That is how Dr. Barry Sears characterized the study published in JAMA yesterday in the Atlanta Journal Constitution article, Atkins Diet Vindicated? Well Maybe.
In the research paper detailing the A to Z Weight Loss Study, his dietary approach (Zone) went head-to-head against Atkins, LEARN and Ornish and had the least influence on weight.
In the AP article, found on MSN, he said the "study had a good concept and incredibly pathetic execution."
Sour grapes?
Let's see what others thought of the same study.
Dr. Dean Ornish has an entire column in Newsweek - Why I Disagree with New Diet Study - where he voiced his concern that "many people may go on a diet that harms them based on inaccurate information;" and complained, as Dr. Sears did in numerous quotes, that study subjects assigned the Ornish diet weren't following the Ornish diet.
In the Forbes article about the study, Dr. Ornish summed up his belief that those on Atkins did better because "[i]t's a lot easier to follow a diet that tells you to eat bacon and brie than to eat predominantly fruits and vegetables."
Two diets, two authors, two not-so-happy campers.
What did Yale University food policy researcher and creator of the LEARN diet, Kelly Brownell, have to say? The study "shows that nothing works very well, [...] it just screams out for the need to prevent obesity."
One thing I do totally agree with - the study was a good concept...but it was poorly executed (Dr. Sears' main gripe).
That was one reason why, yesterday, I decided to forego detailing the data - it wasn't earth-shattering, it wasn't all that exciting and it really only proved - pardon my French - when you do something half-assed you get half-assed results.
I just could not get excited about it. The mouse study - A High Fat, Ketogenic Diet, Induces a Unique Metabolic State in Mice - in the American Journal of Physiology, Endocrine Metabolism; now that was exciting!
But I digress..
While Sears, Ornish and Brownell are all pointing out the lack of adherence to their respective plans, the same can be said of those assigned the Atkins diet; they didn't exactly follow the diet, as written, either.
In fact, at the two-month mark they were already consuming what is known as "pre-maintenance" or "maintenance" level carbohydrate - more than 60g per day on average.
Keep in mind this was during the initial eight week period that was designed to provide intensive support and teach participants about their assigned diets.
Those assigned the Atkins diet were not the only ones who failed to comply with the defined limits of their dietary approach - none of the groups seemed able to follow their diets correctly in the first eight weeks. Those assigned Ornish were to reduce dietary fat to 10% of calories - they ate 20%; those assigned the Zone were to eat 40:30:30 (carbohdyrate:fat:protein) and ate 42:35:23; and those assigned the LEARN diet were to eat what is similar to the Food Pyramid, around 55/60:30:10/15 and ate 50:30:20.
The question then must be asked - what happened in this study that subjects weren't able to follow the basic guidelines of their diets during the period of intense teaching and support? It's our tax dollars - this was an NIH funded study - so, how did a $2-million trial fail to achieve measurable compliance?
Forget about over the long-term, this study failed to achieve compliance out of the gate!
We have to ask, what went wrong?
If don't ask this question and probe the details, we'll just continue to waste money and get nowhere in answering the billion-dollar question - how do we help people lose weight and keep it off?
First let's look at the issue of compliance to an assigned diet protocol in other studies to see if this study is just one more with poor adherence or one more with a problem to resolve to achieve compliance in future studies.
If we look at other published studies for each of the above dietary approaches we find:
ORNISH
In the American Journal of Cardiology, the study - Comparison of coronary risk factors and quality of life in coronary artery disease patients with versus without diabetes mellitus - was published in May 2006. This trial included intensive support from the start to enable patients to modify lifestyle, diet, activity and stress management. Compliance was reported as good with the subjects "able to adhere to the recommended lifestyle."
ZONE - SEARS
In the American Journal of Clinical Nutrition, the study - Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets - was published in May 2006. In the six-week trial we find good food intake was strictly controlled, so good compliance was built into the protocol.
LEARN (FOOD PYRAMID TYPE DIET 55/60:30:10/15)
In JAMA, the study, Low-Fat Dietary Pattern and Risk of Cardiovascular Disease - was published in February 2006. In the seven year trial we find the one year dietary data provided. In addition, we learn from the Dietary Modification Trial data, published in January 2006 (JAMA) that subjects in the intervention group received intensive support to learn their new diet over the first year and the first year data reported shows those in the intervention group consumed, on average, 24.3% of calories from dietary fat, 8.1% of calories from saturated fat, 58.3% of calories from carbohydrate, and the remaining calories - 17.7% from protein.
ATKINS
In the Annals of Internal Medicine, the study - A Low-Carbohydrate Ketogenic Diet versus a Low-Fat Diet to Treat Obesity and Hyperlipidemia - was published in May 2004. Both groups received printed materials and instruction from registered dietitians about their assigned diet protocol. The researchers reported that at the end of six months, the low-carbohydrate group consumed 29.5g of carbohydrate on average and the low-fat group (protocol less than 30% of diet from fat with a calorie deficiet of 500-1000 calories a day) averaged 29% of their calories from dietary fat and an average calorie intake of 1502-calories a day, a level within the desired deficit.
With the above studies, and many others with similar good compliance, one thing is abundantly clear - those tasked with instructing participants about their assigned diets knew the rules of the dietary approach well and were able to communicate, clearly, how to implement the necessary dietary changes to participants in the studies.
So what went wrong with this one?
As much as I hate to say it - if you ask me, it comes down to, as Dr. Sears said "pathetic execution" of the study concept because of a poorly designed protocol.
The researchers recruited women, aged 25 to 50, who had a BMI between 27 and 40, and who wanted to lose weight. This is good because the researchers started with a motivated population of participants. Motivation and desire to lose weight among study participants is a definite plus at the get-go of a study.
Then the researchers, following the gold-standard randomization protocol, blindly randomized participants into one of four groups, each assigned a popular diet book to use - Dr Atkins' New Diet Revolution, Enter the Zone, The LEARN Manual for Weight Management, or Eat More, Weigh Less by Ornish.
This is where I think things started to "go wrong" - those recruited into the study merely wanted to lose weight. Exclusions from the study included those whose weight was not stable over the last two months before the trial (already potentially dieting), those whose medications had changed in the last three months, and those who "self-reported hypertension (except for those whose blood pressure was stable using antihypertension medications); type 1 or 2 diabetes mellitus; heart, renal, or liver disease; cancer or active neoplasms; hyperthyroidism unless treated and under control; any medication use known to affect weight/energy expenditure; alcohol intake of at least 3 drinks/d; or pregnancy, lactation, no menstrual period in the previous 12 months, or plans to become pregnant within the next year."
Unlike other randomized trials with good compliance, these subjects did not have the additional motivation to reverse or improve a medical condition that would over-ride any doubts about a particular dietary pattern assigned to them.
In fact, if we examine the literature, we find when weight loss is the primary objective, compliance within randomly assigned diets is much lower than when subjects choose their diet or have the additional motivation to reverse or improve a medical condition.
We need to learn from this and not chalk it up as one more example that people can't follow a diet.
It's clear to me that blind randomization of subjects, in dietary modification trials, is less effective than allowing subjects to choose their diet if weight loss is the primary objective without specific disease management as a secondary objective.
Next we find in the A to Z Weight Loss Trial that participants did receive some instruction; specifically A) they were provided the book for their assigned diet, B) attanded a 1-hour classes led by a registered dietitian once per week for 8 weeks, and C) each class covered approximately one eighth of their respective books per class.
Curiously, "[t]he same dietitian taught all classes to all groups in all 4 cohorts."
I don't know about you, but I know me...and there is NO WAY I could objectively present and teach four vastly different dietary approaches without some bias seeping into my advice. It wouldn't be intentional either - I could definitely read and regurgitate Ornish's very low-fat, near vegan diet to an audience; I could definitely discuss how to plan a menu, shop and prepare dishes; and I could offer up meaningful suggestions about making good choices.
But....and here is the "but"....what participants would easily pick up on throughout my presentations is my lack of enthusiasm for the dietary approach. They'd also quickly realize I have no appreciable experience myself with eating that way or practical advice since I have not "been there, done that" but expect them to do it.
In this study, the same dietitian was tasked with and expected to provide expert instruction on each diet to each cohort - it's obvious from the abyssimal compliance at two months this approach to instuction about each diet did not work well.
We need to learn from this and not chalk it up as one more example that people can't follow a diet.
It's clear to me, from this study's method of instruction compared with other studies with better compliance, that it is not just knowledge of a diet that is necessary to teach someone how to follow a diet, but actual expertise of the dietary approach is critically important.
The person tasked with instructing a cohort must know not only the diet rules, but also how to plan menus, cook, shop, dine out, overcome objections from family and friends, and have practical advice to overcome obstacles that come along with any diet. Ideally they themself also eat a diet similar to that being taught and therefore have the "been there, done that" enthusiasm that does motivate someone that they can do it too.
After that intial eight weeks of instuction through group classes, we find the only additional communication was to motivate people to show up for follow-up - this communication with participants included telephone calls and emails reminding them of their follow-up appointments and monetary incentives to make their follow-up appointments. From week nine to the end of month twelve, there does not appear to be any additional support by way of classes, group sessions, or consultation to answer questions or provide advice.
We need to learn from this and not chalk it up as one more example that people can't follow a diet.
It's clear to me, from this study's method of follow-up support - or should I say lack thereof - that if we look at studies with good long term compliance, support over the long term goes hand-in-hand with choosing a diet you think you can do and expert instruction about how to do it.
Ask almost anyone who has followed a carbohydrate restricted diet for a long period if they did it without any support and they'll tell you support was critical along the way - whether by online forum, having access to someone expert in the diet rules or doing the diet with a spouse or friend - support got them through frustrations along the way as they learned their new diet.
Each of us, in some small way, through our taxes, paid for this study - a study that cost us $2-million dollars.
A study that tells us that you can lose weight in any diet you're told to follow for a year. Heck, it even tells us you can lose weight if you totally miss the boat with regard to how you're supposed to eat in the assigned diet as long as you don't continue to eat as you did in your habitual diet (baseline diet).
The media is trumpeting this as proof Atkins is better. Sorry, but this wasn't Atkins. It also was not Ornish, Zone or LEARN for that matter.
However, even with this criticism, I think it's safe to say that the study did meet it's primary objective to "test whether any of the 4 diets, representing a spectrum of carbohydrate intake, was more effective than any other in 12-month weight loss."
The carbohydrate intake of those assigned the Atkins diet - even though they did not reduce carbohydrate to Atkins level of intake - did in fact consume significantly less carbohydrate than the other groups while consuming a similar restricted level (without being told to do so) of calories. At each point in time, the Atkins cohort ate less carbohydrate, that correlates with greater weight loss observed at each data collection point. At the period between two months into the diet and one year, the Atkins cohort more than doubled their intake of carbohydrate from 61g at two months to 138g at one year. Even with this higher than encouraged level of carbohydrate, they lost weight - more weight than the other groups consuming more carbohydrate even with similar calorie intakes.
So before we write this one off as one more example of diets not working in the long-term, let's remember the participants did not have an opportunity to review each diet and choose one they felt they could adopt for the long term.
Let's also be aware that while the participants did recieve some instruction about how to follow their assigned diets, it's also fair to say the instruction was probably adequate, but certainly not from the perspective of "domain expertise" that may be critical to learning a new dietary approach in the long-term.
Lastly, let's not lose sight of the fact we'll continue to fail in our quest to find a method of weight loss and health risk improvement if we do not seriously begin to evaluate and understand what leads to good complicance or poor compliance.
Before we spend millions more on poorly executed diet studies, let's seriously evaluate the data and develop a set of best practices to help researchers avoid the pitfalls that are an inherent part of changing someone's diet.
People need motivation and a desire to lose weight.
People need to know their options, have information and make an educated decision about the type of diet they feel they'll do well with based on their dietary preferences and past experiences with different diets.
People need support to get started on a new dietary approach.
People need quality, expert instruction to guide them as they initiate a dietary modification, ideally from someone who is an enthusiastic expert.
People need support throughout the first year - support from experts and from others in the same boat as they are; online support forums, group face-to-face sessions, telephone access and personal consultations all contribute to success and must be considered as a critical component for compliance in dietary trials.
We have before us is a study that really does indicate carbohydrate restriction can work well over a period of one year. Without sub-group analysis to evaluate results tied to compliance (hey, some of the participants had to be doing the various diet right, dontcha think?) we can't know just how effective doing Atkins or any of the diets is with good compliance though since the researchers didn't take their data to that level of analysis in this paper.
What this study cannot tell us is how much better the outcome could have been - for any of the four diets in the trial - if participants had a chance to really have solid instruction and support.
Maybe next time we (taxpayers) fund a diet study, we'll include in the millions spent enough to include important and critical elements for success in the long-term?
Wednesday, March 07, 2007
Tuesday, March 06, 2007
Making the Rounds Around the Research of Low-Carb Diets
Over the coming hours and days, you'll have a smorgasbord of articles to tell you all about the soon-to-be-released study - Comparison of Atkins, Zone, Ornish and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women (aka The A to Z Weight Loss Study) - being published in JAMA later today.
The results are already leaking out in various newspapers, so if you want a preview, you can read here or here or here.
While this study will be a media darling the next few days, I thought I'd highlight some other research that is just as important to our overall understanding of carbohydrate restriction, yet remains virtually ignored by the media!
I'll get to the JAMA study later this week since the findings really are nothing new nor a surprise to those of us who already understand that carbohydrate restriction works.
So, without further ado - in the March issue of Surgical Endoscopy, we find The effect of a low-carbohydrate diet on the nonalcoholic fatty liver in morbidly obese patients before bariatric surgery. In this study researchers investigated the effect of a very low-carbohydrate diet over four-weeks in 14 pre-op patients before bariatric surgery. All were morbidly obese and scans revealed non-alcoholic fatty liver disease (NAFLD).
NAFLD with enlargement of the left lobe of the liver can complicate bariatric surgery, so the researchers wanted to see the effect diet would have on liver density before surgery. After four weeks, there was a statistically significant increase in liver density and statistically significant decrease in liver volume. The researchers concluded, "The findings show that 4 weeks of a very low carbohydrate diet reduces liver fat content and liver size, particularly of the left lobe. This approach may render bariatric surgery or any foregut operations less difficult in morbidly obese patients and may be a useful treatment for nonalcoholic fatty liver disease."
Next up, in the February issue of American Journal of Physiology, Heart & Circulatory Physiology, we find Effects of Low Carbohydrate Diet on Vascular Health: More than just Weight Loss (pubmed citation) reviewing this study, Restoration of Coronary Endothelial Function In Obese Zucker Rats By A Low Carbohydrate Diet, published in the same issue.
In the latter, the study investigated endothelial function in obese rats fed a low carbohydrate or normal rat diet, the researchers concluded that "obesity-induced impairment in endothelial dependent vasodilation of coronary arterioles can be dramatically improved with a low carbohydrate diet most like(ly) through the production of a hyperpolarizing factor independent of NO." In the review (first link above) it was concluded that "Focardi et al demonstrates a novel mechanism of improved coronary vascular function with LC (low-carb) diet during metabolic syndrome. This study implicated a role for EDHF (endothelium derived hyperpolarizinf factors) in dietary interventions that may improve the cardiovascular complications of metabolic syndrome."
