Archive for May, 2006
In the May edition of Diabetologia, researchers from Finland analyzed data from the Finnish Diabetes Prevention Study in the paper High-fibre, low-fat diet predicts long-term weight loss and decreased type 2 diabetes risk: the Finnish Diabetes Prevention Study. The conclusion in the abstract, “Dietary fat and fibre intake are significant predictors of sustained weight reduction and progression to type 2 diabetes in high-risk subjects, even after adjustment for other risk factors” is a text-book example of not letting inconvenient findings get in the way of your hypothesis.
Buried deep within the paper is the sentence, “The highest diabetes risk was seen among the high-fat/high-fibre and not, as would have been expected, among the high-fat/low-fibre consumers.” Interesting, but not the focus of what I’d like to write about today.
Buried even deeper in the data are numbers that defy logic – of the 500 individuals participating in the study, 114 developed diabetes (22.8%) while on average they gained weight, experienced an increase in BMI and waist circumference while they reduced calories! That my friends is in stark contrast to the 386 who did not develop diabetes (77.2%), who also reduced calories but lost weight, reduced BMI and waist circumferance over the three year period.
Those who developed diabetes over the three years also had profound changes in their ability to metabolize glucose effectively – fasting glucose readings shot from 117ml/dL at the baseline to 128ml/dL after three years; and 2-hour glucose readings after an oral glucose challenge were worse too – up from 169ml/dL at baseline to 209ml/dL after three years.The researchers did not seek to investigate why these changes occured – how one gained fat while eating less calories as their glycemic control deteriorated over time.
Something interesting popped out in the discussion however when the reserachers included “In our study we emphasised adequate protein intake (0.8 g/1 kg body weight) but did not advise to increase it more than that. It is impossible to say whether advocating an increase in protein would have led to larger weight reduction than was achieved in our study. We did, however, also analyse the association of the protein intake (E%) quintile with weight reduction and diabetes incidence, but did not see any significant effects (data not shown).”
Why no data?
I did some calculating based on the macronutrients consumed in each group and something very interesting emerged – those who did not develop diabetes, were on average, consuming more protein than those who developed diabetes. In fact, they were consuming more protein even though they were consuming less calories!
It may seem like a very small difference, but the group that did not develop diabetes consumed 0.92g of protein/kg of body weight at baseline – and even with the calorie reduction, consumed 0.92g of protein/kg of body weight at the end of the study term!
Compare this to the group that developed diabetes – at baseline they consumed an average of 0.83g protein/kg of body weight, but by the end of the study had decreased protein intake at just 0.8g protein/kg of body weight.
So while the researchers stated they did an analysis of protein intake – they looked at percentage of energy and determined it wasn’t significant and decided not to include the data.
If they’d taken the time to dig deeper – to see the protein intake by gram/kg-body-weight they might have come to a more interesting conclusion – dietary protein may in fact be correlated with development of diabetes in those with impaired fasting glucose when measured by intake in grams/kg-weight!
Those that did not develop diabetes had, just like those that did develop diabetes, impaired fasting glucose at baseline. Both groups reduced calories, both groups increased fiber intake, both groups lowered fat and carbohydrate intake as a percentage of energy and in real grams consumed – the difference in their macronutrient composition was their intake of protein. Those that did not develop diabetes maintained a constant 0.92g/kg-body-weight intake of protein; those that did develop diabetes reduced their intake of protein from 0.83g/kg to 0.80g/kg and gained weight on less calories!
Not only do we have 2.9-million adolescents at risk for diabetes, if the recent data published in the June issue of Diabetes Care is correct, 33% of adults – 1 in 3 – already have diabetes or are on the path to developing diabetes with impaired fasting glucose levels!
As reported in Forbes, “The number of Americans diagnosed with type 2 diabetes has now topped 19 million, and a new study says a third of adults with the disease don’t even know they have it. The researchers found that another 26 percent of adults had “impaired fasting glucose,” a precursor to diabetes.So, if you add that together with the 9.3 percent of people with diabetes, that means that fully one-third of the adult population — 73 million Americans — have diabetes or they may be on their way to getting it,” said lead researcher Catherine Cowie, director of the diabetes epidemiology program at the U.S. National Institute of Diabetes and Digestive and Kidney Diseases.”
