure or death - diabetes was.
Monday, September 25, 2006
Again it's the Protein
For a number of years now I've been of the belief that at the core of consuming excess calories is inadequate protein and essential nutrients. Basically, those who are obese are in a state of "overconsumptive malnutrition," their hunger driven not by gluttony, but unfulfilled nutrient requirements.
To say hard evidence for this is sparse is an understatment. While there is data which points to nutrient deficiency and data pointing to protein inadequacy, there isn't much out there specifically investigating calorie intake based on nutrient adequacy. Today the Sydney Morning Herald reports findings from researchers at the University of Sydney in Skinniness gene imperils survival of the fattest who studied crickets, cockroaches, rats, minks and even humans in an effort to understand how protein requirements drive food consumption, for some, but not all, humans.
The lead researcher, Dr. Stephen Simpson, found that crickets are driven across the landscape, consuming crop after crop, because they have a fixed protein requirement. To meet that requirement, these pests will cannibalize each other along the way, so the frantic pace to keep moving is a survival mechanism, "stop and you get eaten."
To understand how protein requirements may play in human eating habits, the researchers "incarcerated 10 people in a chalet for six day," to monitor their eating.
For the first two days they could eat what they wanted from a buffet. For the next two days, one group was restricted to high-protein foods, such as chicken and meat, the other to fatty, sugary, low-protein foods, such as croissants.
The first group consumed exactly the same amount of protein as on the first two days. "The second group went way off the mark and just kept on eating until eventually, through their over-consumption of carbohydrate-rich foods, they managed to fill their protein intake."
As Dr. Simpson noted, "A slight shift in the diet towards a lower proportion of protein can have catastrophic effects, your body will stop you eating when you reach the right amount."
In their caterpillar research, they found that the disadvantages of obesity can change the course of evolution in a species. In one experiment, they confined hundreds of caterprillars to a high-carbohydrate diet. Over generations of obesity, the caterpillars slowly became immune to obesity in a high-carbohydrate world; no longer laying the excess carbohydrate down as fat. They also were left with an increased risk of starvation were the world to change and carbohydrates became scarce.
Their cousins, confined to a low-carbohydrate diet showed similar adaptions to their diet and evolved to the opposite, prone to obesity in a carbohydrate-rich environment, depositing excess as body fat when their environment changed.
As Dr. Simpson said "But were they, like we humans, to suddenly find themselves in a world where high-energy foods were abundant, they would be super-prone to becoming obese. This raises the possibility that our diet could significantly influence our genetic evolution over the next few generations."
In Let's Blame Evolution for our Obesity Epidemic, I wrote "it might just be evolution that stops the obesity epidemic for us as we continue our folly with low-fat, fortified, carbohydrate-rich diet recommendations."
I based that on the health of our youth today, where children are already symtomatic with "type II diabetes, atheroclerosis, dyslipidemia, hypertention and cardiovascular disease already present in an alarming number of our youth. Add to that the rising trend of "precocious puberty" where children are maturing much earlier than previous generations."
Survival of the species happens through those endowed with characteristics which improve chances of survival and reproduction, through those who do reproduce and propagate off-spring with heritable characteristics that affect their survival and reproductive success. After millions of years and thousands of generations, today we have inherited a set of characteristics that require, among other things, specific nutrients if we are to reproduce and survive. In a very short time span, we've modified our diet radically from that of our ancestors. If evolution is playing here, it's not playing very nicely in the sandbox of our genes. But, evolution isn't making us fat, we're doing that because we are not "playing within the bounds" of our genetic requirements, especially the requirements for nutrients that optimize reproduction and survival.
The alarming number of children today that are already showing signs of chronic disease and characteristics of infertility is alarming. The stark and painful reality is that this may be evolution exerting influence to limit reproduction potential of those unable to consume a nutritionally complete diet. Without an appropriate and adequate diet, the youngest among us are being afflicted earlier and earlier with chronic disease, characteristics of infertility, and a potentially shorter life-span to be lived battling chronic illness.
What I wrote sounds eerily familiar to what the article stated "This would occur if those with a propensity for stacking on the kilograms cannot reproduce or they have less healthy children, while the lean survive to pass on their skinniness genes.
Signs of this are emerging. Children are developing type 2 diabetes. Overweight women are having difficulty conceiving. "For the first time we are seeing obesity-related health problems affecting significant numbers of reproductive aged and pre-reproductive aged humans," Simpson says.
To say hard evidence for this is sparse is an understatment. While there is data which points to nutrient deficiency and data pointing to protein inadequacy, there isn't much out there specifically investigating calorie intake based on nutrient adequacy. Today the Sydney Morning Herald reports findings from researchers at the University of Sydney in Skinniness gene imperils survival of the fattest who studied crickets, cockroaches, rats, minks and even humans in an effort to understand how protein requirements drive food consumption, for some, but not all, humans.
The lead researcher, Dr. Stephen Simpson, found that crickets are driven across the landscape, consuming crop after crop, because they have a fixed protein requirement. To meet that requirement, these pests will cannibalize each other along the way, so the frantic pace to keep moving is a survival mechanism, "stop and you get eaten."
To understand how protein requirements may play in human eating habits, the researchers "incarcerated 10 people in a chalet for six day," to monitor their eating.
For the first two days they could eat what they wanted from a buffet. For the next two days, one group was restricted to high-protein foods, such as chicken and meat, the other to fatty, sugary, low-protein foods, such as croissants.
The first group consumed exactly the same amount of protein as on the first two days. "The second group went way off the mark and just kept on eating until eventually, through their over-consumption of carbohydrate-rich foods, they managed to fill their protein intake."
As Dr. Simpson noted, "A slight shift in the diet towards a lower proportion of protein can have catastrophic effects, your body will stop you eating when you reach the right amount."
In their caterpillar research, they found that the disadvantages of obesity can change the course of evolution in a species. In one experiment, they confined hundreds of caterprillars to a high-carbohydrate diet. Over generations of obesity, the caterpillars slowly became immune to obesity in a high-carbohydrate world; no longer laying the excess carbohydrate down as fat. They also were left with an increased risk of starvation were the world to change and carbohydrates became scarce.
Their cousins, confined to a low-carbohydrate diet showed similar adaptions to their diet and evolved to the opposite, prone to obesity in a carbohydrate-rich environment, depositing excess as body fat when their environment changed.
As Dr. Simpson said "But were they, like we humans, to suddenly find themselves in a world where high-energy foods were abundant, they would be super-prone to becoming obese. This raises the possibility that our diet could significantly influence our genetic evolution over the next few generations."
In Let's Blame Evolution for our Obesity Epidemic, I wrote "it might just be evolution that stops the obesity epidemic for us as we continue our folly with low-fat, fortified, carbohydrate-rich diet recommendations."
I based that on the health of our youth today, where children are already symtomatic with "type II diabetes, atheroclerosis, dyslipidemia, hypertention and cardiovascular disease already present in an alarming number of our youth. Add to that the rising trend of "precocious puberty" where children are maturing much earlier than previous generations."
Survival of the species happens through those endowed with characteristics which improve chances of survival and reproduction, through those who do reproduce and propagate off-spring with heritable characteristics that affect their survival and reproductive success. After millions of years and thousands of generations, today we have inherited a set of characteristics that require, among other things, specific nutrients if we are to reproduce and survive. In a very short time span, we've modified our diet radically from that of our ancestors. If evolution is playing here, it's not playing very nicely in the sandbox of our genes. But, evolution isn't making us fat, we're doing that because we are not "playing within the bounds" of our genetic requirements, especially the requirements for nutrients that optimize reproduction and survival.
The alarming number of children today that are already showing signs of chronic disease and characteristics of infertility is alarming. The stark and painful reality is that this may be evolution exerting influence to limit reproduction potential of those unable to consume a nutritionally complete diet. Without an appropriate and adequate diet, the youngest among us are being afflicted earlier and earlier with chronic disease, characteristics of infertility, and a potentially shorter life-span to be lived battling chronic illness.
What I wrote sounds eerily familiar to what the article stated "This would occur if those with a propensity for stacking on the kilograms cannot reproduce or they have less healthy children, while the lean survive to pass on their skinniness genes.
Signs of this are emerging. Children are developing type 2 diabetes. Overweight women are having difficulty conceiving. "For the first time we are seeing obesity-related health problems affecting significant numbers of reproductive aged and pre-reproductive aged humans," Simpson says.
Friday, September 22, 2006
Diabetes Control Requires Options Based on Data
Last weekend the European Association for the Study of Diabetes convened in Copenhagen for their 42nd annual meeting. As reported in Zee News, Dr. Targ Elgzyri from Lund University, Malmo, Sweden presented data that found "people who develop type 2 diabetes when they're younger than 50 years of age are more likely to experience a worsening of their disease than those diagnosed at an older age."
He said the study was conducted because "we found, as previously shown, a progressive rise in HbA1c over time in newly diagnosed patients with type 2 diabetes despite different modes of therapy."
To gain an understanding of what drives progressive decline, the researchers investigated non-genetic factors that influence a rise in HbA1c levels. The HbA1c level is blood marker that gives a snapshot of average blood sugar levels over several months. The higher the value, the higher the average blood sugars were in the past few months before testing. It is considered a more precise measure than daily finger testing that those with diabetes do each day as it measures the average blood sugar level throughout the day, which helps determine glycemic control over time.
In this study, the researchers followed more than 1,200 patients with type II diabetes for seven years after their diagnosis. HbA1c improved at 1 year following diagnosis, declining from 7.6 to 6.3 percent. During the subsequent 6 years, however, HbA1c increased from 6.3 to 7.0 percent, as expected.
The patients required insulin therapy after an average of 2.5 years, Elgzyri and colleagues report in a meeting abstract. After 7 years, 47 percent of study subjects were on insulin therapy.
"Among non-genetic factors studied, age at diagnosis showed a significant influence on HbA1c change over time," Elgzyri said.
Specifically, patients younger than 50 years at type 2 diabetes diagnosis experienced a steeper increase in HbA1c than did those 50 years of age or older at diagnosis.
The researchers concluded this was due to a progressive decline in the ability of the pancreas cells to produce insulin in those diagnosed before age 50.
The results of this study confirm findings of other studies, namely the rebound from improvement to decline often seen in those trying to control blood sugars with the recommended diet, exercise and incremental increase in drugs. Back in June I wrote about a study published in the New England Journal of Medicine that found at the six-month and one-year follow-ups there were dramatic changes for those who modified their lifestyle - impressive improvements in fasting blood glucose (FBG).
At baseline those in the lifestyle intervention group had an average FBG of 106.3mg/dL which declined over the first year to just a hair above 100mg/dL. After the first year, their fasting blood glucose levels rebounded however, so for the first year the diet and exercise did have a positive effect - but that was lost over time as fasting blood glucose did a rebound and ended higher at the conclusion of the study than at baseline. So, after three years of the lifestyle intervention, while they weren't diabetic, those in the intervention group experienced an overall negative effect on fasting blood glucose - it worsened over time.
The same disturbing trend is seen with regard to the HbA1c levels. Initially HbA1c improved only to rebound over time with the follow-up levels higher than baseline - HbA1C worsened over time.