In simple English - the rats with metabolic syndrome did significantly better with a low-carb diet than their normal chow.
Another animal model study - A High Fat, Ketogenic Diet, Induces a Unique Metabolic State in Mice - in the American Journal of Physiology, Endocrine Metabolism, was a really cool study. In this study researchers compared the physiologic and metabolic effects of four different diets - normal chow (control group), a high-fat/high-sucrose diet, a ketogenic low-carb diet, and a calorie restricted (66% normal calories) optimal nutrition diet (CRON). The researchers found that the mice on the ketogenic diet ate the same calories as those on the control chow or the high-fat/high-sucrose diet, but their weight dropped and then stablized at 85% of their initial baseline weight - almost identical to those mice fed the CRON diet and allowed just 66% of their normal calories.
Mice grew obese on the high-fat/high-sucrose diet (remember, they were not eating more calories!) and when they were transitioned to a ketogenic diet, they lost their excess weight, improved glucose metabolism and increases energy expenditure. Need I say more?
Back in January, Metabolism published the study, Effects of a carbohydrate-restricted diet with and without supplemental soluble fiber on plasma low-density lipoprotein cholesterol and other clinical markers of cardiovascular risk, in which researchers investigated the effect of dietary fiber in a carbohydrate restricted diet (CRD). The researchers compared two groups of subjects following a carbohydrate restricted diet - group one was given a fiber supplement and group two a placebo; after 12-weeks both groups lost weight and body fat, improved systolic blood pressure, waist circumference and blood glucose levels.
Interesting finding - in both groups HDL and triglycerides improved (10% and -34% in fiber group; 14% and -43% in placebo group); LDL decreased by 17.6% at week 6 and 14.1% at week 12 in the fiber group; and a significant reduction, 6% happened at week 12 in the placebo group. As the researchers concluded, "We conclude that although clearly effective at lowering LDL-C, adding soluble fiber to a CRD during active and significant weight loss provides no additional benefits to the diet alone. Furthermore, a CRD led to clinically important positive alterations in cardiovascular disease risk factors."
So, while the rush will be on later today to pick apart and analyze the JAMA study, keep in mind it's not the first, nor will it be the last that confirms a carbohydrate restricted diet is a scientifically supported dietary approach for weight loss, cardiovascular improvement and improvement to blood sugars, cholesterol and the features of metabolic syndrome. It's also not the only recently published study investigating carbohydrate restriction or comparing it to other dietary approaches.
The results are already leaking out in various newspapers, so if you want a preview, you can read here or here or here.
While this study will be a media darling the next few days, I thought I'd highlight some other research that is just as important to our overall understanding of carbohydrate restriction, yet remains virtually ignored by the media!
I'll get to the JAMA study later this week since the findings really are nothing new nor a surprise to those of us who already understand that carbohydrate restriction works.
So, without further ado - in the March issue of Surgical Endoscopy, we find The effect of a low-carbohydrate diet on the nonalcoholic fatty liver in morbidly obese patients before bariatric surgery. In this study researchers investigated the effect of a very low-carbohydrate diet over four-weeks in 14 pre-op patients before bariatric surgery. All were morbidly obese and scans revealed non-alcoholic fatty liver disease (NAFLD).
NAFLD with enlargement of the left lobe of the liver can complicate bariatric surgery, so the researchers wanted to see the effect diet would have on liver density before surgery. After four weeks, there was a statistically significant increase in liver density and statistically significant decrease in liver volume. The researchers concluded, "The findings show that 4 weeks of a very low carbohydrate diet reduces liver fat content and liver size, particularly of the left lobe. This approach may render bariatric surgery or any foregut operations less difficult in morbidly obese patients and may be a useful treatment for nonalcoholic fatty liver disease."
Next up, in the February issue of American Journal of Physiology, Heart & Circulatory Physiology, we find Effects of Low Carbohydrate Diet on Vascular Health: More than just Weight Loss (pubmed citation) reviewing this study, Restoration of Coronary Endothelial Function In Obese Zucker Rats By A Low Carbohydrate Diet, published in the same issue.
In the latter, the study investigated endothelial function in obese rats fed a low carbohydrate or normal rat diet, the researchers concluded that "obesity-induced impairment in endothelial dependent vasodilation of coronary arterioles can be dramatically improved with a low carbohydrate diet most like(ly) through the production of a hyperpolarizing factor independent of NO." In the review (first link above) it was concluded that "Focardi et al demonstrates a novel mechanism of improved coronary vascular function with LC (low-carb) diet during metabolic syndrome. This study implicated a role for EDHF (endothelium derived hyperpolarizinf factors) in dietary interventions that may improve the cardiovascular complications of metabolic syndrome."
In simple English - the rats with metabolic syndrome did significantly better with a low-carb diet than their normal chow.
Another animal model study - A High Fat, Ketogenic Diet, Induces a Unique Metabolic State in Mice - in the American Journal of Physiology, Endocrine Metabolism, was a really cool study. In this study researchers compared the physiologic and metabolic effects of four different diets - normal chow (control group), a high-fat/high-sucrose diet, a ketogenic low-carb diet, and a calorie restricted (66% normal calories) optimal nutrition diet (CRON). The researchers found that the mice on the ketogenic diet ate the same calories as those on the control chow or the high-fat/high-sucrose diet, but their weight dropped and then stablized at 85% of their initial baseline weight - almost identical to those mice fed the CRON diet and allowed just 66% of their normal calories.
Mice grew obese on the high-fat/high-sucrose diet (remember, they were not eating more calories!) and when they were transitioned to a ketogenic diet, they lost their excess weight, improved glucose metabolism and increases energy expenditure. Need I say more?
Back in January, Metabolism published the study, Effects of a carbohydrate-restricted diet with and without supplemental soluble fiber on plasma low-density lipoprotein cholesterol and other clinical markers of cardiovascular risk, in which researchers investigated the effect of dietary fiber in a carbohydrate restricted diet (CRD). The researchers compared two groups of subjects following a carbohydrate restricted diet - group one was given a fiber supplement and group two a placebo; after 12-weeks both groups lost weight and body fat, improved systolic blood pressure, waist circumference and blood glucose levels.
Interesting finding - in both groups HDL and triglycerides improved (10% and -34% in fiber group; 14% and -43% in placebo group); LDL decreased by 17.6% at week 6 and 14.1% at week 12 in the fiber group; and a significant reduction, 6% happened at week 12 in the placebo group. As the researchers concluded, "We conclude that although clearly effective at lowering LDL-C, adding soluble fiber to a CRD during active and significant weight loss provides no additional benefits to the diet alone. Furthermore, a CRD led to clinically important positive alterations in cardiovascular disease risk factors."
So, while the rush will be on later today to pick apart and analyze the JAMA study, keep in mind it's not the first, nor will it be the last that confirms a carbohydrate restricted diet is a scientifically supported dietary approach for weight loss, cardiovascular improvement and improvement to blood sugars, cholesterol and the features of metabolic syndrome. It's also not the only recently published study investigating carbohydrate restriction or comparing it to other dietary approaches.
Friday, March 02, 2007
Antioxidant Supplements Dangerous?
With some time available last night, I had a chance to finally read through the full-text of the recently published meta-analysis - Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention - published in JAMA this week.
In a WebMD article about the study, Christian Gludd (one of the researchers) was quoted as saying "Anyone is welcome to criticize our research, but my question is, what is your evidence? I think the parties that want to sell or use these antioxidant supplements in the dosages used in these trials, they want [to see only] positive evidence that it works beneficially."
It's funny a researcher would assume criticism is driven by profit motive or desire to believe something is beneficial, and not flawed methodology, overwhelming scope, subjective exclusions or potentially subjective assignment of bias risk.
Here's my take on the review, with first a full disclosure - I do not sell or promote the use of antioxidant supplements; I do not have a financial interest in any supplement company; and I don't take any of the antioxidants included in the meta-analysis except what is included in my daily multi-vitamin. You can see I have no profit motive to criticize the study, nor do I have a blindspot desire to believe that I'm taking particular antioxidants reduce my risk of dying.
I'm interested in the data and the methodology used to reach the conclusion that the researchers did not "find convincing evidence that antioxidant supplements have beneficial effects on mortality. Even more, beta carotene, vitamin A, and vitamin E seem to increase the risk of death. Further randomized trials are needed to establish the effects of vitamin C and selenium."
The stated objective to undertake a meta-analysis of antioxidants was "to analyze the effects of antioxidant supplements (beta carotene, vitamins A and E, vitamin C [ascorbic acid], and selenium) on all-cause mortality of adults included in primary and secondary prevention trials."
Interestlingly, we learn upon reading the full-text that the researchers specifically excluded studies that reported no deaths during a trial period or follow-up. A meta-analysis that seeks to establish effects on mortality but excludes studies with no reported deaths from the pool of data to be analyzed? Hmmm...
Yes, this is the first interesting thing that popped up when I read the paper and learned the researchers conducted an intial search across a number of databases and found 16,111 references that hit their search criteria. Of course many of these were duplicate references (14,003), leaving 2,108 references to review.
The next review led to the exclusion of another 907 references because they included patients with cancer; involved acute and infectious disease; involved infants or children; or involved pregnant or lactating women. These understandable exclusions then left the researchers with 1,201 references (815 trials) to review for inclusion or exclusion from the analysis.
So the researchers moved on and started to excluded based on criteria few can or will agrue with - the trial didn't meet inclusion criteria established for the review; it was not randomized; data was insufficient for review purposes; or a trial was still ongoing.
But then we come to a curious reason for exclusion - a study did not have any deaths during trial or follow-up.
To me this is an odd exclusion criteria for a review specifically looking at mortality.
In fact, this one exclusion removed another 405 studies from the table for the review - almost half the studies that remained after the first round exclusions.
So this now left the researchers with 68 trials, and we know these studies had reported deaths during the trial since the researchers excluded any trials where subjects didn't die during the study or follow-up.
Of these 68 trials that remained, it's now important to understand if and how they differed.
First, 21 were "primary prevention" - that is they were conducted on "healthy" subjects with the trial seeking to establish a benefit to health; the remaining 47 trials were "secondary prevention" - that is the subjects included were diagnosed with disease and the trial was conducted to see if an intervention would slow progression of a disease or reduce risk of death from the disease.
In addition, differences between the studies included in the review help us understand the challenge the researchers set up in what can only be called a broad scope review. We absolutely have to consider all of this to understand just how the data may be confounded in the statistical analysis, so here are the dozen differences that popped out as I read the paper:
1. Primary versus secondary prevention trials
2. Single versus multiple combinations of antioxidants
3. Dose difference in antioxidants administered
4. Mode of administration differences
5. Differences between intervention versus placebo; versus no intervention
6. Absolute risk versus relative risk reporting
7. Duration differences for supplementation and follow-up
8. All cause mortality without cause of death examined in review
9. Synthetic antioxidants
10. Single isomer or full spectrum antioxidants
11. Collateral interventions in some trials
12. Measurement of oxidative stress with and without supplementation not included in review
As the Cochrane Handbook for Systematic Reviews cautions, "[t]he validity of very broadly defined reviews may be criticised for mixing apples and oranges, particularly when there is good biologic or sociological evidence to suggest that various formulations of an intervention behave very differently or that various definitions of the condition of interest are associated with markedly different effects of the intervention. It is fine to mix apples and oranges, if your question is about fruit, but not if your question is about vitamin C and you know that apples and oranges are different with respect to vitamin C."
When we look at the above list of potential confounding variables, it's clear the researchers had apples, oranges, pears, grapes, bananas and more to contend with in analyzing the main outcome endpoint - mortality.
To put it bluntly, the studies used are all over the place, looking at different antioxidants, at different doses, at different durations, with different lengths of follow-up, in different populations - ranging from folks who were incredibly healthy to people with different diseases, with different combinations administered in different trials.
But that's just the beginning.
Where things get really interesting is when we look at just how many various models of analysis worked out to determine risk compared with the warnings in the media.
Let's start by looking at what is called the pooled effect of all the randomized trials included in the review. This part of the analysis looked at all the studies included with all the varying confounders to assess risk.
The findings are interesting:
"The pooled effect of all supplements vs placebo or no intervention in all randomized trials was not significant (RR, 1.02; 95% CI, 0.98-1.06)."
That was step one - an overall analysis of all the data from the 68 trials included. Finding - no statistically significant increase in mortality.
The researchers then took the next step, and examined the effect of dose since the trials included low to mega doses of antioxidants. With this "univariate" (single item, dosage) analysis, they found:
"Univariate meta-regression analyses revealed significant influences of dose of beta carotene (RR, 1.004; 95% CI, 1.001-1.007; P = .012), dose of vitamin A (RR, 1.000006; 95% CI, 1.000002-1.000009; P = .003), dose of selenium (RR, 0.998; 95% CI, 0.997-0.999; P = .002), and bias-risk (RR, 1.16; 95% CI, 1.05-1.29; P = .004) on mortality. None of the other covariates (dose of vitamin C; dose of vitamin E; single or combined antioxidant regimen; duration of supplementation; and primary or secondary prevention) were significantly associated with mortality."
This is critically important to the findings in this meta-analysis because, setting aside "bias risk," the two statistically significant findings of increased mortality risk above regard vitamin A - as vitamin A and as beta-carotene.
A closer look at the studies included shows that the dosage was all over the place for vitamin A - from 2000IU per day to twenty-times the upper tolerable limit (UTL) at 200,000IU per day; and beta-carotene dose ranged from a low of 1.2mg per day to 50mg per day.Just as important to the finding that higher doses statistically increase risk, it is also important to note that there was no increased risk found for vitamin E, vitamin C; single or combined regimen; duration of supplementation; or primary or secondary prevention.
It is also notable that in this univariate analysis, selenium had a statistically significant protective effect by dose, with an RR 0.998 (CI = 0.997-0.999).
But before we get to thinking selenium may be protective, let's see what the researchers next step, multi-variate analysis, found:
"In multivariate meta-regression analysis including all covariates, dose of selenium was associated with significantly lower mortality (RR, 0.998; 95% CI, 0.997-0.999; P = .005) and low-bias risk trials with significantly higher mortality (RR, 1.16; 1.05-1.29; P = .005). None of the other covariates was significantly associated with mortality."
So, here we have a completely different finding - by dose there are increased risks for vitamin A and beta-carotene; a benefit for selenium; and no increased risk for the remaining antioxidants. Do a multi-variate regression and that intial finding of benefit for selenium holds when all studies are examined and disappears to become a statistically significant risk of death when only "low-bias risk" studies are analyzed.
Where before vitamin A and beta-carotene increased risk, now there is no statistical significance; and again, the other antioxidants had no increased risk associated with them.
Not content yet that they'd fully massaged the data every which way they could, they then segregated and analyzed by antioxidant, by single/combination administration, and by "bias risk" that they determined during their review of the trials to include/exclude.