These numbers are downright frightening!
In the Forbes article, Dr. David L. Katz, an associate professor of public health and director of the Prevention Research Center at Yale University School of Medicine said “My hope is that we will do what needs to be done to make healthful diets and activity patterns more accessible to all, and diabetes a bit less so.”
In other words, healthcare professionals like Dr. Katz aren’t considering the possibility that their notion of a “healthful diet” is a contributing factor to these numbers! Dr. Katz is well known for his stance on the low-fat, carbohydrate rich diet – to consider any other approach is a public health threat!
The public health threat is a diet rich with carbohydrates – excessive carbohydrates – which directly and progressively impair the metabolism. The smoke-and-mirrors attempt to convince Americans to continue eating high-carbohydrate diets has to stop. It doesn’t matter if the carbohydrate is simple or complex – excess is still excess! And the definition of excess is very simple – the state or an instance of surpassing usual, proper, or specified limits.
Whether simple or complex, all carbohydrates (with the exception of fiber) are converted to blood glucose which requires insulin to shuttle to the cells for energy. Once the amount available is exceeds what the body knows it needs in the coming hours the excess is shuttled to glycogen and body fat. Eat again and repeat. Eat again and repeat.
But we’re told the problem isn’t too many carbohydrates. Nope – we’re told we eat too much fat…gotta watch the fat, gotta lower consumption of fat, gotta stop eating those foods rich with fat. If only Americans would stop eating so much darned fat they’d not get fat and diabetic. [note sarcasm]
Too much fat with excessive carbohydrate – deadly combination. You’ll get no arguement from me that eating a steady diet with a lot of fat and a lot of carbohydrate will kill you. Slowly. Painfully.
The problem isn’t our fat intake. It’s our carbohydrate consumption – it’s excessive. Our metabolism is designed for us to eat quality protein, good fat and even some carbohydrate. But we’re like drunken sailors binging ourselves silly at every opportunity we find – the indulgence isn’t alcohol, but carbohydrates! And just like the body cannot tolerate excessive alcohol consumption over time, it also cannot tolerate excessive carbohydrates over time!
The solution isn’t reducing fat and eating more carbohydrate – it’s the opposite…reducing the carbohydrate content of our diet and favoring the best quality carbohydrate foods out there – non-starchy vegetables, nuts, seeds, legumes and some fruits. Eat a wide variety of quality protein and choose your fats well and you have a diet designed for your metabolism.
With one-in-three adults now at risk for or already diagnoised with diabetes, and 2.8-million adolescents at risk, we must set aside the dogma and get down to the data and stop this epidemic! We can do it – we have the evidence – it’s been staring us in the face for decades! Are we going to truly take an evidence-based approach now and stop this madness, or are we going to continue down the path of our own destruction?
This morning as I mulled over the news that 2.8-million adolescents are at risk for diabetes, I wondered if the messages we communicate about the disease were part of the problem. I clicked over to the American Diabetes Association (ADA) website, as I often do when seeking some information, and started to poke around.
Within a minute I had what I was looking for – “Type 2 diabetes is serious, but people with diabetes can live long, healthy, happy lives.”
Clearly the message is that even if you have diabetes, you can be healthy and lead a long and normal life. The last time I looked, the definition of health was “the condition of being sound in body, mind, or spirit; especially : freedom from physical disease or pain.”
So if type II diabetes is “not good health” why do we communicate the opposite to those at risk or newly diagnoised?
Secondly, why does the ADA misrepresent the fact that physical degradation, progressive physical disability and premature death goes hand-in-hand with type II diabetes when current treatment protocols are followed? To paint a rosy picture of health and happiness living with type II diabetes may relieve some of the anxiety one will have if diagnoised, but isn’t doing anyone any favors in the long-term if the double-speak “health=disease” corrupts the reality that someone with type II diabetes must make radical changes in their lifestyle to even start to make progress toward regaining their lost health!
