What about the Protein?

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!

Coincidence?

Diabetes Timebomb

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?

Type II Diabetes: Food for Thought

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!

Study: Low-Carb Diet Not Linked to Bone Loss

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?

Does Saturated Fat Increase Health Risks?

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!

Diet Study: Confusing Data Makes Sense!

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!

Protein: Of Primary Importance

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.

Coincidence?

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.

Can Diet Help those with PCOS?

Score one more for controlled carb diets!

Researchers from the University of Alabama Birmingham, led by Dr. Crystal Davis, investigated three dietary approaches in women diagnoised with Polycystic Ovary Syndrome (PCOS) to understand how diet may improve fertility. The diets included:

• a standard diet with 56% carbohydrate, 16% protein and 31% fat
• a high MUFA (mono-unsaturated fat) diet with 55% carbohydrate, 15% protein and 33% fat
• a reduced carbohydrate diet with 43% carbohydrate, 15% protein and 45% fat

The low-carb diet “significantly affected concentrations of fasting insulin, cholesterol, free fatty acids, and acute insulin response to glucose, but circulating concentrations of the reproductive hormones were not significantly affected by the intervention,” wrote the authors in the journal Fertility and Sterility (Vol. 85, pp. 679-688).

From baseline values, levels of fasting insulin decreased by 31 per cent, and the acute insulin response to glucose decreased by 16 per cent for the low-carb diet. The MUFA-enriched diet decreased levels of insulin by 25 per cent, and the acute insulin response to glucose level actually increased by seven per cent.

“Because elevated insulin is thought to contribute to the endocrine abnormalities in PCOS, a reduction in insulin would be expected to ultimately result in an improved endocrine profile.Utilising this low carbohydrate diet in conjunction with a reduced calorie, weight loss regimen may produce additional favourable results in overweight and obese PCOS subjects,” concluded the researchers.

Study: Cholesterol and Glucose Improved by Diet

During my hiatus it seems researchers were busy publishing data that continues to confirm previous findings supporting carbohydrate restricted diets to improve health risk markers!

Yet another study completely ignored by the media - Long Term Effects of Ketogenic Diet in Obese Subjects with High Cholesterol Level - from the April 2006 issue of Molecular Cell Biology. The above link is to the abstract only, the lead author, Dr. Hussein Dashti, was kind enough to send me the full-text of his paper which I'll use to discuss the results below.

The study investigated the effect of a ketogenic diet on two groups of obese subjects - those with normal cholesterol levels and those with high cholesterol levels. Group I had high cholesterol and 35 individuals participating; Group II had normal cholesterol and 31 individuals participating. Both groups were obese with BMI greater than 30. In addition to total cholesterol, LDL, HDL and triglycerides, glucose, creatine, urea and body weight were measured at baseline and weeks 8, 16, 24, 32, 40, 48, and 56 with the findings from the endpoint (56-weeks) compared with baseline in the results. In total, 74% of those participating completed the study term - an impressive number considering the dietary requirements of the study.

Those participating were provided with lists of acceptable foods and allowed to consume as many calories, protein and fat as desired with the only restriction being a limit of 20g of carbohydrate each day at the start with a gradual increase to 40g a day as the study continued. In addition, participants were provided with consultation and a multi-vitamin supplement throughout the study. The foods to avoid included flour, pasta, potatoes, rice, sugar, sweets, honey, cakes, soft drinks and fruit juices.

The results were, in a word, stunning. It's easier to show them visually than detail in numbers:

Body Weight



BMI



Total Cholesterol



LDL Cholesterol



HDL Cholesterol



Triglycerides



TC/HDL Ratio



Glucose



As the saying goes - Ignorance is bliss. As someone commented yesterday, if these results were from a drug study, millions would be spent to get the word out and convince people to use the drug.

Imagine the media blitz! It would overwhelm the senses and ensure vast numbers of people heard or read about the study results. We'd see people lining up at their doctors' office to ask whether the new drug was right for them.

But, a diet that restricts carbohydrate isn't a new and potentially profitable drug. A study such as this one, that results in such impressive data, isn't newsworthy because it isn't providing evidence that supports the current dogma which is deeply entrenched in the minds of consumers, healthcare professionals and government policy makers. This type of data "goes against the grain" (pardon the pun) and will continue to be ignored by the powers that be.

As my readers know, I'm convinced - based on continued review of the evidence - that controlled-carb diets are safe, effective and enhance metabolism to optimize health.

The key is to eliminate the excess carbohydrate from your diet, eliminate the junk foods and refined carbohydrates and choose high quality proteins and fats. One needn't lower carbohydrate to 20g a day for benefit - but that option has repeatedly been shown by the evidence to be extremely effective for weight loss, improvement in cholesterol and reduction of glucose and insulin. As a dietary intervention for diabetes (type II), metabolic syndrome and a host of other metabolic disturbances, a low-carb diet is supported by hard data.

Researching Diet and Saturated Fats Impact on Blood Pressure and Heart Disease

Recently ignored by the media were findings presented at the annual meeting of the American Association of Clinical Endocrinology (AACE) from a study investigating the impact of a diet high in saturated fat on blood pressure. Published in the March/April issue of Endocrine Practice (abstract 201) 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 researchers concluded that their results were consistent with previous studies.

The study included 23 obese, hypertensive patients with documented atherosclerotic cardiovascular disease. The very type of patient who is counseled to eat a low-fat, low sodium diet to reduce their risks. Instead of the traditional dietary recommendation, researchers had these subjects consume a diet high in saturated fat (50% of their total calories) while restricting starches. Yes, a low-carb diet.

Not surprisingly, the group experienced weight loss even while eating whatever they wanted from the allowed foods (ad libitum consumption). In addition, they also lowered their blood pressure (the primary focus of the study) and improved insulin sensitivity. Oh, and did I mention they did this while consuming more sodium too?

