What If Saturated Fat Is Not the Problem?

An article in dLife, written by Richard Feinman, PhD:

Here’s an idea to chew on: The carbs in your diet tell your body what to do with the fat you eat, so it’s the type and amount of carbohydrates that matter when it comes to your weight and health.

Virtually every bit of health information today includes the advice to avoid saturated fat — the so-called evil stuff that lurks in animal foods like steak and eggs. The basis for this recommendation is that research has shown a correlation between saturated fat intake and total cholesterol and LDL (“bad cholesterol”). The problem with these studies is that the effects are not large, there is wide variation among individuals and, in most of these studies, the predicted benefit in incidence of cardiovascular disease did not materialize. In addition, we now know much more about risk factors for cardiovascular disease (CVD) beyond LDL. No assessment of CVD risk can be made without considering HDL (“good cholesterol”), triglycerides, and the size of the LDL particle. Plenty of research shows that these markers can worsen when people reduce their intake of saturated fat and that they can improve by reducing the intake of carbohydrates.

You don’t have to be a medical researcher to recognize that this is a politically charged issue. The thing that is missing for the public is an impartial evaluation of all the data on saturated fat. My personal opinion is that there is much contradictory data and a recent review of the situation suggests that there is not sufficient evidence to make any recommendations.

There is a sense that, in the absence of definitive evidence, lowering saturated fat will at least do no harm. This is not right. The problem for people with diabetes is what happens when saturated fat is replaced with carbohydrate, and research has repeatedly shown that this may actually be harmful. Consider that, according to the Centers for Disease Control and Prevention, during the onset of the current epidemic of obesity and diabetes, almost all of the increase in calories in the American diet has been due to carbohydrate. The percent of total fat and saturated fat in our diet decreased. In men, the absolute amount of saturated fat consumed decreased by 14 percent!

One of the most striking reasons to doubt the across-the-board proscriptions against saturated fat is the report from the large scale Framingham study in the Journal of the American Medical Association, titled “Inverse association of dietary fat with development of ischemic stroke in men.” You read that right: The more saturated fat in the diet, the lower the incidence of stroke.

Perhaps the most compelling research was published in a 2004 issue of the American Journal of Clinical Nutrition by researchers from the Harvard School of Public Health. Their study showed that, in postmenopausal women with heart disease, a higher saturated fat intake was associated with less narrowing of the coronary artery and a reduced progression of disease. Even with similar levels of LDL cholesterol, women with lower saturated fat intake had much higher rates of disease progression. Higher saturated fat intake was also associated with higher HDL (the “good” cholesterol) and lower triglycerides.

If saturated fat isn’t the problem, what is?
In this study, in which greater saturated fat intake was associated with less progression of coronary atherosclerosis, carbohydrate intake was associated with a greater progression. Carbohydrate, through its effect on insulin, is the key player. Insulin not only sweeps up glucose from the blood but it also plays air traffic controller, making the call as to whether that glucose is turned into fat or is used for energy. Most importantly, insulin determines what happens to dietary fat — whether it gets stored or oxidized for fuel. In fact, the fat profile in the blood (cholesterol and triglycerides) is not strongly tied to diet.

A recent study by Jeff Volek at the University of Connecticut compared low-carbohydrate and low-fat diets. Even though the low-carbohydrate diet had three times as much saturated fat as the low-fat diet, levels of unhealthy fats in the blood were lower in the low-carbohydrate group. How is that possible? That is what metabolism does.

What is the best diet?
We don’t know the ideal diet composition. We do know that saturated fat, unlike trans-fat, is a normal part of body chemistry and extreme avoidance is not justified by current scientific data. Removing some saturated fat to reduce calories is good, but adding back carbs appears to be deleterious. It appears that healthy, carbohydrate restriction will trump the effects of any kind of fat. For a person with diabetes, blood glucose must be the first consideration. If you have relatively tight blood sugar control, the amount of saturated fat you eat may be a non-issue. You can do what we did before the diabetes-obesity epidemic: regulate your intake by your taste and your natural appetite. No one ever did want to eat a pound of bacon.

Sources:
1. Food and Nutrition Board: Macronutrients. In: Dietary reference intake: National Academies Press; 2005, p.484.

2. JB German, CJ Dillard: Saturated fats: what dietary intake? Am J Clin Nutr 2004, 80:550-559.

3. MW Gillman, et al. : Inverse association of dietary fat with development of ischemic stroke in men. JAMA 1997, 278:2145-150.

