The Metabolic Magic of Magnesium

I often write about the nutrient-density of low-carb and controlled-carb diets because the evidence continues to highlight the importance of critical essential nutrients consumed more frequently with these eating patterns. Today, the journal Circulation published a study Magnesium Intake and Incidence of Metabolic Syndrome Among Young Adults, that found "young adults with higher magnesium intake have lower risk of development of metabolic syndrome."

Personally I don't necessarily agree with investigating micronutrients in isolation. The vitamins, minerals and trace elements we require for good health work synergistically with each other - so while a chronic deficiency in one micronutrient can wreck havoc on our metabolism, honing in on and focusing on one micronutrient may not do much for us without taking care of the other essentials that come into play when we consume the micronutrient in question.

Put another way - if we're eating the right foods, we're probably going to meet our essential requirements without having to worry about any one nutrient in particular. The foods that are most often recommended as part of a balanced low-carb or controlled-carb diet are the very foods that are rich in micronutrients - non-starchy vegetables, nuts, seeds, fish and some dairy.

Some of your best sources for magnesium are also your best sources of other essential nutrients....pretty convenient, huh?

For example, 1-cup of cooked spinach provides 156mg, or 39.1% of the RDA for magnesium (400mg). Spinach also provides more than 10% of the following essential nutrients too: Vitamin K, Vitamin A, Folate, Iron, Vitamin C, Riboflavin (B2), Potassium, Vitamin B6, Copper, Thiamin (B1), Phosphorus and Zinc.

The list of foods that provide 10% of more of our RDA for magnesium highlights how easy it really can be to meet your nutrient requirements for this essential nutrient each day while following a low-carb or controlled-carb diet. In the list below, I've provided some examples and also included other nutrients in each food that also exceed 10% of the RDA for the amount noted:

• Swiss Chard - 1-cup cooked - 150mg magnesium (37.6% of RDA)
  10% or more of RDA for Vitamins K, A, C, E, Potassium, Copper, Iron and Calcium
• Summer Squash - 1-cup cooked - 43mg magnesium (10%)
  10% or more of RDA for Vitamins C and A, potassium, copper and folate
• Baked Halibut - 4-ounces cooked - 121.3mg (30%)
  10% or more of RDA for Vitamins B3, B6, and B12 and Selenium, Phosporus and Potassium
• Baked Salmon - 4-counces cooked - 138.35mg magensium (35%)
  10% or more of RDA for Vitamins D, B3, B12, and B6 and Selenium and Phosphorus
• Pumpkin Seeds - 1/4 cup - 184.5mg magnesium (46%)
  10% or more of RDA for Phosphorus, Iron, Copper and Zinc
• Other foods that are rich (greater than 10% of RDA) in magnesium along with other essential nutrients include: Almonds, Cashews, Yellowfin Tuna, Scallops, Sesame Seeds, Sunflower Seeds, Flaxseeds, Avocado, Hazelnuts (filbets), Peanut Butter, Walnuts, and Plain Yogurt.

And they're all low-carb too!

All too often we hear misinformation about controlled-carb diets - that they are low in essential nutrients or nutrient deficient. Yet, when we look at the very foods encouraged and recommended, we find they're among the most nutrient dense available and easily integrated into a low or controlled-carb diet.

And, this particular study adds to the evidence from previous studies that found those who consume the most magnesium have lower risks.

From the Nurses' Health Study, Magnesium intake and risk of type 2 diabetes in men and women, researchers reported "a significant inverse association between magnesium intake and diabetes risk. This study supports the dietary recommendation to increase consumption of major food sources of magnesium."

From the Iowa Women's Health Study, Carbohydrates, dietary fiber, and incident type 2 diabetes in older women, researchers found "a protective role for...dietary magnesium in the development of diabetes in older women."

And from the Women's Health Initiative, Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women, researchers concluded that "a protective role of higher intake of magnesium in reducing the risk of developing type 2 diabetes, especially in overweight women."

In my opinion it isn't just the magnesium that's working metabolic magic - it's the combination of essential nutrients that come together in the foods that are rich with magnesium. Foods rich with magnesium are also rich with other essentials - so eat your non-starchy vegetables, nuts, seeds and fish to ensure adequate intake of not only magnesium, but other critical vitamins, minerals and trace elements too!

Getting the Facts About Protein

With evidence continuing to support the critical importance of protein in our diet, it still amazes me how often the media continues to perpetrate the myth that all protein sources have similar value in our diet. Case in point, the CBS Early Show Health Watch article, Protein: Getting It Right.

The article opens with - "Protein is a critical part of a healthy diet and the right amount helps with everything from higher energy to stronger muscles. The trick is knowing the healthiest sources of protein and the right amounts for your body."

So far, so good.

To lend credibility the article offers advice from Elisa Zied, a Registered Dietian and spokesperson for the American Dietetics Association. She correctly includes the reasons why we need protein in our diet, "protein provides the building blocks for our bones, muscles, skin, cartilage, and blood, and helps us make enzymes and hormones that keep our bodies functioning. Protein is the most filling or satiating of all the nutrients and can therefore potentially help us curb our calorie intake and help us achieve or maintain a healthier body weight. Protein can also boost energy by stabilizing our blood sugar levels throughout the day."

Zied's advice is good until she points to which sources of protein provide the best nutritional bang: Zied recommends about five and a half one-ounce equivalents of meat and beans each day in a 2,000 calorie diet. The following equals a 1-ounce equivalent of meat/beans:

• 1 ounce of fish, poultry, or beef
• 1/4 cup beans
• 1 tablespoon of peanut butter or 1/2 ounce (2 tablespoons) nuts
• 1 egg

Three cups of beans per week is the recommended amount, and a great option for vegetarians. "These are great sources that give iron, zinc and healthy fiber which can fill you up as well," said Zied, and also supply folate and antioxidants. She points out, though, that they are very filling and high in calories, so a portion is 1/4 cup.

The quality of protein is measured by its amino acid content. Foods rich with the full spectrum of "essential amino acids" are better than those which have one or more "limiting amino acids" - that is they lack a high enough level of one or more amino acids and therefore require one to eat more or eat another food limited in an amino acid to make up the shortfall. Foods that provide good levels of all the essential amino acids are considered "complete proteins," whereas foods that have a limiting amino acid are considered "incomplete proteins."

Foods are rated according to the Protein Digestibility Corrected Amino Acid Score (PDCAAS). This is a method of evaluating the protein quality based on the amino acid requirements of humans. A PDCAAS value of 1 is the highest, and 0 the lowest. Some ratings of commons foods include eggs (1.0), casein (1.0), milk (1.0), whey (1.0), beef (0.92), kidney beans (0.68), lentils (0.52), peanuts (0.52), wheat (0.25).

So, what's wrong with her list of foods?

The one-ounce equivalents aren't the same for quality protein content. In fact, they're not even close due to the limiting amino acids in the beans, peanut butter and nuts, and also the fact that these items provide less protein per ounce than the eggs, fish, poultry or beef.

Since the article is highlighting the importance of protein, let's take a look at some important differences in each food above and dispel some of the myths put forth.

1. "[P]rotein provides the building blocks for our bones, muscles, skin, cartilage, and blood, and helps us make enzymes and hormones that keep our bodies functioning."

This is the critical reason we need quality protein in our diet each day. When you choose foods with complete proteins, you have a better chance of meeting your requirements for essential amino acids - and you'll consume less calories in the process too - than if you choose foods with limiting amino acids.Just how different is the amino acid profile between two foods?

Take a look at the difference between the egg and a tablespoon of peanut butter:

Egg/Peanut Butter

• Calories: 74/94
• Phenylalanine 0.339g/0.209g
• Valine 0.428g/0.169g
• Tryptophan 0.277g/0.138g
• Isoleucine 0.335g/0.142g
• Methionine 0.190g/0.049g
• Histidine 0.154g/0.102g
• Arginine 0.409g/0.483g
• Lysine 0.455g/0.145g
• Leucine 0.541g/0.262g

Not only does the peanut butter cost you 20-calories more, it's "limited" because of the low level of methionine, and except for arginine, provides much less of every other animo acid considered "essential" - that is, required by humans. In fact, you'd have to eat almost 4-tablespoons of peanut butter, costing you 364-calories, to overcome the limiting amino acid in peanut butter.

2. "These are great sources that give iron, zinc and healthy fiber which can fill you up as well," said Zied, and also supply folate and antioxidants. She points out, though, that they are very filling and high in calories, so a portion is 1/4 cup.

The above statement is a bit misleading, and might lead one to think that eggs, beef, poultry or fish do not contain similar nutrients. This time, let's look at the eggs nutrients and 1/4 cup of pink beans:

Beans/Egg

• Calories: 63/74
• Calcium: 22mg/26mg
• Iron: 0.97mg/0.92mg
• Zinc: 0.41mg/0.55mg
• Phosphorus 70mg/95mg
• Selenium 0.6mg/15.8mg
• Riboflavin 0.02mg/0.24mg
• Vitamin B-6 0.07mg/0.07mg
• Folate 71mg/24mg
• Vitamin E 0.43mg/0.48mg
• Vitamin B-12 0.00/0.64mg
• Vitamin A 0.00/242IU
• Vitamin D 0.00/17IU

With the exception of folate (which you should be getting plenty of from your vegetables) the egg provides more important nutrients than the 1/4 cup of beans! And, like the peanut butter, the amino acid profile of the beans falls short when compared with an egg. To overcome the limiting amino acid in beans, and consume more nutrients, you'd have to eat more than three 1/4 servings - costing you 211-calories - and you'd still not consume any Vitamin D, A or B-12 and still not consume as much selenium or riboflavin as you would with an egg.