Dr. James Hays and colleagues previously reported in the Mayo Clinic Proceedings that the patients achieved significant improvements in a number of cardiovascular risk factors, including reductions in total triglycerides, triglycerides, very low density lipoprotein (vLDL), and vLDL particle size. Additionally, while LDL and HDL concentrations were unchanged, there were significant increases in HDL and LDL particle size.

So, not only did they improve insulin sensitivity, lower blood pressure, and lose weight, they also reduced their risks because their cholesterol levels improved. Add to that those participating either reduced or eliminated their medications during the trial period.

These findings, along with dozens of other studies, continue to support the use of carbohydrate restriction as a dietary intervention for both weight loss and health risk reduction. Taken as a whole body of evidence, the data suggests we must focus our attention not on dietary sodium and fat but on fasting insulin and insulin sensitivity as part of the process to determine the best dietary intervention to reduce health risks and weight.

Remember next time you hear, see or read how deadly saturated fats are that studies continue to show the exact opposite!

It's That Time of the Year

As we head into the season of fun in the sun, get ready for the campaigns to wear sunscreen whenever you go outside. USA Today carried the article, Here comes the sun debate, this morning and I doubt it will be the last one we see in the coming weeks.

Rather than debate the issue, here are the facts:

The sun provides our bodies with a means to make vitamin D. Reasonable exposure to sunshine, sans sunscreen, is necessary for the metabolic pathways that allow the production of vitamin D by the body. The most important aspect in getting adequate exposure to the sun is understanding what is a reasonable amount of time to spend in the sun without sunscreen.

Throughout late spring into early fall, adequate time is fairly minimal - about 10 minutes each day during the mid-day period (10:00 AM until 2:00 PM) in most areas of the United States. That is for a person of medium complexion. For those with fair skin, a bit less time is needed - for those with darker skin, a bit more time is needed; about five minutes more or less.

The rule of thumb is to ensure you do not spend so much time in the sun that you burn!

If you're going to be out in the sun for ANY expended periods, for example going to the beach for the day, you should use sun protection to prevent sunburn - sunscreen, umbrellas, hats, long-sleeve lightweight light colored shirts, and staying in the shade when possible.

The sun is our best source of vitamin D production - you don't have to be afraid of getting reasonable exposure to the sun each day, just don't overdo it!

Getting Caught Up

I'm connected once again to the internet and have access to my blog!

It took a bit longer than anticipated with the move, but slowly but surely I've caught up with things missed over the last two weeks and want to thank my readers for their patience during the move.

New blog entries are on their way!

Off to the Show Me State

With the computer next in line for packing and my internet access limited, my next article will be posted here on May 1, 2006!

Thank you for your patience and I'll be back soon!

AHA Must Stop Endorsing Foods with Trans-Fats!

The American Heart Association (AHA) solicits donations on their website with a powerful few sentences: Cardiovascular disease is the No. 1 killer of American men and women. Your secure online gift will support scientific research, education and programs in your community. Consider it an investment in your own future, as well as the health and well-being of your family and friends.

On their website, their mission is stated on their About Us page as "to reduce disability and death from cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question."

Within the organization's Ethics Policy is the statement that "We pursue our mission with honor, fairness and respect for the individual, ever mindful that there is no 'right way' to do the 'wrong thing.' We uphold the values of the AHA in every action and decision. We are committed to act in good faith, to comply with the rule of law and AHA policies and regulations."

How then does the organization reconcile its inclusion of foods rich with health damaging trans-fats in their book, The No-Fad Diet? How exactly do they reconcile the fact that their list of foods bearing the Heart Check Logo include foods using partially hydrogenated oil as an ingredient?

Just this week, yet another medical journal published the deadly effect of industrial trans-fats on health - as reported on MedPage Today, Trans Fats Judged Major Villain in Cardiovascular Disease.

The article above states, quite clearly, "unhealthy trans fats are found in deep-fried foods, bakery products, packaged snack food, margarines, and crackers, and to try to avoid these foods."

Yet, the AHA No-Fad Diet includes these foods in the sample menus and promotes the book to a public as a diet to improve health and reduce health risks. The AHA list of "heart-healthy" foods on their website also includes these foods.

Just how deadly are industrial trans-fats? Findings in the above review are as follows:

• Lipid Levels: Trans fatty acids have markedly adverse effects on serum lipids. Their consumption raises levels of low-density lipoprotein (LDL) cholesterol, reduces high-density lipoprotein (HDL) cholesterol, and increases the ratio of total cholesterol to HDL cholesterol, a powerful predictor of coronary heart disease risk. Trans fats also increase triglyceride levels, compared with the intake of other fats.
• Potential Molecular Mechanisms: Fatty acids are powerful modulators of cell function, altering membrane fluidity and responses of membrane receptors. They appear to affect lipid metabolism, although these mechanisms are not well established. Cardiovascular Disease: On a per-calorie basis, trans fats appear to increase coronary heart disease risk more than any other micronutrient, conferring a substantially increased risk at levels as low as 1% to 3% of total energy intake. In a meta-analysis of four prospective cohort studies of nearly 140,000 participants, a 2% increase in energy intake from trans fats was linked to a 23% increase in the incidence of coronary heart disease.
• Sudden Death: A large community-based, case-control study found that levels of trans fats in erythrocyte membranes were associated with an increased risk of sudden cardiac death.

Remember - the AHA claims they are working to "to reduce disability and death from cardiovascular diseases and stroke," while asking for donations to "support scientific research, education and programs in your community." They even state one should "Consider it an investment in your own future, as well as the health and well-being of your family and friends."

Why is the AHA ignoring the evidence in their publication of the No-Fad Diet that industrial trans-fatty acids are contributing to cardiovascular disease?

Why does the AHA promote on their homepage, the link A free, heart-healthy grocery list is just a click away where we find a laundry list of foods containing partially hydrogenated oils?