The analysis of the full data from all "low-bias risk" studies revealed "...mortality was significantly increased in the supplemented group (RR, 1.05; 95% CI, 1.02-1.08)" while all "high-bias risk" data, taken together, revealed "...mortality was significantly decreased in the supplemented group (RR, 0.91; 95% CI, 0.83-1.00)"
Is your head spinning yet?
They then analyzed by single or combination administration of antioxidants.
Here come the mental gymnastics and data massaging needed to reach statistical significance:
Beta carotene
Beta carotene used singly significantly increased mortality. RR 1.06 (CI = 1.01-1.11)
This effect was not significant when combined with other supplements. RR 1.01 (CI = 0.94-1.08)
After exclusion of high-bias risk and selenium trials, beta carotene singly or combined significantly increased mortality. RR 1.07 (CI = 1.02-1.11)
Beta carotene by itself, bad; combined, nothing; exlude some study data and again it's bad.
Vitamin A
Vitamin A given singly did not significantly affect mortality. RR 1.18 (CI = 0.84-1.68)
Vitamin A given in combination with the other supplements did not significantly affect mortality. RR 1.03 (CI = 0.90-1.19)
After exclusion of high-bias risk and selenium trials, vitamin A singly or combined significantly increased mortality. RR 1.16 (CI = 1.10-1.24)
Vitamin A alone or in combination, nothing; exclude some study data, bad.
Vitamin E
Vitamin E given singly did not significantly affect mortality. RR 1.02 (CI = 0.98-1.05)
Vitamin E given in combination with the other supplements did not significantly affect mortality. RR 1.01 (CI = 0.95-1.06)
Vitamin E given singly in high (1000 IU) or low dose (greater than 1000 IU) did not significantly affect mortality. RR 1.07 (CI = 0.91-1.25)
After exclusion of high-bias risk and selenium trials, vitamin E given singly or combined significantly increased mortality. RR 1.04 (CI = 1.01-1.07)
Vitamin E alone, in combination, in high dose - nothing; exclude some study data, it's bad.
Vitamin C
Vitamin C given singly was without significant influence on mortality. RR 0.88 (CI = 0.32-2.42)
Vitamin C given in combination with the other supplements was without significant influence on mortality. RR 0.97 (CI = 0.88-1.07)
After exclusion of high-bias risk trials and selenium trials, vitamin C was without significant influence on mortality. RR 1.06 (CI = 0.94-1.20)
Vitamin C alone, in combination and when excluding some study data, nothing.
Selenium
Selenium given singly had no significant influence on mortality when analyzed separately. RR 0.85 (CI = 0.68-1.07)
Selenium given in combination with other antioxidant supplements had no significant influence on mortality when analyzed separately. RR 0.90 (CI = 0.81-1.01)
Selenium given singly or combined significantly decreased mortality when analyzed together. RR 0.91 (CI 0.84-0.99)
After exclusion of high-bias risk trials, selenium given singly or with other antioxidants had no significant influence on mortality. RR 0.90 (CI = 0.80-1.02)
Selenium alone or in combination, nothing; data analyzed together singly or in combination, benefit; exclude some data, nothing.
Interestingly the researchers didn't take the data even further - they didn't investigate causes of death, so no one knows if deaths were related to taking antioxidants, accidents, diagnosed disease or something else. They also did not analyze for potential outcome differences between primary prevention and secondary prevention trials - basically they didn't ask if being sick (secondary prevention trials) influenced mortality outcome differently than being healthy (primary prevention trials) while taking antioxidants.
They provide no context for absolute risk in either setting (primary or secondary prevention) and no context of absolute risk even with their different regression models.
Additionally, each of the above models used highlights the way data can be tweaked a bit here and there - in this case segregated by a subjective determination of "low-bias risk" and "high-bias risk" - to reach different findings that most assuredly will get the media in a tizzy to report the dangers of antioxidant supplements.
As WebMD reported (and pay attention to the wording here) "Use of the popular antioxidant supplements beta-carotene, vitamin E, or vitamin A slightly increases a person's risk of death, an overview of human studies shows. The study also shows no benefit -- and no harm -- for vitamin C supplements. Selenium supplements tended to very slightly reduce risk of death.A new, detailed analysis of human studies of beta-carotene, vitamin A, and vitamin E shows that people who take these antioxidant supplements don't live any longer than those who don't take them. In fact, those who take the supplements have an increased risk of death."
Note WebMD offers no qualification of what part of the analysis finding they refer to that reached statistical significance and then they interject subjectives not normally associated with statistically significant findings; specifically the part where they say "selenium supplements tended to very slightly reduce risk of death" - this is an interpretation. The only question is "was the finding statistically significant?", with the only answer being yes or no, not this "slightly" or "tended to" crap interjected to muddy the water for the consumer.
Now go back and look at the detailed numbers by regression model again.
The full weight of the data analysis in the review certainly does not warrant the quote from Kathleen Zelman, MPH, RD, LD, director of nutrition for WebMD, who said "This is a very comprehensive, to-be-respected analysis. This isn't just another study coming out. The bottom line is that antioxidant supplements are not a magic bullet for disease prevention. We hoped maybe they were, but they are not."
Interesting choice of words considering the review wasn't investigating only primary prevention trials; and that unless you cherry-pick through the data, increased risk of mortality was not a consistent finding throughout the review. While the headlines are pointing to the findings from the group of "low-bais risk" studies within the 68 that showed a relative 16% increase in mortality rates, the statistical difference in the studies analyzed comes down to this:
In a WebMD article about the study, Christian Gludd (one of the researchers) was quoted as saying "Anyone is welcome to criticize our research, but my question is, what is your evidence? I think the parties that want to sell or use these antioxidant supplements in the dosages used in these trials, they want [to see only] positive evidence that it works beneficially."
It's funny a researcher would assume criticism is driven by profit motive or desire to believe something is beneficial, and not flawed methodology, overwhelming scope, subjective exclusions or potentially subjective assignment of bias risk.
Here's my take on the review, with first a full disclosure - I do not sell or promote the use of antioxidant supplements; I do not have a financial interest in any supplement company; and I don't take any of the antioxidants included in the meta-analysis except what is included in my daily multi-vitamin. You can see I have no profit motive to criticize the study, nor do I have a blindspot desire to believe that I'm taking particular antioxidants reduce my risk of dying.
I'm interested in the data and the methodology used to reach the conclusion that the researchers did not "find convincing evidence that antioxidant supplements have beneficial effects on mortality. Even more, beta carotene, vitamin A, and vitamin E seem to increase the risk of death. Further randomized trials are needed to establish the effects of vitamin C and selenium."
The stated objective to undertake a meta-analysis of antioxidants was "to analyze the effects of antioxidant supplements (beta carotene, vitamins A and E, vitamin C [ascorbic acid], and selenium) on all-cause mortality of adults included in primary and secondary prevention trials."
Interestlingly, we learn upon reading the full-text that the researchers specifically excluded studies that reported no deaths during a trial period or follow-up. A meta-analysis that seeks to establish effects on mortality but excludes studies with no reported deaths from the pool of data to be analyzed? Hmmm...
Yes, this is the first interesting thing that popped up when I read the paper and learned the researchers conducted an intial search across a number of databases and found 16,111 references that hit their search criteria. Of course many of these were duplicate references (14,003), leaving 2,108 references to review.
The next review led to the exclusion of another 907 references because they included patients with cancer; involved acute and infectious disease; involved infants or children; or involved pregnant or lactating women. These understandable exclusions then left the researchers with 1,201 references (815 trials) to review for inclusion or exclusion from the analysis.
So the researchers moved on and started to excluded based on criteria few can or will agrue with - the trial didn't meet inclusion criteria established for the review; it was not randomized; data was insufficient for review purposes; or a trial was still ongoing.
But then we come to a curious reason for exclusion - a study did not have any deaths during trial or follow-up.
To me this is an odd exclusion criteria for a review specifically looking at mortality.
In fact, this one exclusion removed another 405 studies from the table for the review - almost half the studies that remained after the first round exclusions.
So this now left the researchers with 68 trials, and we know these studies had reported deaths during the trial since the researchers excluded any trials where subjects didn't die during the study or follow-up.
Of these 68 trials that remained, it's now important to understand if and how they differed.
First, 21 were "primary prevention" - that is they were conducted on "healthy" subjects with the trial seeking to establish a benefit to health; the remaining 47 trials were "secondary prevention" - that is the subjects included were diagnosed with disease and the trial was conducted to see if an intervention would slow progression of a disease or reduce risk of death from the disease.
In addition, differences between the studies included in the review help us understand the challenge the researchers set up in what can only be called a broad scope review. We absolutely have to consider all of this to understand just how the data may be confounded in the statistical analysis, so here are the dozen differences that popped out as I read the paper:
1. Primary versus secondary prevention trials
2. Single versus multiple combinations of antioxidants
3. Dose difference in antioxidants administered
4. Mode of administration differences
5. Differences between intervention versus placebo; versus no intervention
6. Absolute risk versus relative risk reporting
7. Duration differences for supplementation and follow-up
8. All cause mortality without cause of death examined in review
9. Synthetic antioxidants
10. Single isomer or full spectrum antioxidants
11. Collateral interventions in some trials
12. Measurement of oxidative stress with and without supplementation not included in review
As the Cochrane Handbook for Systematic Reviews cautions, "[t]he validity of very broadly defined reviews may be criticised for mixing apples and oranges, particularly when there is good biologic or sociological evidence to suggest that various formulations of an intervention behave very differently or that various definitions of the condition of interest are associated with markedly different effects of the intervention. It is fine to mix apples and oranges, if your question is about fruit, but not if your question is about vitamin C and you know that apples and oranges are different with respect to vitamin C."
When we look at the above list of potential confounding variables, it's clear the researchers had apples, oranges, pears, grapes, bananas and more to contend with in analyzing the main outcome endpoint - mortality.
To put it bluntly, the studies used are all over the place, looking at different antioxidants, at different doses, at different durations, with different lengths of follow-up, in different populations - ranging from folks who were incredibly healthy to people with different diseases, with different combinations administered in different trials.
But that's just the beginning.
Where things get really interesting is when we look at just how many various models of analysis worked out to determine risk compared with the warnings in the media.
Let's start by looking at what is called the pooled effect of all the randomized trials included in the review. This part of the analysis looked at all the studies included with all the varying confounders to assess risk.
The findings are interesting:
"The pooled effect of all supplements vs placebo or no intervention in all randomized trials was not significant (RR, 1.02; 95% CI, 0.98-1.06)."
That was step one - an overall analysis of all the data from the 68 trials included. Finding - no statistically significant increase in mortality.
The researchers then took the next step, and examined the effect of dose since the trials included low to mega doses of antioxidants. With this "univariate" (single item, dosage) analysis, they found:
"Univariate meta-regression analyses revealed significant influences of dose of beta carotene (RR, 1.004; 95% CI, 1.001-1.007; P = .012), dose of vitamin A (RR, 1.000006; 95% CI, 1.000002-1.000009; P = .003), dose of selenium (RR, 0.998; 95% CI, 0.997-0.999; P = .002), and bias-risk (RR, 1.16; 95% CI, 1.05-1.29; P = .004) on mortality. None of the other covariates (dose of vitamin C; dose of vitamin E; single or combined antioxidant regimen; duration of supplementation; and primary or secondary prevention) were significantly associated with mortality."
This is critically important to the findings in this meta-analysis because, setting aside "bias risk," the two statistically significant findings of increased mortality risk above regard vitamin A - as vitamin A and as beta-carotene.
A closer look at the studies included shows that the dosage was all over the place for vitamin A - from 2000IU per day to twenty-times the upper tolerable limit (UTL) at 200,000IU per day; and beta-carotene dose ranged from a low of 1.2mg per day to 50mg per day.Just as important to the finding that higher doses statistically increase risk, it is also important to note that there was no increased risk found for vitamin E, vitamin C; single or combined regimen; duration of supplementation; or primary or secondary prevention.
It is also notable that in this univariate analysis, selenium had a statistically significant protective effect by dose, with an RR 0.998 (CI = 0.997-0.999).
But before we get to thinking selenium may be protective, let's see what the researchers next step, multi-variate analysis, found:
"In multivariate meta-regression analysis including all covariates, dose of selenium was associated with significantly lower mortality (RR, 0.998; 95% CI, 0.997-0.999; P = .005) and low-bias risk trials with significantly higher mortality (RR, 1.16; 1.05-1.29; P = .005). None of the other covariates was significantly associated with mortality."
So, here we have a completely different finding - by dose there are increased risks for vitamin A and beta-carotene; a benefit for selenium; and no increased risk for the remaining antioxidants. Do a multi-variate regression and that intial finding of benefit for selenium holds when all studies are examined and disappears to become a statistically significant risk of death when only "low-bias risk" studies are analyzed.
Where before vitamin A and beta-carotene increased risk, now there is no statistical significance; and again, the other antioxidants had no increased risk associated with them.
Not content yet that they'd fully massaged the data every which way they could, they then segregated and analyzed by antioxidant, by single/combination administration, and by "bias risk" that they determined during their review of the trials to include/exclude.
The analysis of the full data from all "low-bias risk" studies revealed "...mortality was significantly increased in the supplemented group (RR, 1.05; 95% CI, 1.02-1.08)" while all "high-bias risk" data, taken together, revealed "...mortality was significantly decreased in the supplemented group (RR, 0.91; 95% CI, 0.83-1.00)"
Is your head spinning yet?
They then analyzed by single or combination administration of antioxidants.
Here come the mental gymnastics and data massaging needed to reach statistical significance:
Beta carotene
Beta carotene used singly significantly increased mortality. RR 1.06 (CI = 1.01-1.11)
This effect was not significant when combined with other supplements. RR 1.01 (CI = 0.94-1.08)
After exclusion of high-bias risk and selenium trials, beta carotene singly or combined significantly increased mortality. RR 1.07 (CI = 1.02-1.11)
Beta carotene by itself, bad; combined, nothing; exlude some study data and again it's bad.
Vitamin A
Vitamin A given singly did not significantly affect mortality. RR 1.18 (CI = 0.84-1.68)
Vitamin A given in combination with the other supplements did not significantly affect mortality. RR 1.03 (CI = 0.90-1.19)
After exclusion of high-bias risk and selenium trials, vitamin A singly or combined significantly increased mortality. RR 1.16 (CI = 1.10-1.24)
Vitamin A alone or in combination, nothing; exclude some study data, bad.
Vitamin E
Vitamin E given singly did not significantly affect mortality. RR 1.02 (CI = 0.98-1.05)
Vitamin E given in combination with the other supplements did not significantly affect mortality. RR 1.01 (CI = 0.95-1.06)
Vitamin E given singly in high (1000 IU) or low dose (greater than 1000 IU) did not significantly affect mortality. RR 1.07 (CI = 0.91-1.25)
After exclusion of high-bias risk and selenium trials, vitamin E given singly or combined significantly increased mortality. RR 1.04 (CI = 1.01-1.07)
Vitamin E alone, in combination, in high dose - nothing; exclude some study data, it's bad.
