Friday, March 30, 2007
Saturday, May 5
8-8:45 am Low GI and Very Low Carbohydrate Diets for Type 2 Diabetes
Eric C. Westman, MD, MHS
8-8:45 am Low GI and Very Low Carbohydrate Diets for Type 2 Diabetes
Eric C. Westman, MD, MHS
8:45-9:30 am Carbohydrate Restriction for Type 2 Diabetesin Clinical Practice
Mary C. Vernon, MD, FAAFP, CMD
9:30-9:45 am Break
9:45-10:30 am Using the Traditional Diet for Type 2 Diabetes in a Canadian First Nations Community
James A. Wortman, MD
10:30-11:15 am A Review of the American Diabetes Association Recommendations for Dietary Carbohydrate
Judy Wylie-Rosett, EdD
11:15am-Noon Panel Discussion of Morning Speakers
Noon-1:30 pm Lunch & NMS Award Presentation (lunch provided for Obesity Course & NMS attendees)
10:30-11:15 am A Review of the American Diabetes Association Recommendations for Dietary Carbohydrate
Judy Wylie-Rosett, EdD
10:30-11:15 am A Review of the American Diabetes Association Recommendations for Dietary Carbohydrate
Judy Wylie-Rosett, EdD
NMS ATTENDEES ONLY
1:30-2:15 pm Very Low Carbohydrate Diets and Serum Biomarkers of Cardiac Risk
Jeff S. Volek, RD, PhD
2:15-3 pm The Paradox of Fats in the Low Carb Diet
Steven D. Phinney, MD, PhD
3-3:15 pm Break
3:15-3:45 pm Biochemical Aspects of Carbohydrate Restriction
Richard D. Feinman, PhD
3:45-4:30 pm Panel Discussion of Afternoon Speakers
The American Society of Bariatric Physicians (ASBP) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The ASBP designates the NMS Seminar for a maximum of 6.5 credit hours in category 1 credit towards the AMA Physicians Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the educational activity. The program is eligible for AOA-CME credits under category 2-A.
Monday, March 26, 2007
More Science and Less Zealotry, Please.
The controversy over which diet is best for all has again made headlines with the publication of the Stanford University study in the Journal of the America Medical Association March 7, 2007. Since the results are favorable to the low-carbohydrate Atkins diet, the usual criticism can be expected to follow.
Predictably, Dean Ornish has launched a tirade in which he manipulates the study findings to find fault with the low-carb approach and to deflect criticism away from his ultra low-fat diet which did not perform well in the study. Unfortunately, this is an argument based on dogma and not on science. The science speaks for itself.
As scientists and clinicians, we believe that no one dietary approach is going to be ideal for everyone. There is no doubt that, for some, an ultra-low-fat approach may be appropriate. Unlike Dr. Ornish, we recognize that there is no one-size-fits-all approach to the enormously complex problem of obesity and related conditions. Unfortunately, other authoritative sources like the US dietary guidelines also recommend a single lowered fat high-carbohydrate diet approach and have been doing so over the decades that this epidemic has grown.
Gratuitous attacks on the Atkins diet that imply it involves abandonment of wholesome vegetables and fruit for “bacon and brie” are simply wrong. Even in the most restrictive phase it meets the recommended daily guidelines for vegetables and fruits. As one advances through the phases, low-glycemic fruits, more vegetables, legumes and even whole grains are introduced based on an individual’s metabolic tolerance for these foods. One survey found that people who follow the Atkins plan over the long term eat more vegetables than they did before. Another study found that rather than increase the intake of fat and protein to compensate when carbohydrates were reduced, people simply ate less.
The unfortunate reality of today is that too many Americans are eating potato chips and fries and drinking sugar-sweetened beverages. We support the idea that wholesome foods such as meat, fish, cheese and eggs along with vegetables and low glycemic fruits constitute a healthier diet than chips and fries and sodas.
While this study examined four popular dietary approaches, what is clear is that whatever approach one takes to healthy eating, success will depend on how well you can stick to it. In this case, and in many earlier studies, it is clear that the Atkins diet is the one most people can maintain. On the other hand, the extremely low-fat diet advocated by Dr. Ornish is very difficult to follow. In this study, the subjects who were supposed to reduce their fat intake to his recommended intake of 10% could not reach that target.