4. D Mozaffarian, EB Rimm, DM Herrington: Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr 2004, 80:1175-1184.

5. JS Volek, et al. A hypocaloric, very low carbohydrate, ketogenic diet results in a greater reduction in the percent and absolute amount of plasma triglyceride saturated fatty acids compared to a low fat diet. NAASO, Boston, MA, October, 2006.

ADA Revises Nutrition Recommendation for those with Diabetes

I'm still reading through the just released Nutrition Recommendations and Interventions for Diabetes - the 2008 position statement from the American Diabetes Association regarding dietary recommendations for those at risk for or diagnosed with diabetes.

While I finish reading the actual documents and write up what I think of the paper, here are links to what others are saying today:

Jimmy Moore - New 2008 ADA Recommendations Partially Acknowledge Low-Carb Diets

Adam Campbell - Apparently Hell Just Froze Over

Dr. Mary Vernon - HAS THE AMERICAN DIABETES ASSOCIATION SPARKED YET ANOTHER ATKINS REVOLUTION?

Low-Carb Ketogenic Diet - Greater Weight Loss and More...

A neat little study was published in the January 2008 American Journal of Clinical Nutrition - Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum.

In the study, researchers followed seventeen obese men, confined to a metabolic ward, for a month while they consumed either a low-carb ketogenic diet or a moderate carbohydrate diet on an ad libitum basis (eat as much as desired from foods allowed).

Over the course of the study, the protein intake of both dietary regiments was fixed to provide 30% of calories; carbohydrate was restricted to 4% of total calories in the men consuming the low-carb diet and 22% in the men consuming the moderate carbohydrate diet; and fat intake rounded out the calories in each diet with no specific limitation on fat consumption in either.

All meals were prepared and provided as requested by the men and they were allowed to eat whatever they wanted of the allowed foods in each meal with no restrictions other than on their carbohydrate options. The men on the low-carb diet consumed less calories each day on their own and reported higher feelings of satiety while on the diet.

On average, the difference in carbohydrate intake was great - the men on the low-carb diet consumed just 22g of carbohydrate each day, while those on the moderate carbohydrate diet consumed 170g each day. Both levels of intake were significant reductions from baseline, where the men averaged 396g of carbohydrate each day.

Weight loss was greater for the men following the low-carb diet, who averaged a weight loss of 6.34kg (13.95-pounds) compared to the moderate carb diet averaging a loss of 4.35kg (9.57-pounds). Calorie differences between the two groups do not fully explain the greater weight loss in the men consuming the low-carb diet since they ate about 1731-calories a day compared to the men consuming the moderate carb diet consuming about 1898-calories a day. This difference - about 167-calories a day - translates to a month long difference of 5016-calories, or 1.43-pounds....yet the difference between the two groups was 4.38-pounds greater weight loss in those on the low-carb diet.

Digging deeper into the published data we also find that the men on the low-carb diet experienced statistically significant improvements in blood glucose, insulin and HOMA-IR, as well as favorable improvements in their cholesterol levels with a reduction in total cholesterol and LDL, an increase in HDL and a significant reduction in triglycerides.

All of these favorable changes occured while the men consumed a dietary fat intake similar to that at baseline. Where at baseline they consumed an average of 126g of total fat with 43.8g of saturated fat, their dietary intake while following low-carb didn't change much - they averaged 129g of total fat on the low-carb diet and 46.3g of saturated fat. This basically highlights that modifying one's diet to be low-carb does not mean one suddenly increases dietary fat consumption significantly - in this trial, dietary fat was pretty much the same compared to baseline.

So, with this study, we have one more to add to the pile that supports carbohydrate restriction for satiety, ad libitum-spontaneous calorie reduction, weight loss, improvements to glucose, insulin and insulin resistance, along with favorable improvements (although not statistically different from the moderate carbohydrate diet) to lipids.

Low-GI Diet for 1-year Suggests Improvements for T2DM?

As I was browsing through the January issue of the American Journal of Clinical Nutrition this weekend, a perspective written by John Miles caught my attention. In his article, A role for the glycemic index in preventing or treating diabetes, he wrote, "Elsewhere in this issue of the Journal, Wolever et al (7) report the results of the Canadian Trial of Carbohydrates in Diabetes (CCD). Patients with well-controlled type 2 diabetes who were treated with diet alone were randomly assigned to receive either a high-GI diet, a low-GI diet, or a low-carbohydrate, high-monounsaturated fat diet for 1 y.

The study was carefully conducted and of longer duration than many earlier trials. The investigators found no weight loss and a small increase in glycated hemoglobin (HbA1c) in all 3 groups. This increase in HbA1c is what one would expect with no intervention (8). The fact that glucose concentrations 2 h after an oral glucose challenge were significantly lower in persons who had followed the low-GI diet for 1 y than in those who followed the other 2 diets for 1 y suggests improvement in either insulin sensitivity or insulin secretion (or improvements in both)."