This "negative outcome" has led many within the diabetes community to conclude that progression is just part of the disease, there is little that can stop it, and the best course is to initiate pharmaceutical interventions earlier.
The American Diabetes Association [ADA] recently updated their treatment algorithm to include metformin at diagnosis where previously those diagnosed were encouraged to adopt diet and lifestyle modifications as their first line defense to manage the disease.
Other organizations, including the American Association of Clinical Endocrinologists [AACE], are taking a more aggressive approach and recommending intensive intervention to reduce and manage HbA1c when an individual is identified with pre-diabetes (a fasting blood glucose above 100mg/dL and/or impaired glucose tolerance identified with a GTT resulting in blood glucose at or above 140mg/dL after two hours).
The AACE position is that upon diagnosis of pre-diabetes, an HbA1c test is in order and glycemic control, to effectively and safely lower it, specifically below 6.5%, is critical. In their consensus statement, they point to studies that repeatedly find the ADA target of 7% too high to prevent complications and therefore establish a lower target to reduce the risk of complications.
Their "Roadmap to Achieve Glycemic Goals" is comprehensive and starts intervention as early as an HbA1c of 6%.
The reason is found in the translation of HbA1c results as a measure of daily glycemic control:
When we see this type of meaning detailed simply for us, it is easier to understand why glycemic control is so important. It is also clear the ADA target is set too high! An HbA1c of 7% means the person at that target maintains an average blood glucose level of 170mg/dL. It is that ongoing state of hyperglycemia doing damage each day that is leading to complications in the long-term.
The biggest challenge to reducing HbA1c is determining which course of treatment will effectively enable a person with higher than desired blood glucose levels to reduce them and manage them for the long-term in the normal range or as close to normal as possible.
The standard today is to recommend diet, exercise, and more recently medication at diagnosis. However, a growing number of experts within the diabetes community are growing weary from the lack of results when the recommended diet fails and often makes things worse. These failings are not for lack of trying - the problem is the recommended diet exacerbates an already challenged metabolism because it includes too many carbohydrates.
Such a simple reason does not deter the staunch believers of decades old dietary dogma however. Recently this was clear in a dLife segment that featured Dr. Richard K. Bernstein, MD and Hope Warshaw, MMSc, RD, CDE - who are at opposite ends of the dietary spectrum for glycemic control with diet. The transcript of the show may be found here.
As Dr. Bernstein, who recommends a carbohydrate restricted diet in his medical practice, wrapped up his time, he ended by leaving viewers with one simple sentence, someone diagnosed with diabetes is "entitled to the same blood sugars as a non-diabetic and its up to you to get it."
Ms. Warshaw didn't challenge this, but instead opened her time with "I want to make three quick points. Number one, the research shows that low-carb diets don't work. People can't stay on them long-term and they're simply not a healthy way of eating. Number two, people with diabetes deserve to eat healthy and enjoy food. Number three is the carb issue today is not a quantity issue; it is a quality of carbohydrate issue. What we're eating too much of is added sugars, regular soda, fruit drink, and sweets. So what Americans need to do, I believe, is that they need to move those calories into healthier carbs, okay?"
As she continued, she said "[t]he vast majority of people with diabetes need medication. I mean what we know today about diabetes management is that it is good blood glucose control, good lipid control, and good blood pressure control that keeps people healthy long-term. And I feel people need a realistic way of eating."
Evidence versus sophistry; with just enough opinion thrown in to ensure glycemic control remains elusive to those who try their best with the recommended diet.
The available data reminds us that truly isn't a question of "if" but "when" the diet will fail, there is progressive damage as HbA1c rises; this is because the recommended diet makes it impossible to achieve normal blood sugars over the long-term.
Re-read the second part of her statements - she acknowledges that blood glucose, lipid and blood pressure control keeps people healthy long-term but then opines that dietary advice should be "realistic," and from her opening statement, such a diet should be "enjoyable" to the person attempting to use diet as a means of controlling their blood glucose. Forget glycemic control is the priority, it's critically important to eat and enjoy your food even if it is going to kill you slowly with progressive damage.
This type of thinking sets the course for progressive damage because the dietary recommendation includes too much carbohydrate to make glycemic control even remotely possible, even with a high target HbA1c of 7% or less!
Ms. Warshaw's contention that without abundant carbohydrates a person is at risk of consuming a diet that is unhealthy and what matters is the quality of the carbohydrate belies the fact that all carbohydrates (except fiber) are metabolized to glucose - some are just not converted to glucose as quickly as others. While she contends quantity is not the issue, but quality is, the hard fact remains the absolute grams of digestible carbohydrate consumed each day is the number one influence on blood glucose levels.
This isn't opinion, but established metabolic fact.
But those who cling to the orthodoxy that dietary fats are detrimental to health, cannot step back from their position without admitting error; cannot acknowledge that the past is where we can understand how we got into the situation we are in today; and cannot find it within themselves to say "we were wrong, we're sorry," but let's move forward and do the right thing so you can reduce the risk of complications now and tomorrow.
The solution will not be found in simply modifying the type (quality) of carbohydrate consumed. While that will provide a small measure of benefit, at the end of the day, such a modification will not provide enough control unless the total digestible carbohydrate - selected for quality - is reduced significantly in the diet of those with pre-diabetes or type II diabetes.
This month Endocrine Today highlighted the remarks of Ann Albright, PhD, RD (president-elect of the ADA) who said, “When you’re talking about diabetes, there is no ‘one-size-fits-all’ diet. For people with diabetes and those at risk for type 2 diabetes, medical nutrition therapy should be tailored to a person’s specific health issues and personal preferences to help maintain optimum health by controlling blood glucose levels, blood pressure, cholesterol and other risk factors. We hope these recommendations will help people make better choices about what they eat and how they live to maximize their chances of staying healthy.”
It's clear from the MNT document released by the ADA that the personal preference better not be a carbohydrate restricted diet. It's clear from the statements from Ms. Warshaw, with a number of books published and endorsed by the ADA, that such a dietary approach could not be possible nor enjoyable for someone with pre-diabetes or type II diabetes.
I find this only hypocritical, but downright patronizing and limiting patient autonomy!
The "powers that be" are doing all they can to convince the public that a carbohydrate restricted diet is untenable, unhealthy and unrealistic for controlling blood glucose. Just ignore the data and follow their prescription for the long-term; ignore that the data shows their recommendations directly lead to progressive damage, poor glycemic control and progressive increases in medication requirements.
What is so frustrating about this whole situation is that while there will most definitely be a population of those diagnosed with pre-diabetes and diabetes who simply know themselves well enough to know they will not be able to restrict carbohydrate, such stubborn refusal to include carbohydrate restriction as a scientifically supported option is leaving those who would jump at the chance to give it a go from invesitgating it because it's next to impossible to find a physician, healthcare provider or dietitian knowledgable enough in the details about how to follow and monitor a carbohydrate restricted diet properly.
How much longer is the medical community going to stand by and accept less than acceptable results when they have patients fully complying with the recommendations who simply continue to decline because the recommended diet is flawed and is directly contributing to the progressive decline in health?
How much longer will those at risk for or diagnosed with diabetes accept such a guaranteed-to-fail approach from the ADA, the organization they depend on for timely and cutting-edge evidence-based approaches to help them?
I've said it many times before, I do not expect a ringing endorsement from the ADA that a carbohydrate restricted diet is the best dietary approach (even though the evidence clearly points to it as). No, what I expect, and what those at risk for or diangosed with diabetes should expect, is an acknowledgement of the data and a clear, comprehensive guideline provided to those who choose to adopt a carbohydrate restricted diet as their first line defense.
That is true patient empowerment - providing them the options, requirements of each and then allowing them to decide which they will be able to comply with best in the long-term.
It is not up to the ADA to decide what a patient may or may not want to eat - it is the responsibility of the ADA to communicate the findings from studies and communicate how to implement those approaches where statistically significant benefits are found in clear manner so healthcare providers and patients can use the data in their daily management of their disease.
As it stands, the ADA is failing those at risk for or diagnosed with diabetes each day that passes without an honest review of the evidence of carbohydrate restricted diets. It's time for those at risk for or diagnosed with diabetes to stand up and be heard - tell the ADA to get back on track and follow their mission, clearly stated on their website, "to prevent and cure diabetes and to improve the lives of all people affected by diabetes."
A carbohydrate restricted diet has been shown in a number of studies to improve the lives of those with diabetes - and anyone at risk for or diagnosed with diabetes deserves nothing less than full disclosure of the option as a way to manage their blood sugars.
Anything less than a comprehensive guideline is unacceptable and directly causing progressive damage in those denied this critical information to make a choice in their medical care!
That the experts at the ADA find the data hard to digest is of little consequence when we're talking about millions of lives here - they don't have to like the data, findings or results - all that matters is the data is what it is and patients deserve to know what benefit may be possible if they choose a carbohydrate restricted diet.
He said the study was conducted because "we found, as previously shown, a progressive rise in HbA1c over time in newly diagnosed patients with type 2 diabetes despite different modes of therapy."
To gain an understanding of what drives progressive decline, the researchers investigated non-genetic factors that influence a rise in HbA1c levels. The HbA1c level is blood marker that gives a snapshot of average blood sugar levels over several months. The higher the value, the higher the average blood sugars were in the past few months before testing. It is considered a more precise measure than daily finger testing that those with diabetes do each day as it measures the average blood sugar level throughout the day, which helps determine glycemic control over time.
In this study, the researchers followed more than 1,200 patients with type II diabetes for seven years after their diagnosis. HbA1c improved at 1 year following diagnosis, declining from 7.6 to 6.3 percent. During the subsequent 6 years, however, HbA1c increased from 6.3 to 7.0 percent, as expected.
The patients required insulin therapy after an average of 2.5 years, Elgzyri and colleagues report in a meeting abstract. After 7 years, 47 percent of study subjects were on insulin therapy.
"Among non-genetic factors studied, age at diagnosis showed a significant influence on HbA1c change over time," Elgzyri said.
Specifically, patients younger than 50 years at type 2 diabetes diagnosis experienced a steeper increase in HbA1c than did those 50 years of age or older at diagnosis.
The researchers concluded this was due to a progressive decline in the ability of the pancreas cells to produce insulin in those diagnosed before age 50.
The results of this study confirm findings of other studies, namely the rebound from improvement to decline often seen in those trying to control blood sugars with the recommended diet, exercise and incremental increase in drugs. Back in June I wrote about a study published in the New England Journal of Medicine that found at the six-month and one-year follow-ups there were dramatic changes for those who modified their lifestyle - impressive improvements in fasting blood glucose (FBG).
At baseline those in the lifestyle intervention group had an average FBG of 106.3mg/dL which declined over the first year to just a hair above 100mg/dL. After the first year, their fasting blood glucose levels rebounded however, so for the first year the diet and exercise did have a positive effect - but that was lost over time as fasting blood glucose did a rebound and ended higher at the conclusion of the study than at baseline. So, after three years of the lifestyle intervention, while they weren't diabetic, those in the intervention group experienced an overall negative effect on fasting blood glucose - it worsened over time.