Another important aspect of this and earlier studies is the beneficial effect that reducing carbohydrates has on metabolic markers. In his criticism, Dr. Ornish states that the LDL-cholesterol level fell in response to his diet, but does not mention that none of the differences in LDL-C in this study were statistically significant. This is therefore not a scientifically valid criticism. On the other hand, it is widely recognized that elevating the HDL-C, the good cholesterol, is an important factor in reducing cardiovascular risk. In this study there was a highly significant 10% rise in HDL-C in the Atkins group but no such change among those who followed the very high-carbohydrate Ornish diet.
In the same vein, the Atkins group demonstrated a significant (both statistically and clinically) greater reduction in systolic and diastolic blood pressure than the other three diets. A difference in mean arterial pressure of 5 mm Hg is about the response we would expect to see with a first-line pharmaceutical in the clinical setting. Any objective observer would acknowledge this as a major beneficial effect of the Atkins diet.
Dr. Ornish suggests that the positive findings of research such as this that supports the Atkins diet will cause problems, and that “many people may go on a diet that harms them based on inaccurate information.” This is a wildly irresponsible statement, given the consistency with which a reduction in important metabolic and cardiovascular risks are achieved by lowering carbohydrate consumption. It is simply preposterous to suggest that an approach that leads to significant risk factor reduction is unhealthy.
The seriousness of the accelerating epidemic compels us to think outside the box to find new solutions where the status quo has failed. The only approach that will be successful is one that people can actually follow. This study adds to the mounting evidence that the Atkins diet is a healthy choice which should be supported as a viable way to lose weight and improve metabolic and cardiovascular risk factors.
The Real Atkins Lifestyle
Before there was research on the Atkins diet it was commonly criticized in the belief that it would elevate cholesterol, ruin one’s kidneys and bones and cause heart disease. None of this has been borne out by the research.
What is clear from this JAMA study, and others like it, is that cardiovascular risk factors actually improve when controlling carbs. The scientific studies of this approach have shown numerous times that a pattern of rising HDL-C and falling triglycerides is the hallmark of carb restriction and that this benefit occurs even in the absence of weight loss.
Research also shows that rising HDL-C (good cholesterol) and falling triglycerides is correlated with larger LDL-C particles which are less likely to cause heart disease. Even the much touted statin drugs do not deliver this kind of improvement in LDL-C particle size. On the other hand, the research shows that eating a high-carb diet and cutting fat intake results in small dense LDL-C particles that are linked to an increased risk of heart disease.
Importance of Fat
There are other problems associated with extremely low fat diets, as well. Cutting fat intake can lead to deficiencies in fat soluble vitamins, depletion of essential fats such as EPA and DHA, and decreases in the absorption of nutrients. Studies also show that people with cholesterol levels that are too low become prone to depression, suicide and cancer and have higher overall death rates than those who have higher cholesterol levels.
When all is said and done, it behooves us to remember that the diet debate is not a horse race where there is only one winner. We know there is a great variability in metabolic and genetic factors that will determine what dietary approach is best for each individual person. Although, in this and many other studies the Atkins diet worked better for more people, it is also evident that other dietary approaches will work for some people as well. The most important thing we have learned from dietary research is that people need to find the approach that will deliver healthy outcomes for them individually. And, just as the proof of the pudding is in the eating, the proof of a diet's effectiveness is whether it can sustain those benefits over the long haul. Hopefully, the weight of the evidence will now allow the Atkins diet to be recognized and supported as a legitimate option for people who want to improve their health through better nutrition.
On a final note, Dr. Ornish’s repugnant attempt to undermine Dr. Atkins’ credibility by perpetuating the myth that he had heart disease is unconscionable. It is unbecoming of any honorable person to make ad hominem attacks on those who are departed. Enough is enough. Dr. Atkins died of a head injury. He is no longer with us, but the line of scientific inquiry that he started continues to vindicate his dietary approach. And no amount of unfounded criticism will alter the fact that this study, and the 60 others before it, clearly demonstrate that what Dr. Atkins had been telling us all along was right.
- Jacqueline A. Eberstein, R.N. Co-author, Atkins Diabetes Revolution, President, Controlled Carbohydrate Nutrition
- Stephen D. Phinney, M.D. Ph.D Emeritus Professor, Department of Medicine, UC Davis, Elk Grove, Cal
- Mary C. Vernon, M.D., CMD, Co-author, Atkins Diabetes Revolution, President, American Society of Bariatric Physicians
- Eric C. Westman, M.D. M.H.S, Associate Professor of Medicine, Duke University Medical Center
- Jay Wortman, M.D, Department of Health Care & Epidemiology, Faculty of Medicine, University of British Columbia
Monday, March 12, 2007
Today the BBC reports on a very small study - involving four children - who were given fish oil supplements. Tests done at the end of the three-month study found the children showed an increase in reading age of well over a year, their handwriting became neater and more accurate and they paid more attention in class. Brain scans which identified a chemical called N-Acetylaspartate (NAA) which is linked to the growth of nerve fibres in the brain also showed dramatic changes.