Sounds like a compelling study, so intrigued, I clicked open the study mentioned, The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein, and read the abstract.

In it, researchers concluded "In subjects with T2DM managed by diet alone with optimal glycemic control, long-term HbA1c was not affected by altering the GI or the amount of dietary carbohydrate. Differences in total:HDL cholesterol among diets had disappeared by 6 mo. However, because of sustained reductions in postprandial glucose and CRP, a low-GI diet may be preferred for the dietary management of T2DM."

Here I was even more intrigued - a study trial comparing three different dietary approaches, and one low-carb for a year?

But I wondered, how was it that the low-carb diet didn't do as well as other studies would suggest it should have?

Wanting to know this, I opened the full-text to understand how it was possible that greater improvement was not found in the "low-carbohydrate" subjects and why HbA1c didn't remain stable or improve in the course of one year with either low-GI or low-carbohydrate diets. Previous study data published by others would suggest that HbA1c would at least remain stable with low-carb, no?

Well, it took no more than five minutes to fully see why things turned out as they did - the "low-carbohydrate" diet was not a low-carbohydrate diet afterall - at baseline the subjects assigned the low-carb diet ate an average of 210g of carbohydrate each day and during the low-carb diet consumed an average of 199g of carbohydrate each day.

Hello? In whose fantasy world is 199g of carbohydrate each day a low-carb diet?

Ah, but I digress...

While the researchers took pains to measure many risk factors, at the end of the year, the subjects in every group experienced progression of their diabetes risk factors - there simply was no improvement to laud in this trial, no matter how you twist the data.

What's absolutely disappointing in how the findings are presented is that the researchers honed in on two measures of improvement - CRP and post-prandial glucose - to the exclusion of significant declines in other measures that are critically important for those with type II diabetes.

Where do I even begin?

Weight remained fairly stable in all three groups, with only the low-GI group actually gaining some weight, despite no meaningful difference in calorie intake from baseline through one year on the low-GI diet.

Worse though is the lack of critical thought around the marked and significant increase in waist circumference in all three diet groups.

• The high-GI group started with a waist circumference of 99.1cm - it increased over the year to 103.1cm (+1.6 inches) - this despite stable weight on the scale (84.4kg at baseline; 84.3kg after 1-year on the diet).
• The low-GI group started with a waist circumference of 98.3cm - it increase over the course of the year to 104.9cm (+2.6 inches). They also experienced a weight gain, going from 81.1kg at baseline to 83.9kg at the end of the study (+6.2-pounds gained).
• The supposed "low-carbohydrate" group - eating 199g carbohydrate on average - started with a waist circumference of 98.6cm - it increased over the study period to 103.1cm (+1.8-inches) - like the high-GI group, this increase was despite a stable scale weight...they started at 84.7kg and ended the year at 84.3kg.

If that wasn't bad enough - all three groups experienced increases in their HbA1c too.

Those consuming a high-GI diet saw a rise from 6.2 to 6.34; low-GI saw a rise from 6.2 to 6.34; and those on the supposed low-carb diet rose from 6.1 to 6.35.

Over time the researchers reported that this rise was statistically significant - and I'd say clinically significant too!

Now with just these risk measures, you'd think there was enough to maybe, just maybe, inspire the researchers to challenge the efficacy of any of the above diets for those with type II diabetes. Maybe even say that perhaps the level of carbohydrate - despite quality or glycemic index or load improvements - matters; that simply modifying the type of carbohydrate in the diet does NOTHING for glycemic control and if carbohydrate is consumed habitually at levels seen in this study, perhaps someone with type II diabetes should expect a continued progression of their disease?

But, ya know what? They didn't even consider that. And the above problems were not all they reported either.

Let's see what else was reported in the data:

Total cholesterol didn't do much in any of the groups; LDL didn't change significantly in any group....HDL however declined in the low-GI group, but rose in the high-GI and supposed low-carb groups.

Triglycerides fell slightly in the high-GI and supposed low-carb groups, but rose in the low-GI group.

Two more markers of potential health risks found to be problematic in the low-GI diet over a year - and the researchers even noted it in the full-text - "With the low-GI diet, mean triacylglycerol was 12% higher, HDL was 4% lower, and the ratio of apoB to apoA was 4% higher than with the low-CHO diet

But a 12% increase in triglycerides and a 4% drop in HDL didn't set off any alarm bells either.