Vitamin C
Vitamin C given singly was without significant influence on mortality. RR 0.88 (CI = 0.32-2.42)
Vitamin C given in combination with the other supplements was without significant influence on mortality. RR 0.97 (CI = 0.88-1.07)
After exclusion of high-bias risk trials and selenium trials, vitamin C was without significant influence on mortality. RR 1.06 (CI = 0.94-1.20)
Vitamin C alone, in combination and when excluding some study data, nothing.
Selenium
Selenium given singly had no significant influence on mortality when analyzed separately. RR 0.85 (CI = 0.68-1.07)
Selenium given in combination with other antioxidant supplements had no significant influence on mortality when analyzed separately. RR 0.90 (CI = 0.81-1.01)
Selenium given singly or combined significantly decreased mortality when analyzed together. RR 0.91 (CI 0.84-0.99)
After exclusion of high-bias risk trials, selenium given singly or with other antioxidants had no significant influence on mortality. RR 0.90 (CI = 0.80-1.02)
Selenium alone or in combination, nothing; data analyzed together singly or in combination, benefit; exclude some data, nothing.
Interestingly the researchers didn't take the data even further - they didn't investigate causes of death, so no one knows if deaths were related to taking antioxidants, accidents, diagnosed disease or something else. They also did not analyze for potential outcome differences between primary prevention and secondary prevention trials - basically they didn't ask if being sick (secondary prevention trials) influenced mortality outcome differently than being healthy (primary prevention trials) while taking antioxidants.
They provide no context for absolute risk in either setting (primary or secondary prevention) and no context of absolute risk even with their different regression models.
Additionally, each of the above models used highlights the way data can be tweaked a bit here and there - in this case segregated by a subjective determination of "low-bias risk" and "high-bias risk" - to reach different findings that most assuredly will get the media in a tizzy to report the dangers of antioxidant supplements.
As WebMD reported (and pay attention to the wording here) "Use of the popular antioxidant supplements beta-carotene, vitamin E, or vitamin A slightly increases a person's risk of death, an overview of human studies shows. The study also shows no benefit -- and no harm -- for vitamin C supplements. Selenium supplements tended to very slightly reduce risk of death.A new, detailed analysis of human studies of beta-carotene, vitamin A, and vitamin E shows that people who take these antioxidant supplements don't live any longer than those who don't take them. In fact, those who take the supplements have an increased risk of death."
Note WebMD offers no qualification of what part of the analysis finding they refer to that reached statistical significance and then they interject subjectives not normally associated with statistically significant findings; specifically the part where they say "selenium supplements tended to very slightly reduce risk of death" - this is an interpretation. The only question is "was the finding statistically significant?", with the only answer being yes or no, not this "slightly" or "tended to" crap interjected to muddy the water for the consumer.
Now go back and look at the detailed numbers by regression model again.
The full weight of the data analysis in the review certainly does not warrant the quote from Kathleen Zelman, MPH, RD, LD, director of nutrition for WebMD, who said "This is a very comprehensive, to-be-respected analysis. This isn't just another study coming out. The bottom line is that antioxidant supplements are not a magic bullet for disease prevention. We hoped maybe they were, but they are not."
Interesting choice of words considering the review wasn't investigating only primary prevention trials; and that unless you cherry-pick through the data, increased risk of mortality was not a consistent finding throughout the review. While the headlines are pointing to the findings from the group of "low-bais risk" studies within the 68 that showed a relative 16% increase in mortality rates, the statistical difference in the studies analyzed comes down to this:
- there were 15,366 deaths among 99,095 subjects who took antioxidants (15.50%)
- there were 9,131 deaths among 81,343 subjects who did not take antioxidant supplements (11.22%),
- the difference in hard numbers is 4.28% (not quite the frightening 16% relative number the media is headlining)
- the difference did not include any investigation for cause of death
- the studies included in the meta-analysis only included studies in which subjects did die
The problem in a meta-analysis like this is that there are so many pitfalls (identified above) that the researchers do discuss in their paper, but not when they're quoted in the media. It's unfortunate that these researchers are not specific in their quotes in the media, nor doing much to point out all was not "risky" with taking antioxidant supplements.
This meta-analysis had great potential, but was rendered pretty meaningless with all the various regression analyses done and the fact that so much depended on excluding data while mixing the apples-to-oranges study types of primary prevention and secondary prevention.
Thursday, March 01, 2007
Making the Rounds
Yes, life here is a bit busy...but I'd like to point out some interesting reads:
Mike Eades details the findings from Methionine and Vitamin B6 Intake and Risk of Pancreatic Cancer: A Prospective Study of Swedish Women and Men published in Gastroenterology.
Men who consumed the most methionine had under a third the cases of pancreatic cancer as compared to those who are the least. Women with the highest methionine intake had about half the pancreatic cancer rate as those with the lowest intakes. Men and women eating the most methionine, considered together, had only 44 percent of the rate of pancreatic cancer as compared to men and women with the least dietary intake.
Read More...
**********
The International Journal of Obesity published research that found a Blood protein tied to obesity, diabetes in Native Americans, Mexicans - Science Blog provides some insight into the findings.
Lead investigator Gary Nelsestuen, a professor in the College of Biological Sciences’ department of biochemistry, said the abnormal protein may promote metabolic efficiency and storage of body fat when food is abundant. This could have provided a survival advantage to American Indians in the past when food was scarce. The discovery can be used to identify those who are at risk for diabetes and to guide diet and lifestyle choices to prevent diabetes.
Read More...
**********
The Local in Sweden reported that 'Adult diabetes' hits obese Swedish children
Young children suffering with Type-2, or adult-onset, diabetes have been discovered in Sweden for the first time. "We are already seeing the early signs of adult-onset diabetes in five year olds," said professor Claude Marcus, head of the National Centre for Child Obesity in Huddinge, to Svenska Dagbladet. "That means reduced sensitivity to insulin and evident effects on the blood vessels. It's very serious because Type-2 diabetes is an illness which affects the whole system."
This form of diabetes, which is non-insulin-dependent, is becoming increasingly widespread in developed countries. Some 1.2 percent of children at the centre in Huddinge have been shown to have Type-2 diabetes. The first case of adult-onset diabetes in a Swedish teenager was recorded just two years ago.
-----> You may recall Swedish researchers recently found higher incidence of insulin resistance and pre-diabetes in four-year old children consuming a low-fat diet.
**********
Researchers from Harvard School of Public Health published findings that low-fat dairy consumption increased risk of infertility; consumption of whole milk dairy reduced risk.
The scientists, whose work is published in Human Reproduction, say that the total intake of dairy foods shows no link with anovulatory infertility. But when high-fat and low-fat dairy foods were considered separately, a difference emerged. Women consuming at least five portions week of low-fat foods had a higher than average risk of being infertile. If women ate two or more servings of low-fat dairy foods a day, they increased their risk of ovulation-related infertility by more than four fifths (85 per cent) compared with women who ate less than one serving of low-fat dairy food a week.
Read More...
**********
Early next week I should be back!
Mike Eades details the findings from Methionine and Vitamin B6 Intake and Risk of Pancreatic Cancer: A Prospective Study of Swedish Women and Men published in Gastroenterology.
Men who consumed the most methionine had under a third the cases of pancreatic cancer as compared to those who are the least. Women with the highest methionine intake had about half the pancreatic cancer rate as those with the lowest intakes. Men and women eating the most methionine, considered together, had only 44 percent of the rate of pancreatic cancer as compared to men and women with the least dietary intake.
Read More...
**********
The International Journal of Obesity published research that found a Blood protein tied to obesity, diabetes in Native Americans, Mexicans - Science Blog provides some insight into the findings.
Lead investigator Gary Nelsestuen, a professor in the College of Biological Sciences’ department of biochemistry, said the abnormal protein may promote metabolic efficiency and storage of body fat when food is abundant. This could have provided a survival advantage to American Indians in the past when food was scarce. The discovery can be used to identify those who are at risk for diabetes and to guide diet and lifestyle choices to prevent diabetes.
Read More...
**********
The Local in Sweden reported that 'Adult diabetes' hits obese Swedish children
Young children suffering with Type-2, or adult-onset, diabetes have been discovered in Sweden for the first time. "We are already seeing the early signs of adult-onset diabetes in five year olds," said professor Claude Marcus, head of the National Centre for Child Obesity in Huddinge, to Svenska Dagbladet. "That means reduced sensitivity to insulin and evident effects on the blood vessels. It's very serious because Type-2 diabetes is an illness which affects the whole system."
This form of diabetes, which is non-insulin-dependent, is becoming increasingly widespread in developed countries. Some 1.2 percent of children at the centre in Huddinge have been shown to have Type-2 diabetes. The first case of adult-onset diabetes in a Swedish teenager was recorded just two years ago.
-----> You may recall Swedish researchers recently found higher incidence of insulin resistance and pre-diabetes in four-year old children consuming a low-fat diet.
**********
Researchers from Harvard School of Public Health published findings that low-fat dairy consumption increased risk of infertility; consumption of whole milk dairy reduced risk.
The scientists, whose work is published in Human Reproduction, say that the total intake of dairy foods shows no link with anovulatory infertility. But when high-fat and low-fat dairy foods were considered separately, a difference emerged. Women consuming at least five portions week of low-fat foods had a higher than average risk of being infertile. If women ate two or more servings of low-fat dairy foods a day, they increased their risk of ovulation-related infertility by more than four fifths (85 per cent) compared with women who ate less than one serving of low-fat dairy food a week.
Read More...
**********
Early next week I should be back!
Tuesday, February 27, 2007
It's Still a Donut
In the US: Krispy Kreme unveils whole-wheat doughnut
Krispy Kreme Doughnuts Inc., still recovering from the low-carb diet craze that starved the company's earnings, unveiled a whole-wheat doughnut Monday. The 100 percent whole-wheat doughnut - with 180 calories - has a caramel flavoring and is covered with the doughnut maker's original glaze.
This is what happens when "whole grain" is "healthy"...
In the UK: Public want food 'traffic lights'
...simple red, amber and green guide to nutrition.
Under the scheme, cheese gets a red light; avocados get a red light; and a lot of boxed foods (read processed, refined foods) get green lights. One more example of a government pushing processed foods on the public.
Krispy Kreme Doughnuts Inc., still recovering from the low-carb diet craze that starved the company's earnings, unveiled a whole-wheat doughnut Monday. The 100 percent whole-wheat doughnut - with 180 calories - has a caramel flavoring and is covered with the doughnut maker's original glaze.
This is what happens when "whole grain" is "healthy"...
In the UK: Public want food 'traffic lights'
...simple red, amber and green guide to nutrition.
Under the scheme, cheese gets a red light; avocados get a red light; and a lot of boxed foods (read processed, refined foods) get green lights. One more example of a government pushing processed foods on the public.
Wednesday, February 21, 2007
Women Beware: Heart Disease & Stroke Risk
Fox News Nine, out of the Twin Cities headlined 90 Percent of Women at Risk for Heart Disease, Stroke on the heels of the American Heart Association release of updated guidelines for women at risk for heart disease and stroke.
The article opens with an ominous warning, "Michelle Bartell, 43, looks too young and too healthy to have had two heart attacks, and that is exactly the point of a new warning. It happened to her and it will happen to countless others. A new American Heart Association study shows 9 out of 10 women are at risk for heart disease or stroke."
Just nine out of ten?
Truth be told every last person is "at risk" for heart disease or stroke, just as every last person is going to die, life itself comes with a sure "risk" of death - we just don't know when.
The scare tactic headlines get your attention, but do little to help our understanding of real risk, over a lifetime, for women when it comes to heart disease and stroke.
Sadly the updated guidelines are little more than a "how to" manual to initiate drug therapy in every woman in America, as early as age 20 - the age they call for an initial risk assessement and start of intervention and treatment.
Even the recommendations, Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women - 2007 Update, published in Circulation, state that, "...nearly all women are at risk for CVD, which underscores the importance of a heart-healthy lifestyle."
Is it any wonder when you consider the criteria to be found "at risk" and therefore in need of intervention?
Have just one of the following in your initial risk assessment:
The article opens with an ominous warning, "Michelle Bartell, 43, looks too young and too healthy to have had two heart attacks, and that is exactly the point of a new warning. It happened to her and it will happen to countless others. A new American Heart Association study shows 9 out of 10 women are at risk for heart disease or stroke."
Just nine out of ten?
Truth be told every last person is "at risk" for heart disease or stroke, just as every last person is going to die, life itself comes with a sure "risk" of death - we just don't know when.
The scare tactic headlines get your attention, but do little to help our understanding of real risk, over a lifetime, for women when it comes to heart disease and stroke.
Sadly the updated guidelines are little more than a "how to" manual to initiate drug therapy in every woman in America, as early as age 20 - the age they call for an initial risk assessement and start of intervention and treatment.
Even the recommendations, Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women - 2007 Update, published in Circulation, state that, "...nearly all women are at risk for CVD, which underscores the importance of a heart-healthy lifestyle."
Is it any wonder when you consider the criteria to be found "at risk" and therefore in need of intervention?
Have just one of the following in your initial risk assessment:
- Cigarette smoking
- Poor Diet
- Physical Inactivity
- Obesity, especially central adiposity
- Family History of premature CVD (in a male or female relative)
- Hypertension
- Dyslipidemia
- Evidence of subclincal vascular disease
- Metabolic Syndrome
- Poor exercise capacity on treadmill test and/or abnormal heart rate recovery after stopping exercise
Basically no woman will be found who are not at risk if we look at the list above, and then also consider what qualifies as "optimal risk" to remove one from the "at risk" category - a Framingham Global Risk score of less than 10% AND a "healthy lifestyle" AND no risk factors above.
So then we're off and running straight into the lifestyle modifications and intensive medical intervention.
Ah, yes, the lifestyle intervention - it pales in comparison to the intensive pharmacological intervention to be intiated as early as age 20; the treatment algorithm includes diet and exercise, underscored with a true lifestyle change - taking an assortment of drugs for the rest of your life!
This is "prevention"?
This is "risk reduction"?
This is the AHA "solution" to cardiovascular disease in women?
They have the gall to call this "evidence based"?
Just like the recent ADA update for diabetes, we find the AHA is now on the bandwagon to drug America - women in America - for the rest of our lives.
Not only that, they're also intent on getting public policy in line with their insanity, "Population-wide strategies are necessary to combat the pandemic of CVD in women, because individually tailored interventions are likely insufficient to maximally prevent and control CVD. Pulic policy as an intervention to reduce gender-based disparities in CVD preventive care and improve cardiovascular outcomes among women must become an integral strategy to reduce the global burden of CVD."
The media is taking this just as expected, as if it were the best thing next to sliced bread - in the WebMD section, heartwire, this was called a "bold prescription for the prevention of CVD;" and "with the goal to widen the window of opportunity for women to fight their number-one killer..."
A bold prescription? Interesting use of words there since it truly is a bold way to make every woman - healthy or otherwise - a target candidate for lifelong dependancy on prescription drugs!
"All women 20 years and older need initial CVD risk evaluation (medical history, physical exam, fasting glucose, lipids) and Framingham risk assessment; women with CVD need depression screening."