Researcher Basant Puri said of his findings, "In three months you might expect to see a small NAA increase. But we saw as much growth as you would normally see in three years. It was as if these were the brains of children three years older. It means you have more connections and greater density of nerve cells, in the same way a tree grows more branches."
A large placebo controlled study is expected to get underway in the coming months to confirm the findings. On this, Puri said "My view is we can't come to any clear conclusion until a proper trial is done."
Friday, March 09, 2007
You can read her analysis of the presentation at Diabetes Update: Research Gives More Insight into "What is a Normal Blood Sugar"
As Scientific American opened their article about the research, "Could fat be in the brain of the beholder? A new study shows that signals in the brain that warn appetite-modulating neurons of excess fat stores can be suppressed, making the brain unaware of the body's condition. The result: the body becomes completely ignorant about its own makeup and thus makes no attempt to increase energy expenditure or reduce appetite to help shave flab."
The biological sensors in question? A suppressor called SOCS-3, is believed responsible for contributing to a loss of sensitivity to the hormone leptin. The researchers found "leptin binds to a receptor in the arcuate nucleus, triggering a cascade of chemical signals that culminate in the activation of SOCS-3, a suppressor that stops the reaction. The scientists determined that obese animals had an adequate quantity of leptin receptors, but that the quantity of SOCS-3 had risen, likely thwarting any activation of the fat hormone."
Why this may be critically important in our understanding of obesity is that those who are obese often have higher circulating levels of leptin, suggesting something else is limiting it's action. In this animal model it was found that mice consuming identical calorie intakes did not all maintain similar weight - some became obese. After tweaking the macronutrients (in this instance reducing fat since the mice used in this study are bred to grow obese on a high-fat diet) while maintaining the calorie intake, the mice lost weight back to normal - and, the brain control centers regained sensitivity to leptin.
The researchers caution that the study does not necessarily extrapolate well to humans - additional studies are needed since mice overall have a different physiology than humans. But, the study does have value in the scheme of human metabolism and I hope researchers will continue to look at these metabolic pathways and hormones involved in energy regulation in humans.
Like many of us who've continued along over the years as low-carb waxed and waned in the media, but never stopped gaining in the supporting evidence department, she's convinced it's time to set the story straight about carbohydrate restriction - how to do it properly to lose weight, and more importantly, how to maintain weight loss over the years.
She as my vote of confidence - I followed a low-carb diet to lose 80-pounds back in 2001 and have since maintained that weight loss with a basic carbohydrate controlled approach. My husband, Gil, used a low-carb diet to shed over 100-pounds since 2002 and has since maintained that weight loss with the same basic carbohydrate controlled approach. Dana herself has utilized a carbohydrate restricted diet as her eating style since 1995! Twelve years and counting.
I have no doubt there are millions of us out there, across the US and around the world who've lost weight and maintained our loss without much fuss.
The big question - how do we do it?
Everyone says it's impossible to follow a low-carb (carbohydrate restricted) diet for the long-term; that it's boring; that it eventually will lead to declines in health over the long term. Those of us doing it - day to day, year after year - we know it works and we keep at it because it works.
Now it's time to share with others the how and why of long-term success with carbohydrate restriction!
Dana is asking for our help - she'd like to interview everyone she possibly can in the coming months about the how they do it and why they continue with carbohydrate restriction.
She's posed several questions to start a dialogue, initially via email with those interested in participating in this project:
To what do you attribute your success? Was it support from friends? Family? Online support?
Have you learned to cook a wide variety of low carbohydrate meals?
Feeling a lot better?
What do you consider to be the two or three most crucial components in your low carb success?
What were your biggest stumbling blocks? Lack of support, or downright sabotage? Naysaying from your doctor? Boredom with the food? Emotional carb cravings? Discouragement with a plateau? Budget and time constraints? Impulsive eating when junk appears in front of you?
Dana would like to get the project off the ground as soon as possible and is asking for your email replies at firstname.lastname@example.org.
Take a few moments to drop her an email if you'd like to share your success!
She's putting together a proposal and would like to have emails to her by Monday - so what are you waiting for? Email her now!