Within that list we begin to find many foods that use partially hydrogenated oils in the ingredients:

• Kellogg's All-Bran Brown Sugar Cinnamon Bars
• Kellogg's All-Bran Oatmeal Raisin Bars
• Breton Reduced Fat & Sodium Wheat Crackers
• Pepperidge Farm Very Thin Soft 100% Whole Wheat Bread
• Healthy Choice Cheese French Bread Pizza

These are just a sampling from a list online that includes hundreds of products that manufacturers pay the AHA to effectively endorse as healthy with their logo on the box!

The AHA maintains the website HeartCheckMark.org for consumers that states on the homepage "The American Heart Association established its Food Certification Program in 1995 to provide consumers an easy, reliable way to identify heart-healthy foods."

I find it deeply troubling that the foods being promoted as "heart-healthy" are made with heart damaging trans-fats, don't you?

I find it hypocritical that the AHA says they are working to "reduce disability and death from cardiovascular disease and stroke" while at the same time promoting products rich with trans-fats to consumers, don't you?

I think it's downright dishonest for the AHA to promote itself as "trustworthy" and an organization from which one "can count on the information because it comes from America's most reliable source of heart-health information" when the very foods being endorsed contain trans-fats that are known to damage the cardiovascular system!

It's high time the American consumer calls the AHA to task for their contradiction and conflict-of-interest.

As an organization that promotes itself as "trustworthy" it must start to be trustworthy - talk is cheap!

The American Heart Association can redeem itself and earn back the trust it loses each day it promotes foods containing heart-damaging trans-fats if:

• Immediately insist on the removal of its logo from any product containing industrial trans-fats
• Immediately recall the AHA No-Fad Diet book from shelves and re-release only after revisions adequately address the need to eliminate industrial trans-fats from the diet
• Immediately begin a public education campaign to clearly communicate to consumers the heart damaging effects of industrial trans-fats in foods

If you believe the AHA is not doing its part to educate the public about the heart damaging effect of industrial trans-fats and is indeed contributing to their continued use in our food supply and you believe it is time the AHA take responsibility for its endorsement of heart-damaging foods, you can do something about it - stop donating money!

CRP Blocks Action of Leptin in the Obese

Occassionally it happens - I'm stumped by something published in a research paper or from a study. I'm usually stumped because something within the findings or conclusions don't sit right with my understanding of the subject at hand or I don't have enough foundation of the subject at hand to completely "get" the gist of things.

Today, MyDNA's article, What Causes Obesity?, stumped me with the researchers' conslusions. Maybe one or more of my readers will have some insights that will help me better understand why the conclusions are valid - how's that for a teaser? I'm obviously stumped on this one because it's not sitting right with my understanding of the subject at hand!

First though, some background from the article above:

Research data from the University of Pittsburgh suggests that obesity is due — at least in part — to an attraction between leptin, the hormone that signals the brain when to stop eating, and a protein called C-reactive (CRP). The amount of fat regulates the amount of leptin produced by the body: the more fat, the more of the hormone. Obese people produce higher levels of leptin, but somehow they're resistant to its effects. This has led researchers to focus on the interaction between CRP and leptin, which is actually Greek for the word "thin."

Zhao said that the binding of CRP, which is also elevated in obese people, to leptin might help explain why the hormone is not effective.

Zhao said his study suggests researchers should focus their attention on an approach that disrupts the interaction between leptin and CRP, which would allow the hormone to resume its regulatory role.

You may be wondering - why is she stumped?

I'll explain.

Everything above sounds reasonable - someone is obese, they have high levels of leptin being excreted which should be signaling the brain and regulating energy intake well...but CRP is binding the leptin and effectively blocking its path....so, let's block the CRP action and the leptin can get back to doing its job.

Something with this screams out to me this is the wrong and I base that on my understanding of C-Reactive Protein and its role in what's called "complement biology."

As a simple definition, CRP is a plasma protein - an acute phase protein - produced by the liver. It's a marker in the blood that indicates an inflammatory response to injury - like an overt injury when you sprain your ankle or when something is going on internally in your body - an obscure injury or assault - like when you come in contact with bacteria that can make you ill. Both of these inflammatory responses resolve and the levels of CRP decline again once the potential for permanent harm are no longer an issue.

In both cases, the CRP acted in its complementary role with the immune system to target and destroy or neutralize a potentially harmful situation. In the example of the sprained ankle, the inflammatory response was stimulated to help "clean up" the injured site and limit movement during that process - the pain limits mobility to the body can take care of the injury. In the example of the bacteria, the inflammatory response was stimulated to flag the invading microbes for destruction and elimination from the body.

I hope this detail provides some insight to my understanding of the role of CRP - it works together with the immune system to neutralize something that has the potential to negatively affect well being. The target of inflammatory response is any substance that stimulates an immune response. The substance most often the cause, when the injury is not overt physical injury - proteins or polysaccarides (although any type of molecule that has potential for harm can trigger it).

The reason I'm stumped by the idea we should block the CRP if it's binding the leptin is that leptin is a protein, produced by adipose tissue (fat). The more adipose tissue an individual has, the more leptin they secrete. The findings from the University of Pittsburgh tell us that this leptin is being blocked because it is being bound by CRP and the suggestion is that if we can block the action of the CRP, we can allow the leptin to do its work in regulating appetite again.

Why are the researchers not asking the question "is the leptin levels causing the inflammatory response?"

To me, it seems like the assumption is that the higher levels of leptin are good - what's bad is its not able to do its job because the CRP is inhibiting its action when it binds to it.

But what if the higher levels of leptin are bad - harmful - and that is causing the inflammatory response in an effort to limit damage?

What if the inflammatory response is exactly what we are supposed to see - and the cause of that inflammatory response is what we must resolve for the body to regain equilibrium?