Interestingly, on the same page was a brief explanation about what causes the disease to manifest:
“In type 2 diabetes, either the body does not produce enough insulin or the cells ignore the insulin. Insulin is necessary for the body to be able to use sugar. Sugar is the basic fuel for the cells in the body, and insulin takes the sugar from the blood into the cells. When glucose builds up in the blood instead of going into cells, it can cause two problems:
- Right away, your cells may be starved for energy.
- Over time, high blood glucose levels may hurt your eyes, kidneys, nerves or heart.”
Basically the message is the problem is insulin.
Let’s turn that around for a moment and consider the parallel not stated – the body has trouble keeping insulin production at levels to meet the demands of excessive glucose.
Think about how we might consider our diet differently if the message included the damaging effect of a diet that produced high levels of blood glucose. Levels so high that over time the body simply cannot keep up with demand to lower blood sugar repeatedly, day in, day out. If we were to modify the message that when we eat too many foods that make high levels of blood glucose, maybe people might look at the foods they eat differently?
To accomplish this, they’d need a better way to understand which foods elevate their blood sugars and those that don’t. Basically they’d have to understand how carbohydrates, protein and fats affect their metabolism, specifically blood sugar.
These days many are encouraged by the concept of using the glycemic index (GI) and glycemic load (GL) as a way to communicate how various foods stimulate insulin and/or elevate blood sugar. While such an approach works in laboratory and study settings, in real-life it’s more difficult to translate what to eat with the GI/GL approach.
Personally, I think there may just be a much easier and effective way to help the public understand how the food they eat affects their blood sugar and insulin.
By nature, most of us are very visually oriented – when we see things presented simply we understand them quickly. When things are presented in a complicated manner, we tend to just ignore the minutia in favor of the less complicated.
Case in point – food labels today are highly detailed with specifics that we’re encouraged to read, interpret and make educated decisions from. All the details, however, mean food labels are complicated to pick apart and understand. One only has to do a search for “understanding food labels” to find there are tens-of-thousands of articles attempting to educate consumers about how to read and process the information on a package label.
Consumers today are actually more likely to be confused by food labels and packaging than at any time in the past! This in light of the fact that in the last two decades policy makers have attempted to simplify labeling for consumers!
Is there a better way?
How about defining the ingredient most likely to elevate blood sugars simply?
Currently carbohydrates – the macronutrient that is directly converted to blood glucose – is listed by grams per serving. Can anyone tell me how many Americans actually stand in the grocery aisle and do the math to figure out that the 40-grams of carbohydrate in the serving means they’re eating the equivalent of 10-teaspoons of sugar?
Can you imagine the effect of labeling the carbohydrate content in terms of teaspoons of sugar?
Suddenly a can of soda might not seem so thirst-quenching if one visually saw they were consuming the equivalent of 11-teaspoons of sugar in one can; a bowl of raisin bran and cup of skim milk might look less appetizing to start the day if a consumer realized it was the equivalent to 12-teaspoons of sugar; and parents may skip taking junior to the fast food restaurant altogether – the Hamburger Happy Meal at McDonald’s ( plain hamburger with apple juice and apple slices with low-fat carmel dipping sauce) is the equivalent of 20-teaspoons of sugar! Forget the Cheeseburger Happy Meal – it’s even more!
How many parents do you know that would sit and willingly spoon-feed their child 20-or-more-teaspoons of sugar? But that’s exactly what they do each and every time they feed their child something as popular as the Hamburger Happy Meal!
Now imagine the toll on the child’s body trying to lower blood glucose levels with insulin after consuming such a meal!
See what happens when the message is clear and the visual is simple?
Just some food for thought!
Robert H. Eckel, MD, director of the general clinical research center at the University of Colorado Health Sciences Center, Denver and the chairman of the American Heart Association’s Nutrition, Physical Activity, and Metabolism Council has stated that “our worries over the Atkins diet go way past the question of whether it is effective for losing weight or even for keeping weight off. We worry that the diet promotes heart disease. We have concerns over whether this is a healthy diet for preventing heart disease, stroke, and cancer. There is also potential loss of bone, and the potential for people with liver and kidney problems to have trouble with the high amounts of protein in these diets.”