The same disturbing trend is seen with regard to the HbA1c levels. Initially HbA1c improved only to rebound over time with the follow-up levels higher than baseline - HbA1C worsened over time.
This "negative outcome" has led many within the diabetes community to conclude that progression is just part of the disease, there is little that can stop it, and the best course is to initiate pharmaceutical interventions earlier.
The American Diabetes Association [ADA] recently updated their treatment algorithm to include metformin at diagnosis where previously those diagnosed were encouraged to adopt diet and lifestyle modifications as their first line defense to manage the disease.
Other organizations, including the American Association of Clinical Endocrinologists [AACE], are taking a more aggressive approach and recommending intensive intervention to reduce and manage HbA1c when an individual is identified with pre-diabetes (a fasting blood glucose above 100mg/dL and/or impaired glucose tolerance identified with a GTT resulting in blood glucose at or above 140mg/dL after two hours).
The AACE position is that upon diagnosis of pre-diabetes, an HbA1c test is in order and glycemic control, to effectively and safely lower it, specifically below 6.5%, is critical. In their consensus statement, they point to studies that repeatedly find the ADA target of 7% too high to prevent complications and therefore establish a lower target to reduce the risk of complications.
Their "Roadmap to Achieve Glycemic Goals" is comprehensive and starts intervention as early as an HbA1c of 6%.
The reason is found in the translation of HbA1c results as a measure of daily glycemic control:
When we see this type of meaning detailed simply for us, it is easier to understand why glycemic control is so important. It is also clear the ADA target is set too high! An HbA1c of 7% means the person at that target maintains an average blood glucose level of 170mg/dL. It is that ongoing state of hyperglycemia doing damage each day that is leading to complications in the long-term.
The biggest challenge to reducing HbA1c is determining which course of treatment will effectively enable a person with higher than desired blood glucose levels to reduce them and manage them for the long-term in the normal range or as close to normal as possible.
The standard today is to recommend diet, exercise, and more recently medication at diagnosis. However, a growing number of experts within the diabetes community are growing weary from the lack of results when the recommended diet fails and often makes things worse. These failings are not for lack of trying - the problem is the recommended diet exacerbates an already challenged metabolism because it includes too many carbohydrates.
Such a simple reason does not deter the staunch believers of decades old dietary dogma however. Recently this was clear in a dLife segment that featured Dr. Richard K. Bernstein, MD and Hope Warshaw, MMSc, RD, CDE - who are at opposite ends of the dietary spectrum for glycemic control with diet. The transcript of the show may be found here.
As Dr. Bernstein, who recommends a carbohydrate restricted diet in his medical practice, wrapped up his time, he ended by leaving viewers with one simple sentence, someone diagnosed with diabetes is "entitled to the same blood sugars as a non-diabetic and its up to you to get it."
Ms. Warshaw didn't challenge this, but instead opened her time with "I want to make three quick points. Number one, the research shows that low-carb diets don't work. People can't stay on them long-term and they're simply not a healthy way of eating. Number two, people with diabetes deserve to eat healthy and enjoy food. Number three is the carb issue today is not a quantity issue; it is a quality of carbohydrate issue. What we're eating too much of is added sugars, regular soda, fruit drink, and sweets. So what Americans need to do, I believe, is that they need to move those calories into healthier carbs, okay?"
As she continued, she said "[t]he vast majority of people with diabetes need medication. I mean what we know today about diabetes management is that it is good blood glucose control, good lipid control, and good blood pressure control that keeps people healthy long-term. And I feel people need a realistic way of eating."
Evidence versus sophistry; with just enough opinion thrown in to ensure glycemic control remains elusive to those who try their best with the recommended diet.
The available data reminds us that truly isn't a question of "if" but "when" the diet will fail, there is progressive damage as HbA1c rises; this is because the recommended diet makes it impossible to achieve normal blood sugars over the long-term.
Re-read the second part of her statements - she acknowledges that blood glucose, lipid and blood pressure control keeps people healthy long-term but then opines that dietary advice should be "realistic," and from her opening statement, such a diet should be "enjoyable" to the person attempting to use diet as a means of controlling their blood glucose. Forget glycemic control is the priority, it's critically important to eat and enjoy your food even if it is going to kill you slowly with progressive damage.
This type of thinking sets the course for progressive damage because the dietary recommendation includes too much carbohydrate to make glycemic control even remotely possible, even with a high target HbA1c of 7% or less!
Ms. Warshaw's contention that without abundant carbohydrates a person is at risk of consuming a diet that is unhealthy and what matters is the quality of the carbohydrate belies the fact that all carbohydrates (except fiber) are metabolized to glucose - some are just not converted to glucose as quickly as others. While she contends quantity is not the issue, but quality is, the hard fact remains the absolute grams of digestible carbohydrate consumed each day is the number one influence on blood glucose levels.
This isn't opinion, but established metabolic fact.
But those who cling to the orthodoxy that dietary fats are detrimental to health, cannot step back from their position without admitting error; cannot acknowledge that the past is where we can understand how we got into the situation we are in today; and cannot find it within themselves to say "we were wrong, we're sorry," but let's move forward and do the right thing so you can reduce the risk of complications now and tomorrow.
The solution will not be found in simply modifying the type (quality) of carbohydrate consumed. While that will provide a small measure of benefit, at the end of the day, such a modification will not provide enough control unless the total digestible carbohydrate - selected for quality - is reduced significantly in the diet of those with pre-diabetes or type II diabetes.
This month Endocrine Today highlighted the remarks of Ann Albright, PhD, RD (president-elect of the ADA) who said, “When you’re talking about diabetes, there is no ‘one-size-fits-all’ diet. For people with diabetes and those at risk for type 2 diabetes, medical nutrition therapy should be tailored to a person’s specific health issues and personal preferences to help maintain optimum health by controlling blood glucose levels, blood pressure, cholesterol and other risk factors. We hope these recommendations will help people make better choices about what they eat and how they live to maximize their chances of staying healthy.”
It's clear from the MNT document released by the ADA that the personal preference better not be a carbohydrate restricted diet. It's clear from the statements from Ms. Warshaw, with a number of books published and endorsed by the ADA, that such a dietary approach could not be possible nor enjoyable for someone with pre-diabetes or type II diabetes.
I find this only hypocritical, but downright patronizing and limiting patient autonomy!
The "powers that be" are doing all they can to convince the public that a carbohydrate restricted diet is untenable, unhealthy and unrealistic for controlling blood glucose. Just ignore the data and follow their prescription for the long-term; ignore that the data shows their recommendations directly lead to progressive damage, poor glycemic control and progressive increases in medication requirements.
What is so frustrating about this whole situation is that while there will most definitely be a population of those diagnosed with pre-diabetes and diabetes who simply know themselves well enough to know they will not be able to restrict carbohydrate, such stubborn refusal to include carbohydrate restriction as a scientifically supported option is leaving those who would jump at the chance to give it a go from invesitgating it because it's next to impossible to find a physician, healthcare provider or dietitian knowledgable enough in the details about how to follow and monitor a carbohydrate restricted diet properly.
How much longer is the medical community going to stand by and accept less than acceptable results when they have patients fully complying with the recommendations who simply continue to decline because the recommended diet is flawed and is directly contributing to the progressive decline in health?
How much longer will those at risk for or diagnosed with diabetes accept such a guaranteed-to-fail approach from the ADA, the organization they depend on for timely and cutting-edge evidence-based approaches to help them?
I've said it many times before, I do not expect a ringing endorsement from the ADA that a carbohydrate restricted diet is the best dietary approach (even though the evidence clearly points to it as). No, what I expect, and what those at risk for or diangosed with diabetes should expect, is an acknowledgement of the data and a clear, comprehensive guideline provided to those who choose to adopt a carbohydrate restricted diet as their first line defense.
That is true patient empowerment - providing them the options, requirements of each and then allowing them to decide which they will be able to comply with best in the long-term.
It is not up to the ADA to decide what a patient may or may not want to eat - it is the responsibility of the ADA to communicate the findings from studies and communicate how to implement those approaches where statistically significant benefits are found in clear manner so healthcare providers and patients can use the data in their daily management of their disease.
As it stands, the ADA is failing those at risk for or diagnosed with diabetes each day that passes without an honest review of the evidence of carbohydrate restricted diets. It's time for those at risk for or diagnosed with diabetes to stand up and be heard - tell the ADA to get back on track and follow their mission, clearly stated on their website, "to prevent and cure diabetes and to improve the lives of all people affected by diabetes."
A carbohydrate restricted diet has been shown in a number of studies to improve the lives of those with diabetes - and anyone at risk for or diagnosed with diabetes deserves nothing less than full disclosure of the option as a way to manage their blood sugars.
Anything less than a comprehensive guideline is unacceptable and directly causing progressive damage in those denied this critical information to make a choice in their medical care!
That the experts at the ADA find the data hard to digest is of little consequence when we're talking about millions of lives here - they don't have to like the data, findings or results - all that matters is the data is what it is and patients deserve to know what benefit may be possible if they choose a carbohydrate restricted diet.
Thursday, September 21, 2006
On the Trail of e.Coli
Last week the news of a food borne outbreak of E.coli led to the recall of bagged spinach across the nation. It was speculated that the source of contamination was fecal matter, most likely from animal manure used as fertilizer.
In the Fox News article, Robert Brackett, the director of the FDA's Center for Food Safety and Nutrition said that E. coli lives in the intestines of cattle and other animals and typically is spread through contamination by fecal material. He continued to add that the use of manure as a fertilizer for produce typically consumed raw, such as spinach, is not in keeping with good agricultural practices.
Hmm...how in the world did we ever survive before chemical fertilizers?
As the investigation has progressed, a more likely source of contamination has been identified - the water used to irrigate fields, not the fertilizer used to nourish soil and crops. As the LA Times reported today, "Many creeks and streams near the region's spinach fields, including the Salinas River, Gabilan Creek, Towne Creek, Tembladero Slough and Old Salinas River Estuary, are known to be carriers of the E. coli strain implicated in the food poisonings...Although the growers do not draw water from creeks to irrigate their fields, their crops could be tainted by runoff from nearby livestock operations or Central Coast urban areas."
And how about this scary item, "Only one waterway in the lower Salinas River watershed does not violate federal E. coli standards, and it is in a state park, surrounded by natural land. Some waterways are so contaminated they contain 12,000 or more organisms per 100 milliliters of water — 30 times the Environmental Protection Agency's standard. Ingesting just a few organisms can make a person sick."
But experts at the USDA Agricultural Research Service aren't sure irrigation of crops is to blame. "These outbreaks make it appear that the produce was contaminated before harvest. It's a strong suspicion by everyone. So some of the things the investigators will look for is whether certain fields flooded and the quality of the irrigation water used, the location of farms near where animals may be grazing, and whether any wildlife may frequent certain farms," said Robert Mandrell of the USDA.
An interesting Op-Ed, penned by Nina Planck in the New York Times took no prisoners today.
Her view is the contamination "probably has little do with the folks who grow and package your greens. The detective trail ultimately leads back to a seemingly unrelated food industry — beef and dairy cattle."But not just any cattle and livestock farmers, but those who practice what is known as "factory farming" or, more accurately feedlot feeding practices.