On its face, the issue to be resolved is rightly the obesity. What I don't understand is how blocking the action of the CRP binding the leptin will resolve that. Perhaps a better approach isn't to block the inflammatory response that is limiting the high level of leptin, but to resolve the cause of the weight gain in the first place!

The research conclusion leads one to see:

Leptin => Appetite Control => Weight Regulation

CRP blocks Leptin => Block CRP Action => Leptin Appetite Control => Weight Loss

But....what if the path is this instead:

Poor Diet => Weight Gain => Elevated Leptin => Inflammatory Response to limit damage from high Leptin

Food for thought, isn't it?

Level One Evidence to Treat Metabolic Syndrome Largely Ignored

I read with great interest the recent paper by Dr. Scott M. Grundy, Metabolic Syndrome: Connecting and Reconciling Cardiovascular and Diabetes Worlds, published in the March 21, 2006, Journal of the American College of Cardiology. My writing today is going to be long, but I hope you'll bear with me since this is important information.

In part, the summary is short, concise and on point:

The metabolic syndrome is a constellation of risk factors that carry increased risk for cardiovascular disease and type 2 diabetes. These risk factors are atherogenic dyslipidemia, elevated blood pressure, elevated plasma glucose, a prothrombotic state, and a proinflammatory state. The two major underlying risk factors are obesity and insulin resistance. Primary treatment is lifestyle therapy - weight loss, increased physical activity, and anti-atherogenic diet. As the syndrome worsens, drug therapies directed toward individual risk factors might be required. Ultimately, drugs might be developed that will simultaneously modify all of the risk factors, but such drugs are not currently available.

First let me applaud Dr. Grundy's frank discussion of many of the pressing issues clouding progress to effectively diagnose and treat individuals presenting with features of Metabolic Syndrome - ineffective communication and lack of agreement between the diabetes and cardiology researchers and organizations; pharmaceutical agents that only target individual risk factors and often do not ameliorate the features effectively; pointing to the long-term, geometric increases to risk individuals face as each feature of Metabolic Syndrome presents and/or advances; and the continued neglect in clinical practice of the single best intervention - diet and lifestyle.

He makes it a point to state that the long-term risk for antherosclerotic cardiovascular disease is greater than the sum of the risk factors associated with Metabolic Syndrome individually. As Dr. Grundy also points out clearly, "primary treatment is lifestyle therapy - weight loss, increased physical activity, and anti-atherogenic diet."

When Dr. Grundy included a section dedicated to the evidence for lifestyle intervention, I was hopeful he would include evidence that provides a comprehensive presentation of the most effective lifestyle interventions supported by hard data. To sum up my expectations - level one evidence, randomly controlled studies, investigation that includes the primary risk factors (BMI and/or waist circumference; total cholesterol, HDL, LDL, triglycerides, TC/HDL ratio, fasting glucose, insulin levels, and blood pressure) or included individuals with Metabolic Syndrome specifically; studies at least six months in length with good compliance rates and overall statistically significant results.

So, which studies did he include to support his statement that "Beyond reducing risk for cardiovascular disease, weight reduction and increased physical activity slows progression to type 2 diabetes in individuals with the metabolic syndrome."

J. Tuomilehto, J. Lindstrom, J.G. Eriksson et al. and Finnish Diabetes Prevention Study Group, Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, N Engl J Med 344 (2001), pp. 1343–1350.

W.C. Knowler, E. Barrett-Connor, S.E. Fowler et al. and Diabetes Prevention Program Research Group, Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin, N Engl J Med 346 (2002), pp. 393–403.

To say I was disappointed by the two studies he included is an understatement. To be clear, both were indeed level one studies - randomly controlled, long-term and with controls to compare the intervention group results. Neither, however, is clear and convincing that the lifestyle interventions were effective for the features of Metabolic Syndrome.

Let me explain why. In the first, Tuomilehto et al, indeed had two groups with multiple features of Metabolic Syndrome. While the findings support that the intervention group did better than the control, they continued to have Metabolic Syndrome as evidenced by their waist circumferance, cholesterol levels, fasting glucose and blood pressure. This particular study also did not provide enough key data for cholesterol since it did not evaluate impacts on LDL cholesterol.

In the second, Knowler et al investigate how lifestyle intervention compares with a pharmaceutical intervention to delay diabetes and conclude that lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. But, the lifestyle intervention was more effective than metformin. Unfortunately this study, again, did not look at enough risk markers to effectively communicate its value as an intervention for Metabolic Syndrome. The investigators did not look at total cholesterol, LDL, HDL, triglycerides, blood pressure or insulin values. Without a complete investigation of these risk markers, this data lacks and is inappropriate to use in support of lifestyle intervention because it leaves too many questions unanswered.

So, neither of these studies supports the idea that lifestyle intervention can reverse the features of Metabolic Syndrome effectively. The fact that Dr. Grundy didn't include evidence, from trials specifically looking at those with features of Metabolic Syndrome or studies that evaluated enough risk markers to reach conclusions about the features of Metabolic Syndrome begs the question - is there a lack of evidence?

The answer is clearly no!

We have dozens of studies that point to the efficacy of lifestyle interventions that not only delay progression of the features, but that can reverse the features! I am very disappointed that Dr. Grundy failed to include any of them. In fact, I would say, without hesitation, that his omission borders on negligence to his colleagues and those individuals seeking methods to improve their condition!

I know that's a very strong statement. But, it must be said if we are going to start to see evidence-based medicine in practice. Anything other than the use of strong evidence is mere speculation or wishful thinking and is nothing more than lip-service. Dr. Grundy has an obligation to his colleagues, clinicians and the public to fully explore the literature and present those studies that clearly indicate which lifestyle interventions work! He failed to do that. And he didn't just fail to find one study - he failed to find or include dozens of studies.