The dietary recommendations are a guaranteed recipe to induce every symptom needed to score as "at risk" of cardiovascular disease - a low-fat diet, limiting meats and animal foods, that is rich with carbohydrates and completely fails to meet essential nutrients.
The recommendation reads, "[w]omen should consume a diet rich in fruits and vegetables; choose whole grain, high-fiber foods; consume fish, especially oily fish at least twice a week; limit intake of saturated fat to less than 10% of energy, and if possible, less than 7%; cholesterol to less than 300 mg/day; alcohol intake to no more than 1 drink per day and sodium intake to less than 2.3g/day (approximately 1 tsp salt). Consumption of trans-fatty acids shoudl be as low as possible (eg, less than 1% of energy)."
ahem....this is "evidence based"?
Within the statement we find "the summary of evidence used by the expert panel can be obtained online as a Data Supplement at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.107.181546/DC1.
Oddly, on this page referenced as the one to look to for additional information on the data presented in the statement - Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women: 2007 Update - there isn't any file to read to evaluate the so-called evidence used for the development of the dietary recommendations.
Wonder why?
It's because there are no studies that can be used to support the dietary recommendations in the statement!
At the end of the paper we find "Appendix - Bibliography by Topic" and within that section, "Dietary Modification" with a laundry list of studies supposedly supporting the recommendations in the paper, that is followed by "Dietary Modification Meta-Analysis" with one citation as supportive.
This gives any reader the impression that there are mountains of data to support the recommendations.
How about we take a look?
- Abbott et al investigated magnesium in the diet and the risk of cardiovascular disease.
Nope, not evidence to support a low-fat diet. - Willett et al investigated the relationship between calcium intake from diet or supplements and risk of ischemic heart disease in MEN.
Nope, not evidence to support a low-fat diet. - Bazzano et al reported results from a national survey of fiber intake and reduced risk of heart disease.
Nope, not evidence to support a low-fat diet. - Boniface et al reported on 16-year coronary disease mortality in Britain and fat intake.
Intriguing , but nope, not evidence to support a low-fat diet. - Dauchet et al looked at fruit and vegetable consumption.
Nope, not evidence to support a low-fat diet. - Ellingsen et al investigated smoking and dietary advise in MEN.
Nope, not evidence to support a low-fat diet. - Erikka et al looked at vitamin K levels as a potential marker for heart disease, not stroke, in women.
Nope, not evidence to support a low-fat diet. - Howard et al - the Women's Health Initiative null findings from last year are here?
Nope, not evidence to support a low-fat diet. - Hu et all appears in three separate citations - one for overall dietary pattern in MEN, one for alpha-linolenic acid and one for dietary protein.
Nope, not evidence to support a low-fat diet. - Jensen et al was on whole grain intakes
Nope, not evidence to support a low-fat diet. - Knoops looked at the Mediterranean dietary pattern and risk
Nope, not evidence to support a low-fat diet. - Kromhout et al looked at alcohol, fish, fiber and antioxidant vitamins and risk - funny, but the title includes that these "do not explain population differences in coronary heart disease mortality"
Nope, not evidence to support a low-fat diet. - Lee et al looked at vitamin C supplementation and risk
Nope, not evidence to support a low-fat diet. - Liu et al at fruit and vegetable intake, and in a second citation at breakfast cereal intake in MEN
Nope, not evidence to support a low-fat diet. - McCullough et al investigated adhering to the dietary guidelines and risk
Nope, not evidence to support a low-fat diet. - Mukamal et al looked at coffee consumption
Nope, not evidence to support a low-fat diet. - Nestel et al was a drug trial
Nope, not evidence to support a low-fat diet. - Osler et al was a study to look at dietary scoring used in studies
Nope, not evidence to support a low-fat diet. - Sesso et al looked at flavonoid intakes and risk
Nope, not evidence to support a low-fat diet. - Steffen et al looked at whole and refined grains, fuits and vegetables to assess risk
Nope, not evidence to support a low-fat diet. - Trichopoulou et al is cited twice - both studies looking at survival among patients with CHD and the mediterranean diet in Greece
Nope, not evidence to support a low-fat diet. - van der Schouw et al looked at phytoestrogens from diet and risk
Nope, not evidence to support a low-fat diet. - Yano et all looked at coffee and alcohol related to risk
Nope, not evidence to support a low-fat diet.
Notice a pattern here?
How about the Meta-Analysis citation, perhaps that one is convincing enough?
Huxley et al, looked at studies to see the effects of dietary flavonol intake and CHD mortality - and once again, nope, not evidence to support a low-fat diet.
Twenty-nine references cited as supportive evidence for the low-fat diet recommendation within the document - not one actually shows such a diet will prevent cardiovascular disease or stroke in women.
Yet to any casual reader, this list in impressive and is assumed to be support for the recommendations within the document; that's because it's assumed citations are used properly, in context to what's written and because they support of statements.
It's also assumed those writing have the integrity to utilize the evidence accurately and truthfully.But after looking at the citations it's clear this is not the case.
We have before us "evidence-based recommendations" without foundation in the science; without support in the data; being foisted upon us to follow without question because the AHA says it's evidence-based.
As a woman, I am highly offended by these recommendations - they're nothing more than a sure-fire way to make sure every woman in America is classified "at risk" so that intensive intervention and therapy may be initated to "save her" from herself and her poor diet, inactivity and get her on her lifelong pharmaceutical program early.
Tuesday, February 20, 2007
Scare Tactics to Bolster Grain Consumption
Be afraid, very afraid - if you don't eat plenty of folic acid enriched grain products each day, you'll have children with birth defects.
That's the explicit message hot off the press, Could low-carb diets lead to birth defects?
"Blood levels of folate in young women are dropping, a disturbing development that could lead to increased birth defects and may be due to low-carb diets or the popularity of unfortified whole-grain breads."
[...]
"Diet trends may have been be another factor, said Dr. Joseph Mulinare, a CDC epidemiologist who was the study's lead author.
He noted that in 1998, the Food and Drug Administration began requiring that folic acid be added to breads, cereals and other products that use enriched flour. Whole-grain breads were not under that mandate because they already contain some folate.
Low-carb diets increased in popularity during the early 2000s. Women who avoided flour and bread products because of their carbohydrates may have also taken in less folic acid, Mulinare said.Eating certain foods also helps, especially breads, cereals and other products containing enriched flour."
If you could see my face right now, you'd notice a very big eye roll as I shake my head at the insanity of this. Never mind that the survey didn't actually look at the diet of those whose blood samples were found low in folate; never mind this is simply one more excuse to push eating processed grains; and never mind real whole food - vegetables, beans, fruits and some cuts of meat are exceptional foods to meet folate requirements.
One only needs to look at foods routinely consumed on a low-carbohydrate diet and compare them to the "miracle" folic-acid enriched grain products promoted in the above article to see the sham of this scare tactic designed to make you eat more processed grains!
World's Healthiest Foods provides a comprehensive list of foods "rich" with folate - notice the top ten are NOT whole grains or enriched grains, but are real whole foods; in fact, in the longer list toward the bottom of the page, not one of the "excellent sources" are a grain or grain product, not one of the "very good" or even "good" sources are either - they're ALL whole foods - meats, fruits, nuts, vegetables, roots, mushrooms, beans - with almost all of them not only allowed, but encouraged and mandatory in a carbohydrate restricted diet.
On the other hand, the Partnership for Essential Nutrition, an organization that is highly critical of carbohydrate restricted diets includes these foods as good choices to eat:
Bread, enriched white 1 slice 27
Breakfast cereals 1 ounce (approx 1 cup) Approx. 100-400. Check the label
Pasta, enriched ½ cup 53
Rice, white enriched ½ cup 54
No thanks, with just 2 cups romaine, 1 cup cooked spinach I'll easily meet the 400mcg requirement without even specifically trying - if I add in tomatoes, cucumbers, some chickpeas and some more veggies and I can easily double that with real whole food that also come complete with an abundance of other essential nutrients without any added sugars, vegetable oils or processed grains!
UPDATE 02/21/07: A reader emailed with more foods as listed in the USDA Nutrient Database:
Liver – chicken – pan fried per 100mg: Folate, food mcg 560
Chicken liver pate: Folate, food mcg 321
compared with the "wonder" food:
Whole-wheat bread per 100mg: Folate, food mcg 50
That's the explicit message hot off the press, Could low-carb diets lead to birth defects?
"Blood levels of folate in young women are dropping, a disturbing development that could lead to increased birth defects and may be due to low-carb diets or the popularity of unfortified whole-grain breads."
[...]
"Diet trends may have been be another factor, said Dr. Joseph Mulinare, a CDC epidemiologist who was the study's lead author.
He noted that in 1998, the Food and Drug Administration began requiring that folic acid be added to breads, cereals and other products that use enriched flour. Whole-grain breads were not under that mandate because they already contain some folate.
Low-carb diets increased in popularity during the early 2000s. Women who avoided flour and bread products because of their carbohydrates may have also taken in less folic acid, Mulinare said.Eating certain foods also helps, especially breads, cereals and other products containing enriched flour."
If you could see my face right now, you'd notice a very big eye roll as I shake my head at the insanity of this. Never mind that the survey didn't actually look at the diet of those whose blood samples were found low in folate; never mind this is simply one more excuse to push eating processed grains; and never mind real whole food - vegetables, beans, fruits and some cuts of meat are exceptional foods to meet folate requirements.
One only needs to look at foods routinely consumed on a low-carbohydrate diet and compare them to the "miracle" folic-acid enriched grain products promoted in the above article to see the sham of this scare tactic designed to make you eat more processed grains!
World's Healthiest Foods provides a comprehensive list of foods "rich" with folate - notice the top ten are NOT whole grains or enriched grains, but are real whole foods; in fact, in the longer list toward the bottom of the page, not one of the "excellent sources" are a grain or grain product, not one of the "very good" or even "good" sources are either - they're ALL whole foods - meats, fruits, nuts, vegetables, roots, mushrooms, beans - with almost all of them not only allowed, but encouraged and mandatory in a carbohydrate restricted diet.
On the other hand, the Partnership for Essential Nutrition, an organization that is highly critical of carbohydrate restricted diets includes these foods as good choices to eat:
Bread, enriched white 1 slice 27
Breakfast cereals 1 ounce (approx 1 cup) Approx. 100-400. Check the label
Pasta, enriched ½ cup 53
Rice, white enriched ½ cup 54
No thanks, with just 2 cups romaine, 1 cup cooked spinach I'll easily meet the 400mcg requirement without even specifically trying - if I add in tomatoes, cucumbers, some chickpeas and some more veggies and I can easily double that with real whole food that also come complete with an abundance of other essential nutrients without any added sugars, vegetable oils or processed grains!
UPDATE 02/21/07: A reader emailed with more foods as listed in the USDA Nutrient Database:
Liver – chicken – pan fried per 100mg: Folate, food mcg 560
Chicken liver pate: Folate, food mcg 321
compared with the "wonder" food:
Whole-wheat bread per 100mg: Folate, food mcg 50
The Big Fat Joke of our Dietary Recommendations in the US
I've received a number of interesting emails the last few days; asking everything from "where are you going with this?" to "that's not a plant-based diet, and most definitely not a vegetarian diet, so what's your point?"
Patience grasshopper, patience!
My point is this - over the last thirty-odd years we've been repeatedly told to limit meat, consume fewer eggs, choose low-fat dairy, use vegetable oils instead of animal fats for cooking, take the skin off our chicken and eat more chicken and fish; advised to have a few "vegetarian nights" for dinner; told to spread margarine, not butter, on our bread; pressured restaurants and fast food outlets to use partially hydrogenated oils to reduce saturated fat; reminded to eat more grains for fiber; and, at the end of the day, bought - hook line and sinker - the message that how we used to eat was bad, bad, bad and a diet with more plant-based calories was better for us.
Slowly but surely we have modified our diet and more calories now, than ever before, 73% in fact, come from plant-based sources; and we've grown obese, diabetic and disabled with increased incidence of degenerative disease. We're also a nation slowly becoming dependent on prescription medications to relieve the symptoms of our poor dietary habits while we're repeatedly told our health would improve if we just ate less meat, eggs, butter, saturated fat, and cholesterol.
Folks, these are not the problems in our diet.
Oh, we have modified our calories to consume more plant-based sources of calories, but we're not eating closer to a vegetarian diet (nor do I think we have to).
What we're eating is more and more processed foods with the majority of calories coming from three nutritionally poor, calorie dense sources - added sugars, added vegetable oils and refined grain products.
In fact, these three things - added sugars, added vegetable oils and processed grains - made up more than 60% of our daily calories in 2000. By 2004, little changed over four years, these three items still provided more than 60% of our daily calories.
These three items, that are providing most of our calories each day, aren't really "foods" but are better thought of as "ingredients" since no one will readily sit with a sugar-bowl and eat spoon after spoon of sugar, take slugs from a bottle of corn syrup, chow down over a big bowl of flour, or pour a nice big glass of soybean oil to sip at the end of the day.
These ingredients however litter our food supply and are found in virtually all processed foods - those you'll likely find in a box, jar, can or bag; those with a nutrition label on them detailing the fat, carbohydrate, fiber and protein, followed by the ingredients; frozen, refrigerated or stable on the shelf, these foods contain the ingredients that provide the majority of our calories each day.
As the past couple of posts highlighted, the devil is in the details - it's not what you're eating per se that appears to be a problem; but it's what's in what you're eating that is adding not only significant calories each day, but a significant burden on your metabolism.
With more than 60% of calories from nutritionally bankrupt ingredients that provide little more than energy, should we be surprised we're growing obese, diabetic and suffering an increase of degenerative disease?
Take a close look at what our diet looks like from the ERS data - in 2000 averaged 2,739-calories, with those calories coming from:
Patience grasshopper, patience!
My point is this - over the last thirty-odd years we've been repeatedly told to limit meat, consume fewer eggs, choose low-fat dairy, use vegetable oils instead of animal fats for cooking, take the skin off our chicken and eat more chicken and fish; advised to have a few "vegetarian nights" for dinner; told to spread margarine, not butter, on our bread; pressured restaurants and fast food outlets to use partially hydrogenated oils to reduce saturated fat; reminded to eat more grains for fiber; and, at the end of the day, bought - hook line and sinker - the message that how we used to eat was bad, bad, bad and a diet with more plant-based calories was better for us.
Slowly but surely we have modified our diet and more calories now, than ever before, 73% in fact, come from plant-based sources; and we've grown obese, diabetic and disabled with increased incidence of degenerative disease. We're also a nation slowly becoming dependent on prescription medications to relieve the symptoms of our poor dietary habits while we're repeatedly told our health would improve if we just ate less meat, eggs, butter, saturated fat, and cholesterol.
Folks, these are not the problems in our diet.
Oh, we have modified our calories to consume more plant-based sources of calories, but we're not eating closer to a vegetarian diet (nor do I think we have to).
What we're eating is more and more processed foods with the majority of calories coming from three nutritionally poor, calorie dense sources - added sugars, added vegetable oils and refined grain products.