Ms. Planck accurately assesses the situation from the view that e.Coli is indeed abundant in the digestive system of healthy cattle and humans, but when fed an unnatural diet - that is fed grain - the balance of acids in the digestive tract of the cow changes to allow the strain in question, E. coli O157:H7, thrive and be a threat because it is reistant to the acidity of the human digestive tract when present in foods.
As she noted, "Where does this particularly virulent strain come from? It’s not found in the intestinal tracts of cattle raised on their natural diet of grass, hay and other fibrous forage. No, O157 thrives in a new — that is, recent in the history of animal diets — biological niche: the unnaturally acidic stomachs of beef and dairy cattle fed on grain, the typical ration on most industrial farms. It’s the infected manure from these grain-fed cattle that contaminates the groundwater and spreads the bacteria to produce, like spinach, growing on neighboring farms."
Which just confirms my suspicion that when we alter the natural diet of animals, at some point it will come back to haunt us, one way or another. It's one reason why I choose to support local farms and ranches practicing sustainable methods while allowing their animals to graze and forage on their natural diet.
In the Fox News article, Robert Brackett, the director of the FDA's Center for Food Safety and Nutrition said that E. coli lives in the intestines of cattle and other animals and typically is spread through contamination by fecal material. He continued to add that the use of manure as a fertilizer for produce typically consumed raw, such as spinach, is not in keeping with good agricultural practices.
Hmm...how in the world did we ever survive before chemical fertilizers?
As the investigation has progressed, a more likely source of contamination has been identified - the water used to irrigate fields, not the fertilizer used to nourish soil and crops. As the LA Times reported today, "Many creeks and streams near the region's spinach fields, including the Salinas River, Gabilan Creek, Towne Creek, Tembladero Slough and Old Salinas River Estuary, are known to be carriers of the E. coli strain implicated in the food poisonings...Although the growers do not draw water from creeks to irrigate their fields, their crops could be tainted by runoff from nearby livestock operations or Central Coast urban areas."
And how about this scary item, "Only one waterway in the lower Salinas River watershed does not violate federal E. coli standards, and it is in a state park, surrounded by natural land. Some waterways are so contaminated they contain 12,000 or more organisms per 100 milliliters of water — 30 times the Environmental Protection Agency's standard. Ingesting just a few organisms can make a person sick."
But experts at the USDA Agricultural Research Service aren't sure irrigation of crops is to blame. "These outbreaks make it appear that the produce was contaminated before harvest. It's a strong suspicion by everyone. So some of the things the investigators will look for is whether certain fields flooded and the quality of the irrigation water used, the location of farms near where animals may be grazing, and whether any wildlife may frequent certain farms," said Robert Mandrell of the USDA.
An interesting Op-Ed, penned by Nina Planck in the New York Times took no prisoners today.
Her view is the contamination "probably has little do with the folks who grow and package your greens. The detective trail ultimately leads back to a seemingly unrelated food industry — beef and dairy cattle."But not just any cattle and livestock farmers, but those who practice what is known as "factory farming" or, more accurately feedlot feeding practices.
Ms. Planck accurately assesses the situation from the view that e.Coli is indeed abundant in the digestive system of healthy cattle and humans, but when fed an unnatural diet - that is fed grain - the balance of acids in the digestive tract of the cow changes to allow the strain in question, E. coli O157:H7, thrive and be a threat because it is reistant to the acidity of the human digestive tract when present in foods.
As she noted, "Where does this particularly virulent strain come from? It’s not found in the intestinal tracts of cattle raised on their natural diet of grass, hay and other fibrous forage. No, O157 thrives in a new — that is, recent in the history of animal diets — biological niche: the unnaturally acidic stomachs of beef and dairy cattle fed on grain, the typical ration on most industrial farms. It’s the infected manure from these grain-fed cattle that contaminates the groundwater and spreads the bacteria to produce, like spinach, growing on neighboring farms."
Which just confirms my suspicion that when we alter the natural diet of animals, at some point it will come back to haunt us, one way or another. It's one reason why I choose to support local farms and ranches practicing sustainable methods while allowing their animals to graze and forage on their natural diet.
Wednesday, September 20, 2006
People Are Talking...
It's often amusing to trackback links generating traffic to my blog; sometimes it's even an eye-opening experience, where I can read how others interpret what I write from a brutally honest point-of-view - they're simply not worried I'll read their thoughts so they opine freely whether they agree or disagree with me.
Recently, Should we Debate Diet for Diabetes?, caught the attention of the members of a Google Group.
Interestingly, my position that the ADA should, even if cautiously, include the option of a carbohydrate restricted diet for those diagnosed with type II diabetes because it is supported in the scientific literature and hard data, led some to consider me a "fanatic" with "a chip on her shoulder the size of a loaf of bread and drew the same convoluted and biased conclusions," and even "a woman who obviously has an agenda."
Your happy fanatic here is most definitely glad to see, whether you agree with me or not, that out there, in the never-never-land of the internet, people are talking and discussing the situation! Let's not forget we are in the middle of what promises to be a national crisis if we do not find a solution to the alarming and continued increase in the incidence of type II diabetes.
While some see my perspective that those diagnosed with type II diabetes absolutely deserve to know they have dietary options - a number of various approachs to carbohydrate restriction - that have been shown to benefit those with type II diabetes with statistically significant improvements as fanatical; others see it for what it is - a position that is based on an honest review of the data published.
My agenda is simply this - exposing the fact that the ADA is failing those at risk for or diagnosed with diabetes because they have abandon their mission.
The ADA ignoring the weight of the evidence to maintain the status quo; while openly admiting their dietary recommendations are failing to reduce the incidence of diabetes or reverse the alarming trend in the United States. Their solution is to medicate the problem away with the recommendation to begin a pharmacuetical intervention upon diagnosis since the recommended lifestyle intervention is not enough.
The literature highlights there is another option - a carbohydrate restricted diet - and those at risk for or already diagnosed deserve to know this; doctors deserve to know how to monitor progress and make medication adjustments of patients who CHOOSE this option; and dietitians deserve to know how to individualize such a diet based on individual preferences and individual health risk measures.
The ADA position that no one wants to follow a low-carb diet is a patronizing attitude toward patients - a belief that people won't make changes even when presented with hard data and given their options.
I know for a fact there are thousands of renegade, disobedient diabetics out there, controlling their diabetes with a carbohydrate restricted diet.
It is my hope they will start to speak out, loudly, with their numbers and their experiences so those who doubt such an approach works can hear from real, live people that it does; and that when the proof is in the meter, you stick with it.
Here's to continuing the dialogue to bring the science to the public, to those at risk for or diagnosed with type II diabtes - keep the conversation going, it's good to talk about this...maybe, just maybe, we'll make a difference and find a solution together, even with our differences of opinion!
Recently, Should we Debate Diet for Diabetes?, caught the attention of the members of a Google Group.
Interestingly, my position that the ADA should, even if cautiously, include the option of a carbohydrate restricted diet for those diagnosed with type II diabetes because it is supported in the scientific literature and hard data, led some to consider me a "fanatic" with "a chip on her shoulder the size of a loaf of bread and drew the same convoluted and biased conclusions," and even "a woman who obviously has an agenda."
Your happy fanatic here is most definitely glad to see, whether you agree with me or not, that out there, in the never-never-land of the internet, people are talking and discussing the situation! Let's not forget we are in the middle of what promises to be a national crisis if we do not find a solution to the alarming and continued increase in the incidence of type II diabetes.
While some see my perspective that those diagnosed with type II diabetes absolutely deserve to know they have dietary options - a number of various approachs to carbohydrate restriction - that have been shown to benefit those with type II diabetes with statistically significant improvements as fanatical; others see it for what it is - a position that is based on an honest review of the data published.
My agenda is simply this - exposing the fact that the ADA is failing those at risk for or diagnosed with diabetes because they have abandon their mission.
The ADA ignoring the weight of the evidence to maintain the status quo; while openly admiting their dietary recommendations are failing to reduce the incidence of diabetes or reverse the alarming trend in the United States. Their solution is to medicate the problem away with the recommendation to begin a pharmacuetical intervention upon diagnosis since the recommended lifestyle intervention is not enough.
The literature highlights there is another option - a carbohydrate restricted diet - and those at risk for or already diagnosed deserve to know this; doctors deserve to know how to monitor progress and make medication adjustments of patients who CHOOSE this option; and dietitians deserve to know how to individualize such a diet based on individual preferences and individual health risk measures.
The ADA position that no one wants to follow a low-carb diet is a patronizing attitude toward patients - a belief that people won't make changes even when presented with hard data and given their options.
I know for a fact there are thousands of renegade, disobedient diabetics out there, controlling their diabetes with a carbohydrate restricted diet.
It is my hope they will start to speak out, loudly, with their numbers and their experiences so those who doubt such an approach works can hear from real, live people that it does; and that when the proof is in the meter, you stick with it.
Here's to continuing the dialogue to bring the science to the public, to those at risk for or diagnosed with type II diabtes - keep the conversation going, it's good to talk about this...maybe, just maybe, we'll make a difference and find a solution together, even with our differences of opinion!
Researcher Says "If you have a fat waist, then cut the carbs!"
I admit it, I'm a "journal junkie" - my daily data fix is often found in the usual suspects - JAMA, JADA, AJCN, Archives of Internal Medicne, Diabetes Care, Fertility & Sterility, Nature, BJM, Nutrition, Nutrition & Metabolism, the ACOG's "Green Journal," and more.
The other day I happened upon the British Journal of Obestrics & Gynecology while searching for papers related to various supplements and insulin resistance. The first that popped up was the October 2006 publication of Obesity, waist–hip ratio and hunter–gatherers (free full-text), a review article by Dr. LEP Wood, from University Hospitals Coventry and Warwickshire, in Coventry, UK.
It's a fascinating review, with citations I wasn't even aware of, that supports the use of carbohydrate restricted diets in those with "truncal obesity" - that is more fat stored in the middle, than distributed whole body; the "apple" shaped body if you will.
As I read the paper, a number of statements clearly illustrate that no one dietary approach works for everyone, and that for many, a carbohydrate restricted diet is the one best suited to their genetic type.
The full-text paper is worth reading through, it is rich with citations - here I'll share some of the highlights:
Truncal obesity, "is the type of obesity seen in every hunter–gatherer (HG) population around the globe. Such people are intolerant of carbohydrate, especially refined carbohydrate, especially in the excessive amounts typically consumed in affluent societies. In such pure HG communities, rates of diabetes can be as high as 50%, when the 'Western' lifestyle is adopted."
"Quite contrary to the common nutritional dogma of encouraging regular carbohydrates, it is suggested that pregnant women with a high waist-to-hip ratio should be strongly advised to adhere to a low-glycaemic-index diet."
"[Hunter Gatherers] HGs, for instance, are mainly not obese when they live their traditional lifestyle. When such people are exposed to high, refined carbohydrate intake; however, they develop truncal obesity and a vastly increased risk of diabetes—up to 50% in some populations. This tendency to a high WHR and to carbohydrate intolerance is shared by all hunter–gatherer (HG) populations throughout the world: Canadian Inuit, Native Americans, Mexican Indians, Pima Indians, South American Indians, Middle-Eastern Nomads, African Pygmies, Australian Aborigines, Maoris, South Sea Islanders, etc."