Case in point: Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. A randomized trial of a low-carbohydrate diet for obesity N Engl J Med. 2003;348:2082–2090

Key aspects of the above study - one year, randomly controlled trial; measured cholesterol, insulin, blood pressure, weight, insulin response and glucose levels. The results are best summed up in a graphic:



Golay A, Eigenheer C, Morel Y, Kujawski P, Lehmann T, de Tonnac N. Weight-loss with low or high carbohydrate diet? Int J Obes Relat Metab Disord. 1996;20:1067–1072

Key aspects of the above study - one year, randomly controlled trial; compared low carbohydrate with a low fat diet; measured cholesterol, BMI, glucose, cholesterol, insulin and blood pressure. Again, the results are best summed up in a graphic:



Late last year, Volek & Feinman published a comprehensive review of the literature and found that the degree of carbohydrate restriction directly parallels improvement in the features of metabolic syndrome. As part of their paper, Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction, they included a table of one dozen studies of varying time lengths:



Notice in the above graphic the stunning improvements, across the board, when carbohydrate restriction is used as the dietary intervention.

They also review fourteen studies of ad libitum consumption of carbohydrate restricted diets compared with low-fat diets. The results again strongly support the use of carbohydrate restricted diets to specifically reduce or reverse the features of Metabolic Syndrome:



Now you may be thinking this is all fine and dandy, but surely the conventional wisdom and recommendation to follow a low-fat diet must have merit, otherwise the leading health organizations would stop recommending them since we're told things now are strictly evidence-based?

Unfortunately, the dogma that supports the low-fat paradigm finds little support in the evidence for the features of Metabolic Syndrome. And, sadly, the negative effect of low-fat diets on the risks have been long-known and ignored.

Our first key date in the history of understanding the negative effects of low-fat diets on the features of Metabolic Syndrome comes from data from none other than the "Father of Metabolic Syndrome," Gerald Reaven's work. In 1986, Dr. Reaven published Effect of dietary carbohydrate on the metabolism of patients with non-insulin dependent diabetes mellitus. (Nutr Rev. 1986;44:65–73) and found reducing carbohydrate to 40% of the calories improved individuals to a greater degree than when they consumed 55% of their diet as carbohydrate.

Little research was done to replicate the results or to explore if further reductions of carbohydrate would result in even greater improvements. The biggest reason for the stall in the research was, and remains, the fear of dietary fat. Yet, in 2004, Gannon and Nuttall published, Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. (Diabetes. 2004;53:2375–2382) and found that when carbohydrate is reduced to 20% of calories, the improvements exceed those seen in Reavens' work where carbohydrate was restricted to just 40% of calories! Numerous other studies - from Gannon, Nutall, Westman, Volek, Noakes, Phinney, Yancy, Stern, Brehm and others resulted in similar findings. Yet, these studies continue to be omitted from reviews and analysis of effective lifestyle interventions! This is not only neglectful, it's shameful.

In the United States, we have a real crisis today - 25% of all adults are estimated to already have Metabolic Syndrome; another 20-30% are at risk for developing Metabolic Syndrome; and some 4% of all adolescents and 30% of overweight adolescents meet the criteria for Metabolic Syndrome. If we do not do something now to educate those already affected or at risk for the disorder - and do it quickly - these numbers will continue to grow with pre-mature death the end result of our failure to act from an evidence-based approach.

When compared side-by-side - carbohydrate-rich, low-fat diets and carbohydrate restricted diets - we see dramatically different results. The low-fat diets often raise LDL and triglycerides, lower HDL, have little impact on glycemic control, and minimal effect on blood pressure. These effects are negative impacts that increase the risk of progression of Metabolic Syndrome. While the low-fat diet can and often will result in weight loss, the long-term the benefit of weight loss is negated as weight is re-gained and completely offset by the negative effect on the risk markers for Metabolic Syndrome.

On the other hand, a carbohydrate restricted diet - whether fat or protein or a combination of both is substituted for calorie requirements - has a profound effect on triglycerides, significantly lowering them, raising HDL, improving TC/HDL ratios, increasing insulin sensitivity and glycemic control, reducing blood pressure and reducing weight. Again, in the long-term, it is not certain if the weight loss can be sustained as we have few studies to date that meet the standard of level one evidence. However, the positive impacts on the risk markers of Metabolic Syndrome are promising, especially given the fact that recent data suggests that even without weight loss, such improvements to the various risk factors are seen when carbohydrate restriction is followed.

The bottom line is that a large number of researchers have invested years of time studying diet and nutrition to learn how different macronutrient ratios affect the risk markers associated with Metabolic Syndrome. We have level one evidence that points clearly to carbohydrate restriction as an effective lifestyle intervention.

We have millions of people in the United States today who are being denied this evidence each time a review is published and the author omits the data from these gold standard studies because they counter the established dogma.

I've said it before and I'll say it again - DOGMA IS NOT EVIDENCE!

I implore you to take the time to read the paper published by Dr. Jeff Volek and Dr. Richard Feinman - Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction - and review the 112 references included in their extensive review of the literature.

If you do that - take the time - I think you'll find yourself asking the same question I do - When will the leading medical organizations and experts finally take an evidence-based approach to making recommendations for those at risk for or already presenting features of Metabolic Syndrome?

AHA Gets a Pass on Health Damaging Trans-fats

In July 2005 I wrote a scathing review of the American Heart Association's "No-Fad Diet," a book promoted as "weight-loss strategies...based on reliable scientific research and are backed by respected medical professionals. The American Heart Association has the information you can trust."

The main thrust of my criticism was that here we have the AHA including foods rich with trans-fats in their sample menus and advice, yet the scientific evidence is clear that trans-fats are a detriment to health. The sample menus in the book included things like fast food bacon biscuits, donuts, animal crackers, fast food sub sandwiches, and microwave popcorn. All foods notorious for high levels of trans-fats.

Recently two publications have mentioned my review in their own review of the book. Souix Valley Hospital & Health System Newsletter, Winter 2006 and the March 16, 2006 edition of The Mountain Times.