Neither did the fact the low-GI group saw an increase in their fasting plasma glucose over the year, which was also noted and basically disregarded.

With regards to the main focus in the abstract, C-Reactive Protein, the researchers did find a significant difference between the low-GI diet and the high-GI diet, but also noted that between the low-GI diet and the supposed "low-carb" diet there was no significant difference.

Yet, they chose to focus on the low-GI diet as better for a type II diabetic, despite the fact it led to

• weight gain
• waist circumference increase
• increase in HbA1c
• increase in fasting plasma glucose
• a marked rise in triglycerides
• and a decline in HDL

The conclusion here speaks volumes when taken in context to the carbohydrate intake in each group, "In subjects with T2DM managed by diet alone with optimal glycemic control, long-term HbA1c was not affected by altering the GI or the amount of dietary carbohydrate."

Better stated might be, with no meaningful change in absolute carbohydrate consumption, even with improvement in quality of carbohydrate - it is likely a type II diabetic will experience progressive decline in glycemic control along with other declines in risk factors over a year.

The data is published right in the full-text - the glycemic index as a means to reverse or prevent diabetes is no solution.

In this study, those who followed the low-GI diet had the worst overall outcome - they gained weight, increased waist circumference, saw triglycerides rise while HDL fell, and experienced a decline in glycemic control as evidenced by their increased HbA1c.

Yet you wouldn't know it from the abstract which focuses instead on "sustained reductions in postprandial glucose and CRP" and then concludes that "a low-GI diet may be preferred for the dietary management of T2DM."

And then back to the article from John Miles, who said this study "suggests improvements" in those who followed the low-GI diet for one year. Who's he kidding?

ADA Says Low-Carb Okay for Weight Loss, So What?

An article published today in Diabetes Health, ADA Now Supports Low-Carb Diets, reminded me that I have not yet posted my thoughts on the updated guidelines for Medical Nutrition Therapy (MNT) recently issued by the American Diabetes Association (ADA). This will probably be longer than usual, so bear with me!

On December 28, 2007, the ADA issued a press release to highlight the publication of and changes within their clinical practice recommendations, better known as the Standards of Care in Diabetes.

Each year the guidelines are updated and this year was no exception - as noted in the press release, "Until now, the ADA did not recommend low carbohydrate diets because of lack of sufficient scientific evidence supporting their safety and effectiveness. The 2008 Recommendations include a statement recognizing the increasing evidence that weight-loss plans that restrict carbohydrate or fat calorie intake are equally effective for reducing weight in the short term (up to one year). The "Standards of Medical Care in Diabetes--2008" document reviews the growing evidence for the effectiveness of either approach to weight loss. In addition, there is now evidence that the most important determinant of weight loss is not the composition of the diet, but whether the person can stick with it, and that some individuals are more likely to adhere to a low carbohydrate diet while others may find a low fat calorie-restricted diet easier to follow."

There are two main issues I'll look at in the above statement today:

1. that low-carbohydrate diets are as effective as low-fat calorie restricted diets for weight loss for up to one-year

2. that composition of diet is less important than whether a person can stick with the dietary approach for weight loss.

In order to fully understand exactly what the ADA is saying with regard to the first issue, we need to return to the August 2006 issue of Diabetes Care, where an updated consensus statement was published, Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy: A consensus statement from the American Diabetes Association [ADA] and the European Association for the Study of Diabetes [EASD]

As I noted in my review of that consensus statement "Rather than question the dietary recommendations, or explore emerging data supportive of dietary interventions that are different from the recommendations, the statement instead concludes that "the limited long-term success of lifestyle programs to maintain glycemic goals in patients with type 2 diabetes suggests that a large majority of patients will require the addition of medications over the course of their diabetes."

The final sentence in the section discussing medications, which followed the section on lifestyle intervention, sets the stage for what is to come, "addition of medications is the rule, not the exception, if treatment goals are to be met over time."

In August 2006 the ADA, along with the EASD, threw up their hands and decided that dietary and lifestyle intervention was futile, therefore the only logical place to go was intensive pharmaceutical intervention at diagnosis.

The authors wrote, in the paper's conclusion, "We now understand that much of the morbidity associated with long-term complications can be substantially reduced with interventions that achieve glucose levels close to the nondiabetic range. Although new classes of medications, and numerous combinations, have been demonstrated to lower glycemia, current-day management has failed to achieve and maintain the glycemic levels most likely to provide optimal health care status for people with diabetes."

On this the ADA remains steadfast - pharmacological intervention is the first step with lifestyle intervention upon diagnosis. The freely available full-text of the Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy clearly continues with the August 2006 consensus that lifestyle intervention for those diagnosed with diabetes will not work, therefore medication must be initiated upon diagnosis.

