Red Meat and Saturated Fat: a Tasty but Cautious Combo?

So if carbohydrates are the suspects, what should we replace them with? Most people naturally gravitate towards a Low Carb High Fat diet (LCHF) but even that can be ambiguous due to what kinds of fats should be selected. While browsing through the American Journal of Clinical Nutrition TheFatNurse found an interesting study about low carbohydrates, saturated fats and beef.

This study, which involved Dr. Krauss (famous for differentiating LDL particles and risk), decided to look at how much of a role red meat and its association with saturated fat plays in CVD risk. Red meat is often thought of as a CVD risk from the questionable lipid hypothesis due to the amount of saturated fat it has.

Free Beef to be a research subject? LETS DO IT

Participants were given a baseline diet that consisted of 50% carbohydrates before being divided up into a Low Carb High Saturated Fat group (LCHSF) or Low Carb Low Saturated Fat (LCLSF) group for another 3 weeks. Both groups dropped to 31% of their energy from carbs but increased their protein consumption to 31% of energy and fat to 38% of energy. The differences between the groups occurred in the percentage of saturated fat (made up from dairy). The Low Carb High saturated fat group took in 15% of their energy from saturated fat whereas the low carb low saturated fat group only took in 8% (with an increase in monounsaturated fat to keep the total fat even). So what were the results?

***Atherogenic dyslipidemia is often associated with elevated triglycerides, low HDL cholesterol and more small LDL particles***

Triglycerides: Baseline diet (1.22+/-0.61), LCHSF (1.10+/-0.61), LCLSF (1.05 +/- 0.49)

HDL-C: Baseline diet (1.08+/-0.27), LCHSF (1.07+/-0.30), LCLSF (1.04 +/- 0.27)

So based off those results it seems that both Low Carb options here perform much better than the Baseline diet that was higher in carbohydrate right? Not so fast. While it’s true that the LCHSF yielded much lower triglycerides, it also yielded increases in LDL than the baseline group. This shouldn’t be surprising tho due to the saturated fats. However, what concerns TheFatNurse is the types of LDLs raised. The LCHSF group had increases in the large LDLs and medium LDLs (as expected) but also in the small LDLs!

This is a bit concerning since Krauss had shown through previous studies that it’s the small LDL particles that are associated to CVD risk and not so much the larger ones (Recent findings are also suggesting its the total particle count that matters most). Perhaps the saving grace for LCHSF is that it did yield a smaller result for “very small LDLs” but this was not statistically significant (p=0.23).

In his study, Krauss reports previous studies showing saturated fats raising LDLs and total cholesterol but not contributing towards levels of small LDL particles. Could the results of this study have been due to the type of protein eaten with the saturated fat? Additionally, could these results have been due to the substitution of monounsaturated fats for the LCLSF group? Krauss addresses these points and remarks that the difference in this study was the strict use of beef as the protein source. Does this mean it’s the beef protein itself with saturated fat that is causing these changes to LDLs? Krauss remarks that it can be due to other factors such as iron which has been shown to contribute with lipid metabolism as well.

The Bottom Line: So while some previous studies did not show any cardiovascular risk with saturated fat intake…does this study mean that people should be careful if they are eating lots of saturated fat with red meat (specifically beef)? Maybe, maybe not. As Krauss notes, more studies are definitely needed, and this experiment had people eating more beef than what is typically normal. TheFatNurse think the biggest thing to take away for now is more evidence that carbohydrates are a risk factor since both low carb diets in the study yielded lower triglycerides. As for the increase in small LDLs from the higher saturated fat diet? Just cut out a little saturated fat from red meat in your diet and replace with non red meat saturated fats if this one study makes you cautious. In the meantime, TheFatNurse is gonna go fry up a steak.