3. Zied recommends about five and a half one-ounce equivalents of meat and beans each day in a 2,000 calorie diet.

This is one recommendation I take issue with repeatedly as it fails to provide adequate intake of complete protein. Because the current dietary recommendations base intake of carbohydrate, protein and fat on percentage of calories this type of simplistic advice is provided again and again without considering the potential danger to the individual following the advice.

Quite frankly, for most men 5.5-ounces of protein-rich foods in a day is simply inadequate, regardless of the source, for overall total protein intake at the end of the day. For a good number of women, it's also inadequate - especially if one is choosing incomplete protein sources more than complete protein sources, which is currently the recommendation (eat more plant based foods instead of aminal foods).

The Institutes of Medicine (IOM) consider quality protein to be critical and are clear in their recommendations - protein must provide adequate intake of all indispensible amino acids and care must be taken when protein sources are limited in amino acid content. In addition, they set the minimum intake of complete protein at 56g for men and 46g for women. And, let's be clear - that's "complete" protein, not "total protein" in a day from all sources. They also carefully calculated amino acid requirements based on quality protein intake for each of the essential amino acids which is based on miligrams (mg) of amino acid required for each gram (g) of protein consumed.

So, just how risky is the advice to consume just 5.5-ounces of meat and beans with the emphasis on the beans?

In a single day eating 3-ounces of cooked beef (ground, lean, broiled), 1/4 cup of pink beans, a tablespoon of peanut butter and 1/2 ounce of almonds would fulfill the recommendation based on "ounce equivalents" but falls short on actual protein consumed - just 30g - and is deficient in essential amino acids, specifically falling short for phenylalanine and methionine. Including the beef simply wouldn't overcome the limiting amino acids in the other foods. If you followed the advice and consumed no other "protein-rich foods" - that is no more beans or eggs or meats - but relied on other foods like vegetables, fruits, and grains to round out your menu and provide your calories, you'd still fall short for protein and amino acids no matter how many calories you ate.

The bottom line is that when it comes to protein in your diet - quality counts!

Not only will you cosume complete proteins with eggs, meats, poultry, fish, and dairy, you'll also consume higher amounts of vitamins and minerals critical for good health. These foods are and should be recommended as the "gold standard" for quality protein and should be your first choice for protein!

Hitting Below the Belt...

Today Dr. Mike Eades brilliantly [that is the only way to describe his article] takes readers through the Lancet publication of A Life Threatening Complication of the Atkins Diet.

The comedy of errors he points out are funny, yet disturbing when you really think about it - had the media paid better attention to the facts, the headlines would have read "Buffoons misdiagnose mild gastroenteritis, costs patient thousands."

Then again, had the peer reviewers at the Lancet paid attention, the case report never would have been published - but that's another story!

I hope you enjoy Dr. Eades article, Low-carb diet takes one below the belt.

Talk About Creativity!

Usually when researchers find no measurable differences between groups they're observing, they'll either choose to tell it like it is and reach the honest conclusion that there was no difference, or they'll simply not publish their findings.

This month however, it appears researchers got creative to find statistically significant differences in the publication of Weight gain over 5 years in 21,966 meat-eating, fish-eating, vegetarian, and vegan men and women in EPIC-Oxford, published in the International Journal of Obesity.

I say "creative" because the research team abandon the traditional measurements of pounds and/or kilograms and instead reported their findings in grams! Not only did this sleight-of-hand help massage the data to statistically significance, it also got the attention of the media as we see in the Globe and Mail article, Need a carrot to stick to vegetarian eats?

Creative statistics may get you in the media, but it's intellectually dishonest and purposely misleading. In two words, bad science.

So, what's the hub-bub about?

The researchers purport to show there is a statistically significant difference between different dietary habits on weight gain over a period of five years. The dietary patterns observed included meat-eaters, fish-eaters, vegetarians and vegans. At the end of the five years, there was no difference between the groups. This is stated, very clearly, in the abstract: The differences between meat-eaters, fish-eaters, vegetarians and vegans in age-adjusted mean BMI at follow-up were similar to those seen at baseline.

But then we find creativity at work with the data - after massaging the data to death, it's finally found that vegans gained less weight annually than fish-eaters; who in turn gained less weight than meat eaters. The conclusion - During 5 years follow-up, the mean annual weight gain in a health-conscious cohort in the UK was approximately 400g. Small differences in weight gain were observed between meat-eaters, fish-eaters, vegetarians and vegans. Lowest weight gain was seen among those who, during follow-up, had changed to a diet containing fewer animal food.

How much weight are we talking here? Oh, an ounce or so. So completely insignificant and totally able to be skewed by something as benign as a participant drinking a glass of water before they weighed.

But, convert the ounces to grams and, viola!, you have differences that suddenly reach statistical significance deemed worthy of publication, press releases and media attention!

What we really have here is data that's completely worthless - it offers us nothing more than a lesson in data massage and creative presentation. At the end of five years there was no statistical difference between the groups in pounds or kilograms, and there certainly was no clinical significance to support the media attention or recommendations making the rounds to eat less animal foods.

Metabolic Syndrome - Which Came First, the Chicken or the Egg?

At the annual meeting of the American College of Cardiology earlier this month, some startling figures were presented - there's an alarming rise in the number of people with the constellation of heart-disease risk factors known as the metabolic syndrome: the presence of at least three of the following risk factors: obesity, high blood pressure, high triglycerides, low HDL cholesterol, or high fasting blood sugar.

Additionally some clinicians also consider high LDL, high insulin, and waist-hip ratio or abdominal adiposity as risk factors. Some are also measuring inflammatory markers like C-Reative Protein (CRP).

The incidence of metabolic syndrome hasn't just increased - it is skyrocketing. As reported on WebMD - Metabolic Syndrome Skyrocketing - Despite the improvements seen in some heart disease risk factors, a survey of nearly 80,000 people showed that rates of the metabolic syndrome continued to rise both in the United States and in Europe.

The surge is driven mainly by the epidemic of obesity in the Western world, says researcher Benjamin A. Steinberg, a Sarnoff fellow at Brigham and Women's Hospital in Boston.

We're not doing much better with cardiovascular disease either. The survey estimates that in 1998, 61.4 million American adults were estimated to have cardiovascular disease or risk factors for coronary heart disease. That figure rose to 66.7 million in 2001 and to 67.2 million in 2004.

This is in light of the improvements seen with cholesterol levels across the board!

During the six-year period, some major gains were made in reducing the number of people with heart disease risk factors.

For example:

• The percentage of people with high triglyceride levels dropped from 46% to 40%.
• The number of people with low HDL cholesterol levels decreased from 35% to 33%.
• During this time frame the use of cholesterol-lowering statin drugs increased from 37% to 52%.

Yet despite these improvements, the rates of the metabolic syndrome rose from 36% to 44% during the same period.

So, what do the "experts" tell us is driving the alarming rate of metabolic syndrome?

Obesity.

That means the rise [in the metabolic syndrome] is primarily driven by the skyrocketing rates of obesity -- from 30% to 48% -- during the six-year period, says America Heart Association president Robert Eckel, MD, professor of medicine at the University of Colorado Health Sciences Center in Denver.

"Although several components of the metabolic syndrome are better off, people are still much more likely to be obese," he tells WebMD. "We have to continue to target obesity to reverse these trends."

Yes, I'm shaking my head here, wondering if they'll ever "get it."

Metabolic syndrome is one of those "chicken and egg" disorders - which came first, the metabolic dysfunction or the obesity, dyslipidemia, hypertension, insulin resistance, or high fasting blood sugars? The American Heart Association (AHA) apparently believes it is the obesity driving the disorder. Their recommendation - a low-fat diet to reduce weight coupled with increased physicial activity.

The problem with that recommendation? Data from numerous trials shows that a low-fat carbohydrate rich dietary pattern actually worsens the other risk factors for metabolic syndrome with increased triglycerides, decreased HDL. Without significant weight loss, such a diet may also increase insulin resistance and worsen fasting blood sugars due to the high carbohydrate intake required to achieve a fat intake less than 30% of total calories.

The AHA is fully aware of this, yet continues to ignore the data that clearly points to a low-carb diet as a better approach to tackle ALL the risk factors with dietary modification. The Nutrition & Metabolism Journal recently published the review, Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction, that included 112 references.

The bottom line? The review summary stated: Five symptoms common to most definitions of MetS are those that are reliably improved by CHO restriction. Carbohydrate restriction is one strategy for weight loss but, in addition, improves glycemic control, insulin levels, TAG and HDL levels even in the absence of weight loss. We suggest that response to CHO restriction may, in fact, be an operational definition of MetS. Its underlying basis would rest on the idea that the features of MetS are associated with a disruption in insulin metabolism which is strongly influenced by dietary CHO. The extent to which this definition is useful may depend on its application by individual practitioners. Experimental studies that follow its lead or conversely disprove its fundamental premise should advance our understanding of obesity, diabetes and CVD. Dismissing CHO restriction without evidence, or expressing "concerns" rather than offering data will probably be less productive.

Folks, obesity is indeed contributing to the increase in metabolic syndrome. However, the answer to reverse the trend is not as simple as losing weight. The only way to reverse the trend is to identify the driving factor behind our obesity AND metabolic dysfunction issues - resolve the underlying reason for our weight gain and identify what is disrupting our metabolic pathways so negatively.

The AHA takes the simplistic approach - eat less and exercise more - as the solution.

I'd like to know just how many people haven't already heard that advice and tried it only to fail again and again as their metabolic dysfunction worsens and their risk factors increase?

Until we move past the deeply rooted dogma that preaches the carbohydrate rich low-fat diet as the end-all-be-all and actually move instead toward an evidence-based approach, we're going to continue to see the alarming rate of metabolic syndrome rise higher and higher.