Yet we find the ADA falling all over itself to tout its position change for weight loss - that now a low-carbohydrate diet is considered as effective as a low-fat calorie restricted diet for weight loss? And somehow we're supposed to be jumping for joy that they made this change?

If we take the entire package of documents published in the Diabetes Care Supplement, we cannot reach any conclusion other than the ADA has made up its mind and is not going to review the evidence. They may concede that a low-carbohydrate diet can help with some loss of weight, but nothing else - and even that carries the caveat that one must be intensely monitored if they do decide to follow a low-carb diet.

But, going back to the first point - the concession that low-carbohydrate diets and low-fat calorie restricted diets are both effective for weight loss over the short-term.

Quite frankly this statement by the ADA is meaningless when we consider the full context of their position because they hold that "current-day management has failed to achieve and maintain the glycemic levels most likely to provide optimal health care status for people with diabetes."

While many lauding the change as a step in the right direction for the ADA, I'm not impressed, nor convinced - if anything, the ADA only confirmed what they've already said previously.

We only need to go back to the publication of a 22-month study, in which diabetic subjects were found to have significant health improvements following a low-carbohydrate diet, to read the ADA reaction in an article at WebMD - "While agreeing that carbohydrate restriction helps people with type 2 diabetes control their blood sugar, ADA spokesman Nathaniel G. Clark, MD, tells WebMD that the ADA does not recommend very low-carb diets because patients find them too restrictive. "We want to promote a diet that people can live with long-term," says Clark, who is vice president of clinical affairs and youth strategies for the ADA. "People who go on very low carbohydrate diets generally aren't able to stick with them for long periods of time."

Which brings us to issue two above - diet composition does not matter as much as a diet one can follow, a theme the ADA has been hot and heavy on for at least two years now.

Let's review the sentence in the ADA press release carefully, "In addition, there is now evidence that the most important determinant of weight loss is not the composition of the diet, but whether the person can stick with it, and that some individuals are more likely to adhere to a low carbohydrate diet while others may find a low fat calorie-restricted diet easier to follow."

Evidence? What evidence?

The Standards of Medical Care in Diabetes 2008 includes this sentence, "Although numerous studies have attempted to identify the optimal mix of macronutrients for meal plans of people with diabetes, it is unlikely that one such combination of macronutrients exists. The best mix of carbohydrate, protein, and fat appears to vary depending on individual circumstances. For those individuals seeking guidance on macronutrient distribution in healthy adults, the Dietary Reference Intakes (DRIs) may be helpful;" referencing the IOM documents published back in 2002.

The Nutrition Recommendations and Interventions for Diabetes: A Position Statement of the American Diabetes Association 2008 includes "Nutrition counseling should be sensitive to the personal needs, willingness to change, and ability to make changes of the individual with pre-diabetes or diabetes. (E)"

Note with that the letter "E" assigned to it, classing it as "expert opinion" - so again, where is the evidence? Each study referenced dates between 1997 and 2004 - so what exactly is the new evidence alluded to in the updated documents?

Oh, that's right, there is NONE...this is simply an opinion and has already been stated numerous times before.

I've said it before, "evidence versus sophistry; with just enough opinion thrown in to ensure glycemic control remains elusive..."

The ADA refuses to acknowledge that diabetics deserve clear statements about how to achieve normal blood sugars, and instead continues headlong on this path that they somehow deserve to eat like anyone else in the population and can mediate the effects of carbohydrate-rich food with medications.

:::sigh:::

So yeah, the ADA now says one can try a low-carbohydrate diet for weight loss, for the short-term (up to 1 year) and that some will somehow manage to follow such a diet. But let's not forget, if you do decide to follow a low-carbohydrate diet, you're also going to be subjected to much more intense monitoring than your low-fat calorie restricted peer and you're left with no advice other than the same-old same-old once your year is up.

Then what?

The failed ADA diet?

Lifelong medication with continued stepped-up pharmaceutical requirements with each passing year until you're dependent upon insulin injections?

The ADA, even with this new position that a low-carbohydrate diet may be used for up to one year for weight loss, still continues to fail in their mission - to prevent and cure diabetes and to improve the lives of all people affected by diabetes - because they refuse to actually review the hard data available; and instead continue in this sophistry that dietary recommendations need to be based upon what one wants to eat rather than what one should eat based upon metabolic, hormonal and physiological facts.

Animal products are ‘whole foods,' too

Dana Carpender's latest - I couldn't have said it better myself!