***Of note, some people would consider the 31% of calories from carbohydrates in the Low carb groups not low enough to be considered a “true low-carb” diet***

Steak

Changes in Atherogenic Dyslipidemia Induced by Carbohydrate Restriction in Men Are Dependent on Dietary Protein Source

Lara M MangraviteSally ChiuKathleen WojnoonskiRobin S Rawlings, et al. The Journal of Nutrition. Bethesda: Dec 2011. Vol. 141, Iss. 12; pg. 2180, 6 pgs
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Fat Research During the MadMen Era

My friends keep obsessing over the new season of MadMen, so lets take a look at some of the landmarks of obesity related topics in this era. This era is well known for establishing Ancel Key’s Lipid hypothesis which states saturated fat increases cholesterol and increased cholesterol is a risk for heart disease therefore reduction of cholesterol and saturated fat reduced heart disease. This hypothesis is still widely accepted today. However, contradictory evidence was emerging around the same time. Two notable scientists providing an alternate hypothesis to heart disease at this time were Peter Ahrens and John Gofman.

John Gofman is famous for pioneering cholesterol research. While everyone was focusing on cholesterol as the circulating fat during the 50s, Gofman pointed out that the body circulated more lipid like substances than just cholesterol such as triglycerides. Additionally, there was also the lipoproteins that were involved in these lipids. This discovery naturally lead to the question: is there more to this story than just cholesterol? However, due to the technology at the time, it was only feasible to measure cholesterol (total).

With time, scientists eventually discovered three important Lipoproteins involved with cholesterol: HDL (the so called good one), LDL (what we commonly think of as the bad one) and VLDL (which carries most of the triglycerides). While everyone else was concerned about total cholesterol, Gofman realized that LDL seemed to be in larger amounts in patients with atherosclerosis independent of their total cholesterol. Therefore, Gofman pointed out that measuring total cholesterol was useless. However, even more compelling, was Gofman’s research on VLDL.

Gofman discovered that eating saturated fats could raise LDL which would fall in line with our current way of thinking. However, he also discovered that eating more carbohydrates would raise VLDL levels! The implications of this finding showed the potential dangers of using a low fat – high carbohydrate diet. For example, Gofman pointed out that the substitution of saturated fats for carbohydrates (the “carbohydrate factor” as he put it) could potentially cause more harm for individuals if it elevated their VLDL levels too high. This was of particular concern since cholesterol levels during this era was measured as total cholesterol and not into more specific subsets.

John W. Gofman

“If LDL was abnormally elevated, then this low-fat diet might help, but what Gofman called the ‘carbohydrate factor’ in these low-fat diets might raise VLDL so much that the diet would do more harm than good.”

– Gary Taubes, Good Calories Bad Calories

Another prominent scientist at this time was Peter Ahrens who is associated with terming the phenomenon of carbohydrate-induced lipemia. Simply put, this is circulation of fatty triglycerides in the blood (carried by VLDLs as shown from Gofman’s research) which is a risk for heart disease. The question is: was a person more likely to have this circulating systemically on a high carb or a high fat diet?

Since VLDLs were more likely to increase under carbohydrates consumption, you would be right if you said a diet focused more on carbohydrates. Ahrens demonstrated this by showing blood serum from the same patient following a high fat or high carbohydrate meal. The test tube was cloudy with triglycerides if they had eaten the carbohydrate diet but clear if they had eaten the high fat diet. However, during this period, having a high triglyceride level was still being questioned whether or not to play a role in heart disease. Ahrens warned the lipid hypothesis needed more questioning before low-fat diets (which would mean an increase of calories from carbohydrates) should be recommended since they did not know whether carbohydrates, fats or some other factor played a role in heart disease.
***Of note, Ahrens showed that a high carbohydrate diet would have less triglyceride levels if the total caloric intake was very low. A point he used to argue certain Asian countries having lower heart disease despite having a high carbohydrate diet at the time.

Margaret Albrink, at the metabolic division of Yale Medical School would provide some observations on the importance of triglycerides. Her findings showed high triglycerides were more common than elevation of cholesterol in patients with cerebral, coronary and aortic atherosclerosis. And that potential accumulation of triglycerides may be the most common lipid derangement in coronary artery disease.