The Souix Valley Health Newletter

The book relies heavily on the credibility of the AHA, and one internet blogger, Regina Wilshire, criticizes Dr. Eckels for including some sample menus that contain unhealthy trans-fats. What the book proposes, more than anything else, however, is a practical approach to diet that may involve compromises. While there may be no safe level of trans fats, a low level is better than a high one.

The Mountain Times

The No-Fad Diet book gains a great deal of credibility from its explicit association with the American Heart Association, which is highlighted in large type on the back cover. However, Regina Wilshire, an internet blogger who says she has lost weight successfully through the low-carbohydrate Atkins approach, takes the AHA to task for using sample menus that encourage the eating of foods containing trans-fats.

“On page 35 they provide a bullet point with ‘Avoid trans fats’ and then include foods notorious for their trans-fat content in their sample menus, giving a greenlight to eating them,” Wilshire writes. Wilshire’s examples, taken from the book, include: low-fat graham crackers, light microwave popcorn, whole wheat English muffins, reduced fat vanilla wafers, a six-inch fast food ham submarine sandwich and a glazed doughnut.

Dr. Eckel and the AHA are certainly not endorsing trans-fats, and they might well be embarrassed by such criticisms. What the book proposes, more than anything else, is that any effort to lose weight is bound to involve some compromises between the ideal and the practical. While there may be no safe level of trans fats, a low level is better than a high one.

These excuses mix just enough fact with fiction to sound halfway credible! Sure trans-fats are unhealthy they say. But instead of stating the hard truth - one should not eat any man-made trans-fats, they give consumers a false sense of security, give the manufactuers of this poison a free pass, and excuse the AHA from responsibility for promoting the junk food! This sets the lay public up for poor health as many will not be able to distinguish these few facts from the unsubstantiated bunk.

And the bunk here is that "a little" trans-fat is better than a lot.

The long-term health effects are disregarded and the science that concludes man-made trans-fats are detrimental to health are dismissed.

The reviews state that including foods with trans-fats is not an endorsement. Double-speak. The idea that the AHA and the author, Dr. Eckel, aren't "endorsing" trans-fats is without merit - if they're in the book, specifically included in a sample menu for one to follow if they can't make a menu themself or want a simple easy exmple to follow - that's an endorsement no matter how you slice it. It's myopic to think it's not.

Let's not forget, the long-term health effects are specficially negative to the cardiovascular system - the very thing the AHA purports to be providing evidence-based information about in an effort to reduce the risk of cardiovascular disease! The data clearly shows that man-made trans-fats (partially hydrogenated oils) elevate LDL and lower HDL - two things everyone, even the general public, understands increases the risk of cardiovascular disease!

Yet, the AHA gets a free pass for including foods with trans-fats from almost every reviewer of the book. I find this unacceptable and will continue to maintain that the book is not based on evidence, is not healthy, is certainly not going to reduce one's risk for cardiovascular disease, and is a hazaard to follow in umpteen ways. More distrubing is that it is nothing more than lip-service to an unwitting public - the public trusts the AHA and the AHA is promoting a diet that includes a class of fats that the Institutes of Medicine (IOM) concluded have "no safe level" of consumption for humans.

The idea that the public simply won't accept a diet that isn't littered with foods that are unhealthy is not a reason to lie to them, pacify them and tell them they can have their cake and eat it too. Instead of attempting to engage in a meaningful dialogue where facts based on facts are exchanged, the AHA pushes emotional buttons in an attempt to sway readers from the task at hand - eliminating man-made trans-fats from the diet. It's a pitiful and pathetic act and not worthy of any attention by those who are looking to engage in that meaningful dialogue in pursuit of truth about diet and health.

In fact, what we need is a scientific community dedicated to neutralizing harmful ingredients we have inflicted on ourselves; not endorsing and recommending ones we know are harmful. If America is craving healthy snack foods let them eat organic fruit and nuts. Is that such a difficult idea or what?

If we are going to make a difference we must start by taking the path of truth and stop lying to the American public that junk food is acceptable in moderation.

The hawked book promises “don’t give up your favorites." Instead of evoking integrity, the book is schizophrenic - promoting a "no fad" approach to diet while also promoting foods known to be damaging to health.

By refusing to support industry that is detrimental to our health we can send a message to the puppets we have sitting in many of the leading health organizations: health does not come out of a can, a bottle, or any other man made disposable. Health does not come from chemistry. Health comes from the soil - from real whole foods that served us well for millenia that too many today wouldn't even recognize if itwere on their plate.

We have all heard the saying, "Think globally, Act locally." Well, your own body is as local as you can get. Everything you consume is a personal statement of how you view your body and health.

This is a personal challenge to any and all of my friends and readers who see the irony of the AHA encouraging donuts, fast food bacon biscuits and other assorted junk food - Let's all take a stand for ourselves, our health and say "enough is enough." Put down the soda, the chips, and donuts and declare your body a toxin-free zone. If you're not up to this challenge, ignore me and belly up to the bar. It was the wise bartender who said "name your poison."

Aren't we lucky to have so many to poisons to choose from?

Fools Folly

Shame on Dr. John G. Sotos, a cardiologist whose Op/Ed "A Modest -- and Slimming! -- Proposal" appeared in today's Washington Post.

In it, he suggests we adopt a public policy for the food industry modeled on our current encironmental policy, better known as "Tradable Emission Allowances" that allow companies who pollute less to credit companies that pollute more. He thinks basing such a credit system on calories per ounce would solve our growing obesity problem.

A program for tradable emission allowances could target foods with a high caloric density, that is, foods with a high number of calories per ounce. These foods are more likely to produce weight gain than foods with a low density of calories. It's easier to eat 1,000 calories in dessert than in vegetables, because the calories in dessert are concentrated.A food's caloric density generally depends on its water and fat content. Dry, fatty foods have the highest caloric density, because water has weight but no calories and because fat has more calories per ounce than proteins and carbohydrates. For example, butter, which is fatty and dry, has 195 calories per ounce. Frozen spinach has seven calories per ounce.