"...reduced carbohydrate in the diet has been shown to have beneficial effects in certain circumstances."
"...exercise is an important trigger to the key element of weight control—heat production. Anything, which influences this metabolic process will also affect weight. Thus, dietary carbohydrate in HGs might not only cause the tendency to obesity (and glucose intolerance) by excess calories, but also by a downregulation of metabolism."
"It seems very sensible to suggest, therefore, that women with a tendency to glucose intolerance should limit the total amount of carbohydrate they eat."
"Given the multifaceted nature of insulin resistance, if any single intervention can be shown to make a difference by itself, then that intervention should be worthy of close scrutiny, even if it is a nutrient."
"Much information has come from studying the diet of HGs, which is naturally anti-diabetic."
"However, the message can be put more simply: if you have a fat waist, then cut the carbs!"
The other day I happened upon the British Journal of Obestrics & Gynecology while searching for papers related to various supplements and insulin resistance. The first that popped up was the October 2006 publication of Obesity, waist–hip ratio and hunter–gatherers (free full-text), a review article by Dr. LEP Wood, from University Hospitals Coventry and Warwickshire, in Coventry, UK.
It's a fascinating review, with citations I wasn't even aware of, that supports the use of carbohydrate restricted diets in those with "truncal obesity" - that is more fat stored in the middle, than distributed whole body; the "apple" shaped body if you will.
As I read the paper, a number of statements clearly illustrate that no one dietary approach works for everyone, and that for many, a carbohydrate restricted diet is the one best suited to their genetic type.
The full-text paper is worth reading through, it is rich with citations - here I'll share some of the highlights:
Truncal obesity, "is the type of obesity seen in every hunter–gatherer (HG) population around the globe. Such people are intolerant of carbohydrate, especially refined carbohydrate, especially in the excessive amounts typically consumed in affluent societies. In such pure HG communities, rates of diabetes can be as high as 50%, when the 'Western' lifestyle is adopted."
"Quite contrary to the common nutritional dogma of encouraging regular carbohydrates, it is suggested that pregnant women with a high waist-to-hip ratio should be strongly advised to adhere to a low-glycaemic-index diet."
"[Hunter Gatherers] HGs, for instance, are mainly not obese when they live their traditional lifestyle. When such people are exposed to high, refined carbohydrate intake; however, they develop truncal obesity and a vastly increased risk of diabetes—up to 50% in some populations. This tendency to a high WHR and to carbohydrate intolerance is shared by all hunter–gatherer (HG) populations throughout the world: Canadian Inuit, Native Americans, Mexican Indians, Pima Indians, South American Indians, Middle-Eastern Nomads, African Pygmies, Australian Aborigines, Maoris, South Sea Islanders, etc."
"...reduced carbohydrate in the diet has been shown to have beneficial effects in certain circumstances."
"...exercise is an important trigger to the key element of weight control—heat production. Anything, which influences this metabolic process will also affect weight. Thus, dietary carbohydrate in HGs might not only cause the tendency to obesity (and glucose intolerance) by excess calories, but also by a downregulation of metabolism."
"It seems very sensible to suggest, therefore, that women with a tendency to glucose intolerance should limit the total amount of carbohydrate they eat."
"Given the multifaceted nature of insulin resistance, if any single intervention can be shown to make a difference by itself, then that intervention should be worthy of close scrutiny, even if it is a nutrient."
"Much information has come from studying the diet of HGs, which is naturally anti-diabetic."
"However, the message can be put more simply: if you have a fat waist, then cut the carbs!"
Monday, September 18, 2006
Diabetes Prevention - What's the Bottomline?
Imagine for a moment you are at your doctors' office for a check-up.
While reviewing the various tests, your doctor's face shows his concern as he tells you your blood sugars worry him, they show you are "pre-diabetic;" when he factors in your weight, blood pressure and cholesterol levels, he's even more concerned for your long term health, especially your risk for diabetes and cardiovascular disease.
This scenario is one millions face each year in the United States.
Now imagine you're faced with the decision about what to do to reduce your risk for progressing to diabetes. Your doctor presents you with the following information:
While reviewing the various tests, your doctor's face shows his concern as he tells you your blood sugars worry him, they show you are "pre-diabetic;" when he factors in your weight, blood pressure and cholesterol levels, he's even more concerned for your long term health, especially your risk for diabetes and cardiovascular disease.
This scenario is one millions face each year in the United States.
Now imagine you're faced with the decision about what to do to reduce your risk for progressing to diabetes. Your doctor presents you with the following information:
- Dietary modification to reduce fat, especially trans and saturated fat; basic calorie restriction within the recommendations
- Lifestyle modification to start an exercise program;
- Pharmaceutical intervention with a medication, rosiglitazone, shown to reduce the risk of progressing to diabetes in a recent study.
Your doctor tells you quickly about some of the side effects of the drug, but says that the latest trial using the medication showed it reduced the risk of developing diabetes in the study by 66%.
Do you do it?
Most people in such a situation would; without knowing that there are other, clinically effective interventions they might want to consider as their first line defense.
While the media is hot on reporting the recent study, Effect of Rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomized controlled trial, that found a reduction in the risk of progression to diabetes in those treated with rosiglitazone, much of the important data is being lost in the hype.
Lost in the frenzy to report the results of the study is the side effects of rosiglitazone:
- upper respiratory tract infection
- headache
- back pain
- hyperglycemia
- fatigue
- sinusitis
- diarrhea
- hypoglycemia
- mild to moderate accumulation of fluid (edema); can lead to heart failure
- weight gain
- potential for liver injury
- elevated total and low-density cholesterol (LDL)
Also lost is the number of people who would have to follow the course of treatment for three years to prevent one case of diabetes.
Bottom line from the study - for every seven people compliant with treatment for three years, one case of diabetes may be prevented.
In other words, the treatment will not prevent diabetes in six out of seven people of those who modify their lifestyle, diet and take the prescribed rosiglitazone for three years when compared with those who only modified their diet.
Now that doesn't sound quite as impressive as the first statistic - a 66% reduction of risk of developing diabetes in those treated - does it?
That's because it's not.
The current hype also doesn't tell you that those taking the rosiglitazone - those without cardiovascular disease in this trial - also had an "excess" of 4 to 5 cases of congestive heart failure compared with those not taking the drug.
But, when you want to promote a pharmaceutical intervention, it's a very effective way to present findings in a positive light.
Really, who would take the time to hype an intervention that works for only one in seven who follow it or come right out and say the risk for congestive heart failure increases?
No one.
So, instead of taking such an honest approach, the tact is to hype the risk reduction compared to the control group, then take it a step further and compare it to other miserable trial results!
Within the published study, the researchers compare their results with those found in trials in the US and Finland. In those trials, both reported a 58% reduction of risk when subjects followed a lifestyle intervention; in both that translated to the intervention working for one in five, or 20% of those who made the changes recommended. Stated another way, a failure rate of 80% that is easily glossed over when one highlights the reduction in risk rather than absolute numbers of prevention.
So what we have here are three trials being promoted as evidence that one can reduce their risk of developing diabetes if they follow the recommendations for diet, lifestyle and/or include medications too. It will only work 14% to 20% of the time over a period of three to five years, but hey it sounds so much better if stated as a risk reduction of 58% to 66%!
This is nothing more than doublespeak - failure is being hyped as success; failure is being hyped as prevention.
Let's also not forget the side effects reported by those who follow the lifestyle intervention promoted - weight loss, hunger, fatigue, strict calorie counting, strictly limiting many foods like eggs, headache, increased triglycerides, reduced HDL, reduced LDL, and loss of lean body mass with fat loss. Add to this, if you take this new course - the lifetyle, diet and rosiglitazone intervention, you also have to remember to take your medication as prescribed in addition to any other medications you're already taking.
Now take a look again at the side effects listed above if you follow the intervention to include rosiglitazone too. Consider those together with the lifestyle changes....now consider you're presented with an alternative with these side effects:
- Weight loss
- Loss of body fat, sparing lean body mass
- High satiety (loss of hunger)
- Headache
- Normalized triglycerides
- Increased HDL
- LDL change uncertain
- Total:HDL improvement
- Improved glycemic control
- Fatigue
- Improved HbA1c
- Bad breath
- Constipation
- Reduced blood pressure
- Reduction in inflammatory markers
- Reduction in use of medications
Would you rather try the drugs with the recommended diet, or the dietary intervention above, alone without additions to any medications you are already taking?
No matter which you would choose, don't you think you should be told about both options so you can decide which one may be easier for you to follow, stay compliant with longer? The one that may work better for you and your lifestyle and eating preferences?
Six Weeks to Goal
Last week I didn't update my weight loss since I was in the middle of making a few more adjustments for the longer term - namely making some changes to the supplements I take each day. None of the changes was to try to enhance weight loss - the modifications were more quality changes and adjustments to target nutrients rather than take a shot-gun approach with a multi-vitamin plus other nutrients. This is because my menus are darn high for nutrient-density and some of the vitamins in the multi seem like overkill!
On the weight loss front, I have now reached my goal of losing 20-pounds within eight weeks. It took just six weeks! Now that I'm at this weight, I'll just continue eating as I have been the last few weeks and make adjustments as needed to keep my weight stable.
Good luck to everyone continuing toward their goal!
On the weight loss front, I have now reached my goal of losing 20-pounds within eight weeks. It took just six weeks! Now that I'm at this weight, I'll just continue eating as I have been the last few weeks and make adjustments as needed to keep my weight stable.
Good luck to everyone continuing toward their goal!
Wednesday, September 13, 2006
Diabetic Complications Inevitable? Not So Fast...
In the September issue of Diabetes Care, a study published - Treating Postprandial Hyperglycemia Does Not Appear to Delay Progression of Early Type 2 Diabetes - had an ominous conclusion:
"Ameliorating postprandial hyperglycemia did not appear to delay progression of early type 2 diabetes. Factors other than postprandial hyperglycemia may be greater determinants of progression of diabetes. Alternatively, once FPG exceeds 126 mg/dl, ß-cell failure may no longer be remediable."
Now how is that for a conclusion? Pretty depressing if you ask me!
But this conclusion is totally understandable if you consider the perspective of those doing the research. They believe the dietary intervention used in this study was a proper diet for those with type II diabetes. The conclusion is that it's a losing battle to try to slow progression in those with diabetes who follow the dietary intervention with or without including acrabose. For those not aware of what acrabose is - it's a starch blocker designed to slow carbohydrate digestion and absorption. From my understanding, it effectively can block about 10-15g of carbohydrate when taken before a meal.
So, after five years of following the two groups, both given the same dietary intervention - with one group, the treatment group, given acrabose and the control group given a placebo - there was no statistically significant differences between the groups in rates of progression to "frank fasting hyperglycemia."
Some background on the study - the researchers investigated whether an intervention with acarbose in subjects with early diabetes (fasting plasma glucose greater than 140mg/dl and two-hour postprandial glucose of greater than 200mg/dl) would prevent or delay progression to "frank fasting hyperglycemia."