You don't have to wait for the "experts" to finally "get it" - your long-term health depends on educating yourself about what the science says, what the research data shows us and making an informed decision about taking control of your diet to improve your risk factors. A controlled-carb approach offers improvements in weight, HDL cholesterol, blood pressure, triglycerides, insulin senstivity and glycemic control.

If you're waiting for the leading organizations to suddenly accept and take the evidence-based approach any time soon and give you a greenlight to follow a controlled-carb diet - well, let's just say you might not want to hold your breath. There is way too much invested in the dogma and things will not change until the perspective is changed to focus on public health instead of the bottom-line dependent on the status quo.

Cholesterol & Food

On March 9, 2006 I wrote about the findings from a study using a "portfolio" of foods in an attempt to use a low-fat diet to lower cholesterol. Today, the Washington Post carried Sally Squires take on that study in the Lean Plate Club - Portfolio Diet: Tough to Stay Invested In.

As is often the case, I have to wonder if Ms. Squires read the full-text of the study or not. More troubling is her recommendations to swap the foods that were part of the study for other foods, even though those foods were not part of the trial!

My article on the study is here: This is Success?

I'll add today, that the results were not impressive when you consider that 70% of those who followed the diet enthusiatically did not see a benefit. In reviewing various dietary interventions, a low carbohydrate diet has a much more dramatic effect on cholesterol levels and ratios in a much shorter period of time. Diet can indeed be used to effectively improve cholesterol - a low-fat diet is not the best option however.

Ketoacidosis - A Complication of Atkins' Diet?

Today's headline in Bloomberg caught my attention - Low-Carb Atkins Diet Isn't Safe for Losing Weight, Doctors Say - sounds like the same old, same old warning, huh?

The opening sentence is certainly alarming: The low-carbohydrate Atkins diet, which experienced a peak of popularity two years ago, isn't safe and shouldn't be recommended for weight loss, according to doctors writing in The Lancet.

And once you get past the first few paragraphs you find the cause for this 'sounding the alarm bells' - In a case report, doctors including Klaus-Dieter Lessnau, clinical professor of medicine at New York University School of Medicine, described a 40-year-old white female patient from February 2004 who was vomiting as often as six times daily and had difficulty breathing after strictly following the Atkins diet for a month. She reported a weight loss of 9 kilograms (20 pounds) while on the diet.

I really had to go read the case study for myself since the media reports, found in literally hundreds of sources today - from the Chicago Sun Times to Forbes, from ABC Online to USA Today - are carrying the story with scant details.

The details from the media include: the woman was 40-years old, obese, vomiting six times a day, and the Atkins Diet caused her to develop ketoacidosis.

The case study was published in the Lancet. Fortunately for all the alarmists, it's within the confine of "premium content" so it's not publically accessible without paying to read it. I'll just say here that limited access must go by the way-side if we're going to advance evidence-based medicine...full open-access is the way to do this, but that's an entirely different subject!

So, what did the case study tell us that the media isn't? More importantly, does the information contained within justify the frenzy of alarm today?

Let's tackle the first question first. Within the case report are the following details: the woman was 40-years old, obese with a BMI of 41.6, who'd followed the 1972 version of the Atkins diet for one-month before she lost her appetite and started to feel nausea. During that time before she started feeling ill, she was eating meat, cheese and salads daily, was taking an assortment of nutritional supplements and lost about 20-pounds in the month. Five days prior to her emergency room visit for shortness of breath, she'd vomited four to six times a day.

The report notes that other than the mild distress, clinical examination was "unremarkable" with normal vital signs. Blood tests showed a high level of lipase (indicative of pancreatitis) with normal amalyse, which confuses things since both are elevated with pancreatitis - sometimes this type of reading is actually suggestive of something more sinister happening, specifically cancer. But we find no mention of that possibility in the case report.

The report does state, clearly, that a CT scan of her pancreas on admission was normal. Interesting, at least to me, is that with ketoacidosis her glucose would be high (at a level greater than 14mmol/l - hers was 4.2mmol/l) and her sodium would be abnormal, yet it was normal according to the report. But, hey, what do I know?

The diagnosis of ketoacidosis in this woman was based on "The differential diagnosis of high-anion-gap metabolic acidosis includes ingestion of methanol, ethylene glycol, or salicylate, L- or D-lactate acidosis, and ketoacidosis due to diabetes mellitus, alcohol, or starvation." It's clearly stated that "Our patient denied alcohol use; her serum osmolar gap was 0, which excludes the presence of unmeasured osmotic agents such as methanol or ethylene glycol; L-lactate concentration was normal; and salicylate was undetectable. D-lactate acidosis was unlikely without antibiotic use or bowel surgery. Serum was positive for acetone, and ß-hydroxybutyrate was high at 390 µg/mL (normal 0–44 µg/mL), consistent with ketoacidosis."

Quite frankly, the level of ketones in her urine are not alarming for someone who is not diabetic or someone properly following a low-carb diet...but let's keep moving forward and get through this report. The author states that in trials where children are fed a ketogenic diet for epilepsy ketoacidosis is a complication.

Unfortunately, the reference he cites as his evidence, did not have ketoacidosis due to diet as a complication. Nice try though - Fanconi's renal tubular acidosis, reported as a complication in one patient in his citation, is a disorder that may be inherited as a primary disorder or may be one symptom of a disease that affects many parts of the body. Researchers have now discovered the abnormal gene responsible for the inherited form. More often, however, classic distal renal tubular acidosis is a complication of diseases that affect many organ systems (systemic diseases), like the autoimmune disorders Sjögren's syndrome and lupus.

Gotta give him credit for trying! I check referenced citations specifically because I see, too often, a study referenced and when you read through the data, the data doesn't support the use of the citation in context to support an assertion.

Here's the main problems with the case report.

The symptoms of acute methanol poisoning are shortness of breath, vomiting, headache, with metabolic acidosis occuring often. The course of treatment for her was dextrose and sodium bicarbonate infusion - the course of treatement for methanol poisoning.

She'd been vomiting for days - that alone will upset her electrolyte levels and cause dehydration. Five days of vomiting - well, you can imagine just what state her body was in by that time. The vomiting and dehydration are glossed over as inconsequential to make the case it was the diet - and only the diet.

So what's that now? Two possibilities besides the diet?

How about another - maybe she did drink alcohol and that disturbed her metabolism leading to the acidosis state. Yes, alcohol can do this to a person, regardless of the diet they consume!

Lastly, she may have actually had undiagnoised diabetes and/or a cancerous tumor that would have also served as the catalyst for her symptoms.

We just don't know since none of the other possibilities were explored - the diet was the cause in the mind of her physician, so there was no further investigation.

That troubles me - we have thousands of participants from hundreds of studies to date and not one incident of ketoacidosis. Is it possible this woman's ketoacidosis was a result of her diet? I would say it's not impossible, but very highly improbable given the reams of data from clinical trials to date that have not found ketoacidosis as a complication, even in diabetic patients following a low-carb diet.

The reason it isn't a complication is that dietary ketosis, in and of itself, does not cause ketoacidosis. More likely this woman experienced ketoacidosis as a result of something else and unfortunately her diet placed an obstacle in front of a complete investigation as to its cause.

That said, I cannot state strongly enough that one person is not evidence to indict a low-carb diet as dangerous. Which leads to my answering the second question above - does the information contained within justify the frenzy of alarm today?

We do not see this frenzied alarm when someone in a statin trial experiences complications which may or may not be related to the drug nor do we see such alarm when someone participating in a low-fat diet trial experiences a complication which may or may not be due to their diet.

In the real world, one person in a case study presenting information about one person is considered to be the "n of 1" - meaning there is no other person to compare them to - their symptoms and course of treatment are in isolation to a greater population and highly dependent on the investigation, or lack thereof, of causes related to the symptoms.

While this particular case study was interesting, it remains an "n of 1" since there are no other reports of this type of complication from any other clinician in the world, and the physician did not, in my opinion, explore all avenues for cause since he believed it could only be her diet - short-sighted and a headline grabber to be sure.

Good science? No.

Correction: In the originial publication of this article I noted the woman's blood pH was normal. In reviewing the case report again, I realize I read through the details too quickly and was incorrect - her pH was lower than normal, suggestive of acidosis. The sentence was edited out for accuracy.

Revisiting the Glycemic Index

Last month the British Journal of Nutrition published a study, Towards understanding of glycaemic index and glycaemic load in habitual diet: associations with measures of glycaemia in the Insulin Resistance Atherosclerosis Study, that concluded "The present results call into question the utility of GI and GL to reflect glycaemic response to food adequately, when used in the context of usual diet."

Today, an article about the study is found in The State that opens with "It’s trendy, it’s diet-y and it’s hard to understand. So naturally, the glycemic index has inspired all kinds of “expert” commentary and plenty of confusion among consumers. But a USC researcher says the glycemic index is so flawed, it’s pretty much useless for people trying to lose weight."

So, just what did this study investigate and what were the findings? More importantly, are the findings useful?

As I read through the full-text of the study, something immediately popped-out - the calculations for the food values were based on faulty assignment of glycemic index values. For example, cheese was arbitrarily assigned the same value as milk. Milk in the United States has a glycemic index value of 40 - low GI. Cheese hasn't been assigned a value, and you'd be hard pressed to find someone who would consider cheese as having a GI of 40 due to its protein and fat content, which makes it nearly impossible to test.

The reason it is difficult to test cheese is that consuming enough to reach the "test-load" intake - that is, eating 50g of digestible carbohydrate to reach the level to test - means you'd have to find enough people able to actually eat 8.6-pounds of cheese! So, that alone makes the data suspicious in my mind - assigning a value to an untested food, bad science!

