Every other week it seems we hear another media report of how saturated fat, once the villain, is now good for us.  

The latest study to hit the airways purportedly addressed the question of which diet is better for weight loss and reducing cardiac risk, a high-fat/low-carb diet or a low-fat/high-carb diet.  Its conclusions favored a high-fat/low-carb diet, which, being contrary to time honored wisdom, no doubt explains why the media has flocked like flies on garbage to report these“novel” findings.  Apart from the fact that this study does little to addt o our knowledge of dietary approaches to weight loss, of concern is that it provides yet more dangerous justification for eating foods that appeal to our primal instincts, i.e. foods that are nutrient dilute and calorically dense. 

The study I am referring to is one that was recently published in the Annals of Internal Medicine. It was reported in the New York Times under the headline “A Call for a Low-Carb Diet that Embraces Fat”.  

Dr. David Katz, director of Yale University’s Prevention Research, roundly criticized both the journal for publishing the study and the question the study set out to answer. He called the study design both pre-historic and propaganda. The question being asked, he said, was “egregiously silly” and “disingenuous”.  He went on to say that it was a comparison of two bad diets (he called it “a comparison of the best low-carb/high-fat diet to the worst low-fat/high-carb diet”). Its conclusions, he said, were both misleading and potentially harmful.  I couldn’t agree more.  

Low in Fat?

The first criticism is that the low-fat diet in this study was not even close to being low in fat. Those on the high-fat diet increased their fat intake about 5% to 40%, while those in the ‘low-fat’ group reduced their fat intake to 30%, about 5% lower than their baseline.  A 30% fat diet is not low in fat.  A15% fat diet is closer to the mark.  (For a review on why 30% was never considered to be the low-fat standard, click here.)  

Additionally, fiber intake for both groups was about the same, 15-16 grams per day. For any diet, high-carb or otherwise, that is less than ideal. At a minimum we need over twice that amount (40-50 g/day).  This tells me that the quality of the high-carb/low-fat diet was indeed quite poor.  I think there is one thing upon which we can all agree, a diet full of poor-quality carbs is not healthy, regardless of how much fat you are consuming.  

But this is only a sub-plot of a greater egregious error, and that is lumping a vast array of foods into a single food category--carbs.  This is probably the biggest ‘beef’, no pun intended, which I have with low carb advocates. Black beans and jelly beans, both high in carbs, are not the same foods. In order for nutrition research to be advanced we need to depart from this pre-historic reductionist approach and look at the effect of actual foods on health outcomes, not just the macronutrient content of a particular diet.  

But apart from all this, how could it be that eating a slightly higher fat diet resulted in more weight loss than a slightly lower fat diet?  The answer to this is blindingly simple.  Over the course of the study, the low-carb group took in about 100 fewer calories a day. They ate fewer calories and they lost more weight. Funny how that works.  This fact was never mentioned in the NY Times article.

All this tells me is that it is possible to lose weight independent of the macronutrient make-up of the diet as long as you are restricting calories.  But I think this has already been well established.  And lest you think that eating more fat magically means you will eat fewer calories, consider this--if I eat 5% more fat and a whole lot fewer low-quality carbs, I will likely eat fewer calories than eating 5% less fat and a whole lot more low-quality carbs.  

But evenmore disturbing is the claim that the low-carb/high-fat diet improved cardiac risk factors.

Reduced Cardiac Risk?

First it is important to note that neither group saw reductions in LDL cholesterol, total cholesterol or blood pressure.  Given that both groups experienced weight loss one would expect these biomarkers to improve.  Maybe all that fat in the diet prevented this.  LDL cholesterol is the primary atherogenic sub-fraction, and reducing LDL is the target of both drug and dietary interventions. So given that LDL did not improve it is difficult to understand why this study was heralded as improving cardiac risk.  Unless a dietary intervention gets most of its obese high-risk patients to an LDL level that is under 70 mg/dl, I don’t get too excited.  Not lowering LDL at all is something of a failure.  