In fact, these three things - added sugars, added vegetable oils and processed grains - made up more than 60% of our daily calories in 2000. By 2004, little changed over four years, these three items still provided more than 60% of our daily calories.
These three items, that are providing most of our calories each day, aren't really "foods" but are better thought of as "ingredients" since no one will readily sit with a sugar-bowl and eat spoon after spoon of sugar, take slugs from a bottle of corn syrup, chow down over a big bowl of flour, or pour a nice big glass of soybean oil to sip at the end of the day.
These ingredients however litter our food supply and are found in virtually all processed foods - those you'll likely find in a box, jar, can or bag; those with a nutrition label on them detailing the fat, carbohydrate, fiber and protein, followed by the ingredients; frozen, refrigerated or stable on the shelf, these foods contain the ingredients that provide the majority of our calories each day.
As the past couple of posts highlighted, the devil is in the details - it's not what you're eating per se that appears to be a problem; but it's what's in what you're eating that is adding not only significant calories each day, but a significant burden on your metabolism.
With more than 60% of calories from nutritionally bankrupt ingredients that provide little more than energy, should we be surprised we're growing obese, diabetic and suffering an increase of degenerative disease?
Take a close look at what our diet looks like from the ERS data - in 2000 averaged 2,739-calories, with those calories coming from:
- dairy, 285-calories (10.4%);
- fruits 80-calories (2.9%);
- vegetables, including potatoes and legumes, 133-calories (4.9%);
- nuts, including peanuts, 90-calories (3.3%);
- eggs 27-calories (1%);
- meats, poultry and fish combined provide 374-calories (13.6%)
red meats, including beef, pork, lamb and veal, 248-calories (9%);
poultry, including chicken and turkey, 110-calories (4%)
fish 16-calories (less than 1%) - grains, 634-calories (23%)
whole grains, 32-calories (1.1%)
refined grains, 602-calories (21.9%) - added sugars, 502-calories (18.3%)
- added fats, 650-calories (23.7%)
vegetable oils (mostly soybean), 276-calories (10%)
shortening, 238-calories (8.7%)
margarine, 40-calories (1.5%)
To determine the ratios of whole grain versus refined grain, I based the above calorie intakes on a 2002 Nutrition Research Newsletter that included the following, "Grains account for approximately 25% of energy consumption in the United States. However, an estimated 95% of grain available for consumption is refined."
Our diet is appalling - not because we eat too much meat, not because we can't give up eggs, and not because we love our butter...but because we're replacing "real food" with processed foods rich with added sugars, added vegetable oils and refined grains!
And we're eating like this thinking we're choosing healthy foods because we're told these foods are healthier for us - when we reach for the whole grain crackers, whole grain breads, ready-to-eat breakfast cereals touting whole grains, reduced fat salad dressings, and other "foods" we're encouraged to eat - almost all contain one, two or all three of the offending ingredients.
Want an example of just how we're encouraged to eat foods with these ingredients? The Mayo Clinic says "For a healthy breakfast on the go, munch dry, ready-to-eat cereal with a banana and drink a small carton of low-fat or skim milk. The best cereals are those that are higher in fiber. If counting calories, choose cereals that are lower in calories."
Among the options suggested by the Mayo Clinic?
Basic Four
INGREDIENTS include: Sugar, Rice, Brown Sugar, Crisp Rice (Rice Flour, Malt Extract, Sugar, Salt),Corn Syrup, Partially Hydrogenated Soybean Oil, Corn Syrup Solids, Dextrose, Malt Syrup, Dried High Maltose Corn Syrup, and High Maltose Corn Syrup
With 200-calories per serving, 41.5% of those calories are from added sugars and added vegetable oil (partially hydrogenated vegetable oil); if 50% of the grains are refined, as the ingredients suggest, than another 12.5 grams of carbohydrate, or 25% more of the calories, are from refined grains, bringing the total calories from three ingredients - added sugars, added oils and refined grains - to 66.5% of the total calories in a serving.
It's not just the Mayo Clinic serving up advice that leads directly to higher than anticipated consumption of added sugars, added vegetable oils and processed grains.
The 2005 Dietary Guidelines for Americans maintains a document "Food Groups to Encourage" that reads "Consume 3 or more ounce-equivalents of whole-grain products per day, with the rest of the recommended grains coming from enriched or whole-grain products. In general, at least half the grains should come from whole grains;" an implicit nod to continue eating processed foods, now just look for whole grain in the ingredients!
The American Heart Association makes the same recommendation and even offers manufacturers an opportunity to have the AHA Heart Check Mark on their products for consumers to identify those that are "heart healthy" - among those promoted as "heart healthy" - breads with added sugars and partially hydrogenated oils; ready-to-eat breakfast cereals including Lucky Charms, Cocoa Puffs, Berry Berry Kix, and Trix; chocolate and strawberry flavored milks; microwave popcorn; and reduced fat crackers. The No-Fad Diet, an AHA publication, specifically includes donuts, fast food bacon biscuits and other fare as "healthy" when it is clearly the opposite!
And yet we blame Americans for being unable to make good choices?
The American Dietetics Association, in their Nutrition Facts Sheets, maintains a document, targeted toward the consumer, titled "Whole Grains Made Easy" - within it, a weeks menu with granola bars, pretzels, cornbread, ready-to-eat cereal, graham crackers, tortilla chips, veggie burgers and waffles; all included as "whole grain" foods to choose each day! Ignore that each is processed and includes one or more of the three ingredients above.
The American Diabetes Association (ADA) includes sugar, processed foods and copious amounts of vegetable oils in their advice to those at risk for or diagnosed with diabetes. In their latest update to their Nutrition Recommendations and Interventions for Diabetes - 2006, they specifically state a low-carbohydrate diet (less tahn 130g of carbohydrate each day) is to be avoided and that "Individuals at high risk for type 2 diabetes should be encouraged to achieve the U.S. Department of Agriculture (USDA) recommendation for dietary fiber...and foods containing whole grains (one-half of grain intake);" and "people with diabetes are encouraged to choose a variety of fiber-containing foods such as legumes, fiber-rich cereals..., fruits, vegetables, and whole grain products because they provide vitamins, minerals, and other substances important for good health."
More food products, with added sugars, added vegetable oils and refined grains, encouraged as good choices.
And yet we blame Americans for being unable to make good choices?
While we're repeatedly told to limit our consumption of red meat, butter, eggs and other animal foods, we're also specifically encouraged to consume processed food products disguised as "healthful" because they're a "source" of whole grains, low-fat, no cholesterol.
Ignore the added sugars, ignore the vegetable oils, ignore how much of a product is not whole grain...just don't eat animal foods!
Our current diet is wrecking havoc on our metabolism; its nothing more than excessive sugars, oils and processed grain products, which leave our bodies wondering what its supposed to do with these calories coming in that do not include much in the way of essential nutrients to work with.
We're reminded it's all about calories, without much said about meeting essential nutrient requirements; we're reminded to limit saturated fat, without much said about the detriments of excess polyunsaturated fatty acids providing excess omega-6 and the nutrient deficiency risk when limiting or replacing one type of food with another; and when we hear "food" mentioned by experts, it's often a "food product" with little distinction between real whole food versus processed foods.
We're left totally confused within the grocery store as more and more packages have labels touting their food product as superior to another because "insert health claim here;" manufacturers and retailers are gearing up to confuse us further with in-store promotions of whole grain products and other such "healthful" selections, totally ignoring the added sugars, vegetable oils and processed grains in those products you'll be directed toward because they're "healthier" for you.
Nutrition advice in the United States is a total joke, yet no one is laughing at the consequence of our folly that has resulted in an explosion of obesity, diabetes and other degenerative diseases.
Yet we continue down the path, warning incessantly about the terrible things in real whole food - saturated fat in meats and coconut oil; cholesterol in animal foods, especially eggs and butter; too much fat in nuts and seeds, too much fat in milk and cheese; while encouraging the consumption of vegetable oils, processed grains, fruits & vegetables and legumes; in a continued attempt to modify our dietary habits to include more plant-based foods, more vegetarian selections and include even fewer animal foods each day.
Just get with the program and all with be well.
But if you look at our food intake, and look at where it was forty years ago, thirty years ago, even twenty years ago, we're eating similar levels of animal foods - what we've increased, significantly, is added sugars, processed grains and vegetable oils.
We do this without much thought, eat without realizing just how much more we are consuming calorie-wise, because added sugars, vegetable oils (soybean) and processed grains do not offer satiety or a level of nutrients our metabolism can use; all these ingredients offer is additional calories which short-circuit our metabolism and cause a host of problems from insulin resistance, high blood pressure, dyslipidemia, high triglycerides, elevated blood sugars and more.
Over time these disturbances lead to diabetes, heart disease and some cancers.
If we seriously want to halt the trends in obesity, reverse the epidemic of diabetes and stop the continued rise in degenerative diseases, we must - must - stop promoting processed food products as "healthful" options; better for us than real, whole foods that happen to include meat, dairy, eggs, oatmeal, qunioa, vegetables, fruits, nuts, seeds, etc.
For over thirty years we've been sold a bill of goods that is directly causing our poor health and growing obesity - processed foods that contain added sugars, vegetable oils and processed grains - are adding significant hidden calories to our diet and not providing for essential nutrients that are critical for our health.
The experts wring their hands over the obesity epidemic while they refuse to consider the source of our inability to regulate appetite; they blame the population for making poor choices and lacking willpower; and they ignore that the foods they're specifically encouraging are the problem. Until the powers that be have the guts to address the issue of processed foods and the damaging effects of excess ingredients in packaged foods, little is going to change regarding obesity or diabetes.
But you - you can read the consumption data yourself and begin to see exactly how our eating pattern has changed in ways no one is talking about. You can see with your own eyes just how much more added sugars, vegetable oils and processed grains we're consuming in this country and then look at the various recommendations being made to consume that foodstuff.
Then, you can evaluate your own diet - see where you can make improvements to eliminate these ingredients adding calories, these foods that are not healthful to you and begin to eat a diet that truly is healthy....one rich with nutrients, rich with real, whole foods.
Saturday, February 17, 2007
Diet Pattern from Another Perspective
The Economic Research Service of the USDA released food consumption data that provided the following in the overview, "In 2002, total meat consumption (red meat, poultry, and fish) amounted to 200 pounds per person, 23 pounds above the level in 1970. Americans consumed, on average, 18 pounds less red meat (mostly less beef) than in 1970, 37 pounds more poultry, and 4 pounds more fish. The types and amounts of food an individual chooses to eat not only affect his or her well-being, but also have implications for society as a whole."
In the spreadsheets online, the ERS data for 2000 includes calorie consumption of 2,739-calories each day (not including alcohol). Because the data is presented differently than the FAO data I used in a previous post, it's not an easy cut & paste into a spreadsheet to see where the calorie differences are found. After reviewing both sets of data however, the ERS data shows consumption of significantly less calories than FAO data for these items:
Added sugars ERS = 502-calories - FAO = 666-calories
Cereal GrainsERS = 635-calories - FAO = 869-calories
DairyERS = 285-calories - FAO = 387-calories
Other food consumption differences are minor, like butter is listed in the FAO data as 55-calories per day and 32-calories in the ERS data; FAO says fish in the US is 30-calories a day, the ERS says 16-calories a day.
The discrepancy is due to the calculation methods - the FAO calculates consumption based on production, imports, exports, wholesale waste and clearance from supply chain; the ERS takes that a step further and calculates estimated plate/kitchen waste along with surveys from eating habits (like what percentage of the population is known to toss egg yolks before making an omelet). In addition, unlike the FAO data which assumes, for example, "dairy is dairy" globally, the ERS bases the consumption estimate on type of dairy consumed (whole, low-fat, skim, etc.), so it more refined than the FAO data.
So, before I continue, I'm also going to present a quick scenario of a day of eating created from the ERS data since it also works out to 73% of calories from plant-based sources and 27% of calories from animal foods. Interestingly, if we use the ERS data, the calories from added sugars, cereal grains and vegetable oils now exceeds 60% of total calories per day.
So, based on the ERS dataset, the menu for a day might look like this:
Breakfast
1 serving frozen waffles
Pancake syrup
2-oz pork sausage
Coffee with sugar and non-dairy creamer
1 cup orange juice
Snack
Low-fat fruit yogurt
Bottled water
Lunch
1 cup mixed salad greens, tomatoes, slice onion, salad dressing (composite to type)
Roast beef (3-oz) sandwich with mayonnaise, 1 slice nonfat american cheese
1 cup potato salad
1 can regular soda
Snacks/Beverages
1 apple
8 reduced fat Wheat Thins
1.5 tablespooon peanut butter
Dinner
2.5-oz chicken breast, skinless, sauted in vegetable oil (soybean)
1 cup broccoli with margarine
1 cup brown rice (long grain)
1 cup lemonade (from powder mix)
Total Calories = 2738
Fat = 102g (34%)
Carbohydrate = 370g; Fiber = 23g; Net = 347g (51%)
Protein = 99g (15%)
The above menu is off by 3-calories, and like the FAO data menu is exact for meat, poultry, eggs, etc.
Like the previous menu, it is startlingly "healthy" if we measure healthfulness based on dietary guidelines in America - it contains low-fat dairy, reduced fat crackers, lean meats and favors margarine and vegetable oil for cooking.
Yet, it too is a nutritional nightmare - deficient now in Potassium, Vitamin D, and Vitamin K; with excessive intake of sodium (63% more than recommended) and contains less fiber than recommended.
It also contains an unacceptably high 7.48g of trans-fatty acid - but hey, saturated fat only provides 8% of total calories.
I've added this post to add to our understanding of how we eat in the United States and to begin the next step of analysis of why this type of eating pattern may be directly related to our obesity epidemic and exploding prevalence of metabolic syndrome and diabetes.
We'll begin to tackle that issue next week!
In the spreadsheets online, the ERS data for 2000 includes calorie consumption of 2,739-calories each day (not including alcohol). Because the data is presented differently than the FAO data I used in a previous post, it's not an easy cut & paste into a spreadsheet to see where the calorie differences are found. After reviewing both sets of data however, the ERS data shows consumption of significantly less calories than FAO data for these items:
Added sugars ERS = 502-calories - FAO = 666-calories
Cereal GrainsERS = 635-calories - FAO = 869-calories
DairyERS = 285-calories - FAO = 387-calories
Other food consumption differences are minor, like butter is listed in the FAO data as 55-calories per day and 32-calories in the ERS data; FAO says fish in the US is 30-calories a day, the ERS says 16-calories a day.
The discrepancy is due to the calculation methods - the FAO calculates consumption based on production, imports, exports, wholesale waste and clearance from supply chain; the ERS takes that a step further and calculates estimated plate/kitchen waste along with surveys from eating habits (like what percentage of the population is known to toss egg yolks before making an omelet). In addition, unlike the FAO data which assumes, for example, "dairy is dairy" globally, the ERS bases the consumption estimate on type of dairy consumed (whole, low-fat, skim, etc.), so it more refined than the FAO data.
