Archive for September, 2006
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.
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!
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
- 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!”
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
Recent Headlines I Don’t Have Time to Write About:
Food Navigator USA
Nutrition labels may confuse public
International Herald Tribune
WHO: Fight against chronic diseases, obesity can use anti-smoking campaigns as models
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
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.
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:
- 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.