To understand why both groups experienced a continued progression, the researchers didn't consider the diet - 55% carbohydrate, 30% fat and 15% protein - as a potential problem in the equation. Why should they? It is, after all, the recommended diet for those with type II diabetes!
In fact, while the researchers did include the potential of the dietary intervention as a possible confounder in the results, it wasn't because the diet was problematic and raised blood sugars too high, but because "the dietary suggestions provided to both groups were potent and overwhelmed any effects of acarbose on ß-cell function."
The researchers simply could not wrap their heads around the idea the diet itself is the problem, so they totally failed to consider the negative effect the diet itself had on glycemic control (or lack thereof). Here is the paragraph the researchers included in their full-text paper:
It is possible that the dietary suggestions provided to both groups were potent and overwhelmed any effects of acarbose on ß-cell function. However, postprandial glucose was significantly lower in the acarbose group, and acarbose lowered A1C slightly but significantly over the first several years, suggesting that the drug itself had a superior effect on glycemia. In addition, the dietary intervention was no more potent than that provided to the placebo arms in studies such as the DPP and STOP-NIDDM.
To give you some perspective here, the diet was the standard carbohydrate:fat: protein ratio of 55:30:15. So, if a meal is 55% carbohydrate, 30% fat and 15% protein and provides 600-calories, it would provide 83g of carbohydrate. If acrabose is taken and actually reduces absorption of carbohydrate in the meal by 15g, the meal still provides 68g of carbohydrate that will be converted to glucose by the metabolism. Such a meal is not unreasonable if one is consuming 2,000-calories a day with three meals at 600-calories and two snacks at 100-calories each.
How great is the difference between a carbohydrate load of 83g versus 68g?
Quite frankly, not much when one considers each gram of carbohydrate converts to blood glucose and that rise in blood glucose must be reduced as much as the body can do with its insulin and medications. In those with type II diabetes, the ability to lower blood sugars is impaired and blood sugars stay elevated longer than they should. Basically their metabolism is doing the best it can with what it has and dietary carbohydrate strongly influences how high blood sugars rise since all carbohydrates (expect fiber) are converted to glucose - the more you consume carbohydrate, the higher blood sugars rise and over time, the less the body is able to reduce them effectively.
As Dr. Richard K. Bernstein illustrates this in what he calls the Laws of Small Numbers for controlling blood sugars - in type II diabetics, who still make insulin, it's common for a gram of carbohydrate to potentially raise blood glucose by 3mg/dl. I'll be clear here - how high blood sugars do rise is highly individual and based on insulin and insulin sensitivity. I'm going to use the 3mg/dl as an example to highlight how the current dietary recommendations can potentially raise blood sugars in someone with type II diabetes.
With that in mind, in this study, if 83g were consumed in the control group with an average fasting blood sugar of 126mg/dl, after the meal with 83g of carbohydrate their blood glucose would rise to 249mg/dl; those in the treatment group taking acrabose with absorption reduced to 68g would have blood sugars rise to 204mg/dl.
Lower? Yes.
Normal? No.
And it's because blood sugars were not normalized by the diet or the addition of the acrabose, the researchers really did reach the only logical conclusion one could reach when the perspective is that the dietary approach was a correct dietary intervention for those with diabetes - progression happens, not much we can do, life goes on.
Can we do better? Absolutely!
To do better we must evaluate interventions that specifically result in a normalization of blood sugars naturally.
In this study we find that the data speaks volumes of the inability of the current dietary recommendations with or without acrabose to normalize blood sugars. Both groups continued to deteriorate and it wasn't because that's what happens with diabetes - it was because they were consuming too many carbohydrates which kept blood sugars too high!
Is there a better way to use diet as an intervention?
From numerous studies we find that carbohydrate restriction can reduce blood sugars more effectively than the current dietary guidelines offered by the American Diabetes Association.
In this study the researchers truly missed a golden opportunity in the five years of time spent following these folks. They failed to discuss the very real problem their data shows clearly - the dietary intervention held near and dear is ineffective at normalizing blood sugars in those with type II diabetes. Even adding acrabose had little effect in the long-term. It did lower postprandial blood sugars, but not enough to reduce risks or slow progression. The reason is because neither the diet nor the diet and acrabose effectively reduced blood sugars to the normal range. Simply reducing blood sugars isn't enough - reduction must bring blood sugars back into the normal range!
It's only when we carefully consider the implications of this data that we see it tell us an important piece of the puzzle - progression is inevitable if control of post-prandial blood sugars is not normalized.
Over the long term, this continuous hyperglycemia leads to progression and is damaging and deadly to beta-cell function, kidneys, cardiovascular system, eyes and nerves.
The problem isn't that the diet and acrabose are ineffective to slow progression thus we just have to accept the inevitable - the problem is that the diet isn't restricting the very foods that are producing hyperglycemia after each meal, day after day after day.
The diet includes too many carbohydrates for the metabolism of those with type II diabetes to effectively deal with each day.
So, while the take home message to many physicians and healthcare professionals reading this study will be "reducing postprandial hyperglycemia doesn't slow progression in those with type II diabetes" the real finding here is that unless postprandial glucose is NORMALIZED one will continue to experience progressively worse deterioration as hyperglycemia takes its toll throughout the body and damages nerves, the cardiovascular system, kidneys, retinas and more.
What this study tells us is that simply lowering fasting and post prandial sugars is not good enough - we must establish dietary recommendations with the goal to normalize blood sugars as much as possible in those with type II diabetes if we are to have any hope of slowing progression and possibly reversing damage from hyperglycemia.
"Ameliorating postprandial hyperglycemia did not appear to delay progression of early type 2 diabetes. Factors other than postprandial hyperglycemia may be greater determinants of progression of diabetes. Alternatively, once FPG exceeds 126 mg/dl, ß-cell failure may no longer be remediable."
Now how is that for a conclusion? Pretty depressing if you ask me!
But this conclusion is totally understandable if you consider the perspective of those doing the research. They believe the dietary intervention used in this study was a proper diet for those with type II diabetes. The conclusion is that it's a losing battle to try to slow progression in those with diabetes who follow the dietary intervention with or without including acrabose. For those not aware of what acrabose is - it's a starch blocker designed to slow carbohydrate digestion and absorption. From my understanding, it effectively can block about 10-15g of carbohydrate when taken before a meal.
So, after five years of following the two groups, both given the same dietary intervention - with one group, the treatment group, given acrabose and the control group given a placebo - there was no statistically significant differences between the groups in rates of progression to "frank fasting hyperglycemia."
Some background on the study - the researchers investigated whether an intervention with acarbose in subjects with early diabetes (fasting plasma glucose greater than 140mg/dl and two-hour postprandial glucose of greater than 200mg/dl) would prevent or delay progression to "frank fasting hyperglycemia."
To understand why both groups experienced a continued progression, the researchers didn't consider the diet - 55% carbohydrate, 30% fat and 15% protein - as a potential problem in the equation. Why should they? It is, after all, the recommended diet for those with type II diabetes!
In fact, while the researchers did include the potential of the dietary intervention as a possible confounder in the results, it wasn't because the diet was problematic and raised blood sugars too high, but because "the dietary suggestions provided to both groups were potent and overwhelmed any effects of acarbose on ß-cell function."
The researchers simply could not wrap their heads around the idea the diet itself is the problem, so they totally failed to consider the negative effect the diet itself had on glycemic control (or lack thereof). Here is the paragraph the researchers included in their full-text paper:
It is possible that the dietary suggestions provided to both groups were potent and overwhelmed any effects of acarbose on ß-cell function. However, postprandial glucose was significantly lower in the acarbose group, and acarbose lowered A1C slightly but significantly over the first several years, suggesting that the drug itself had a superior effect on glycemia. In addition, the dietary intervention was no more potent than that provided to the placebo arms in studies such as the DPP and STOP-NIDDM.
To give you some perspective here, the diet was the standard carbohydrate:fat: protein ratio of 55:30:15. So, if a meal is 55% carbohydrate, 30% fat and 15% protein and provides 600-calories, it would provide 83g of carbohydrate. If acrabose is taken and actually reduces absorption of carbohydrate in the meal by 15g, the meal still provides 68g of carbohydrate that will be converted to glucose by the metabolism. Such a meal is not unreasonable if one is consuming 2,000-calories a day with three meals at 600-calories and two snacks at 100-calories each.
How great is the difference between a carbohydrate load of 83g versus 68g?
Quite frankly, not much when one considers each gram of carbohydrate converts to blood glucose and that rise in blood glucose must be reduced as much as the body can do with its insulin and medications. In those with type II diabetes, the ability to lower blood sugars is impaired and blood sugars stay elevated longer than they should. Basically their metabolism is doing the best it can with what it has and dietary carbohydrate strongly influences how high blood sugars rise since all carbohydrates (expect fiber) are converted to glucose - the more you consume carbohydrate, the higher blood sugars rise and over time, the less the body is able to reduce them effectively.
As Dr. Richard K. Bernstein illustrates this in what he calls the Laws of Small Numbers for controlling blood sugars - in type II diabetics, who still make insulin, it's common for a gram of carbohydrate to potentially raise blood glucose by 3mg/dl. I'll be clear here - how high blood sugars do rise is highly individual and based on insulin and insulin sensitivity. I'm going to use the 3mg/dl as an example to highlight how the current dietary recommendations can potentially raise blood sugars in someone with type II diabetes.
With that in mind, in this study, if 83g were consumed in the control group with an average fasting blood sugar of 126mg/dl, after the meal with 83g of carbohydrate their blood glucose would rise to 249mg/dl; those in the treatment group taking acrabose with absorption reduced to 68g would have blood sugars rise to 204mg/dl.
Lower? Yes.
Normal? No.
And it's because blood sugars were not normalized by the diet or the addition of the acrabose, the researchers really did reach the only logical conclusion one could reach when the perspective is that the dietary approach was a correct dietary intervention for those with diabetes - progression happens, not much we can do, life goes on.
Can we do better? Absolutely!
To do better we must evaluate interventions that specifically result in a normalization of blood sugars naturally.
In this study we find that the data speaks volumes of the inability of the current dietary recommendations with or without acrabose to normalize blood sugars. Both groups continued to deteriorate and it wasn't because that's what happens with diabetes - it was because they were consuming too many carbohydrates which kept blood sugars too high!
Is there a better way to use diet as an intervention?
From numerous studies we find that carbohydrate restriction can reduce blood sugars more effectively than the current dietary guidelines offered by the American Diabetes Association.
In this study the researchers truly missed a golden opportunity in the five years of time spent following these folks. They failed to discuss the very real problem their data shows clearly - the dietary intervention held near and dear is ineffective at normalizing blood sugars in those with type II diabetes. Even adding acrabose had little effect in the long-term. It did lower postprandial blood sugars, but not enough to reduce risks or slow progression. The reason is because neither the diet nor the diet and acrabose effectively reduced blood sugars to the normal range. Simply reducing blood sugars isn't enough - reduction must bring blood sugars back into the normal range!