A specific example illustrates how tradable emission allowances could work. Suppose the calorie-emission allowance is set to 100 calories for each ounce of food emitted into the environment (i.e., sold). A four-ounce food item having more than 400 calories could not, therefore, be sold unless "calorie credits" were purchased to cover the excess calories. So a standard four-ounce stick of butter, containing 780 calories, could not enter the marketplace until the butter producer acquired 380 additional calorie-credits from someone having credits to sell.

On the other hand, the producer of a four-ounce block of frozen spinach would emit only 28 calories into the environment and could sell the unused 372 calorie-credits to the butter producer.With such a program, high-density foods would become more expensive and low-density foods would become cheaper. Unlike a tax, the program could be designed so the net cost change to consumers was zero. Thus, consumers who alter their eating habits need pay no more to eat the same number of calories. The hope, which should be tested, is that the number of calories eaten would drop, owing to the difficulty of consuming large numbers of calories from low-density foods. This would then reduce food costs and, ultimately, health-care costs.

As a cardiologist, Dr. Soto should know it's not just about calories. While his idea is certainly novel, it fails at the very core of our nutrient requirements - actual micronutrients - vitamins, minerals, trace elements, amino acids, and fatty acids - in a food per ounce!

Some examples of foods that would fall under those with too many calories per ounce:

• almonds, walnuts, peacans, sunflower seeds - basically all nuts and seeds
• nut & seeds butters
• natural cheese
• any natural oil or fat, including those that are essential
• fatty fish
• some fruits, like avocados and coconut
• poultry, like duck
• natural sweeteners, like honey

The list is by no means inclusive of all the natural, whole foods that would fall into the "over 100 calories per ounce" folly. I don't know about you, but I see such a system as harmful to farmers and growers who are producing these very foods - foods that are healthy and good in our diet. While Dr. Soto may think he's on to something here - I think it's an unworkable idea that isn't going to make a dent in our eating habits or obesity epidemic.

What will work is for the American population to be told the truth about what the evidence tells us about diet, health and weight gain or loss; and provide them with usable tools - including a variety of dietary options that are scientifically supported - to get their weight down and improve their health.

The message "eat less and move more" doesn't work, isn't going to work and the evidence shows there are alternatives to the carbohydrate-rich, low-fat diet repeated day-in-day-out to the public, that work better, faster and with greater improvements in health risks!

Diabetes: Are we Angry Yet?

The National Health and Nutrition Examination Survey (1988–1994 and 1999–2002) and the Behavioral Risk Factor Surveillance System (1995 and 2002) reveal that not much has improved for diabetics in the United States in the last decade. On some measurements of diabetic control, things have actually gotten worse. But, you wouldn't know that from the conclusions found in the abstract of Improvements in Diabetes Processes of Care and Intermediate Outcomes: United States, 1988–2002 that states: "Diabetes processes of care and intermediate outcomes have improved nationally in the past decade. But 2 in 5 persons with diabetes still have poor LDL cholesterol control, 1 in 3 persons still has poor blood pressure control, and 1 in 5 persons still has poor glycemic control."

The American Diabetes Association (ADA) and the National Diabetes Eduction Program both are clear - an HbA1c higher than 7 indicates "poor control" of diabetes. Yet the data in the above full-text article shows that poor glycemic control is prevalent not in 20% of those with diabetes, but 58.7% of diabetics!

What's more, some organizations like the International Diabetes Federation (IDF) actually set the bar lower - to 6.5 or less as the target for controlled blood sugar. But for now let's not bicker about which is a more accurate measure over the long-term for health complications - something more troubling is found in the data - the number able to maintain an HbA1c of 6 or less has fallen considerably - from 23.4% of those with diabetes in the 1990's to just 16.4% in the most recent survey.

Add to that, the overall average HbA1c didn't change at all - it remained steady at 7.7% - poor control.

That, my friends, is not an improvement by any stretch of the imagination!

So while some are patting themselves on the back for "improvements" over the last decade, I implore you to look beyond the headlines and read the data and the tables in the full article. It is only with this full information can you begin the task of asking "why, with all of our advances in medicine, do we still have those with diabetes unable to adequately control their blood sugar?"

"Why do so many still have very high LDL levels (37% greater than 130), low HDL levels (68% less than 50) and often alarming levels of triglycerides (53% higher than 150)?"

"Why do one in three have high blood pressure?"

Many will challenge these questions with "well, that's the path of complications with diabetes - all we can hope to do is slow it down."

My retort - poppycock!

I'm going to state this very clearly - the ADA diet, the carbohydrate-rich, low-fat diet preached to every type II diabetic in this country - is a death sentence!

Over time it leads to less and less ability to control blood sugar adequately, leading to increased reliance on medications, increased complications and side-effects from both the poor glycemic control and medications, which in turn leads to further worsening of the condition. It's a vicious cycle and it starts with the insane recommendation to eat a low-fat, carbohydrate rich diet upon diagnosis of type II diabetes.

Back in January I wrote that Diabetics Must Demand Accountability from the ADA because "The ADA survives because we, as a nation, are not demanding they be accountable to every diabetic out there who has followed their recommendations and still are declining each day. The ADA continuing to promote the idea of managing the disease symptoms and progressive complications is NOT good enough anymore."

"Only an aggressive campaign that openly and honestly reviews every last piece of scientific data available and comprehensively details exactly what metabolic and/or endocrine improvement is seen with each option will be an acceptable start."

In the above survey data, evey last item reviewed points to problems with the recommended diet, yet there is no mention of this in the paper - the discussion is limited to medical interventions and slowing the progression of the disease rather than asking the hard question - why with all of our medical advancements, interventions and intensive education programs are we getting nowhere with glycemic control?