But, that wasn't the only issue I had with the design of this study. The researchers used data from Food Frequency Questionaires (FFQ) not designed to measure glycemic index and/or glycemic load. Whether the assigned values are correct or not (I think they were inaccurate), those considered to be consuming a "low glycemic index" diet were in fact still eating a high level of carbohydrate at baseline and after five years.

One red flag that makes this an easy conclusion is the low amount of fiber in the diets - at baseline 16g on average and at the five-year evaluation 15g on average. This level was in the context of a high intake of carbohydrate - at baseline the average intake was 235g of carbohydrate, at five years it was 222g of carbohydrate.In looking at the assigned values from low to high for glycemic index - each level was HIGH, therefore the data was really only evaluating the effect of a high GI diet with a higher GI diet with an even higher GI diet, not a low GI against a high GI diet.

That's an important distiction here - and it is further supported by looking at the Glycemic Load (GL) levels assigned and assessed.

It is believed that GL is much more important at the end of the day than the GI of any one food or an entire day's GI measure. That's because the GI is not based on serving size of a food, but rather consumption of a specific level of digestible carbohydrate - 50g - in one sitting. With some foods a very small portion reaches this 50g intake, for others, like the cheese example above, the portion is so enormous it makes testing the food impossible and unnecessary. GL, on the other hand, is a calculation based on actual serving size of a particular food. For example, carrots have a high GI, but because you'd have to eat such a large portion to consume 50g of digestible carbohydrate, the actual serving size of a portion is measured and carrots are ranked as having a low GL.

I was happy to see that the research team tried to evaluate both the GI and GL because it provides support to my contention that few were following a low GI diet since only a small number actually fell into the low GL category - of the five groupings from low to high for GL, only one was calculated to consume less than the GL target of 100 to be considered consuming a low GI/GL diet. All the other groups ranked well above that 100 GL mark, so they were all consuming a higher GL diet. So again, we find comparison between high GL with high GL for the vast majority of those evaluated and for the one group that did seem to consume below the target GL level of 100, there is question with that due to the arbitrary assignment of GI values for untested foods as mentioned above.

My own opinion about the glycemic index is that it is very complicated and not really a very useful tool for the average dieter trying to lose weight. There is a lot of picking and choosing based on GI or GL numbers instead of nutrient-density. That said though, if one does follow it correctly - strive to maintain a low glycemic load each day by picking nutrient-dense selections - you're much better off than just eating a calorie restricted diet consuming whatever with only calories as your focus.

I personally think there are easier ways to plan what you're going to eat each day - simple basics - like real whole foods as the foundation of each day with lots of non-starchy vegetables, limit sugars and skip the processed junk food. Odds are high that if you're doing that, you're consuming a low GI diet anyway!

Here's an idea for researchers serious about investigating the efficacy of a low GI/GL diet - deisgn a study specifically to measure two or more groups consuming different levels over a period of time. Give the low GI/GL group specific foods allowed with instuctions on how to be compliant with the diet, the next group same thing, but higher value for GI/GL allowed and then have a control group eating whatever they want. Follow them for five years and then get back to us with REAL DATA!

Findings from Crestor [Statin] Study

While the headlines are screaming out for your attention to highlight all the 'benefits' of taking a statin cholesterol medication for reducing the risk of a heart attack, let's step back a moment and take a closer look!

The very convincing headline on MSNBC yesterday - Statin drug shown to reverse heart disease - might lead you to believe taking a statin may be a good preventative step to reduce your risk of heart disease. The actual study remains unpublished as it is scheduled for release in JAMA in the April 5, 2006 edition.

From the March 13, 2006 JAMA press release about the study, we learn that the trial included participants with coronary artery disease, specifically atherosclerosis. The study was designed to determine the effects of high-intensity statin therapy on IVUS-derived measures of coronary atherosclerosis regression. This is the first critical item in the study - patients in the study already had established coronary disease. If you read through the MSNBC article however, this tidbit is missing - nowhere in the article are readers informed the study was conducted on those with established coronary artery disease.

The findings are quite impressive - the therapy, which included high doses of Crestor (rosuvastatin) reduced LDL, increased HDL and also resulted in a slight demonstrated regression of their atherosclerosis. On average, LDL fell from 130mg/dL to 60.8mg/dL; HDL rose from 43.1mg/dL to 49mg/DL; and "[f]or the primary efficacy parameter of change in PAV, the average decrease was -0.98 percent and 63.6 percent of patients showed regression of atherosclerosis. For the second primary efficacy parameter, change in atheroma volume in the 10-mm subsegment with the greatest disease severity, there was a median (midpoint) reduction of 9.1 percent in atheroma volume, and 78.1 percent of patients demonstrated regression of atherosclerosis. The secondary efficacy parameter, change in total atheroma volume, showed a 6.8 percent median reduction."

Did you catch those numbers? I hope you did - the study subjects already had pretty good cholesterol levels. While 130mg/dL is the level at which the American Heart Association recommends one consider drug therapy for those with existing coronary heart disease, the participants in this study did not have an alarming LDL level - they were, on average, just at the level to consider a drug intervention. More important, the participants' HDL level was well within the "normal" range of 40-50mg/dL with an average of 43mg/dL.

This leaves me with a question - I wonder if cholesterol really is the end-all-be-all measure in the process of coronary disease as we're repeatedly told? I've wondered this for quite some time actually - and this study just reinforces my doubts. Had the average patient in this study walked into their doctor's office, alarm bells would not have been sounding all that loudly about their cholesterol levels. Even if their clinician was a bit concerned about their LDL, a level of comfort would have come from the HDL readings. Add to that our knowledge that 50% of people who have heart attacks have a normal level of cholesterol.

Hmm...might be easy to say our target levels are still too high. But, to answer that, we also must consider that our target levels truly are accurate and cholesterol isn't really the issue - something else is and we're still missing what that is.With this study we are still missing critical pieces of data - we have no idea what their total cholesterol was, nor do we have any clue what their triglycerides were. We're left in the dark about other known risk factors - like blood pressure, inflammatory markers, weight and activity levels.

Until the publication of the paper, we'll just have to be patient - this additional information is critical to effectively analyze the total effect on cholesterol - did the therapy result in an improved cholesterol ratio? Did it improve triglycerides? Did it have an effect on blood pressure? Did it reduce inflammation? Did participants actively seek to normalize their weight? Were these folks active?

Without the additional data, we simply cannot make a judgement about whether this therapy provided real improvements and/or if there were confounding variables to consider. Yes, the therapy improved LDL and HDL and led to a small regression - but what does that mean for the long-term? At this point, I'm fairly certain that in the long-term, this therapy is not going to be as effective as the headlines want us to believe - it's notable that the press release stated that "[a]dverse events were infrequent and similar to other statin trials."

So, during the term of this study, adverse events [read: deaths and/or other complications or compromises in health] were similar to other studies. At the end of the day, this means that the therapy had little effect on quality of life or whether one would die without the therapy when compared with those using the therapy. Hey, they did improve some measures of their cholesterol and had a regression - but they didn't live longer or better, did they?

I'm not surprised the numerous articles in the media aren't including this information though - it might make someone think twice about whether the positives of the therapy outweigh the negatives. I'm also not surprised that the media isn't highlighting that this was designed as a "secondary prevention" trial - that is to evaluate if a therapy can cut your risk of having another "adverse event" when you've already had one.

This type of study is very different from those designed to evaluate a therapy for "primary prevention" - that is to answer the question of whether a therapy will be effective to reduce the risk of having the first-time "adverse event."

Basically, if a study is not designed to measure primary prevention, its data should not be extrapolated as evidence of efficacy for a healthy population or even a population with a few risk factors who have not yet experienced an adverse event. But, I can almost guarantee that's what's going to happen with this study - we're going to start to see the recommendations call for more aggressive drug intervention in the near future. Just pay no mind to the fact that "[a]dverse events were infrequent and similar to other statin trials."

At least one of the study co-authors did issue a caution in another press release from JAMA regarding the study - Editorial co-author Navin K. Kapur, M.D., a clinical research fellow at Hopkins, adds that, “Researchers’ next steps have to determine whether these very promising results translate into greater reductions in future heart attacks and strokes.”

When Will We Change Course for Metabolic Syndrome?

The current approach to treating Metabolic Syndrome - a constellation of metabolic maladies in concert together - dyslipidemia (low HDL, high triglycerides, and/or high LDL), obesity, high blood sugars, high insulin levels, high blood pressure - is basically "isolation" treatment. That is, each feature is treated on its own rather as a single problem, rather than a more comprehesive approach that recognizes the reality that these features are not occuring in isolation, but are red flags to a systemic issue of metabolism dysfunction.

For example, if you have high blood pressure, obesity and dyslipidemia, the approach is often a statin to tackle the cholesterol problem, a blood pressure medication to bring BP under control and recommendation to lose weight.

This, in my opinion, is only placing a band-aid on the problem and not taking the critical step necessary to reverse the metabolic dysfunction at the root of the problems.

Will medication lower the cholesterol? Perhaps - but it isn't addressing why the cholesterol is rising or forcing a change to actively resolve the cause and may have side effects that cause another problem.

Will medication lower the blood pressure? Perhaps - but it isn't addressing the cause of the elevation, only managing the problem and may have side effects that cause another problem.

Will losing weight make a difference? Perhaps - but even that too isn't addressing the underlying cause of the obesity in the first place. With the failure rate as high as it is, without establishing a long-term eating pattern to not only lose weight, but keep it off, is only a short-term fix.

The same holds true for the two items I didn't include in my example - blood sugars can be "controlled" with medication and/or insulin injections, but these do not fix the metabolic disturbance - these act only as a band-aid and do not improve the metabolic function of the body.

With the recent findings, presented at the 55th Annual Meeting of the American College of Cardiology (ACC), that since 1998 there has been a 50% rise in the incidence of Metabolic Syndrome, we must begin to demand accountability and establish standards of care that require improvement in whole body metabolism, not just management of the syndrome.