So, before I continue, I'm also going to present a quick scenario of a day of eating created from the ERS data since it also works out to 73% of calories from plant-based sources and 27% of calories from animal foods. Interestingly, if we use the ERS data, the calories from added sugars, cereal grains and vegetable oils now exceeds 60% of total calories per day.
So, based on the ERS dataset, the menu for a day might look like this:
Breakfast
1 serving frozen waffles
Pancake syrup
2-oz pork sausage
Coffee with sugar and non-dairy creamer
1 cup orange juice
Snack
Low-fat fruit yogurt
Bottled water
Lunch
1 cup mixed salad greens, tomatoes, slice onion, salad dressing (composite to type)
Roast beef (3-oz) sandwich with mayonnaise, 1 slice nonfat american cheese
1 cup potato salad
1 can regular soda
Snacks/Beverages
1 apple
8 reduced fat Wheat Thins
1.5 tablespooon peanut butter
Dinner
2.5-oz chicken breast, skinless, sauted in vegetable oil (soybean)
1 cup broccoli with margarine
1 cup brown rice (long grain)
1 cup lemonade (from powder mix)
Total Calories = 2738
Fat = 102g (34%)
Carbohydrate = 370g; Fiber = 23g; Net = 347g (51%)
Protein = 99g (15%)
The above menu is off by 3-calories, and like the FAO data menu is exact for meat, poultry, eggs, etc.
Like the previous menu, it is startlingly "healthy" if we measure healthfulness based on dietary guidelines in America - it contains low-fat dairy, reduced fat crackers, lean meats and favors margarine and vegetable oil for cooking.
Yet, it too is a nutritional nightmare - deficient now in Potassium, Vitamin D, and Vitamin K; with excessive intake of sodium (63% more than recommended) and contains less fiber than recommended.
It also contains an unacceptably high 7.48g of trans-fatty acid - but hey, saturated fat only provides 8% of total calories.
I've added this post to add to our understanding of how we eat in the United States and to begin the next step of analysis of why this type of eating pattern may be directly related to our obesity epidemic and exploding prevalence of metabolic syndrome and diabetes.
We'll begin to tackle that issue next week!
Friday, February 16, 2007
What Does our Diet Look Like?
On Wednesday I ended my post with:
The changes in our diet over the last forty years begs an important question - how are we able to consume copious and increasing amounts of sugar, vegetable oils and cereal grains while continuing to eat a similar level of animal foods?
Just what is going on in our metabolism that even makes that possible?
That was written after detailing how our diet changed between 1961 and 2000 - changes that included an increase of 934-calories; 80% of them from increased consumption of added sugars, cereal grains and vegetable oils; all while we ate less red meat, butter, and eggs.
The shocker - as a nation we consumed an average 3,817-calories per person each day in 2000.
So, I had to wonder, what does 3,817-calories in a day look like?
Using the FAO data for each food group and type, I pulled a menu together in an attempt to reach 3,817-calories with, as per the consumption data, 156g of fat, 115g of protein, 20g of alcohol and 450g of carbohydrate.
In the process I had to choose foods rich with soybean oil, added sugars and include an adequate level of cereal grains to try to match the consumption pattern suggested in the data; I also limited animal fats and proteins to align with the data to reach the dietary pattern the FAO data suggests we consumed each day in 2000.
Lastly, I attempted to make this menu as realistic as possible, where an individual might think they're eating healthy since recent surveys show the majority of people - 75% - actually do think they're eating healthy.
What does such a day of eating potentially look like if we create a menu based on the consumption data from 2000?
Breakfast
1 serving frozen pancakes, microwaved
2.5 small brown-and-serve pork sausage links
Pancake syrup
Coffee with sugar and non-dairy creamer
1/2 cup orange juice
Morning Snack & beverage
Low-fat Fruit Yogurt
Lemonade
Lunch
1 cup mixed greens salad, 1/2 cup diced tomatoes, 1 medium slice onion
2 TBS salad dressing (composite to type, soybean oil based)
2-oz lean roast beef, 1 slice american cheese (plastic wrap type), 2 regular slices rye bread, mayonnaise
3/4 cup potato salad
1 small apple
Lemonade (made from powdered mix)
Afternoon Snack(s) & beverages
1-ounce tuna in water mixed with mayonnaise
6 reduced fat Wheat Thins
1 can regular soda
1 peanut butter cookie (packaged, soft style)
Lemonade
Bottle of water
Dinner
3.9-oz chicken, white meat, skinless (vegetable oil, soybean, used in pan to saute chicken)
1 cup noodles, 1 tsp butter
1 cup green beans with onions, from frozen, margarine in ingredients
7.5 ounces red or white wine
After Dinner Snack
1 cup skim milk
Pretzels, reduced fat dip
Total Calories = 3,830
Fat = 152g
Carbohydrate = 472g; Fiber 21g; Net 451g
Protein = 125g
Alcohol = 20g
Just a bit over the estimated calorie intake (+13 calories), but the menu is exact for intake of beef, fish, poultry, pork, butter and eggs; notable is that there isn't an egg on the menu, it's in the prepared foods.
In this menu, the cereal grains, added sugars and soybean oil is very very close to the consumption estimate from the FAO.
Overall, in the above menu, almost 57% of the calories come from three things - cereal grains, vegetable oils and added sugars.
Yet it doesn't look like there are 4.5-tablespoons of soybean oil or a bit more than 3/4 of a cup of added sugars and with seven servings of grains, it's well within the dietary recommendation of six to ten servings each day.
It's also within the recommendation to keep saturated fat intake at or below 10% of calories, coming in with just 9% of calories from saturated fat.
But consider this - even with this level of calorie intake, the above menu does not meet the recommended intake for Potassium, Vitamin A, Vitamin D, Magnesium or Fiber! All those calories and anyone eating it is still deficient for essential nutrients, and even would consume 2.75-times the sodium without adding one shake of salt at the table!
And, while this menu contained just 9% of calories from saturated fat - a target most agree is desirable, no one would say the almost 12g (11.58g) of trans-fatty acids are acceptable, yet the above menu contains that much trans-fat!
This is but one scenario of a typical day's menu that might align with the consumption data for the United States in 2000; few eat all types of meat and fish in one day; the FAO data and ERS data is based on consumption averages - so while in the real world one day may be chicken and fish and another day beef or pork, over a week or month we consume an average number of calories from those foods.
The scary thing is the above menu isn't unreasonable for an average person to consume throughout the day, and many of the items I selected are considered "healthier" choices as per the dietary recommendations - the lowfat yogurt, wheat thins, tuna, rye bread, pretzels, skinless chicken breast, salad and green beans with onions, non-dairy creamer, skim milk, lean roast beef, and an apple - yet this menu is a nutritional nightmare - is it any wonder What We Eat in America, a report compiled using NHANES data, found chronic population-wide nutrient deficiency when published in 2005?
Which brings us to the second question asked above - just what is happening in our metabolism that allows us to eat that many calories?
We'll explore that question next week...
The changes in our diet over the last forty years begs an important question - how are we able to consume copious and increasing amounts of sugar, vegetable oils and cereal grains while continuing to eat a similar level of animal foods?
Just what is going on in our metabolism that even makes that possible?
That was written after detailing how our diet changed between 1961 and 2000 - changes that included an increase of 934-calories; 80% of them from increased consumption of added sugars, cereal grains and vegetable oils; all while we ate less red meat, butter, and eggs.
The shocker - as a nation we consumed an average 3,817-calories per person each day in 2000.
So, I had to wonder, what does 3,817-calories in a day look like?
Using the FAO data for each food group and type, I pulled a menu together in an attempt to reach 3,817-calories with, as per the consumption data, 156g of fat, 115g of protein, 20g of alcohol and 450g of carbohydrate.
In the process I had to choose foods rich with soybean oil, added sugars and include an adequate level of cereal grains to try to match the consumption pattern suggested in the data; I also limited animal fats and proteins to align with the data to reach the dietary pattern the FAO data suggests we consumed each day in 2000.
Lastly, I attempted to make this menu as realistic as possible, where an individual might think they're eating healthy since recent surveys show the majority of people - 75% - actually do think they're eating healthy.
What does such a day of eating potentially look like if we create a menu based on the consumption data from 2000?
Breakfast
1 serving frozen pancakes, microwaved
2.5 small brown-and-serve pork sausage links
Pancake syrup
Coffee with sugar and non-dairy creamer
1/2 cup orange juice
Morning Snack & beverage
Low-fat Fruit Yogurt
Lemonade
Lunch
1 cup mixed greens salad, 1/2 cup diced tomatoes, 1 medium slice onion
2 TBS salad dressing (composite to type, soybean oil based)
2-oz lean roast beef, 1 slice american cheese (plastic wrap type), 2 regular slices rye bread, mayonnaise
3/4 cup potato salad
1 small apple
Lemonade (made from powdered mix)
Afternoon Snack(s) & beverages
1-ounce tuna in water mixed with mayonnaise
6 reduced fat Wheat Thins
1 can regular soda
1 peanut butter cookie (packaged, soft style)
Lemonade
Bottle of water
Dinner
3.9-oz chicken, white meat, skinless (vegetable oil, soybean, used in pan to saute chicken)
1 cup noodles, 1 tsp butter
1 cup green beans with onions, from frozen, margarine in ingredients
7.5 ounces red or white wine
After Dinner Snack
1 cup skim milk
Pretzels, reduced fat dip
Total Calories = 3,830
Fat = 152g
Carbohydrate = 472g; Fiber 21g; Net 451g
Protein = 125g
Alcohol = 20g
Just a bit over the estimated calorie intake (+13 calories), but the menu is exact for intake of beef, fish, poultry, pork, butter and eggs; notable is that there isn't an egg on the menu, it's in the prepared foods.
In this menu, the cereal grains, added sugars and soybean oil is very very close to the consumption estimate from the FAO.
Overall, in the above menu, almost 57% of the calories come from three things - cereal grains, vegetable oils and added sugars.
Yet it doesn't look like there are 4.5-tablespoons of soybean oil or a bit more than 3/4 of a cup of added sugars and with seven servings of grains, it's well within the dietary recommendation of six to ten servings each day.
It's also within the recommendation to keep saturated fat intake at or below 10% of calories, coming in with just 9% of calories from saturated fat.
But consider this - even with this level of calorie intake, the above menu does not meet the recommended intake for Potassium, Vitamin A, Vitamin D, Magnesium or Fiber! All those calories and anyone eating it is still deficient for essential nutrients, and even would consume 2.75-times the sodium without adding one shake of salt at the table!
And, while this menu contained just 9% of calories from saturated fat - a target most agree is desirable, no one would say the almost 12g (11.58g) of trans-fatty acids are acceptable, yet the above menu contains that much trans-fat!
This is but one scenario of a typical day's menu that might align with the consumption data for the United States in 2000; few eat all types of meat and fish in one day; the FAO data and ERS data is based on consumption averages - so while in the real world one day may be chicken and fish and another day beef or pork, over a week or month we consume an average number of calories from those foods.
The scary thing is the above menu isn't unreasonable for an average person to consume throughout the day, and many of the items I selected are considered "healthier" choices as per the dietary recommendations - the lowfat yogurt, wheat thins, tuna, rye bread, pretzels, skinless chicken breast, salad and green beans with onions, non-dairy creamer, skim milk, lean roast beef, and an apple - yet this menu is a nutritional nightmare - is it any wonder What We Eat in America, a report compiled using NHANES data, found chronic population-wide nutrient deficiency when published in 2005?
Which brings us to the second question asked above - just what is happening in our metabolism that allows us to eat that many calories?
We'll explore that question next week...
Thursday, February 15, 2007
Time Crunch...
Yesterday I wrote that I'd continue with a follow-up to my post - for those awaiting that post, please forgive my delay, an unanticipated schedule change here means I won't be able to complete the post until later tonight!
Thanks for your patience!
Thanks for your patience!
Wednesday, February 14, 2007
Do we need more plant-based calories in our diet?
Eat a plant-based diet.
It's a message we're bombarded with almost daily in the media and from health experts.
Carefully packaged within the message are subtle cautions about our omnivore ways - meat is loaded with "artery clogging" saturated fat, so are dairy products; eggs are rich with that deadly stuff called cholesterol; and, my favorite, we eat too much protein anyway, so limiting or eliminating animal foods will somehow resolve this problem in our diet.
A recent article in Pipe Dream, sums up our wayward diet nicely, "we are here to tell you to relax and put down the t-bone, as you're probably getting enough protein to feed a small family...of lions.
[...]
Although protein is an essential macronutrient which plays many key roles in the way our bodies function, we do not need huge quantities of it...Given the content of a Western diet, getting enough protein is no challenge. Unlike carbohydrate centered diets of China and Italy, protein is a huge part of our diet. From pork chops to hamburgers to filet mignon, meat is everywhere...You don't have to become a vegetarian to combat the protein craze, but consider rethinking the amount of animal protein you ingest."
Another site, The Body Fat Guide, explains that "Looking first at the role of animal fat in producing disease, one comes across a contradiction to the conventional wisdom: the French Paradox. If eating animal fat produces heart disease, why do the French, who eat plenty of saturated animal fat, have lower rates of heart disease?
The explanation that is consistent with the research on animal protein is that the French consume animal fat largely in the form of butter and cream, which is very low in animal protein. When considering the overall diet of the French, one sees that it is much lower in total animal protein then the Western diet, even though it is higher in animal fat."
Articles like these try convince you that the problem in our diet is animal foods - and that if we eliminate or limit animal foods, we'll see better health because we'll be eating less animal protein and animal fat.
The question then is, are we really eating too much animal protein and fat?
In order to answer that question, we need to first look at our dietary habits before the "diet-heart theory" (aka the lipid hypothesis) took off in the popular media; before the messages to eat less fat really took hold in the minds of the American public; to a time when people just ate their food and didn't think much of it other than did it taste good?
To do that we'll look back at data from the 1960's - the period right before health organizations and the government sought to modify our eating habits toward a plant-based diet....so let's look at the year, 1961 - the earliest date available for complete data from the Food and Agriculture Organization (FAO) of the UN.
From the food balance sheets (which calculates production, exports, imports, waste, spoilage and other factors that determine final consumption of a given population) we find that in 1961 the calories in our diet came from mostly plant-based foods; 65% of total calories were plant-based and 35% were animal-based sources.
Of the 2882.50-calories each day, we consumed 13.2% of our calories from protein, 34.4% from fat, 48.7% from carbohydrates and 3.7% from alcohol.
Of those calories, animal protein accounted for 8.7% of our total calories and also accounted for 66.1% of our total protein intake.
Animal fats provided 21.7% of our total calories, and also accounted for 66% of our total fat consumed.
Pretty shocking, isn't it?
By today's dietary standards, that's a diet that's going to kill you - and given the level of noise about our "poor diet" these days, we must be eating more animal fat and protein - so you'd think?
Well, we're most definitely eating more calories - in 2000 we consumed an average of 3816.71-calories each day; an increase of 934.21 calories over 40-years.
Where things get interesting though, is how our diet has changed in those years.