Animal products are 'whole foods,' too
Dana Carpender

The nutritional buzz phrase is 'whole foods.' This is encouraging. I've been watching the nutrition scene long enough to remember when people who insisted that whole-grain bread was more nutritious than enriched bread were scorned as 'food faddists.'

But the admonitions to eat whole foods seem to apply only to grains, fruits and vegetables. Officialdom still recommends discarding large fractions of animal foods. Yet few see these fractionated animal foods as the refined, depleted foods they are.

Take dairy. Virtually all recommendations for dairy products include the qualifiers 'low-fat' or 'fat-free.' But that's not the way it comes out of the cow. Yes, whole milk has more calories than skim. It also has far more vitamin A, because it's carried in the butterfat. (Some skim milk is fortified with vitamin A —- the equivalent of adding a few vitamins back to nutritionally depleted white flour.) Because fat aids in calcium absorption, you'll get more calcium from whole milk. Whole milk from grass-fed cows supplies CLA, a fat that increases fat-burning and reduces heart disease and cancer risk, and omega-3 fats, which reduce inflammation, and heart disease and cancer risk. It is worth paying premium prices for such milk.

And eggs. Oh, poor eggs. There they are, just about the most perfect food in the world, and what do people do? They throw away the yolks. The part with almost all the vitamins, including A, E, K and the hard-to-come-by D, not to mention brain-enhancing choline and DHA. Eggs from pastured chickens also have yolks rich in omega-3. Better to throw away the whites, not that I'd recommend that, either. Just eat whole eggs, will you?

Then there's chicken. When did 'chicken' become synonymous with 'boneless, skinless chicken breast?' Chicken breast is a good food, but the whole chicken is better. Dark and white meats both have nutritional strengths. They are not identical in vitamin and mineral content. Chicken skin is a good source of vitamin A, again because it's fatty. I wrote recently about liver's nutritional bonanza, and hearts are nutrient-rich as well, making giblet gravy a great idea. Simmering the leftover chicken bones yields flavorsome broth rich in highly absorbable calcium and joint-building gelatin. (I save my steak bones, too, for beef broth.)

Our ancestors, ever mindful of where their next meal was coming from, relished every edible part of every animal they killed. Indeed, paleoanthropologists assert that hunter-gatherers ate the rich, fatty organ meats first, preferring them to muscle meats, and smashed bones to eat the marrow. As recently as a century ago, marrow was such a popular food that special spoons were made for scooping it out of bones. I love the stuff. I've been sucking the marrow out of lamb-chop bones since I was a tyke. A 1997 article in the journal Nature asserts that human brain capacity decreased at the dawn of agriculture 10,000 years ago, very likely because of a reduction in animal-fat consumption. Whole animal foods are part of our nutritional heritage.

My low-carbohydrate eating habits are often referred to as a 'fad.' Whatever. If it was good enough for my hunter-gatherer ancestors, it's good enough for me. Do you want to know what's really a fad? Removing the fat from milk and the yolks from eggs, and discarding three- quarters of the chicken, all organ meats and most bones. There's not a culture in the world where our narrow, refined, low-fat, flavorless versions of animal foods are part of the traditional diet.

Continuing reading for recipe included in original article!

Two-Fold Reduction in Triglycerides! How? Low-Carb!

In a recent study - Metabolic Effects of Weight Loss on a Very-Low-Carbohydrate Diet Compared With an Isocaloric High-Carbohydrate Diet in Abdominally Obese Subjects, published in the Journal of the American College of Cardiology, researchers reported favorable results for obese adults randomly assigned a low-carbohydrate diet for 24-weeks (six months).

As reported in heartWire, "After six months, isocaloric energy-restricted very-low-carbohydrate, high-fat and high-carbohydrate, low-fat diets produced similar weight loss and substantial reductions in a number of cardiovascular disease risk markers," write Jeannie Tay (Flinders University, Adelaide, Australia) and colleagues in the January 1, 2008 issue of the Journal of the American College of Cardiology.

"Neither diet displayed adverse effects, suggesting diverse dietary patterns, including very-low-carbohydrate, high-fat diets, may be tailored to an individual's metabolic profile and dietary preference for weight management."

The investigators note that while the traditional diet reduced LDL-cholesterol levels, the low-carbohydrate, high-fat diet resulted in greater increases in HDL cholesterol and singificantly larger reductions in triacylglycerol levels (a two-fold greater reduction compared to the traditional low-fat diet).