Albrink presented her results to the association of the American Physicians but was met with anger and disbelief. This occurred only recently after the American Heart Association decided to accept and endorse Ancel Key’s idea of saturated fat and cholesterol (Lipid hypothesis) being the culprit. Albrink would continually be attacked by proponent’s of the lipid hypothesis. However, she would receive more support from other scientists later such as Nobel laureate Joseph Goldstein who found elevated triglyerides just as common if not more so than cholesterol in over 500 patients with heart disease. Even more interesting was a study done by Peter Kuo which showed:

More than 90% of the 286 patients were found to have hyperglyceridemia derived from increased endogenous lipogenesis from carbohydrate. This abnormal carbohydrate sensitivity was revealed with an ad libitum carbohydrate (35% to 40%) diet. Since lipoproteins synthesized from carbohydrates were shown to be rich in both triglyceride and cholesterol, carbohydrate-sensitive hyperglyceridemia was frequently found in association with hypercholesteremia. The abnormal metabolism was controlled by a sugar-free diet, with a carbohydrate allowance of 125 to 150 gm supplied as starches.

So 90% of the subjects had elevated triglycerides related to carbohydrate consumption. Additionally, since VLDLs carry triglycerides and cholesterol (majority triglycerides), that could potentially mean increases in cholesterol levels could be related to carbohydrate consumption as well. Interestingly enough, the elevated triglycerides and cholesterol were controlled when patients were put on limited carbohydrates…

Even more interesting was an editorial put out by the Journal of the American Medical Association about these new discoveries:

“Research,like therapeutics, experiences cyclic fads. These are characterized by a rush of investigators towards an avenue of research initiated by publication of a few promising studies. For nearly fifteen years, an almost embarrassingly high number of researchers boarded the “cholesterol bandwagon” in pursuit of understanding of atherosclerosis. This fervent embrace of cholesterol to the exclusion of other biochemical alterations resulted in a narrow scope of study of a disease which is probably multifaceted in causation. Fortunately, other fruitful approaches have been made possible in the past few years by identification of the fundamental role of such factors as triglycerides and carbohydrate metabolism in atherogenesis.”

Somehow tho, saturated fats and cholesterol being the culprit behind heart disease has still become unquestionable medical facts to many practitioners and thus society. Just how sure are we of this?

Peter Ahrens

“Some thought him to be obtuse or stubborn, as he refused to endorse claims that changing our diets by lowering cholesterol intake would be the sole and most effective weapon to win the battle against heart disease. He was indefatigable in pointing out the necessity of additional clinical research in human subjects to delineate individual differences in response to diet. Unpopular as these views may have been, time has revealed the correctness of his views.
http://www.jlr.org/content/42/6/891.full

Serum Lipids and Cerebral Vascular Disease
ROBERT G. FELDMAN, MD; NEW HAVEN; MARGARET J. ALBRINK, MD
Arch Neurol. 1964;10(1):91-100.

Hyperlipidemia in Coronary Heart Disease I. Lipid levels in 500 survivors of  Myocardial InfarctionJOSEPHL.GOLDSTEIN,WILLIAMR.HAzzmm, HELMUTG.ScinoTT, EDWINL.BIERMAN,andARNoG.MOTULSKYwiththeassistanceof MARYJoLEVINSKIandELLEND.CAMPBELL

Hyperglyceridemia in Coronary Artery Disease and Its Management
Peter T. Kuo, MD JAMA.1967;201(2):87-94. doi: 10.1001/jama.1967.03130020033007

CORONARY HEART DISEASE AND CARBOHYDRATE METABOLISM JAMA.1967;201(13):1040-1041. doi:10.1001/jama.1967.03130130066017CORONARY HEART DISEASE AND CARBOHYDRATE METABOLISM JAMA.1967;201(13):1040-1041. doi:10.1001/jama.1967.03130130066017

Eat your Bacon

If someone were to ask, “what is healthier bacon or a bowl of cheerios?” What would you say? Well in theory…Bacon. I know I know, MIND = BLOWN. About half the fat is monounsaturated, the kind found in olive oil, which is suppose to help with HDL and LDL. Additionally, a third of the saturated fat is stearic acid which can potentially increase HDL cholesterol. Compared with eating a bowl of cereal or bread for breakfast, does this mean Bacon is actually better at reducing the risk of…heart disease!? If you prescribe to the carbohydrate hypothesis (where it is carbs and not fat or cholesterol that cause heart disease and other chronic illnesses) it just might.