It's easy to blame the person with diabetes as the culprit here - if only they'd follow the guidelines - instead of asking if the guidelines are contributing to the problem. When the assumption is that the guidelines are accurate it's difficult to ask the question and even harder to persue an answer which could throw everything you think you know out the window.

I'll close here with the same challenge I wrote in Janaury:

Type II Diabetics, ask yourself, do you want to have to take medication every day for the rest of your life and progressively add more and more as the years go by?

No? Well...Demand the ADA begin to tell you the truth about restricting carbohydrate in your diet!

Demand the ADA begin to give you actual IMPROVEMENT in, not just medical management of, your metabolism, endocrine system and thus, your diabetes!

Alarming Rates of Childhood Obesity & Related Diseases

The other day, WebMD reported newly released CDC statistics in "Obesity Epidemic Balloons to New Girth," that show 70% of adults are overweight or obese in the United States. Of that, 32% obese with a BMI greater than 30 and 5% super-obese with a BMI greater than 40. As stunning as those statistics are for the adult population - the statistics regarding the rates of obesity amongst our children are downright frightening!

Children:

• aged 2-5 years, 26% currently have a body weight in the 85th percentile or higher, with 14% of all children of this age group in the 95th percentile or higher
• children aged 6-11 years, 37% have a body weight in the 85th percentile or higher, with 19% of all children of this age group in the 95th percentil or higher
• children aged 12-19 years, 34% have a body weight in the 85th percentile or higher, with 17% of all children of this age group in the 95th percentile or higher

Add to this, a study, Worldwide trends in childhood overweight and obesity, published in the premier issue of the International Journal of Pediatric Obesity this month - it paints a bleak picture of where we are and where we're headed with our children and their growing girth.

From the 1970s to the end of the 1990s, the prevalence of overweight or obesity in school-age children doubled or tripled in several large countries in most regions, such as Canada and the United States in North America; Brazil and Chile in South America; Australia and Japan in the Western Pacific region, and Finland, Germany, Greece, Spain and the UK in Europe.

Based on the secular trends reported here, and assuming they continue on a linear basis, we estimate that over 46% of school-age children will be overweight...in the Americas by 2010; ...[b]y 2010, one in seven children in the Americas is predicted to be obese. The implications for local health services as these children develop obesity-related chronic diseases in later adolescence and early adulthood, are difficult to estimate, but planning for this disease burden needs to be undertaken urgently. For some countries the costs may not be easily absorbed into the domestic economy, and health outcomes may be correspondingly poor.

Folks, within the next four years, if we continue on the current path, 50% of our children will be overweight with one in seven obese! I don't even want to imagine what these statistics translate to in terms of type II diabetes, metabolic syndrome and other obesity related disorders for our children in the future.

To me, this is appalling and a clear indication we are failing our children.

We're quick to blame the marketers, manufacturers, television, fast food restaurants, childrens' characters, not having enough time, lack of safe play space outside and more - but the hard truth is, as parents, we control every last thing our children eat, do and see each day! Ultimately it is the parent who is responsible when their child has learned out-of-control eating habits and sits idle each day.

Am I being too hard on parents?

I don't think so - I speak from experience as a mom and understand the difficulty we parents face in maintaining healthy eating habits and levels of activity in an environment that encourages the exact opposite. But it is my responsibility as a parent to be up to the challenge and do the hard work necessary for my childs health and well-being.

If I don't step up and take that responsibility seriously, why would anyone else? Think about it - if marketers and manufaturers are working hard to convince my child to eat junk food and I buy it for him, are the marketers and manufacturers responsibile when he eats it, or am I when I buy it and subsequently feed it to him?

In my mind, the only person responsible in such a scenario is me - I bought the junk food and I fed it to my child...no one made me do it, no one forced my hand and, conversely, no one can make me buy or feed it to my child.

So while many are quick to blame everyone and anyone to absolve themself - the hard truth is that we parents make the final choice of how and what to feed our kids, how often they get outside to play, and how often they're allowed to sit around doing nothing more than watching television or playing video games.

The statistics cited in the above two articles are frightening for our future. We are raising a generation of children who are getting fatter by the day - not only does the excess weight present a challenge for our children today, it is setting the stage for ill-health in the long-term! The Kansas City Star reported today "Study: More children using drugs that treat Type 2 diabetes" that researchers reviewing prescriptions dispensed in the last four years showed that drugs used to treat and prevent Type II Diabetes IN CHILDREN doubled in the last four years. Four years! Doubled!

Sadly, I'm not surprised. I am however concerned that many parents are ignoring the obvious - the lifelong complications they are imposing on their children because they aren't paying attention to the details and making their childrens' short and long-term health priority number one.

Yes, it's often easier to believe you don't have time, you are doing all you can and that somehow your child will be insulated from harm - obesity and type II diabetes only happens to other kids. The numbers tell us that we're in trouble in the United States - not impending, soon-to-happen if we do nothing trouble - but deep trouble today.

We're pretty good at wringing our hands and hoping someone will do something to reverse the trend. The truth is that only you - the parent - can do the hard work necessary to ensure your child is eating a healthy diet and is active every day!

Waiting for the government, schools, daycare, health organizations, politicians, doctors, the food industry or others to fix the problem for you is no longer an option any parent should consider viable for the long-term health of their child. It's time we parents step up to the plate and take responsibility for what we're feeding our kids, what messages we allow marketers to ingrain in their minds, and what activities we encourage them to engage in each day.

More importantly, it's time we parents stepped up to be the role model our kids need to learn from and want to emulate. It's time to put down the big gulp and bag of chips, grab a bottle of water and a bag of blueberries and go take a walk with you child, run with your child at the park and laugh together as you decide what the clouds look like today as you kick back, enjoy your snack and rest from all that fun together!

Trust me - your kids are worth the effort!