Thursday, March 08, 2007
The results show the Atkins diet is a reasonable choice for short-term weight loss, said Gardner, a vegetarian.
But the study's lead author warns that the research does not mean dieters should go on the Atkins diet."No, no, no," said Dr. Christopher Gardner, an assistant professor of medicine at the Stanford Prevention Research Center. "This is not a vindication of the Atkins diet."
Can you see him pulling out his hair?
"You lose weight if you have cholera too,'' said Dr. David Katz, director and co-founder of the Yale Prevention Research Center and a longtime critic of the Atkins diet. "You can't measure overall health by a few cardiac risk factors.''
"It's flawed,'' Katz said."Nothing in this study will change nutritional recommendations I make to my patients,'' Katz said.
Katz argues the debate over best types of nutrition should be over. People need fresh fruits and vegetables and should stay away from saturated fats and junk food, he said.
And your evidence is?
"Once the weight-loss stops, the effect of saturated fat would be negative," said James O. Hill, director of the Center for Human Nutrition at the University of Colorado at Denver.
Say it isn't so....
"This study confirms the importance of reducing carbohydrates in the diet," said Dr. Frank Hu, associate professor of nutrition and epidemiology at the Harvard School of Public Health, who was not involved in the research.
"There has been too much emphasis on saturated fat," he said. "Bagels, white bread, potatoes and soft drinks are the real bad guys in our diet."
Did Ornish really just admit Atkins' is easier....?
"It's a lot easier to follow a diet that tells you to eat bacon and brie than to eat predominantly fruits and vegetables," said Dr. Dean Ornish, creator of the Ornish diet.
Keep repeating after me....
Though the study shows Atkins is a safe and effective approach to weight loss, Rex Healthcare registered dietician Natalie Newell still has concerns."You're eliminating a majority of the grain products, fruits and even some vegetables," she said. "So, the major concern I looked at was 'What are you eliminating from your diet?' Vitamins and minerals that come from fruits and vegetables are very important."
I have a hammer....
Dr. Alice Lichtenstein, a nutrition expert at Tufts University, said she thinks too much is made of the amounts of carbohydrates and fats in people's diets as they try to shed weight. “There is no magic combination of fat versus carbs versus protein,” she said. “It doesn't matter in the long run. The bottom line is calories, calories, calories.”
What part of the improvement to risk factors did you miss?
"If they go on an Atkins style diet, there is not going to be negative consequences to their health," says Sheah Rarback, Nutritionist.
Ya Don't Say....
"I think the one thing that really stands out about that Atkins diet was how simple it was," said Dr. Gardner. "Just drastically limit your carbohydrates, with the emphasis being on refined carbohydrates - white bread, white sugar, soda pop, the high fructose corn syrup."
Wonder if anyone else said this...
Dr. Yoni Freedhoff of the Bariatric Medical Institute said [...] “The currency of weight at the end of the day isn’t carbohydrates or proteins or fats, the currency of weight is calories,” he said. “This study proves that too. You can lose weight on any of these approaches. They all have vastly different distributions of carbs, proteins and fats.”
“What matters are the calories in your food.”
Allow me to speculate...
"It shows that people will steadily go back to their old habits," said Dr. Lawrence J. Cheskin, director of the Johns Hopkins Weight Management Center. "After two years, you might find that everybody has regained everything."
Let me try this one again...
"Health is not measured as the combination of several cardiac risk markers and weight over the course of a year," says Dr. David Katz, director of the Prevention Research Center at Yale University School of Medicine. "If it were, every patient getting chemotherapy would be 'healthy.'"
Did anyone else say this?
"Some heart indicators were better, but what about the mountains of evidence about high consumption of fruits and vegetables to promote overall health?" says Keith-Thomas Ayoob, associate professor at the Albert Einstein College of Medicine's department of pediatrics in Bronx, N.Y.
"The public may not realize that keeping weight off for one year is no indication of permanence," says Carla Wolper of the Obesity Research Center at St. Luke's Hospital in New York City.
Let me throw this out and see if it sticks....
"Numbers don't lie, but they don't tell the whole story — by a mile," says Jackie Newgent, instructor at the Institute of Culinary Education in New York City. "There are more than just a couple numbers that determine your overall health. And as cholesterol numbers and blood pressure levels improve, it doesn't mean other heart-health indicators improve."
Oh, did I forget to add...
"A healthy diet is the same as it ever was," Katz says. "Focus on health, and the long term, and your weight will take care of itself."
Hmmm, the hammer, OK, I'll swing...