We've got a lot of band-aids out there, but still have an alarming surge in the rates of Metabolic Syndrome. We're doing something wrong here and instead of wringing our hands and continuing down the path to nowhere, it's time to step back and re-evaluate the evidence that clearly shows marked improvement in those with Metabolic Syndrome when they are placed on a low-carb diet.

While such a diet is politically incorrect, there is no denying the strong support in the data from numerous trials that found significant improvements in all features of Metabolic Syndrome when the dietary approach was low in carbohydrate (60g net or less carbohydrate a day). Not only does the diet appear to effectively reverse the features of Metabolic Syndrome, it also reduces or eliminates the need for many of the medications used to manage the features of the disorder.

So, why does the medical establishment continue to dismiss the findings and continue with medical management and less effective dietary intervention? At this point in time, I can only reach one conclusion - profitability. A patient is simply not as profitable to a medical practice, pharmaceutical company or other corporate interests if they are able to reverse their metabolic disorder by implementing a controversial, yet scientifically supported, dietary approach.

Do I think those making recommendations are consciously thwarting the dissemination of this critical evidence?

Honestly, probably not - I think it's more likely from years of deeply rooted dogma driving the decision making process more than a purposeful attempt to keep people sick. But, at this point in time, with the alarming rates continuing to rise even further, we seriously need to step back from our assumptions and stick with the evidence and not our consensus driven dogma that simply does not have a foundation in the evidence.

Low-Carb Menu Planning Made Easy

So, you need to plan a low-carb menu for yourself and are at a loss where to start?

Over the years I've played with various approaches to creating menus and I've found the easiest place to begin is with your carbohydrate allowance for the day.

For the purpose of this article I'll use 20g net carbs as is allowed during the first two weeks of the Atkins diet - but the principles of menu planning detailed here are the same regardless of low-carb diet you're following.

To be clear, "net carbs," is the total carbohydrate minus fiber. I do not recommend subtracting carbohydrate from other sources often recommended - sugar alcohols, inulin, glycerine, etc. Also, the following menu is for illustrative purposes to take you step-by-step in the process of menu planning. To be sure you're choosing nutrient-dense foods, I recommend using online software (free) at FitDay.com which has a reporting feature that determines your nutrient intake and keeps track of carbs, protein and fat!

No matter which low-carb diet you follow, one half of your net carbohydrate (total minus fiber) should be from non-starchy vegetables and/or salad greens. This "rule of thumb" - 50% of net carbohydrate each day from non-starchy vegetables - holds true until you reach a point where you're consuming 40g net carbs each day. After that time, you still plan for 20g net carbs as your foundation each day, but can choose from other carbohydrate foods to increase your carb intake to add variety!

To do this, you start by selecting choices that will give you a 10g net minimum for the day and place them into your menu.....as you do this, note how many net carbs each selection has.....and for now plan ONLY carbs from salads and veggies at this point...

Breakfast
Spinach, 1/4 cup cooked - 0.6g
Net Carbs = 0.6g

Lunch
3 Cups Lettuce - 1.2g net
3 Cherry Tomatoes - 1.8g net
1/4 Cucumber - 1g net
Net carbs = 4g

Dinner
1 Cup Green Beans - 5.8g net
Net Carbs = 5.8g net

Net Carbs so far = 10.4g

Not bad - you have now planned for 10.4g net carbs just from your veggies/salads. If you need more after you plan other things, add them later......but at this point, move on to plan your protein sources now.....at this point, only add in those things you'll be eating that are protein rich...adjust your net carbs for each meal where appropriate.

Breakfast
Spinach, 1/4 cup cooked - 0.6g
2 Eggs - 1.2g
3 Slices Bacon - 0.3g
Net Carbs = 2.1g

Lunch
3 Cups Lettuce - 1.2g net
3 Cherry Tomatoes - 1.8g net
1/4 Cucumber - 1g net
6oz can tuna in water - 0g
2 TBS Shredded cheddar cheese - 0.2g
Net carbs = 4.2g

Dinner
1 Cup Green Beans - 5.8g net
6oz hamburger - 0g
2/3 oz real American cheese (1 slice) - 0.3g
Net Carbs = 6.1g net

Total net for the day so far = 12.4g

But now you need to include fats and fat sources that may have carbs too.....again, add to the menu, this time your fats/oils and fat sources...again, add additional carbs where appropriate to the meal totals and the day's total so far.....

Breakfast
Spinach, 1/4 cup cooked - 0.6g
2 Eggs - 1.2g
3 Slices Bacon - 0.3g
1 Tsp butter to cook eggs - 0g
Net Carbs = 2.1g

Lunch
3 Cups Lettuce - 1.2g net
3 Cherry Tomatoes - 1.8g net
1/4 Cucumber - 1g net
6oz can tuna in water - 0g
2 TBS Shredded cheddar cheese - 0.2g
3 TBS Creamy Dressing for salad - 1.5g
2 TBS Mayonnaise for tuna - 0.9g
Net carbs = 6.6g

Dinner
1 Cup Green Beans - 5.8g net
6oz hamburger - 0g
2/3 oz real American cheese (1 slice) - 0.3g
1 TBS butter for green beans - 0g
Net Carbs = 6.1g net

Total net for the day so far = 14.8g

So, now you have your meals planned, but you have not included "extras" you might have like beverages, artificial sweetener, etc. Plan these now....(and add carbs where appropriate.

Breakfast
Spinach, 1/4 cup cooked - 0.6g
2 Eggs - 1.2g
3 Slices Bacon - 0.3g
1 Tsp butter to cook eggs - 0g
6oz decaf coffee - 0.5g
2 TBS Half & Half - 1g
1/2 Packet Splenda - 0.5g (1/2 AS)
Net Carbs = 4.1g

Lunch
3 Cups Lettuce - 1.2g net
3 Cherry Tomatoes - 1.8g net
1/4 Cucumber - 1g net
6oz can tuna in water - 0g
2 TBS Shredded cheddar cheese - 0.2g
3 TBS Creamy Dressing for salad - 1.5g
3 TBS Mayonnaise for tuna - 0.9g
Net carbs = 6.6g

Dinner
1 Cup Green Beans - 5.8g net
6oz hamburger - 0g
2/3 oz american cheese (1 slice) - 0.3g
1 TBS butter for green beans - 0g
1 oz slivered macadamias in green beans - 0.9g
Net Carbs = 7g net

After dinner you want a sugar-free jello - 1g (1 AS)
2 TBS Heavy cream whipped up with - 0.8g
1/2 Packet Splenda - 0.5g (1/2 AS)
Net Carbs = 2.3g

Total net for the day so far = 20g net carbs, with 10.4g from veggies and salad greens, you get in 52% (most) of your carbs from veggies/salads. If you do this for each meal each day and plan this ahead of time, you have a much easier time with how many carbs you're eating each day - you'll know ahead of time if you're on track for the day.

Insuring Diet Failure

Quick - what's the best way to keep an obese person obese in the long-term?

Have them diet with starvation level calorie restriction!

That we understand starvation doesn't work in the long-term (unless you can live the rest of your life hungry) doesn't seem to matter - Blue Cross Blue Shield is shelling out $5-million to study weight loss in the obese with pharmaceuticals and starvation diets in an effort to "measure the safety, cost and effectiveness of the more traditional approaches against those of the surgery," according to an article on MSNBC.

They need to spend $5,000,000 to find this approach isn't going to work in the long-term? Have all previous studies on the subject been for naught? Is this study really any different - so different that it's bound to find something new and exciting?

Those taking part in the study will be divided into four groups. Two groups will consume 800 calories a day, with most calories coming from a packaged, nutritionally dense powder to be mixed into shakes, soups and other foods. The other groups will consume 1,200 to 1,500 calories a day. Half of the participants will take an FDA-approved appetite suppressant or fat-blocker while the other half receives no medication. All will receive behavioral treatment to learn how to manage their diets, prevent relapses and stay motivated, and all will be encouraged to walk daily, eventually three miles.

I don't know about you, but I can already tell BCBS what their result will be - initially those participating will lose weight, a portion will become dependent on the stimulants and require rehab, there will be a high drop-out rate overall and those that manage to stick it out, they'll gain the weight back once they increase calories to what should be "normal intake" for their new weight.

There is a better way - yet this study, like so many others - fails to consider including it.

A carefully planned, nutrient-dense low-carb diet ad libidum (eat as much as you want from the allowed foods). Calorie intake will take care of itself and those following such a dietary approach will have a better chance of losing the weight while not feeling hungry, thus reducing the risk of failure!

This is Success?

Today a study was published in the American Journal of Clinical Nutrition, touting the benefits of a diet rich with plant sterols, almonds, and soy - Assessment of the longer-term effects of a dietary portfolio of cholesterol-lowering foods in hypercholesterolemia - that concluded "More than 30% of motivated participants who ate the dietary portfolio of cholesterol-lowering foods under real-world conditions were able to lower LDL-cholesterol concentrations more than 20%, which was not significantly different from their response to a first-generation statin taken under metabolically controlled conditions."

Wow - so 70% of motivated participants apparently didn't have the same "beneficial" outcome.

But, let's see just how the data in this study bears out, shall we?

At baseline, the profile of the participants shows they were consuming well within the "heart healthy" guidelines already, consuming on average, 25.2% total fat, just 6.8% saturated fat, just 141.3mg of cholesterol daily on average (89.5mg/1000 calories, 1579 calories a day average) and the requisite 55% carbohydrate (54.6%).

The cholesterol at baseline - one word - horrible, even with their "heart healthy" eating habits:

TC = 261
LDL-C = 173
HDL-C = 48
TG = 203
TC/HDL Ratio = 5.76 (actual as reported by the researchers)

So, then, what happened at the end of a year?