In fact, if we go to the full-text, we find the researchers went so far as to write "consistent with other recent studies, the VLCHF (very-low-carb high-fat) diet produced greater reductions in TAG and increases in HDL-C than the HCLF (high-carbohydrate low-fat) diet. This suggests that the VLCHF diet as a weight loss strategy may confer the greatest clinical benefits in patients who present with hypertriglyceridemia, low HDL levels, abdominal adiposity, and insulin resistance"

Did you catch that - "greatest clinical benefits" - part?

In the paper we learn that subjects were randomly assigned to either of the moderately energy-restricted diet plans for 24 weeks. For those assigned to the very-low-carbohydrate, high-fat diet, 4% of total calories were obtained from carbohydrates, 35% from protein, and 61% from fat, including 20% of total calories from saturated fat. Subjects randomized to the high-carbohydrate, low-fat diet followed a more traditional macronutrient profile, with 46% of calories obtained from carbohydrates and 30% from fat, including <8% from saturated fat.

Now we all know the American Heart Association insists we must keep saturated fat at less than 7% of our calories because intakes higher than that will kill us (eye roll) - yet here we have stunning improvements with saturated fat intake at/above 20% daily for six months! If you haven't read it yet, Dr. Richard Feinman wrote a good article about saturated fat recently.

So, what gives? It seems the subjects in this study significantly reduced their carbohydrate, and that carbohydrate does matter. Also, this study confirms previous data published that found similar improvements in those restricting carbohydrate.

Slowly but surely more data is coming forward that validates carbohydrate restriction for not only weight loss, but health improvements!

Insulin Resistance and Cardiomyopathy

An interesting abstract was published in the recent issue of the Journal of the American College of Cardiology - Insulin-Resistant Cardiomyopathy, Clinical Evidence, Mechanisms, and Treatment Options.

Increasing evidence points to insulin resistance as a primary etiologic factor in the development of nonischemic heart failure (HF). The myocardium normally responds to injury by altering substrate metabolism to increase energy efficiency. Insulin resistance prevents this adaptive response and can lead to further injury by contributing to lipotoxicity, sympathetic up-regulation, inflammation, oxidative stress, and fibrosis.

Animal models have repeatedly demonstrated the existence of an insulin-resistant cardiomyopathy, one that is characterized by inefficient energy metabolism and is reversible by improving energy use. Clinical studies in humans strongly support the link between insulin resistance and nonischemic HF.

Insulin resistance is highly prevalent in the nonischemic HF population, predates the development of HF, independently defines a worse prognosis, and predicts response to antiadrenergic therapy.

Potential options for treatment include metabolic-modulating agents and antidiabetic drugs. This article reviews the basic science evidence, animal experiments, and human clinical data supporting the existence of an "insulin-resistant cardiomyopathy" and proposes specific potential therapeutic approaches.

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Protein Provides Satiety Through PYY

In our strange world, we have researchers now promoting the idea that a pharmaceutical version of the gut hormone PYY may offer a solution to help individuals lose weight.

In the MSN article, Natural Gut Hormones May Provide a Treatment for Obesity, we learn that researchers are seeking to develop a pill to provide the satiety hormone PYY.

"The advantage of developing weight loss medications based on gut-derived satiety hormones is that they enhance a process that occurs naturally. It is expected, therefore, that side effects will be minimal," says Dr Sainsbury-Salis.

Folks, we're not PYY deficient; in fact, I'd argue we're not eating the foods that stimulate PYY to effectively sate appetite naturally.

As I noted in a previous blog post about research investigating PYY, "A high protein diet led to spontaneous calorie reduction as PYY increased. The phenomenon was consistent with both the animal model using mice and in human studies used to validate the mice model. Over a longer term, the higher protein diet stimulated weight loss and enhanced PYY synthesis and secretion in mice."

As I noted in that post, the study I wrote about included quite specific detail about how diet influences the release of PYY in humans - "The ready availability of carbohydrate-rich grains and cereals has been a recent development in human nutrition with the onset of organized agriculture. Many of the physiological systems that regulate food intake were probably established and may function better under lower-carbohydrate and higher-protein dietary conditions."

Those were not my words, but the words of the researchers!

And now we have researchers looking to design a pill to provide what we already have naturally - if we eat adequate protein and fat. But, let's not go there and discuss diet, let's just pop a pill and continue along with the supposed "healthy diet" that obviously is not sating out appetite!

The future of Oracle APEX - aka Oracle APEX 4.0

In case you haven't read it on Marc Sewtz blog or in the newest edition of the German Oracle APEX community newsletter, on Friday July 25th at 14:00 (German time) there will be a WebCast about the features the Oracle APEX team is currently working on for Oracle APEX 4.0! The WebCast will also cover some tips & tricks for APEX 3.1.1.

Get the details about how to join the WebCast at the German Oracle APEX Community web site.