I’ll never doubt you again

How Much Longer Can We Expect To Live By Cutting Out the Saturated Fat?

Interesting tidbit I found in Good Calories Bad Calories from page 65:

“Between 1987 and 1994, independent research groups from Harvard Medical School, the University of California, San Francisco, and McGill University in Montreal addressed the question of how much longer we might expect to live if no more than 30 per cent of our calories came from fat, and no more than 10 percent from saturated fat, as recommended by the various government agencies…

“The Harvard study, led by William Taylor, concluded that men with a high risk of heart disease, such as smokers with high blood pressure, might gain one extra year of life by shunning saturated fat. Healthy nonsmokers, however, might expect to gain only three days to three months …

“The UCSF study, led by Warren Browner, was initiated and funded by the Surgeon General’s Office. This study concluded that cutting fat consumption in America would delay 42,000 deaths each year, but the average life expectancy would increase by only three to four months. To be precise, a man who might otherwise die at 65 could expect to live an extra month if he avoided saturated fat for his entire adult life. If he lived to be 90, he could expect an extra four months. The McGill study, published in 1994, concluded that reducing saturated fat in the diet would result in an average life expectancy of four days to two months.”

“Michael McGinnis, the deputy secretary for health, then wrote to JAMA trying to prevent publication of Browner’s article, or at least to convince the editors to run an accompanying editorial that would explain why BRowner’s analysis should not be considered relevant to the benefits of eating less fat.”

Now if these studies are true (and to be honest I haven’t gone through them personally), they were not the only ones at the time down playing the dangers of saturated fat. However, the fact that the McGovern report chose to test a low fat hypothesis without conclusive evidence as recommendations for the US people…and only for the government to try and silence research that downplayed their own recommendations decades later….sounds fishy. More importantly, the rage I feel for denying myself bacon and eggs for breakfast all these years cannot be understated!

Unintended consequences of Medical Dogma

So what do people know about heart disease? Well that is often determined by what their healthcare providers tells them. And what is their healthcare provider likely to tell them? Well, unless they constantly keep up with the latest research, they are likely to tell them the knowledge they were educated with themselves. For myself, I was taught to inform patients that they should eat a low fat (especially of animal fats) and low cholesterol diet (along with low sodium but that’s for another discussion) if they wanted to reduce their incidence of developing heart disease. From my Pathology and Nutrition textbooks:

“A major intervention related to atherosclerosis is encouraging the consumption of a low-fat diet, with those fats being primarily polyunsaturated (from vegetable sources as opposed to animal). Additionally, exercise and weight control are effective in improving lipid profiles. Pharmacologic management of elevated serum lipids is encouraged as a prophylactic intervention”

“Saturated fats are of animal origin. Fats from plant sources usually are unsaturated fats and help reduce health risks (notable exceptions are coconut and palm oil).” 

By now this is common sense right? After all, everybody knows that eating fats is unhealthy and will clog your arteries. But in case you forgot, celebrity doctors like Dr. Oz was on the other day informing viewers that “cutting the fat in half saves a lot of lives.” So how do we know all this? There must be thousands of research studies that show consumption of fat and cholesterol is bad right? Actually…not really.

The connection between heart disease with cholesterol and saturated fat is often taught as eating saturated fat raises cholesterol (LDL) which ends up clogging your arteries. This connection is often cited as if it were unquestionable medical dogma but the evidence of this ever being clear cut is shaky at best. Much has been discussed at length about this by other medical professionals such as the bloggers in my dispatch link. If this is the first time you’ve heard about this, an entertaining documentary about the matter can be found in Fathead by Tom Naughton. For those who want more details, Good Calories, Bad Calories by Gary Taubes provides much more detail about the matter. So instead of going over the subject matter I thought I’d share my thoughts on the unintended consequences of this.