Well, there was improvement in their cholesterol:

TC = 234
LDL-C = 150
HDL = 49
TG = 175
TC/HDL Ratio = 5.03 (actual reported by researchers)

First let me say - these "improvements" were unimpressive - on average the group still had borderline high total cholesterol, LDL-C and triglycerides and only minor movement with their HDL-C. Their TC/HDL ratio remained way too high.

The researchers concluded that it was the dietary portfolio of almonds, soy, oats and other foods with plant sterols that was responsible for the improvement.

I wondered, did anything else change?

Interestingly, the percentage of saturated fat in their diets did decrease, but the actual amount eaten remained exactly the same at one-year as it was at baseline because they increased their calorie intake over the year.

Not only did they increase calories, they increased fiber, fat, polyunsatured and monounsaturated oils, and significantly decreased their intake of cholesterol.So the question begs - were the results due to the "dietary portfolio" of almonds, oats and soy, or the other dietary modifications that occured? Or, something else?

Sadly, the researchers don't explore the confounding variables in their data. They also failed to have a control group to compare the dietary intervention group against and instead compared results the effect of statins for cholesterol reduction. Also noteworthy is the study is one-year and cannot accurately predict long-term outcomes or even show long-term outcomes from such a diet - will a diet like this reduce heart attacks, will it reduce all cause mortality over the long-term?

Who knows?

Cut the Carbage!

The other day, I wrapped up my column, Repetition Turns Myths into Truths if You Can Just..., with the promise to continue with a definition of a controlled-carb diet and highlight the "how to" of the approach to help with understanding its superiority as a dietary defense for long-term health.

After years of reviewing the literature, the only conclusion I can honestly reach is that neither the carbohydrate-rich low-fat diet (what we're told to eat) or the Standard American Diet (what we actually eat) is optimal - on a population-wide basis - for our long-term health. We have thousands of studies comparing the two diets - in the hope one day it will be clear that a carbohydrate-rich low-fat diet is better for us. The problem is, that no matter how many studies are done, the data remains very clear that there is little difference in long-term outcomes for those eating either diet.

What those same studies do provide us though are clues to the optimal diet for humans. We keep finding, for instance, that those who consume more vegetables and fruits tend to live longer, healthier lives; higher intake of whole grains often translate to better health; eating less sugar tends to protect us from obesity; adequate intake of protein offers reduction in health risks...the list goes on, but clearly points to the obvious - if you eat higher quality, whole food, you're healthier than your neighbor eating a steady diet of fast food and processed food.

But, because the data is viewed from a fat-phobic perspective - that is already biased to find support that low-fat diets are optimal - we've lost sight of the truth - whole, nutrient-dense food is optimal.

The best definition of controlled-carb is that it is a dietary approach that offers the best chance to meet or exceed essential nutrients because it provides a wide range of nutrient-dense selections from all the food groups while also enhancing metabolic function because it is balanced.

The *limited* macronutrient in a controlled-carb diet is not fat, it's carbohydrate - where carbohydrates provide up to, but no more than, 40% of total calories each day. Controlled-carb diets also include low-carb diets, those that strictly limit carbohydrate intake, for one reason or another, but always include at least 20g of net carbohydrate each day (net = total carbohydrate minus fiber).

So, controlled-carb diets are a dietary approach with a range of carbohydrate intake - from as low as 20g net carbs, or less than 5% of calories each day, up to 40% of calories each day from carbohydrate. Unlike the carbohydrate-rich low-fat diet, controlled-carb diets are highly individualized - if you like eating or can tolerate a higher intake of carbohydrate you eat more, if you prefer less or have metabolic challenges with more carbohydrate, you eat less each day.

What is consistent within all the ranges of carbohydrate intake is that non-starchy vegetables MUST be the foundation of your daily diet...no if's, and's or but's about it. This is conveniently ignored by those who are convinced a carbohydrate-rich low-fat diet is optimal.

Rather than acknowledge the requirement of controlled-carb diets to increase (substantially) intake of non-starchy vegetables, they focus on the diets' allowing one to eat red meat, bacon or butter.

Yet, if you read through the dietary recommendations made by the various authors of different controlled-carb plans, you'll not find one that requires you to eat red meat, bacon or butter. These foods are allowed, they're not mandatory!

In fact, you can even follow a controlled-carb approach as a vegetarian or vegan.

Remember, the foundation of a controlled-carb diet is whole nutrient-dense food, with the foundation of non-stachy veretables, not just meat and fat.

Controlled-carb diets do allow you to eat a wide-variety of meats, game, poultry, and seafood, along with eggs and dairy. In fact, these protein foods are the "bricks" - the building blocks - added to the foundation of the diet - the non-starchy vegetables.

Together non-stachy vegetables and protein foods "pack-a-punch" nutritionally - these two foods together can provide all your essential nutrients without any other additions to your menu. Something none of the naysayers will tell you because they want you to believe you must eat fruit, grains, roots, nuts and seeds, and soy products to complete your nutrient requirements each day. The truth is, you don't have to - these other foods offer a variety in your menus, but are not *required* to meet your nutritional needs each day.

At the end of the day, the macronutrient ratio matters much less than the nutrient-density of your food intake. Controlled-carb dietary approaches give you the best chance of meeting and exceeding your nutrient requirements - carbohydrate-rich low-fat diets limit your potential nutrient intake. Period.

Want to know how to create a controlled-carb menu? Come back tomorrow when I'll take you step-by-step to creating a nutrient-dense low-carb menu and explain how to modify that to include more carbohydrate for a controlled-carb menu!

Evidence-Based Medicine - Science for a Change!

It may be surprising to learn that the gold standard of clinical guidelines - evidence-based medicine - is a recent concept. In the last decade, the idea that we must use hard data as the basis for medical decisions has taken root as our years of "that's the way it's done" tradition-based approaches are falling by the wayside.

The evidence-based approach took hold as our understanding that 'all evidence is not created equal' took hold and standardization of study design and weight came to be accepted. Studies are now subject to review to determine the "level" of weight the data should carry in assessing the conclusions and subsequent recommendations borne from that data. The highest level of evidence is "Level 1" evidence - these trials are considered the gold-standard and employ strict randomization and controls and are prospective - that is, looking forward.

Data gathered from studies that are retrospective, or less controlled, are weighted as less rigorous, thus not considered as highly as Level 1 evidence. These studies are still important though - they provide perspective and a different measure of findings. If you were to review the entire body of medical literature, most studies fall into the categories of Level 2 to 3 evidence since Level 1 data is more time consuming, costly and requires stricter control to take a study from start to finish.

Evidence-based medicine has taken hold in a wide range of specialties. Imagine my surprise though when my husband, Dr. Gil Wilshire, MD, FACOG, was invited to write an editorial in the journal, Age Management Medicine, on the topic of evidence-based approaches in anti-aging medicine. His editorial, The Evidence-Based Nature of Age Management Medicine, highlights how far we still must go to employ evidence-based medicine for our aging population.

The field of Anti-Aging Medicine, as perhaps no other, has been fraught with wild claims and unsupported assertions. In preparing to write this editorial, I randomly read through a sampling of various popular websites. As you can confirm for yourself, the “literature” is full of case studies (“N’s of one”), cross-species inferences, improper use of surrogate markers, and lack of proper control groups. I do not mean to disparage this entire field. By definition, the study of the medical issues of aging requires a long time to study! The testing of some of the most important currently contested hypotheses may potentially take generations to be done properly and effectively. The field of Age Management Medicine will present enormous challenges to the courageous investigators who choose to work in this field. For these reasons, the advent of this new, evidence-based journal represents a tremendous advancement for this specialty and for the advancement of human health in general.

His article is rich with information for any reader to develop their own critical analysis skills when reading a study. In it, you'll find information about common words that should be considered 'red flags,' common errors that appear in many studies, how to tease out conflicts-of-interest and some basic rules of thumb that will help you understand what you're seeing in a published study.

Enjoy!

Repetition Turns Myths into Truths if You Can Just...

..."Pay no attention to the man behind the curtain!"
The Wonderful Wizard of Oz

A month has passed since the publication of the null findings from the Women's Health Initiative Dietary Modification Trial and the media continues, in earnest, to try to convince you to stick with a carbohydrate-rich, low-fat diet. The repeated myths continue with a strong emphasis on eating less total fat but more monounsaturated and polyunsaturated fats in liquid vegetable oils instead of saturated fats in butter or meat. Emphasis is also placed on eating less animal foods and more plant foods with grains highlighted.

A few individuals are pointing out the flaws in the reasoning used to convince us that we should ignore the WHI null findings and continue to believe instead a low-fat diet is better for us in the long-term - the fatal flaws include things like trends are not useful, obesity remained an issue in both groups, risks increased in some women in the intervention group, etc. But this isn't stopping the "old guard" from basically telling us to ignore the evidence, just dismiss the fact that the study found no differences between the groups!

That very fact - that there was no difference - should be setting off alarm bells!

Basically, the Standard American Diet (SAD) is no worse than a low-fat diet - or conversely - a low-fat diet is no better than the SAD.

So, the one thing I totally agree with in all the media reports is this - the findings aren't a license to go out and eat whatever thinking it doesn't matter in the long-term. It does - and I'll tell you why...what few are willing to state is the obvious - neither diet is good for you or your long-term health.

And that is what you should care about!

We know, without a doubt, that the standard American diet, as it is today, is unhealthy for long-term health. Just look around you - two out of three adults are overweight, one of the two is obese. An estimated 25% of all adults have features of Metabolic Syndrome. Millions have Type II Diabetes. Cancer is now the leading cause of death in the United States. Cardiovascular disease is a close second. And now our children are out-pacing adults in diseases once thought to be only effecting the aged.