Overlapping labels in an Oracle APEX pie chart

Ever had the problem of overlapping labels in a pie chart which you used in an Oracle Application Express (APEX) application? Have a look at Gary Myers excellent tip to avoid collisions by using analytic functions to sort the data. It's another great example of using the built-in power of the Oracle database.

Two new Oracle APEX whitepapers

Ok, they are not brand new anymore, they have already been released last month. But in case you are not reading David Peake's blog or checking regularly the Oracle APEX website on OTN, the APEX team has published the following two new whitepapers:

• NTLM Authentication (a PL/SQL only solution) and
• Oracle APEX with RAC (Real Application Cluster)

Oracle APEX team needs your help!

It's your chance to help the Oracle APEX team to spreading the word about Oracle APEX. They want to convince the Oracle eBusiness Suite/Oracle Applications team to formally legitimize the use of Oracle Application Express with the Oracle eBusiness Suite/Applications. I think that would be another huge step to get Oracle APEX into more companies if it can be officially used to write custom applications in that environment.

But they need your help! Check out David Peake's blog posting for more details.

What's next on the Oracle APEX roadmap? Oracle APEX 3.2!

Just read on David Peake's blog that he has updated the Statement of Direction for Oracle Application Express (APEX).

What has changed?

They are planing to release Oracle APEX 3.2, which will be Oracle APEX 3.1 + The Oracle Forms Migration Tool. If you are a Forms guru, they are looking for beta testers! Get the details at David's blog.

I think the Forms Migration Tool will be another major step for Oracle APEX to get the Forms developers into the APEX boat. These two tools have a lot of similarities (declarative, PL/SQL, ...) and the same kind of productivity to develop database driven applications. Forms developers can re-use their existing skills and companies protect there investment by using the same business logic (if written in database packages) as for there Forms applications. Compared to learning or migrating an application into a new language (eg. Java/.Net) this can be a huge time safer.

Oracle APEX 3.1.2 is out!

The Oracle APEX team has released a new patchset for Oracle Application Express (APEX). According to the readme file the new version 3.1.2 contains 28 new bug fixes (Note: the list also contains the bugs from the previous patchset).

The full release can be downloaded from the OTN download side.
The patchset with just the changed files can be found on Metalink with the patch number 7313609.

Number of displayed Records of Oracle APEX Popup LOV

Recently I answered a question about where to change the number of displayed records of a Popup LOV in Oracle APEX and I thought it could be of general interest.

The behavior of Popup LOVs can be changed through the Popup Lov template. You can find it at
Shared Components\Templates\Popup LOV.

In the Pagination section you will find the property Display which defines how many records are displayed at once.

The Popup LOV template also contains other interesting settings like the icon which is used for the popup lov field or the text for the search button, the width and height which is used to display the popup lov window and much more. Just have a look!

DOAG Regionaltreffen in München zum Thema Oracle APEX

Just a quick announcement about an Oracle APEX meeting of the German Oracle Usergroup in Munich. The rest of the posting will be in German.

Termin: Mittwoch, 17.09.2008, 17:00 - 19:00 Uhr

Geplante Vorträge:

1. Professionelle APEX Entwicklung - Projektbeispiele und Lessons Learned
Referent: Dietmar Aust, OPAL Consulting

2. Möglichkeiten mit Oracle TEXT (Volltextsuche) und APEX
Referent: Carsten Czarski, ORACLE Deutschland GmbH

Ab ca. 19:00 Uhr wird der Meinungsaustausch dann im Löwenbräukeller am Stiglmeierplatz fortgesetzt.

Weitere Details und die Anmeldung auf den Seiten der DOAG.

Übrigens, die Teilname ist kostenlos.

Pro Oracle Application Express finally shipping?

Is John Scott's long awaited book Pro Oracle Application Express finally shipping?

It looks like!

There are reports on the OTN APEX forum that they have received a mail from Amazon that they have shipped the book. I also checked the order page of Amazon and it shows that the book is on stock.

You will not guess where I'm! ;-)

On the other side it's not very hard to guess. I'm there where most of the Oracle blogging and Oracle APEX community currently is. I'm at Oracle Open World in San Francisco.

I'm not sure how often I will blog, because I have a tight time schedule. But if you want to get hold of me, I will try to visit most of the Oracle APEX sessions.

On Tuesday, between 14:30 and 15:30 I'm doing my own presentation titled The Power of the Oracle APEX Repository (Session Id: 300210). It's currently booked out, but you might get a chance to still get in.

Enough for now, I have to listen to Tom Kyte's "Efficient Schema Design" now.