With everybody believing saturated fat and cholesterol are the culprits without solid evidence what has happened?

We now have supermarkets filled with low-fat options that substitute the fat with more carbohydrates when some research is showing carbohydrates as the original culprit.

We’ve developed drugs (Statins) which are now one of the most prescribed medicines that are believed to reduce risks of heart attacks since they lower cholesterol. However, if cholesterol was never a cause for heart disease, then patients have been taking a drug they have never needed while being exposed to adverse risks such as cognitive dysfunction and increased risk of diabetes from these drugs.

We can’t be objective because everything is viewed through this diet-heart hypothesis. A good example of this is the “best diets” list by U.S News which seems to have diets ranked upon how little saturated fat and cholesterol they compose of. It doesn’t bother asking whether the assumption of saturated fat and cholesterol being bad is valid in the first place.

It’s created an obesity stigma where people who can’t lose weight are viewed upon as lazy, incompetent and lack will power. However, if carbohydrates are the original cause, their obesity may have been contributed because they were informed to eat less fat and more carbohydrates!

Defining cholesterol and saturated fats in this manner without reexamining them focuses a lot resources used in research on potentially the wrong cause and treatment.

More importantly, if everything was based on the wrong hypothesis, then the rises in obesity, diabetes, childhood obesity, heart disease, metabolic syndrome, and etc were the cause of unintended consequences!

“When you cut the fat in half you save a lot of lives” – Dr. Oz 5:03

Dr. Oz, arguably more influential than the US Surgeon general, is seen here vilifying fat again. “When you cut the fat in half you save a lot of  lives,” has a lot of implicit meaning and portrays fat in a conclusive manner as harmful.

It’s interesting to see that he has made up his mind about the manner even tho the evidence is so controversial with experts arguing on both sides. Oz has already interacted with Gary Taubes twice on national TV about the manner, as seen below, so he has been exposed to the arguments. While I am not saying Taube’s is right, vilifying fat in such a conclusive manner often closes the door for further investigation and brings with it unintended consequences and the creation of medical dogma.

Math clogs people’s brains

One of the most common drugs people have is Atorvastatin known more popularly as Lipitor:

Hmm…misleading?

I can’t speak for everyone else, but when I see a number like that it makes me think that you can prevent a heart attack in more than 1 out of 3 people. But four years ago, Businessweek pointed out the details of the fine print below the glaring asterisk of the 36% number.

“That means in a large clinical study, 3% of patients taking a sugar pill or placebo had a heart attack compared to 2% of patients taking Lipitor”

What that boils down to is maybe one fewer heart attack per 100 people. What wasn’t covered in the article was how such a huge number came to be. That 36% is a real number and this is how its done.

In statistics it’s known as relative risk and compares the ratio of heart attacks between both groups. I’ll just use the 2 and 3 percent numbers they provided instead of looking up the actual study. That breaks down to:

Lipitor: 2 heart attacks per 98
Sugar Pill: 3 heart attacks per 97

So the odds of heart attack for the Lipitor group is 2:98 which is 0.02041 and the odds of heart attack on sugar pill is 3:97 which is 0.03093. Next, you take these two numbers and you do (odds with Lipitor)/(odds with sugar pill) which is (0.02041)/(0.03093). This comes out to 0.66 which means the odds of a heart attack on Lipitor is 66% to the odds of having one with a sugar pill. You then subtract 1.00 from the percent: 1.00-0.66 and you get 34% lower. The reason it is not 36% exactly is because the 2 and 3 percent numbers used were probably rounded.

The confusion comes because we don’t often think in terms of relative risks but absolute risk instead. Was that Ad portraying the 36% as a relative risk instead of an absolute risk? Hmm, that depends on the reader but I definitely thought it was absolute risk when I first saw it.

BTW if sugar really is the culprit behind heart disease and not fat….maybe they shouldn’t be giving sugar pills to control groups in these sort of studies!