It's only when we carefully consider the implications of this data that we see it tell us an important piece of the puzzle - progression is inevitable if control of post-prandial blood sugars is not normalized.
Over the long term, this continuous hyperglycemia leads to progression and is damaging and deadly to beta-cell function, kidneys, cardiovascular system, eyes and nerves.
The problem isn't that the diet and acrabose are ineffective to slow progression thus we just have to accept the inevitable - the problem is that the diet isn't restricting the very foods that are producing hyperglycemia after each meal, day after day after day.
The diet includes too many carbohydrates for the metabolism of those with type II diabetes to effectively deal with each day.
So, while the take home message to many physicians and healthcare professionals reading this study will be "reducing postprandial hyperglycemia doesn't slow progression in those with type II diabetes" the real finding here is that unless postprandial glucose is NORMALIZED one will continue to experience progressively worse deterioration as hyperglycemia takes its toll throughout the body and damages nerves, the cardiovascular system, kidneys, retinas and more.
What this study tells us is that simply lowering fasting and post prandial sugars is not good enough - we must establish dietary recommendations with the goal to normalize blood sugars as much as possible in those with type II diabetes if we are to have any hope of slowing progression and possibly reversing damage from hyperglycemia.
Thursday, September 07, 2006
Protein Study Uncovers Role of PYY and, Gasp! - Bias!
Quite a buzz was created by the publication of a study in the September issue of Cell Metabolism, Critical role for peptide YY in protein-mediated satiation and body-weight regulation.
From the summary section of the paper:
Dietary protein enhances satiety and promotes weight loss, but the mechanisms by which appetite is affected remain unclear. We investigated the role of gut hormones, key regulators of ingestive behavior, in mediating the satiating effects of different macronutrients. In normal-weight and obese human subjects, high-protein intake induced the greatest release of the anorectic hormone peptide YY (PYY) and the most pronounced satiety. Long-term augmentation of dietary protein in mice increased plasma PYY levels, decreased food intake, and reduced adiposity. To directly determine the role of PYY in mediating the satiating effects of protein, we generated Pyy null mice, which were selectively resistant to the satiating and weight-reducing effects of protein and developed marked obesity that was reversed by exogenous PYY treatment. Our findings suggest that modulating the release of endogenous satiety factors, such as PYY, through alteration of specific diet constituents could provide a rational therapy for obesity.
Cliff notes version:
A high protein diet led to spontaneous calorie reduction as PYY increased. The phenomenon was consistent with both the animal model using mice and in human studies used to validate the mice model. Over a longer term, the higher protein diet stimulated weight loss and enhanced PYY synthesis and secretion in mice.
To better understand the role of PYY, the researchers used mice where the PYY coding region was deleted and found that without PYY, the mice, even on a high protein diet, gained weight and experienced hyperphagia (eating an excessive amount of food beyond needs).
Basically the PYY-null mice were resistant to the satiating effects of dietary protein.
The media quickly picked the findings of the study up and ran attention grabbing headlines:
From the summary section of the paper:
Dietary protein enhances satiety and promotes weight loss, but the mechanisms by which appetite is affected remain unclear. We investigated the role of gut hormones, key regulators of ingestive behavior, in mediating the satiating effects of different macronutrients. In normal-weight and obese human subjects, high-protein intake induced the greatest release of the anorectic hormone peptide YY (PYY) and the most pronounced satiety. Long-term augmentation of dietary protein in mice increased plasma PYY levels, decreased food intake, and reduced adiposity. To directly determine the role of PYY in mediating the satiating effects of protein, we generated Pyy null mice, which were selectively resistant to the satiating and weight-reducing effects of protein and developed marked obesity that was reversed by exogenous PYY treatment. Our findings suggest that modulating the release of endogenous satiety factors, such as PYY, through alteration of specific diet constituents could provide a rational therapy for obesity.
Cliff notes version:
A high protein diet led to spontaneous calorie reduction as PYY increased. The phenomenon was consistent with both the animal model using mice and in human studies used to validate the mice model. Over a longer term, the higher protein diet stimulated weight loss and enhanced PYY synthesis and secretion in mice.
To better understand the role of PYY, the researchers used mice where the PYY coding region was deleted and found that without PYY, the mice, even on a high protein diet, gained weight and experienced hyperphagia (eating an excessive amount of food beyond needs).
Basically the PYY-null mice were resistant to the satiating effects of dietary protein.
The media quickly picked the findings of the study up and ran attention grabbing headlines:
- Probable Mechanism Behind Atkins Diet Revealed
- 'Proof' behind high protein diets
- Atkins-style diets suppress slimmers' hunger, says study
- Eat more meat to cut obesity
- Stomach growling? Eat a burger, study finds
Of course that last one made me laugh considering the headline last month that claimed A Bite Of Burger Can Cause Heart Attack!
The above headlines are designed to capture your attention and it's only when you read the article that you find the good examples of disconnect between the study published and what's put out there for public consumption.
Case in point, in the Nature article High-protein diet reduces appetite: Eggs, meat and cheese trigger a protein that makes us eat less, we find the lead researcher, Dr. Rachel Batterham quoted within the following paragraph:
[S]he cautions, that doesn't mean the Atkins diet is a good idea: "No medical person is going to tell you to have all that saturated fat in your diet and no carbohydrates." In its early stages, the regime causes a condition called ketosis, in which the liver, deprived of glycogen from carbohydrates, switches to its starvation mode and begins to metabolize fatty compounds. "The problem is that it makes you feel terrible," Batterham says.
Followed by, [s]he now plans to organize a long-term study of the effects of a high-protein diet in humans, which might feature foods such as lean meat, soy, tofu and egg.
Compare this with the full-text paper - The ready availability of carbohydrate-rich grains and cereals has been a recent development in human nutrition with the onset of organized agriculture. Many of the physiological systems that regulate food intake were probably established and may function better under lower-carbohydrate and higher-protein dietary conditions. This might explain the effects of protein on satiation and PYY release and the marked phenotype caused by the deletion of the Pyy gene.
To her peers, she writes about how our metabolism and the systems that regulate food intake may function better under carbohydrate restriction; the the public she perpetuates the myth that the Atkins diet (or an Atkins type diet) provide "no carbohydrate" and is one long saturated-fat-fest. ::::big eye roll:::::
I highlight the disparity to show readers how what they read in the media isn't always in synch with the primary source - the full-text paper that is published.
But that's not all.
Interestingly there is subtle bias that emerges in the full-text of the paper, which helps explain the public statements made regarding dietary fat.
Within the discussion, the citations of support for the satiety effect of protein include:
There is some limited evidence from human studies that these acute effects on satiety translate into longer-term benefits. For example, a 6 day intervention study examining the effects of a normal-protein (15%) low-fat American Heart Association diet compared with high-protein (31%) low-fat diet found that ad libitum caloric intake was reduced by 25% with the increased protein content diet (Dumesnil et al., 2001). In a randomized 6 month trial comparing ad libitum high-protein (25%) low-fat diet with a normal-protein (12%) low-fat diet for 6 months, Skov et al. demonstrated improved weight loss and fat mass loss with enhanced-protein diet, an effect attributed to reduced food intake (Skov et al., 1999). Furthermore, increasing the protein content of the diet from 15% to 18% during weight maintenance after weight loss has been shown to halve the amount of weight regained (Westerterp-Plantenga et al., 2004). Protein-rich diets caused the greatest satiation in our acute human and rodents feeding studies and the greatest reduction in weight gain in our chronic rodent diet studies, consistent with these published studies on the beneficial effects of dietary protein.
What's missing from the above citations?
The data from studies where protein and fat were consumed ad libitum - specifically the studies investigating carbohydrate restricted diets where subjects were allowed to consume protein and fat without limitation.
This very subtle bias doesn't change the data, but it does help us understand how preconceived notions enter into interpretation of the findings and the recommendations for additional research studies.
In this instance, it seems, the lines of scientific thought and inquiry are open for further exploration, as long as the researchers start with the assumption dietary fat, especially saturated fat, is bad.
It's an assumption that the diet-heart theory is not only valid, but infallible, that leads to limited lines of research inquiry - it's based on "let's ignore the fact that protein rich animal foods, in their natural state, often are packed with saturated fats - along with monounsaturated and polyunsaturated fats. Let's not look at data from studies where subjects were allowed to eat these sources of protein, and thus also consumed saturated fat; even the findings with beneficial improvements are unimportant here because of the saturated fat in the diet of these subjects. In fact, let's just contradict ourselves and our citation of Loren Cordain, his work exploring hunter-gatherer diets, and let's go investigate soy!"
So while this research expands our understanding of the role PYY plays in satiety, we see the researchers already setting the stage to investigate further within the dogmatic paradigm that dietary saturated fat is bad...forget the context of the diet, just don't explore the possibility that saturated fat may be a player here too! Go look at soy for goodness sake - there is just no way saturated fat may be beneficial....enough said.
Wednesday, September 06, 2006
Let's Blame Evolution for our Obesity Epidemic
As the 10th Internation Congress on Obesity opened in Sydney, Australia, experts from around the world gathered to collaborate to understand the global rise in obesity and explore potential solutions. In an article this week in Reuters, Evolution led to obesity pandemic, it's speculated that Evolution and the environment, not just gluttony, has led to a global obesity pandemic, with an estimated 1.5 billion people overweight -- more than the number of undernourished people.
Health experts at the week-long congress said calls for the past 30 years for people to eat less fatty foods and exercise more had failed to combat global obesity.
Obesity had become an "insidious killer and the major contributing cause of preventable diseases such as diabetes and heart disease," said conference co-chair Paul Zimmet. "It is a disease with disastrous health, social and economic consequences."
Kate Steinbeck, also co-chair of the conference said, "We know this is not about gluttony -- it is the interaction of heredity and environment."
Based on research studies and the growing incidence of obesity around the world, the experts gathered at the conference believe that too little sleep and too much fatty fast food are altering human biology. They also contend that weight loss diets, supplements and treatments promising weight loss have "no effect because they cannot match evolutionary influences that cause the body to conserve energy in times of famine."
So, let's blame evolution.
Dr Anne-Thea McGill told the conference "Early humans sought energy-dense food with high levels of fats, starches and sugars. We are genetically programmed to find foods with these qualities appealing. However, highly energy-dense Western diets have had many of the flavour and micronutrients processed out of them. The artificial replacements in starchy, fatty and sugary foods make them over-palatable and easy to eat quickly."
Long story short, McGill sees this as too much processed food that provides excess energy while deficient in essential nutrients - chronic malnutrition which causes the body to perceive a state of famine and store energy. Dieting to lose the excess weight doesn't work because it does not address the nutrient imbalance created by a poor diet.
Hmm...that sounds familiar! Ah, yes, I've written about this before....
For years I've been saying much of our weight problems are intricately linked to chronic nutrient deficiency. I also contend that within the framework of the current dietary guidelines, it is impossible to meet essential nutrient requirements from food. The current guidelines are designed in a way that reinforces an eating pattern that dooms our health and well-being.
So, it's not evolution that is causing our obesity epidemic, we've created this all on our own.
Unfortunately, it might just be evolution that stops the obesity epidemic for us as we continue our folly with low-fat, fortified, carbohydrate-rich diet recommendations.