We also know, without a doubt, that a carbohydrate-rich, low-fat diet reduces intake of essential nutrients - especially fat soluable vitamins D and E, preformed vitamin A and often vitamin K; limited intake of animal foods limits our intake of complete protein (the best source for our essential amino acids) and vitamin B-12; and that switching to liquid vegetable oils significantly increases our intake of omega-6 and may disrupt the balance of our intake of omega-3 fatty acids negatively. Add to this our knowledge that a carbohydrate-rich, low-fat diet lowers HDL and increases triglycerides while also, often, increasing glucose and insulin and you start to understand the growing prevalence of Metabolic Syndrome, obesity and diabetes in this country.

Whether you eat the SAD or the recommended and highly touted carbohydrate-rich, low-fat diet, your chances of optimizing your health in the long-term are just not happening. Period. The proof is in the pudding - and the pudding is the WHI Dietary Modification Trial and numerous other studies - including, but not limited to the Nurses' Health Study, the Framingham Heart Study, MRFIT, the MRC trial, the Malmo Diet and Cancer Study, the Puerto Rico Heart Health Program, and the Caerphilly Study among others.

Taken together - the high number of studies that find a low-fat diet is not protective and/or does not reduce the risk of disease in the long-term and the known health related problems that crop up repeatedly if you eat the Standard American Diet - the findings should be making us dig deeper to find the answers to what type of diet really does give us a better chance to optimize our health in the long-term!

It's not like we're clueless - there are thousands of studies out there (yes, thousands) that keep telling us the same thing again and again:

• Essential Fatty Acids (EFA's) are critical, especially omega-3 fatty acids
• Intake of the full spectrum of Essential Amino Acids (EAA's) is critical
• Meeting nutrient requirements for vitamins, minerals and trace elements daily is critical and some, like vitamin B-12, are best met with quality animal food sources
• Non-starchy vegetables are rich in nutrients and fiber
• Body weight is important but not the end all be all of long-term health - interestingly, when we meet our basic nutritional requirements, weight often takes care of itself
• Stress is damaging both to our mental health and our endocrine system, increasing our nutrient requirements
• Low-level, chronic inflammation is deadly
• Failing to get adequate sleep and rest is damaging to our body
• Physical activity in our daily life keeps our body "tuned" and "toned"

With this simple list - the question is, how does one eat and what lifestyle modifications will lead to a good chance of long-term health?

To start to answer that, let's step back for one moment and ask a better question first - what type of dietary approach reduces the risk of overeating with the highest odds of meeting critical nutrients that provide long-term health benefits?

This question, instead of the first one, addresses two issues - weight and meeting nutritional requirements.The answer to that question is easy - a controlled-carb dietary approach.

A controlled-carb approach offers an opportunity for nutrient-density that is superior to a low-fat diet along with a high level of satiety that is missing in a low-fat diet. Tomorrow we'll go step-by-step with a definition and comprehensive look at what a controlled-carb nutritional approach looks like and tap the evidence to see just how strong the data is and why the evidence supports it as the one dietary approach that can optimize health in the long-term!

Unlocking the Cause of Inflammation

For years the question was "why do those who are overweight (or obese) have a higher risk to their health than their lean counterparts?"

It was believed that the excess weight itself was the problem - greater demand on the whole body system to support the higher weight and maintain mobility of a heavier body.

In the last decade our understanding of the many things contributing to that higher risk have evolved and developed. As if on a collision course within itself, the body system - with ever increasing fatness - seems to turn on itself when the delicate balance between "health" and "illness" is tipped: insulin resistance, high blood sugars, hypertension, dyslipidemia, hyperinsulinemia, and inflammation - errupt and cascade in a domino effect leading to our worst health problems - diabetes, cancer, and heart disease.

But, as I noted in an article last week, it is not just the overweight and obese who get snagged in this domino effect of health ills - those who are considered normal weight - lean - can find themselves in the same boat as those who are much heavier. Being thin, it seems, does not automatically confer protection against long-term health problems.

This has led researchers to dig deeper to understand what is happening and why. The most recent addition on the list of potential warning signs of impending health problems is waistline circumferance and waist-hip ratio. These two measures offer warning to the lean that they may be developing "central adiposity" - that is belly or middle-torso fatness - even when they're normal weight and slim.

As reported by the USDA Agricultural Research Service this month - Inflamatory News about Fat Cells - scientists have uncovered why "fatness" - not simply overweight and/or obesity - matters. Researchers from the Obesity and Metabolism Laboratory, at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, Massachusetts identified key mechanisms in fat cells that cause chronic low-level inflammation in the body.

Deep within bone marrow, spleen, and lymph nodes lie a form of large white blood cells. As part of the immune system, these “macrophages,” as they are called, circulate within blood to seek out and devour bacteria, other foreign invaders, and cellular debris. Scientists have known that macrophages also appear in adipose, or fat, tissue. But their role in the tissue was once thought to be inconsequential.

Now, a new study explains important aspects of these immune cells in body fat, such as why they infiltrate, how they function, and just where they gather.

A number of researchers in the past few years have 'red flagged' inflammatory markers as one more marker to measure when assessing an individuals risk for heart disease or diabetes. This is because inflammatory markers like C-Reactive Protein are repeatedly observed in those with heart disease, cancer and diabetes. How the inflammation develops and continues to increase in the body has remained largely unknown.

This study shows that more than 90 percent of the macrophages in adipose tissue of obese mice and humans are located around dead fat cells. As the fat cells get bigger within fat tissue, the prevalence of macrophages increases proportionally. These new findings may partly explain the mechanisms inside the adipose tissue that cause the cells to secrete the inflammatory chemicals. These immune cells appear to be rushing to fat cells after their death to mop them up. When this happens, the macrophages may emit potentially dangerous amounts of inflammatory chemicals.

“When fat cells die, macrophages surround the dead lipids the same way white cells surround a wooden splinter in your skin,” Greenberg says. “The immune system is essentially surrounding and sequestering the dead fat cells and gorging on the leftover lipids and cellular debris.”

The macrophages identify the leftover insoluble lipid droplets as foreign bodies. In a case of molecular rescue gone awry, the findings may explain how enlarged fat cells, as found in obesity, promote obesity-related complications such as arthritis, insulin resistance, diabetes, or heart disease.

Diet for Metabolic Syndrome?

While doing a search last night for some information about one of the complications of Metabolic Syndrome, I stumbled upon an interesting review in the World Journal of Gastroenterology - Non-alcoholic fatty liver disease and the metabolic syndrome: Effects of weightloss and a review of popular diets. Are low carbohydrate diets the answer?

Researchers at the University of Connecticut Health Center, in Farmington, Connecticut, reviewed the role of the metabolic syndrome, especially insulin resistance and obesity in the development of non-alcoholic fatty liver disease (NAFLD), to investigate the effect of weight loss on NAFLD and, finally, to evaluate popular diets and compare them with regard to their effects on the metabolic syndrome and NAFLD.

The above article is fairly long, but the researchers take things step by step and review the degeneative processes that occur in metabolic syndrome. They then look at the various therapies that have been evaluated, "Therapies that have been evaluated include lifestyle changes such as diet and exercise, antioxidants like vitamin E and betaine, cytoprotective agents such as ursodeoxycholic acid, lipid-lowering agents, anti-diabetics, weight-loss agents like orlistat and iron reduction therapy, i.e. phlebotomy. The management of associated conditions, such as diabetes, obesity and hyperlipidemia, is especially important, given their association with more advanced liver disease."

The most common of these therapies is weight loss since it, by itself, often leads to improvements in insulin sensitivity, choleseterol, blood pressure and glycemic control - all problems associated with metabolic syndrome. Their concern, however is that "Improvement in liver biochemistry and ultrasonographic appearance is a consistent finding with moderate weight reduction. However, serum aminotransferases are unreliable markers for follow-up, and do not provide accurate data on prognosis. Worsening of fibrosis can occur even as the levels of transaminases decline. A few studies have evaluated and shown histologic improvement."

After a review of traditional weight loss recommendation studies, they move to "popular diets."
The effects of many popular diets on fatty liver are not known. However, metabolic improvements related to dietary weight reduction may favorably influence NASH. If dietary intervention can positively affect insulin resistance and other features of the metabolic syndrome, it would be important to know which particular diet is most beneficial.

One of the most startling statements in the review "A diet high in carbohydrates results in an increase in blood glucose, insulin and triglycerides, all of which are risk factors for the development of NAFLD."

This was stated after a favorable look at studies that used traditional dietary therapies!
Most researchers are well aware of the danagers of low-fat carbohydrate rich diets and I have to applaud these researchers for stating it here simply - the literature is rich with data that clearly shows low-fat diets do not result in significant improvements, but few will state it - it there in their data, but they simply omit any questions or concerns with "unfavorable" outcomes from low-fat diets.

These researchers continue, "Carbohydrate restriction leads to ketosis resulting not only in weight loss, but also a decrease in blood glucose, insulin and triglyceride levels. Studies have shown these diets to be effective in short-term weight loss. Early weight loss is a result of diuresis associated with ketone and urea nitrogen excretion. However, over time, weight loss is a result of loss of body fat. Proponents believe that these diets have a high satiety level, which make them easier to adhere to. This is very important, as dietary adherence is one of the main challenges faced by dieters. Questions with regard to their nutritional adequacy and long-term effects have been raised. In the short-term, these diets have been found to be safe. "

When reviewing studies that compared a low-fat diet to a low-carb diet, it was found that "Effects on biochemical markers associated with the metabolic syndrome appear to be more favorable with low-carbohydrate diets. In general, these diets show greater improvements in insulin sensitivity, triglyceride and high-density cholesterol levels. It is possible that for patients with the metabolic syndrome, a low-carbohydrate diet may be more advantageous. This, in turn, may positively affect NAFLD."