Over the years, even in light of numerous studies demonstrating low-carb diets are effective for weight loss, improving HDL and triglycerides, improving insulin sensitivity and glycemic control and even sparing lean body mass, Dr. Eckel has maintained his position that low-carb diets are not healthy.
Now human data, published in the journal Osteporosis International, highlights (once again) the superiority of low-carb diets for weight loss while also providing concrete evidence that the diet does not lead to bone loss. The study’s lead author, Dr. John D. Carter, an assistant professor at the University of South Florida College of Medicine, was surprised since “people on low carbohydrate diets absorb less calcium through the gut and excrete more calcium in the urine, so you’d expect they would be leaching their bones.” However tests conducted on those following a low-carb diet found there was “no significant change in the bone turnover ratio.”
I’m not surprised by the findings since the warning that high protein intake will leech calcium from bones was based on a hypothesized “potential” taken together with animal model data rather than hard data from human studies. In fact, we’ve had the data for quite some time that shows higher consumption of protein may actually be beneficial to bone health!
Just last year a study published in the American Journal of Clinical Nutrition examined the relationship between protein consumption and bone health in 1,000 women averaging 75 years in age. Higher protein intakes were associated with improvements in the bone density in the hip, and the quality of the bone in the heel.
The researchers in this latest study concluded “Although the patients on the low-carbohydrate diet did lose significantly more weight than the controls did, the diet did not increase bone turnover markers compared with controls at any time point. Further, there was no significant change in the bone turnover ratio compared with controls.” I wonder what Dr. Eckles has to say now?
MSNBC carried the column of registered dietian Karen Collins last week – Saturated Fats are Worse than You Think – that set out to convince readers that consuming saturated fat increases the risk of cancer, diabetes, infertility and heart disease. On her list of foods to avoid or strictly limit – the usual suspects: red meat, full-fat dairy products and butter.
While Ms. Collins states this is based on recent findings that saturated fat increases risk, and claims it as fact, she offers no references to published studies. In her article she writes “Now research suggests that too much saturated fat may be problematic, even if your cholesterol isn’t high, because of its possible effects on insulin functions, potentially raising the risk of diabetes, cancer, ovarian disorders and other health problems.”
She continues later with “One of the new studies that links saturated fat consumption with problems in proper functioning of insulin suggests that initially too much saturated fat might decrease the pancreas’s secretion of insulin. Less insulin might then cause a chain of events that leads to over-production of insulin, resistance to its functioning and ultimately to the most common form of diabetes.”
I wondered, what new data was published investigating the effect of saturated fat on insulin in healthy individuals with normal cholesterol?
A quick search in PubMed.com was all it took to find the study that seems a likely fit with what Ms. Collins wrote. Differential effects of monounsaturated, polyunsaturated and saturated fat ingestion on glucose-stimulated insulin secretion, sensitivity and clearance in overweight and obese, non-diabetic humans is published in the June issue of Diabetologia.
An interesting study indeed, but it seems Ms. Collins committed the ultimate faux pax of many in the popular press who write about research studies – she took the study abstract and ran with it rather than take the time to read the full-text and data published to understand where the conclusions in the abstract came from.
The conclusion in the abstract stated “Oral ingestion of fats with differing degrees of saturation resulted in different effects on insulin secretion and action. PUFA ingestion resulted in an absolute reduction in insulin secretion and SFA ingestion induced insulin resistance. Failure of insulin secretion to compensate for insulin resistance implies impaired beta cell function in the SFA study.”
A pretty powerful conclusion. The question begs – did the study design provide the power to extrapolate the findings to a wide population reading Ms. Collins colum?
In a word – no.
There are a number of profound limitations with the study – the study included just seven individuals; the macronutrient mix of the test beverages was insanely high in fat content providing 89% of calories (238g of fat over 24-hours) and bankrupt for protein with a mere 1.74% of calories (just 10g) consumed over the test period; one specific type of fat – palm oil – tested as the saturated fat; and each of the fat types tested – monounsaturated, polyunsaturated and saturated – had negative impacts on risk markers which were neglected in the conclusions but included in the full-text.