That's a pretty scary thought, isn't it?
But it's not much of a leap when we consider the health of our children today - type II diabetes, atheroclerosis, dyslipidemia, hypertention and cardiovascular disease already present in an alarming number of our youth. Add to that the rising trend of "precocious puberty" where children are maturing much earlier than previous generations.
As Dr. Steinbeck said in the Reuters article, "This is the first generation in history where children may die before their parents."
The reason they may have a shorter life expectancy is because they're in poor health and they're in poor health because they're not eating a nutrient-rich diet that provides for all their essential nutrients! They're chronically malnourished!
Let's be clear, malnutrition isn't just not having enough food or calories each day. It's much more than that - consuming excess calories from food with inadequate essential nutrients is also malnutrition. Nutritional surveys show that we're chronically malnourished in the United States.
When we consider evolution - in particular natural selection - it's important to remember that "survival of the fittest" isn't the necessarily the strongest, fastest or most weight stable among us. Survival of the species happens through those endowed with characteristics which improve chances of survival and reproduction, through those who do reproduce and propagate off-spring with heritable characteristics that affect their survival and reproductive success. After millions of years and thousands of generations, today we have inherited a set of characteristics that require, among other things, specific nutrients if we are to reproduce and survive. In a very short time span, we've modified our diet radically from that of our ancestors. If evolution is playing here, it's not playing very nicely in the sandbox of our genes. But, evolution isn't making us fat, we're doing that because we are not "playing within the bounds" of our genetic requirements, especially the requirements for nutrients that optimize reproduction and survival.
Consider the alarming number of children today that are already showing signs of chronic disease and characteristics of infertility. The stark and painful reality is that this may be evolution exerting influence to limit reproduction potential of those unable to consume a nutritionally complete diet. Without an appropriate and adequate diet, the youngest among us are being afflicted earlier and earlier with chronic disease, characteristics of infertility and a potentially shorter life-span to be lived battling chronic illness.
Some contend that recent adaptions exhibited in finches of the Galapogos Islands highlight that adaption to foods like grains is likely due to the 10,000-year inclusion in our diet. As Kevin Dill said " are we to believe that human beings are incapable as a species of successfully incorporating into our diet, the most abundant food source available on the planet today? What exactly does that say about our future as a species?"
What this view fails to appreciate is that the finches were undergoing what is called "characteristic displacement" which happens when change is driven by competition among species for a limited resource like food. As an article at Fox News in July quotes Dr. Peter Grant (who published findings from observations of the finches) "The recent immigrant species had almost eaten the supply of food themselves, so they almost went extinct. The resident species, the species that was there before the new species arrived, underwent a large shift toward small size in beaks."
The reason - smaller beaked birds were better able to meet their nutritional requirements from smaller seeds, thus that characteristic - a smaller beak - was passed to the next generation because those birds with smaller beaks could reproduce.
Why? Those finches with smaller beaks were able to meet their nutritional requirements where those with larger beaks couldn't as large seed availability dwindled. Those with the smaller beaks didn't radically alter their diet to consume a different set of nutrients - in fact, they adapted to the food source available, smaller seeds, within the same context of nutrients as their previous diet contained with larger seeds. Those finches who were at a disadvantage with smaller beaks unable to extract nutrients from larger seeds were now at an advantage when the larger seeds were limited, and their characteristics prevailed as they reproduced with off-spring having smaller beaks.
Such a character displacement isn't expected in a species that fails to consume a diet that is nutritionally adequate.
As Dr. Grant stated, "It's a very important one in studies of evolution, because it shows that species interact for food and undergo evolutionary change, which minimizes further evolution."
Humans, as a species, are forcing the hand of evolution these days - we're consuming a diet that is nutritionally bankrupt. Are we to expect evolution to step in and favor a diet that sets up disease, disrupts our metabolism, and does not provide for our essential nutrients?
I think not.
What evolution is going to do is step in and stop our madness - those who are unable to secure and consume a nutrient-dense diet will continue to develop chronic diseases and infertility issues earlier and earlier in their life. As a species, we cannot expect to be able to reproduce and survive long with a less than optimal diet.
It's futile to blame evolution for our woes - we're working against our genetic requirements and we're seeing the results of our folly.
Fortunately it's not too late - if we're to reverse obesity, optimize our health and survival, we must - absolutely must - abandon this thinking that a "healthful diet" is based on these insane, man-made macronutrient ratios and get back to the important and critical aspects of dietary requirements at the micronutrient level.
Only when we finally go back to the drawing board and take a long hard look at meeting essential nutrient requirements and reverse the chronic state of nutrient deficiency we are in, can we expect to see a reversal in the current trends that promise to be our undoing as a species.
Health experts at the week-long congress said calls for the past 30 years for people to eat less fatty foods and exercise more had failed to combat global obesity.
Obesity had become an "insidious killer and the major contributing cause of preventable diseases such as diabetes and heart disease," said conference co-chair Paul Zimmet. "It is a disease with disastrous health, social and economic consequences."
Kate Steinbeck, also co-chair of the conference said, "We know this is not about gluttony -- it is the interaction of heredity and environment."
Based on research studies and the growing incidence of obesity around the world, the experts gathered at the conference believe that too little sleep and too much fatty fast food are altering human biology. They also contend that weight loss diets, supplements and treatments promising weight loss have "no effect because they cannot match evolutionary influences that cause the body to conserve energy in times of famine."
So, let's blame evolution.
Dr Anne-Thea McGill told the conference "Early humans sought energy-dense food with high levels of fats, starches and sugars. We are genetically programmed to find foods with these qualities appealing. However, highly energy-dense Western diets have had many of the flavour and micronutrients processed out of them. The artificial replacements in starchy, fatty and sugary foods make them over-palatable and easy to eat quickly."
Long story short, McGill sees this as too much processed food that provides excess energy while deficient in essential nutrients - chronic malnutrition which causes the body to perceive a state of famine and store energy. Dieting to lose the excess weight doesn't work because it does not address the nutrient imbalance created by a poor diet.
Hmm...that sounds familiar! Ah, yes, I've written about this before....
For years I've been saying much of our weight problems are intricately linked to chronic nutrient deficiency. I also contend that within the framework of the current dietary guidelines, it is impossible to meet essential nutrient requirements from food. The current guidelines are designed in a way that reinforces an eating pattern that dooms our health and well-being.
So, it's not evolution that is causing our obesity epidemic, we've created this all on our own.
Unfortunately, it might just be evolution that stops the obesity epidemic for us as we continue our folly with low-fat, fortified, carbohydrate-rich diet recommendations.
That's a pretty scary thought, isn't it?
But it's not much of a leap when we consider the health of our children today - type II diabetes, atheroclerosis, dyslipidemia, hypertention and cardiovascular disease already present in an alarming number of our youth. Add to that the rising trend of "precocious puberty" where children are maturing much earlier than previous generations.
As Dr. Steinbeck said in the Reuters article, "This is the first generation in history where children may die before their parents."
The reason they may have a shorter life expectancy is because they're in poor health and they're in poor health because they're not eating a nutrient-rich diet that provides for all their essential nutrients! They're chronically malnourished!
Let's be clear, malnutrition isn't just not having enough food or calories each day. It's much more than that - consuming excess calories from food with inadequate essential nutrients is also malnutrition. Nutritional surveys show that we're chronically malnourished in the United States.
When we consider evolution - in particular natural selection - it's important to remember that "survival of the fittest" isn't the necessarily the strongest, fastest or most weight stable among us. Survival of the species happens through those endowed with characteristics which improve chances of survival and reproduction, through those who do reproduce and propagate off-spring with heritable characteristics that affect their survival and reproductive success. After millions of years and thousands of generations, today we have inherited a set of characteristics that require, among other things, specific nutrients if we are to reproduce and survive. In a very short time span, we've modified our diet radically from that of our ancestors. If evolution is playing here, it's not playing very nicely in the sandbox of our genes. But, evolution isn't making us fat, we're doing that because we are not "playing within the bounds" of our genetic requirements, especially the requirements for nutrients that optimize reproduction and survival.
Consider the alarming number of children today that are already showing signs of chronic disease and characteristics of infertility. The stark and painful reality is that this may be evolution exerting influence to limit reproduction potential of those unable to consume a nutritionally complete diet. Without an appropriate and adequate diet, the youngest among us are being afflicted earlier and earlier with chronic disease, characteristics of infertility and a potentially shorter life-span to be lived battling chronic illness.
Some contend that recent adaptions exhibited in finches of the Galapogos Islands highlight that adaption to foods like grains is likely due to the 10,000-year inclusion in our diet. As Kevin Dill said " are we to believe that human beings are incapable as a species of successfully incorporating into our diet, the most abundant food source available on the planet today? What exactly does that say about our future as a species?"
What this view fails to appreciate is that the finches were undergoing what is called "characteristic displacement" which happens when change is driven by competition among species for a limited resource like food. As an article at Fox News in July quotes Dr. Peter Grant (who published findings from observations of the finches) "The recent immigrant species had almost eaten the supply of food themselves, so they almost went extinct. The resident species, the species that was there before the new species arrived, underwent a large shift toward small size in beaks."
The reason - smaller beaked birds were better able to meet their nutritional requirements from smaller seeds, thus that characteristic - a smaller beak - was passed to the next generation because those birds with smaller beaks could reproduce.
Why? Those finches with smaller beaks were able to meet their nutritional requirements where those with larger beaks couldn't as large seed availability dwindled. Those with the smaller beaks didn't radically alter their diet to consume a different set of nutrients - in fact, they adapted to the food source available, smaller seeds, within the same context of nutrients as their previous diet contained with larger seeds. Those finches who were at a disadvantage with smaller beaks unable to extract nutrients from larger seeds were now at an advantage when the larger seeds were limited, and their characteristics prevailed as they reproduced with off-spring having smaller beaks.
Such a character displacement isn't expected in a species that fails to consume a diet that is nutritionally adequate.
As Dr. Grant stated, "It's a very important one in studies of evolution, because it shows that species interact for food and undergo evolutionary change, which minimizes further evolution."
Humans, as a species, are forcing the hand of evolution these days - we're consuming a diet that is nutritionally bankrupt. Are we to expect evolution to step in and favor a diet that sets up disease, disrupts our metabolism, and does not provide for our essential nutrients?
I think not.
What evolution is going to do is step in and stop our madness - those who are unable to secure and consume a nutrient-dense diet will continue to develop chronic diseases and infertility issues earlier and earlier in their life. As a species, we cannot expect to be able to reproduce and survive long with a less than optimal diet.
It's futile to blame evolution for our woes - we're working against our genetic requirements and we're seeing the results of our folly.
Fortunately it's not too late - if we're to reverse obesity, optimize our health and survival, we must - absolutely must - abandon this thinking that a "healthful diet" is based on these insane, man-made macronutrient ratios and get back to the important and critical aspects of dietary requirements at the micronutrient level.
Only when we finally go back to the drawing board and take a long hard look at meeting essential nutrient requirements and reverse the chronic state of nutrient deficiency we are in, can we expect to see a reversal in the current trends that promise to be our undoing as a species.
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