In their conclusions - "Traditionally, a low-fat diet has been recommended, but recent studies, show greater short-term weight loss and greater improvement in markers of the metabolic syndrome without significant adverse effects with low-carbohydrate diets. This raises the question of whether low-carbohydrate diets should be recommended as part of a weight loss strategy for our patients. At this point, questions regarding the nutritional adequacy and long-term safety remain. While studies have evaluated the effect of these diets on weight loss, cardiovascular and metabolic marker studies are needed to evaluate the effect of these diets specifically on NAFLD."

Metabolic Madness

Nowadays, with heightened concern about obesity, people who are lean might feel complacent: If excess weight means disease, then normal weight must mean health.

Not so fast - a silent killer called the metabolic syndrome can strike anyone, overweight or not. Metabolic syndrome is a set of disorders that significantly increases the risk of heart disease. Its biochemical underpinnings are tremendously complicated and are still being worked out.

Among the major features of Metabolic Syndrome we find, in parallel with each other, various warning signs - only a few need to be present for a diagnosis of Metabolic Syndrome:

• excess weight or accumulation of abdominal fat
• waist-hip ratio and/or large waistline
• high blood pressure
• dyslipidemia (high triglycerides and/or LDL and/or low HDL)
• insulin resistance
• high blood sugars
• inflammation

Individually, each is a risk factor for heart disease, but a person with several of these - that is, a person with metabolic syndrome - is at a higher risk. Increasingly, the medical community is identifying and treating people with the metabolic syndrome.

In practice, diagnosis is based on easily measurable parameters: fat accumulation around the waist, blood pressure, levels of key lipids, and levels of glucose. We've come to understand that lifestyle contributes enormously to abnormalities in these parameters, and doctors typically admonish patients to "eat right and exercise" as the first line of defense.

But even for people who dutifully eat a low-fat, carbohydrate rich diet (the current recommendation) and exercise, those measures often do not halt the progression of metabolic syndrome.

In the US, it is estimated that 25% of adults - some 47 million people - are likely to have metabolic syndrome. With the rapidly rising incidence of obesity among children and youth, the number of people with metabolic syndrome is likely to swell.

According to the CDC, about 16% of 6-to-19-year-olds in 1999–2002 (more than 9 million youngsters) were overweight. Studies find that in this group, metabolic syndrome is already highly prevalent.

The causes of the syndrome are not yet fully understood but we have an understanding of some influencial factors.

Genetics is a factor. A recent study has shown that a cluster of abnormalities similar to those in metabolic syndrome can be caused by a single mutation in a mitochondrial gene.

Lifestyle is a factor. Physical inactivity and diets that generate high levels of fat in the blood and accumulation of central fat on the torso correlate strongly with metabolic syndrome.

Age is a factor. If you are at least 35 years old, there is a 25% probability that you have the syndrome; by age 60, the probability increases to 40%.

Several mechanisms may operate concurrently to give rise to the features of metabolic syndrome. Obesity is high on the list of some researchers, mainly because anyone who has a large waist circumference that meets the criteria is almost always obese. But, let's be clear, obesity is not just a matter of excess weight, we now recognize the deadly relationship between a larger waist and accumulation of fat in the middle. Metabolic syndrome occurs in people who are lean and people who are obese - the data shows that 18% of men and 22% of women who are of normal weight or slightly overweight have the metabolic syndrome.

So, you can be of normal weight but have a high percentage of body fat - what matters is how much of that fat is visceral and how much is subcutaneous. This central fatness is harmful because fat cells do not merely store fat - they send out bioactive molecules with powerful effects throughout the body. Some of these are low-molecular-weight proteins that induce inflammation, now understood to be a major cause of cardiovascular disease.

Fat in the deep visceral area is the most dangerous. Unlike the fat under the skin, visceral fat is more easily mobilized and is a richer source of proinflammatory proteins. When hydrolyzed, visceral fat releases free fatty acids. When these reach the liver, they are converted to triglycerides and stored.

Researchers agree that insulin resistance is central to metabolic syndrome. When cells are unresponsive to insulin, the pancreas responds by pouring even more insulin into the bloodstream, leading to high levels of the hormone in the blood, a condition called compensatory hyperinsulinemia. The high level of insulin in the blood forces glucose into cells but also begins the process of events leading to arterial damage and eventually a heart attack. Under these conditions, a person may not manifest either diabetes or heart disease but could well be on the way to either or both.

In general, excess insulin causes problems because insulin affects many other processes. For example, it stimulates the uptake of amino acids and increases the permeability of cells to key ions, such as potassium. In muscle cells, it promotes storage of glucose as glycogen. It also induces the secretion of angiotensin II, a peptide hormone that constricts arteries and raises blood pressure, so when insulin levels go up, hypertension follows.

In the liver, insulin promotes the synthesis of free fatty acids. However, excess fat makes liver cells insulin resistant. When free fatty acids are exported from the liver, they are taken up by other tissues, including fat (adipose) tissue, which stores free fatty acids as triglycerides. Couple that with the inhibition of the breakdown of fat in adipose tissue because insulin spares fat - more insulin means more fat sparing and fat storage - more fat produce fewer insulin receptors and increase insulin resistance. In a vicious cycle, the pancreas responds by pumping more insulin until the insulin-producing cells die from exhaustion. Type 2 diabetes ensues.

Under conditions of insulin resistance and compensatory hyperinsulinemia, the liver makes more very low density lipoprotein (VLDL). Among the lipoproteins that the body uses to transport fat, VLDL contains the greatest amount of triglycerides. Release of VLDL from the liver raises the levels of trigylcerides in the blood - and when VLDL is converted to low-density lipoprotein, levels of LDL rise. VLDL also tends to exchange some of its triglycerides with the cholesterol contained in high-density lipoprotein (HDL), the so-called "good cholesterol." This reduces the levels of HDL cholesterol. High triglycerides, high LDL, and low HDL all increase the risk of a heart attack.

The impact of fat on insulin resistance is even more pronounced during periods of stress, which releases the stress hormones adrenaline and cortisol. Adrenaline in turn stimulates the hydrolysis of fat in fat tissue, raising the amount of free fatty acids in circulation, which eventually end up in the liver. On the other hand, cortisol builds back the fat in fat tissue.

Left unchecked, insulin resistance will progress to diabetes because glucose will increasingly flood the bloodstream as insulin resistance increases. People with diabetes are likely to suffer damage to the eyes, nerves, and kidney; be more susceptible to infection, ulceration, and gangrene; are at a high risk for limb amputation and eventually will develop heart disease.

These complications are probably due to the reactivity of the excess glucose in the bloodstream because of a reaction called glycation, where glucose attaches to various proteins and causes them to cross-link and form so-called advanced glycation end products. These are known to trap LDL particles in artery walls and have been linked to cataract formation and reduced kidney function. Glycation also releases reactive oxygen radicals, which damage many entities, such as LDL. Oxidized LDL particles are very atherosclerotic - that is, they contribute significantly to the formation of plaque in arterial walls.

This oversimplified picture of the metabolic syndrome belies the complexity of the interconnections among insulin action, fat storage, energy metabolism, and cardiovascular disease. Diagnosis of metabolic syndrome is based on comparing a patient's values for risk factors against levels defined by several bodies. The most widely cited set of criteria is that of the U.S. National Cholesterol Education Program Adult Treatment Panel III (ATP III). According to ATP III, a patient has metabolic syndrome if he or she meets the criteria for at least three of five parameters:

• Waist circumference 40+ inches (men) or 35+ inches (women)
• Triglycerides 150+ mg/dL
• HDL cholesterol -40 mg/dL (men) or -50 mg/dL (women)
• Blood pressure 130/85 mm Hg
• Fasting glucose 110+ mg/dL

That definition is straightforward, but not everyone is happy with it. For example, among many of its shortcomings - the definition does not work well with certain ethnic groups, it gives equal weight to each parameter, it does not factor in the effect of age or gender and it does not address the core issues of insulin resistance or inflammation.

As for treatment, doctors overwhelmingly recommend losing weight through a "balanced diet" and regular exercise. "Eating right" means eating modest amounts of food and avoiding foods that contain high levels of fat. Physical activity is thought to ensure that calories consumed are expended.

But, as numerous dietary and lifestyle intervention studies show, a carbohydrate rich diet that is low in fat may exacerbate metabolic syndrome, even when weight is lost following the diet used as intervention. You may recall last week one study I reviewed from the American Journal of Clinical Nutrition (November 2005) and the editorials that followed - these clearly pointed out that low-fat diets are counter productive for those with insulin resistance and metabolic syndrome.

Numerous other studies point to an alternative dietary approach - a controlled-carb diet - that reverses the features of metabolic syndrome! Findings from dozens of studies show marked improvement in insulin sensitivity, decreased fasting glucose, increased HDL, significantly reduced triglycerides, stablized blood pressure, reduced inflammatory markers and weight loss too.

An extensive review was published last November in the Nutrition & Metabolism Journal - Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction.

Yet the powers that be - the established medical and scientific organizations tasked with providing the public with accurate, objective information in an evidence-based manner - simply dismiss this data and continue with the entrenched dogma that a diet with 30% or less calories from total fat and 10% of less calories from saturated fat is optimal for everyone. It's not - I know and they know it - now you know it too.

If you have metabolic syndrome or think you may be at risk - see your physician and find out for sure. Metabolic syndrome really is a silent killer - it's progressive and leads to poor long-term health and quality of life. Even if you're thin, you may already have the features of metabolic syndrome - and you can do something about it now to start to reverse the deadly effects on your long-term health...a well designed low/controlled-carb diet can and will offer you improvements.