That doesn’t mean the study doesn’t have merit. In fact, there are a number of questions left unanswered that should be pursued in the future to understand the results from this study. For example:
- did the type of saturated fat – palm oil – influence the results?
- would butter, coconut oil or lard result in similar findings?
- did the short-term deficiency in essential amino acids influence the results?
- would longer-term testing find different effects with time for metabolic homeostasis?
- would a different macronutrient mix, while remaining high in fat but adequate for essential amino acids, result in similar findings?
The researchers in this study sought to understand the effect of different fat types on metabolic markers. While tightly controlled, the sample size and number of potential confounding variables make it too small with too many questions to be a source to write a column stating that eating saturated fat will raise your risk “for diabetes, cancer, ovarian disorders and other health problems.”
Simply put – the data in this study has no weight to make such an interpretation, especially when there are numerous other studies finding the exact opposite effect. Let’s not forget the recent study A High Fat Diet in Obese Patients Induces Weight Loss, Leads to Improved Insulin Resistance, and Lowers Systolic Blood Pressure Despite Marked Increase in Dietary Sodium I wrote about in Researching Diet and Saturated Fats Impact on Blood Pressure and Heart Disease earlier this month!
After scratching my head for a few days trying to tease out just what it was in the recent study, Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia, that was so baffling, I found the likely explanation.
What baffled me was that the researchers concluded in their abstract that “Moderate carbohydrate restriction and weight loss provide equivalent but nonadditive approaches to improving atherogenic dyslipidemia. Moreover, beneficial lipid changes resulting from a reduced carbohydrate intake were not significant after weight loss.”
In the results section of the full-text of the paper however, it’s clear the low-carb diets induced greater improvements in cholesterol and weight. As the researchers stated in the full-text:
“In the initial diet, stable-weight phase of the study, the 26%-carbohydrate, low-saturated-fat diet resulted in reductions from baseline in total cholesterol, triacylglycerol, apo B, and total:HDL cholesterol that were greater than the changes observed in the group remaining on the 54%-carbohydrate diet. However, the difference in the change in LDL cholesterol between the 26%-carbohydrate diet and the control diet was not significant by post hoc analysis (P = 0.13). Despite our effort to maintain constant weight, the 26%-carbohydrate, low-saturated-fat diet group lost more weight than did the 54%-carbohydrate group during the stable-weight period. There was also a trend for a greater reduction in percentage body fat with the lower-carbohydrate diets (P less than 0.02, analysis of variance). The significance of the lipoprotein differences between the 26%- and 54%-carbohydrate groups persisted after adjustment for the change in body weight for total cholesterol (P = 0.01), triacylglycerols (P = 0.02), apo B (P = 0.001), and total:HDL cholesterol (P = 0.002), whereas differences in LDL cholesterol and LDL-IV between groups became marginal (P = 0.09 and P = 0.11, respectively).”
Where the findings get confusing is when the researchers continue:
“In contrast with the findings during the initial diet, stable-weight phase, weight loss and stabilization led to reductions in each of these variables that were significantly greater with the 54%-carbohydrate diet than with the 26%-carbohydrate, low-saturated-fat diet.”
How does that happen? I wondered if it really was just the weight loss – not the macronutrient composition – that truly was responsible in the various findings to date that were so favorable for low-carb diets. Then again, study after study also shows data that low-fat macronutrient mix diets – those that are high in carbohydrate – have a negative effect on HDL and triglycerides.
So what gives?
As I said above, I think I’ve found the likely explanation, and it’s from Dr. Mike Eades. He too read and re-read the paper, crunched the numbers over and over and then after some head-scratching – viola! – a very interesting and likely explanation.
I couldn’t explain it better, so I hope you’ll take some time to head over to Dr. Mike’s Blog and have a read yourself!