By 2000, however, our diet looked very different from the sixties; in fact, our dietary intake from plant-based foods increased to account for 73% of our calories each day, animal food sources provided just 27% of our calories.
Must make the "plant-based diet is all that" crowd pretty darn happy - we've most definitely migrated toward eating more calories from plant-based foods than animal foods!
But, in 2000 we did eat more calories - we consumed just 12% of our calories from protein, 36.7% from fat, 47.3% from carbohydrate and 4% from alcohol.
Shifts in protein consumption also are found in the data - where before 8.7% of our total calories were from animal proteins, in 2000, just 7.6% of calories came from animal protein; and animal protein now accounted for 63% of our total protein versus 66% previously.
So while we're told we're in the middle of an obesity epidemic, an explosion of diabetes and a healthcare crisis - remember this fact: while the powers that be are trying desperately to convince you to restrict or eliminate animal foods - today we're eating less protein as part of our total diet than other countries with less heart disease - including Japan!
In countries with enviable low mortality rates from heart disease, protein accounts for
It's a message we're bombarded with almost daily in the media and from health experts.
Carefully packaged within the message are subtle cautions about our omnivore ways - meat is loaded with "artery clogging" saturated fat, so are dairy products; eggs are rich with that deadly stuff called cholesterol; and, my favorite, we eat too much protein anyway, so limiting or eliminating animal foods will somehow resolve this problem in our diet.
A recent article in Pipe Dream, sums up our wayward diet nicely, "we are here to tell you to relax and put down the t-bone, as you're probably getting enough protein to feed a small family...of lions.
[...]
Although protein is an essential macronutrient which plays many key roles in the way our bodies function, we do not need huge quantities of it...Given the content of a Western diet, getting enough protein is no challenge. Unlike carbohydrate centered diets of China and Italy, protein is a huge part of our diet. From pork chops to hamburgers to filet mignon, meat is everywhere...You don't have to become a vegetarian to combat the protein craze, but consider rethinking the amount of animal protein you ingest."
Another site, The Body Fat Guide, explains that "Looking first at the role of animal fat in producing disease, one comes across a contradiction to the conventional wisdom: the French Paradox. If eating animal fat produces heart disease, why do the French, who eat plenty of saturated animal fat, have lower rates of heart disease?
The explanation that is consistent with the research on animal protein is that the French consume animal fat largely in the form of butter and cream, which is very low in animal protein. When considering the overall diet of the French, one sees that it is much lower in total animal protein then the Western diet, even though it is higher in animal fat."
Articles like these try convince you that the problem in our diet is animal foods - and that if we eliminate or limit animal foods, we'll see better health because we'll be eating less animal protein and animal fat.
The question then is, are we really eating too much animal protein and fat?
In order to answer that question, we need to first look at our dietary habits before the "diet-heart theory" (aka the lipid hypothesis) took off in the popular media; before the messages to eat less fat really took hold in the minds of the American public; to a time when people just ate their food and didn't think much of it other than did it taste good?
To do that we'll look back at data from the 1960's - the period right before health organizations and the government sought to modify our eating habits toward a plant-based diet....so let's look at the year, 1961 - the earliest date available for complete data from the Food and Agriculture Organization (FAO) of the UN.
From the food balance sheets (which calculates production, exports, imports, waste, spoilage and other factors that determine final consumption of a given population) we find that in 1961 the calories in our diet came from mostly plant-based foods; 65% of total calories were plant-based and 35% were animal-based sources.
Of the 2882.50-calories each day, we consumed 13.2% of our calories from protein, 34.4% from fat, 48.7% from carbohydrates and 3.7% from alcohol.
Of those calories, animal protein accounted for 8.7% of our total calories and also accounted for 66.1% of our total protein intake.
Animal fats provided 21.7% of our total calories, and also accounted for 66% of our total fat consumed.
Pretty shocking, isn't it?
By today's dietary standards, that's a diet that's going to kill you - and given the level of noise about our "poor diet" these days, we must be eating more animal fat and protein - so you'd think?
Well, we're most definitely eating more calories - in 2000 we consumed an average of 3816.71-calories each day; an increase of 934.21 calories over 40-years.
Where things get interesting though, is how our diet has changed in those years.
By 2000, however, our diet looked very different from the sixties; in fact, our dietary intake from plant-based foods increased to account for 73% of our calories each day, animal food sources provided just 27% of our calories.
Must make the "plant-based diet is all that" crowd pretty darn happy - we've most definitely migrated toward eating more calories from plant-based foods than animal foods!
But, in 2000 we did eat more calories - we consumed just 12% of our calories from protein, 36.7% from fat, 47.3% from carbohydrate and 4% from alcohol.
Shifts in protein consumption also are found in the data - where before 8.7% of our total calories were from animal proteins, in 2000, just 7.6% of calories came from animal protein; and animal protein now accounted for 63% of our total protein versus 66% previously.
So while we're told we're in the middle of an obesity epidemic, an explosion of diabetes and a healthcare crisis - remember this fact: while the powers that be are trying desperately to convince you to restrict or eliminate animal foods - today we're eating less protein as part of our total diet than other countries with less heart disease - including Japan!
In countries with enviable low mortality rates from heart disease, protein accounts for
- 13.2% of calories in Japan
- 13.2% of calories in Sweden
- 13.1% of calories in France
- 12.5% of calories in Italy
- 13.1% of calories in Spain
- 13.5% of calories in Greece
We consume just 12% of our calories each day from protein - and here's an interesting fact: we're not eating more red meat or eggs.
In fact, consumption of both red meat and eggs has decreased over 40-years, along with consumption of butter.
In 1961 red meat (beef, lamb, and goat) provided about 140-calories each day; in 2000 these same foods now provided an average of 123-calories a day. Pork consumption didn't change much, but poultry consumption increased significantly - in 1961 poultry accounted for an average 64-calories a day; by 2000 it accounted for 186-calories a day.
So, while we're eating less red meat and about the same amount of pork, we're eating a heck of a lot more poultry!
Eggs used to provide an average 67-calories a day (about six eggs a week on average per person); in 2000 that had declined to 55-calories a day (less than five eggs a week on average per person).
And, butter - that "bad boy" everyone keeps insisting we must eat less of - well, we are...a lot less. In 1961 we averaged 65-calories a day from butter (about 4.5 tablespoons a week) - in 2000 that was down to just 40-calories a day (about 2.8 tablespoons a week).
So, while we're eating the same calories from animal fat - most of it today is from poultry, not butter, eggs and red meat - and 36 more calories from animal protein, is again from increased consumption of poultry, not red meat or eggs.
But still, if you're advocating a plant-based diet, that's not much of an "advance" toward a "healthier" diet is it?
And, well, we are eating 934 more calories a day! That can't be a good thing.
So, if just 36 of those calories are from animal foods, what the heck explains the other 898-calorie increase?
Sugar, vegetable oils and cereal grains.
Yes, a full 80% of our calorie increase - 750.48 calories - comes from just three sources: sugar, vegetable oils and cereal grains.
Over the period of 40-years, we've increased our added sugars by about 30%, adding 150-calories a day (from 515.75 calories to 665.82 calories); increased our consumption of vegetable oils almost two-fold, adding 358.78-calories a day (from 276.15 calories to 634.93 calories); and increased our consumption of cereal grains by 38%, adding 241.7-calories a day (from 627.32 calories to 869.05 calories).
Sugar, vegetable oil and cereal grains - the base ingredients of many packaged, processed foods in America.
The changes in our diet over the last forty years begs an important question - how are we able to consume copious and increasing amounts of sugar, vegetable oils and cereal grains while continuing to eat a similar level of animal foods?
Just what is going on in our metabolism that even makes that possible?
Those questions will be explored tomorrow!
Friday, February 09, 2007
Adaptive Thermogenesis Can Impede Weight Loss
A calorie is a calorie is a calorie; so we're told.
Calories in - calories out matter when it comes to our weight; so we're told.
Eat less and move more, reduce calories and increase calories used, the secret to weight loss; so we're told.
Back in 2004, Drs. Feinman and Fine offered up a paper, published in Nutrition & Metabolism, "A calorie is a calorie" violates the second law of thermodynamics.
Within that paper, it was noted that, "A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law. Homeostatic mechanisms are able to insure that, a good deal of the time, weight does not fluctuate much with changes in diet – this might be said to be the true "miraculous metabolic effect" – but it is subject to many exceptions. The idea that this is theoretically required in all cases is mistakenly based on equilibrium, reversible conditions that do not hold for living organisms and an insufficient appreciation of the second law. The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a "calorie is a calorie" violates the second law of thermodynamics, as a matter of principle."
While the paper has been cited a number of times over the years, no other major study or paper has challenged the idea that weight loss is mostly dependent on "calories in calories out" - so lacking is any question of this belief that many continue to hold the not-so-subtle idea that if someone isn't losing weight on a calorie restricted diet, then they are not restricting calories enough or they're cheating and just won't admit it.
Well folks, get ready to read an eye-popping study published this month in the International Journal of Obesity, Clinical significance of adaptive thermogenesis. (full text)
The conclusion?
In conclusion, based on studies that have shown a greater than predicted decrease in EE under energy restriction circumstances, this review presented arguments in support of the potential of adaptive thermogenesis to impede obesity treatment on a short- and long-term basis, at least in some individuals. In some cases, the adaptive decrease in thermogenesis was shown to be significantly related to a single cycle of body weight loss and regain, an increase in plasma organochlorine concentration following weight loss, and a lower than predicted EE was also shown to be associated with severe nocturnal oxygen desaturations in OSAS. This suggests that energy metabolism might be sensitive to stimuli of different physiological nature and that adaptive thermogenesis could be quantitatively more important than what is generally perceived by health professionals and nutrition specialists. However, from a clinical point of view, several issues remain to be investigated in order to more clearly identify adaptive thermogenesis determining factors and to develop strategies to cope with them. Along these lines, it is concluded that unsuccessful weight loss interventions and reduced body weight maintenance could be partly due, in some vulnerable individuals, to the adaptive thermogenesis, which is multicausal, quantitatively significant, and has the capacity to compensate for a given prescribed energy deficit, possibly going beyond any good compliance of some patients. [emphasis mine]
Weight loss impeded, even with restricting calories and good compliance?
Who'da thunk it possible?
Calories in - calories out matter when it comes to our weight; so we're told.
Eat less and move more, reduce calories and increase calories used, the secret to weight loss; so we're told.
Back in 2004, Drs. Feinman and Fine offered up a paper, published in Nutrition & Metabolism, "A calorie is a calorie" violates the second law of thermodynamics.
Within that paper, it was noted that, "A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law. Homeostatic mechanisms are able to insure that, a good deal of the time, weight does not fluctuate much with changes in diet – this might be said to be the true "miraculous metabolic effect" – but it is subject to many exceptions. The idea that this is theoretically required in all cases is mistakenly based on equilibrium, reversible conditions that do not hold for living organisms and an insufficient appreciation of the second law. The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a "calorie is a calorie" violates the second law of thermodynamics, as a matter of principle."
While the paper has been cited a number of times over the years, no other major study or paper has challenged the idea that weight loss is mostly dependent on "calories in calories out" - so lacking is any question of this belief that many continue to hold the not-so-subtle idea that if someone isn't losing weight on a calorie restricted diet, then they are not restricting calories enough or they're cheating and just won't admit it.
Well folks, get ready to read an eye-popping study published this month in the International Journal of Obesity, Clinical significance of adaptive thermogenesis. (full text)
The conclusion?
In conclusion, based on studies that have shown a greater than predicted decrease in EE under energy restriction circumstances, this review presented arguments in support of the potential of adaptive thermogenesis to impede obesity treatment on a short- and long-term basis, at least in some individuals. In some cases, the adaptive decrease in thermogenesis was shown to be significantly related to a single cycle of body weight loss and regain, an increase in plasma organochlorine concentration following weight loss, and a lower than predicted EE was also shown to be associated with severe nocturnal oxygen desaturations in OSAS. This suggests that energy metabolism might be sensitive to stimuli of different physiological nature and that adaptive thermogenesis could be quantitatively more important than what is generally perceived by health professionals and nutrition specialists. However, from a clinical point of view, several issues remain to be investigated in order to more clearly identify adaptive thermogenesis determining factors and to develop strategies to cope with them. Along these lines, it is concluded that unsuccessful weight loss interventions and reduced body weight maintenance could be partly due, in some vulnerable individuals, to the adaptive thermogenesis, which is multicausal, quantitatively significant, and has the capacity to compensate for a given prescribed energy deficit, possibly going beyond any good compliance of some patients. [emphasis mine]
Weight loss impeded, even with restricting calories and good compliance?
Who'da thunk it possible?
Gluten-Free Labeling, Proposed Rules, Open Comment Period
On January 23, 2007 the FDA opened a comment period on proposed rules for labeling products 'gluten-free'. The agency accepting comments and feedback from consumers on several issues relating to a gluten-free diet and how individuals make choices about gluten-free products.
If you would like to comment, the page is HERE.
The proposed rule summary was published as follows:
2005N-0279 - Food Labeling; Gluten-Free Labeling of Foods
FR Type: Proposed Rules
Action: Other
RIN Number: 0910-ZA26
SUMMARY: The Food and Drug Administration (FDA) is proposing to define the term "gluten-free" for voluntary use in the labeling of foods, to mean that the food does not contain any of the following: (1) an ingredient that is any species of the grains wheat, rye, barley, or a crossbred hybrid of these grains (all noted grains are collectively referred to as "prohibited grains"); (2) an ingredient that is derived from an prohibited grain and that has been processed to remove gluten (e.g., wheat flour); (3) an ingredient that is derived from a prohibited grain and that has been processed to remove gluten (e.g., wheat wheat starch), if the use of that ingredients result in the presence of 20 parts per million (ppm) or more gluten in the food; or (4) 20 ppm or more gluten. A food that bears the claim "gluten free" or similar claim in its labeling and fails to meet the conditions specified in the proposed definition of "gluten free" would be deemed misbranded. FDA also is proposing to deem misbrand
If you would like to comment, the page is HERE.
The proposed rule summary was published as follows:
2005N-0279 - Food Labeling; Gluten-Free Labeling of Foods
FR Type: Proposed Rules
Action: Other
RIN Number: 0910-ZA26
SUMMARY: The Food and Drug Administration (FDA) is proposing to define the term "gluten-free" for voluntary use in the labeling of foods, to mean that the food does not contain any of the following: (1) an ingredient that is any species of the grains wheat, rye, barley, or a crossbred hybrid of these grains (all noted grains are collectively referred to as "prohibited grains"); (2) an ingredient that is derived from an prohibited grain and that has been processed to remove gluten (e.g., wheat flour); (3) an ingredient that is derived from a prohibited grain and that has been processed to remove gluten (e.g., wheat wheat starch), if the use of that ingredients result in the presence of 20 parts per million (ppm) or more gluten in the food; or (4) 20 ppm or more gluten. A food that bears the claim "gluten free" or similar claim in its labeling and fails to meet the conditions specified in the proposed definition of "gluten free" would be deemed misbranded. FDA also is proposing to deem misbrand
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