"It's not about demonizing whole food groups," Ayoob says. "It's about how much and how often, and learning to strike a balance between what we know we need, and what we don't want to live without."
Ouch, that's gotta hurt....
"I'm tired of these diet wars," Ornish says. "It's not low-fat versus low-carb. It's both."
Wait, let me re-phrase that....
Previous studies have shown the Ornish diet and lifestyle program could also reverse progression of prostate cancer and diabetes while the Atkins diet has been proved to worsen heart disease, Ornish said. [...] All nutritionists have or should have concerns over the Atkins diet. High fat diet is in no way a healthy diet.
And I'll add...
That dismays Dr. Dean Ornish, [...] "I'm concerned that this study may cause people to forgo eating a healthy diet for one that's actually harmful for them," he said.
The key word is "boring," said Kathryn Sucher, a nutrition and food science professor at San Jose State University. That, she said, is the reason so many people drop off the Atkins diet and other highly restrictive eating plans.
[Gary] Foster [...] cautioned, "The lipid story is gradually emerging, but it's still unresolved."
I'm so confused....
"It's news that contradicts current healthy-eating advice — a diet heavy on meat and cheese and void of whole grains and fruit can help you lose weight and may even help reduce heart-disease risk, according a study released this week," Leslie Beck "The surprising findings suggest that dieters who lost faith in the low-carbohydrate regime out of concern for their health, might want to reconsider the weight-loss plan."
Finers in my ears....la la la la la la
"This is the message of this article -- focus on lifestyle and environmental factors and don't worry about the macronutrient composition of the diet, particularly if you can achieve the NHLBI guidelines of a 5 to 10 percent weight loss," says Dr. George Blackburn, chair in nutrition medicine at Harvard Medical School. "I think that was my message for the past 20 years."
Tell us what you really think....
Canada.com - One day they're in, the next day they're out again. But whether we're talking about Atkins or South Beach, low-carb diets are one kind of fad that never seems to die.
[and....GASP!....] If you haven't tried a low-carb diet, you may not know that many of these programs restrict all kinds of carbohydrates, and not just the obvious ones, such as bread, rice, and pasta. For example, Atkins, perhaps the best-known low-carb diet around, also excludes most grains, beans, fruits, potatoes, and starchy vegetables, while allowing lots of beef, pork, chicken, eggs, and butter.
A diet that's rich in meat and high in fat can take a toll on your health. [emphasis theirs]
Are you paying attention yet?
Dr. Gardner, [...] still thinks his study is "neat."
"The low-fat message that we had for a long time backfired on us. It was overly simplistic. People went out and bought low-fat cookies and ate the whole box. Maybe this is another piece of evidence that a general, low-carbohydrate message has more merit than people might have given it before."
Just don't do it as recommended....
Gardner said Atkins might work because of its simplicity. Carbohydrates typically account for the biggest proportion of the North American diet. The Atkins diet is also high in protein, which makes people feel fuller longer."Just to say (eat) low carbohydrates doesn't mean anything under the sun goes, including butter and pork rinds and steak and whip cream," Gardner said.
Get it? Got it? Good!
"We've all been worried that the high saturated fat content of Atkins would be bad for you," said study author Christopher Gardner, an assistant professor of medicine at Stanford. The plan's high-fat levels "still make us nervous," he said, "but I think the weight loss that comes with the diet must be more powerful" in keeping cholesterol and other heart risk factors at bay.
File this under I just won't believe it...
''But all diets work. It doesn't really matter which program you're using. When you reduce your calories and get more exercise, you lose weight,'' Burke said. ''Atkins might have had the best results, but I'd like to see what would happen a year from now, or two years from now.''
But of course...
"Yes, on the Atkins diet, the women may have lost a little bit more weight, but I'm not so sure about their quality of life - that's the kind of information that just isn't in here," said dietitian Bonnie Taub-Dix, a New York City weight-control specialist and spokeswoman for the American Dietetic Association.
Keep repeating the message again and again....
Because blood glucose reacts particularly strongly to excessive carbohydrate intake, lowering carbs "might assist blood sugar control," said Harvard endocrinologist Dr Barbara Kahn. "But the [potentially] harmful part has to do whether all those fats over the years are going to lead to more cardiovascular disease. That's the next thing that needs to be studied."
So have you read any other notable quotes? If you have one, share it in the comments!
Wednesday, March 07, 2007
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."
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:
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.
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?
Tuesday, March 06, 2007
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
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 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 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 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 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 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
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.
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.
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.
Early next week I should be back!