The word “protein” is rooted in the Greek “protas,” meaning “of primary importance.” Proteins are involved in practically every function performed by a cell, including regulation of metabolism. Proteins control almost all the molecular processes of the body and are the actors that do everything that happens within us. Yet, protein is perhaps the most undervalued macronutrient in our dietary recommendations. How much we should eat isn’t well defined but recommended as a default percentage of calories based on consumption of 55-60% carbohydrate and less than 30% fat. Basically we’re told to consume 10-15% of our diet as protein.
But, not all protein sources are created equal. Within our food supply there are foods rich with complete protein – that is containing all of the essential amino acids required by humans; then there are foods that contain protein but are incomplete sources due to one or more amino acid being deficient to meet human requirements for amino acids.
Now one would think that since we have essential requirements for specific amino acids, the advice we receive would include a recommendation to eat those foods rich with our required amino acids. Unfortunately the opposite is true – we are specifically encouraged to eat sources of incomplete proteins rather than rich sources of complete proteins!Which foods are our best sources of complete protein? Animal foods – meat, poultry, fish, game, and dairy products. The very foods our dietary recommendations implore us to avoid or strictly limit in our diet.The question begs – what does the research data tell us?
Again and again we find that protein rich foods – specifically those foods that contain complete proteins – protect us from overeating. Two new studies recently published highlight the importance of protein in our diet and the effect amino acids have on our appetite.
The first study, conducted at the Genome Research Institute, demonstrated that the signaling pathway known as mTOR, plays a role in the brain’s ability to sense how much energy the body has available. It is activated by nutrient and hormonal signals, and suggests that very specific micronutrients drive these pathways in the brain and help regulate body weight.
Which micronutrient was the center of the study? Leucine – an essential amino acid found in high amounts in meat, fish, poultry and dairy products like cheese. As Dr. Randy Seeley, PhD, lead author of the study said “Rather than basing our diets only on macronutrients like fat or carbohydrates, we might one day be designing diets based on micronutrients like amino acids.”
The second study, conducted by researchers at from Imperial College London, investigated the effect of oxyntomodulin – an amino acid peptide hormone. Not only did the hormone reduce appetite, it also increased energy expenditure in study subjects. The effect of oxyntomodulin did this – not specific direction to increase activity levels or specific dietary advice to eat less food!
These two studies add to the data from previous studies that find protein – specifically amino acids from protein rich foods – plays an important part in our metabolism. Add to this the fact that our level of satiety when we eat directly influences our calorie intake at the meal we are consuming and also directly influences when we will feel hungry again and one must ask why our recommendations are encouraging consumption of carbohydrate to the detriment of protein!
When we eat excessive carbohydrate – and 55-60% of calories from carbohydrate IS excessive – we limit our consumption of other sources of nutrients, specifically fats and protein. Those foods that have the highest amounts of complete protein also come packed with fat.
I don’t think so. I believe that our food chain specifically provides for our dietary requirements if we eat foods our metabolism is “programmed” to use efficiently. It’s no coincidence that diets that restrict carbohydrate and allow ad libitum consumption of fats and protein result in a reduced calorie intake.
The reason is simple – such diets stabilize the hormones responsible for hunger and appetite. I’ve been saying it for years – the Standard American Diet (how most Americans eat) and the US Dietary Guidelines (how Americans are told to eat) – are nutrient-poor diets that lead to overeating. Until we step back from our assumptions about “healthy eating” and actually recommend eating a nutrient-dense diet based on human metabolism we’re not going to reverse the obesity epidemic that plagues us.
We have the necessary information to make a difference in the lives of millions of people in the United States who are obese, overweight and/or suffering the effects of their poor diet. We can reverse the obesity epidemic – with the truth.
And that truth is that we must recommend a reduction in the level of carbohydrate in our diet to allow for adequate consumption of essential amino acids (protein) and adequate consumption of essential fatty acids (fats). We have no requirement for carbohydrate – we do however have essential requirements for amino acids, fatty acids and micronutrients such as vitamins and minerals. We do not need to be consuming excessive carbohydrate to meet those dietary requriements – non-starchy vegetables and some fruits, nuts and seeds with perhaps occassional legumes or whole grains can and will provide all essential micronutrients when one is also consuming adequate levels of complete protein and fat containing foods.