LDL Subtype a Valid Predictor?

However, the New York Times article, in an attempt to gloss over this point, went down the “small dense vs. large fluffy LDL” path.  Incidentally, the type of LDL particle was not measured in this study, so to try to use this to further support the study’s finding is a bit disingenuous.  Nevertheless, this was a tack the article took.  

The argument goes something like this--greater carb consumption makes LDL particles smaller and denser.  This is bad because the smaller particles can more easily get into the arterial wall.  Saturated fat, on the other hand, results in more LDL particles that are large and fluffy.  These are too large to get into the sub-endothelial space and are thus benign.  Hence carbs make LDL atherogenic and saturated fat doesn’t.  This would make for a compelling argument except that this is not well supported in the research. 

We’ve known for a while that particles as large as 70 nm can enter the arterial wall.  The largest LDL particles (including the large puffy LDL particles) are only around 25-27 nanometers (nm), well below 70 nm.  Thus both smalland large LDL particles are atherogenic.  To quote one paper, “incorrect conclusions may have been drawnregarding the potential importance of certain “novel” risk factors.…The former observation led to the belief that small LDL particles are inherently more atherogenic than large ones, a conclusion not supported by recent analyses.” Identifying LDL particle size does not appreciably improve risk prediction above and beyond what total LDL cholesterol does.  Both types of LDL phenotypes (large and small alike) are atherogenic and are associated with increased risk. (For a good review on this watch this video presentation).

A better tack might have been to measure something called flow-mediated dilation (FMD), a reliable measure of arterial health.  Reduced FMD has been shown to be a strong predictor of future cardiac events.  A 2008 study which compared a lower-fat calorie restricted diet to a high-fat calorie restricted diet, and one where both groups lost weight, did exactly this. Weight loss should improve FMD.  However, in this study, only the lower fat group showed improvements in FMD.  The high fat group had worsened FMD, this in spite of losing slightly more weight than the low-fat group.  Point being that not all weight loss is created equal and eating more fat generally makes things worse, even when weight is lost.  

Does Increased HDL Mean Decreased Risk?

The purported reduction in risk in this study was due to increased levels of HDL. High fat diets do tend to raise HDL levels, but the real question is, does this result in reduced risk?  This is debatable.  Evidence suggests that elevations in HDL cholesterol don’t necessarily correspond with improved protection, i.e. animproved ability to perform reverse cholesterol transport or anti-inflammatory functions.  It is not so much the amount of HDL that is important, but rather its ability to exert its protective effects, i.e. not all HDL is created equal, the HDL you do have needs to be effective.  A recent (2014) study highlighted the fact that HDL can befunctionally impaired due to oxidative modification.  They found that,similar to oxidized LDL, oxidized HDL also induced significant oxidative stress and release of pro-inflammatory cytokines. Oxidized HDL is essentially HDL gone bad, and, as it turns out, can potentially increase risk, not reduce it.  This might help explain why those living in western countries have the highest HDL levels yet also have the highest rates of heart disease.

Diets low in antioxidants (i.e. low in whole plant foods) and high in fat and cholesterol promote oxidation of both LDL and HDL.  Diets high in meat, eggs and dairy promote inflammation via bacterialendotoxins and TMAO production, both of which impair HDL function.  People eating antioxidant rich diets (i.e.plants) may reduce apo-A1 oxidation thus protecting HDL and preserving its protective functions.  Thus, I would view any purported improved cardiac risk outcomes reported by this study with a degree of skepticism, especially when the HDL elevations occurred as a result of eating more fat and fewer poor quality carbs.  

In conclusion, if we truly want to be enlightened on how to best reduce risk for arterial disease, we need to highlight those papers and researchers who have clinically shown reversal of heart disease.  The only diet to date that has proven to do this effectively is one that is low in fat (<15%), high in fiber and rich in anti-oxidants; a whole-foods, plant-based diet.