Tuesday, June 23, 2009

Benefits of High-Saturated Fat Diets (Part IV): REGRESSION IN HEART PATIENTS

Few studies review the benefits of high-saturated fat diets in actual heart disease patients. Perhaps, researchers worry about... M A L P R A C T I C E . . . ?

Like urban myths, do such studies exist?

Indeed studies of high saturated fat diets in heart disease patients IN FACT do EXIST.

LA...la la la... I feel on top of the world... (LMFAO)

The diagram exemplifies a normal coronary artery, with a large.. wide diameter... spacious... flexible.. lumen (Courtesy: medicinenet.org). The diameter of the artery can be measured accurately down to fractions of a millimeter via angiography.

It was observed that in post-menopausal women with documented heart disease from the Estrogen Replacement and Atherosclerosis (ERA) trial, a multicenter clinical trial evaluating the effects of hormone replacement therapy on atherosclerotic progression, in the group consuming the highest-saturated dietary fat diet (12.0% Sat Fat), an enlargement in coronary diameter of 0.01 mm and a 0.1% regression in coronary artery stenosis.

Quoted to Men's Health, "In the nutrition field, it's very difficult to get something published that goes against established dogma," said Dr. Dariush Mozaffarian MD MPH, assistant professor, Harvard. "The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence." Mozaffarian says he believes it's critical that scientists remain open minded. "Our finding was surprising to us. And when there's a discovery that goes against what's established, it shouldn't be suppressed but rather disseminated and explored as much as possible."

In a year during my pharmacy student training at Stanford, I worked with Dariush on an internal med rotation for 4wks. I think I learned more about drugs and how to use them than some of my preceptors combined. His teaching approaches were usually articulate, concise and patiently provided. Gosh, can I say, I've had serendipity with many mentors in my little drug journey so far. *haa*

Dividing the saturated fat intake into quartiles, the individuals at the highest quartile (dietary saturated fat intake: 12.0%) demonstrated the least progression on angiogram of coronary diameter. In fact, this was the only group that exhibited REGRESSION.

This group was also characterized as having the:
--least medications, including lipid-lowering medications
--the least medications and the higher the saturated fat, the more coronary artery widening in coronary artery diameter
--highest LDL (low density lipoprotein) measurements
--highest HDL (high density lipoprotein 'good cholesterol)
--highest HDL2 (the regressive particle)
--lowest Trigs
--highest dietary fat intake (32%)
--highest monounsaturated fat intake
--lowest dietary carbohydrate intake (47.1% v. (!!) 69%)

Improved Anti-Atherogenic Lipoproteins
"A higher saturated fat intake was associated with a more favorable lipoprotein profile, including higher HDL,HDL2, and HDL3 cholesterol; higher apoprotein A-I; lower triacylglycerolc oncentrations; and a lower ratio of total cholesterol(TC) to HDL cholesterol (TC:HDL cholesterol). Women who consumed more saturated fat consumed less carbohydrate and dietary fiber and more total fat, protein, cholesterol, polyunsaturated fat, trans fatty acids, and monounsaturated fat."

Lipid-Lowering Drugs: The Less, The More Regression
The researchers astutely noticed that "among the women not taking lipid-lowering medication at baseline or during follow-up, there was 0.22 mm less progression for each 5% greater energy intake from saturated fat, compared with 0.09 mm less progression for each 5% greater energy intake from saturated fat among women taking lipid-lowering medication (P = for interaction 0.008)."

Omega-6 PUFAs: Highly Associated with Progression
After the Lyon-Diet Heart trial was completed and showed a dramatic reduction in all-cause mortality, cardiac death and events with simple reductions in omega-6 PUFAs and increase omega-3 from fish and ALA sources like olive oil, I think this trial hits it home again that any increase in dietary PUFAs are extremely pro-inflammatory leading to progression of coronary artery diameter reductions. The lowest quartile consumed less than 3.9% PUFA which was positively (see above) associated with less of a decline of average minimal coronary artery diameter (P for trend =0.04) compared with other quartiles. Clearly, a dietary PUFA concentration greater than 3.9% was highly statistically correlated to angiogram progression. The highest quartile that consumed 7.5% PUFA in the diet this was shown to produce the second highest amount of artery diameter constriction in this trial.

FIGURE 1 (divided, above, below). Mean (SE) change in minimal coronary artery diameter according to intake of different nutrients, with adjustments as in Table 2 (see footnote 1), except that total fat was not adjusted for carbohydrate, and carbohydrate and protein were also adjusted for polyunsaturated fat. These models estimate the effect of saturated fat replacing other fats (monounsaturated or polyunsaturated),monounsaturated fat replacing other fats (saturated or polyunsaturated), polyunsaturated fat replacing other fats (saturated or monounsaturated), total fat replacing carbohydrate, carbohydrate replacing saturated or monounsaturated fat, and protein replacingsaturated or monounsaturated fat.

Median intakes(% of energy) for quartiles 1–4 were as follows:
saturated fat*** (6.1, 7.8, 9.5, and 12.0),
monounsaturated fat (6.9, 8.6, 10.7, and 13.0),
polyunsaturated fat** (3.9, 5.2, 6.1, and 7.5),

total fat (17.6, 21.7, 27.0, and 31.9),
carbohydrate* (47.1, 55.6, 60.5, and 68.9)
protein (12.7, 15.8, 18.0, and 21.2).

P for trend = 0.001 (**saturated fat), 0.40(monounsaturated fat), 0.04 (**polyunsaturated fat), 0.48 (total fat), 0.20 (protein), and 0.001 (*carbohydrate).

High Carbohydrate Intake: Associated with Coronary Plaque Progression
The authors also found that "Carbohydrate intake (see above) was strongly positively associated with progression, with a 19-mm greater decline in mean minimal coronary artery diameter in a comparisonof extreme quartiles of intake (P for trend = 0.001)."

The design of this particular study was novel in examining multiple dietary components against a validated heart disease marker for progression. Obviously, prospective RCTs utilizing high-saturated fat, low carb, low PUFA diets would constitute the best scenarios to show unequivocal heart disease reversal. Am I going to hold my breath?

R e g r e s s i o n
With a high-saturated fat diet in documented heart disease patients... coronary artery stenosis regression occurred shockingly in individuals who took less lipid-lower drugs, smoked more, and basically were hedonistic beyond a conventional cardiologist's belief. Should we live life a little dangerously... disobey the 'rules'?


katherine said...

so does this mean I don't have to worry about quitting smoking? sweet! if they could only do something about the cigarette smell... :P

all joking aside, it is reassuring that the dietary changes I've made in the past two years probably mitigate SOME of the damage done by this habit I'm trying to kick. thanks for the info, love your blog!

Calvin said...

Hey G,

As usual, another great post!

BTW: I love your last sentence-- "Should we live life a little dangerously... disobey the 'rules'?"


Dr. B G said...

Hey Calvin,

Yes that is the wicked question posed...!


That is why I like TYP... it is outrageously aTYPical... with outrageously aTYPical outcomes.

Miki said...

Here is an interesting finding by Volek et al.
"Despite a threefold higher intake of dietary saturated fat during the CRD (carb restricted diet), saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD (low fat diet)
1: Lipids. 2009 Apr;44(4):297-309. Epub 2008 Dec 12.Links
Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet.
If I understand this correctly eating saturated fats and having them in your blood are two different thing and the sat fat in your blood actually comes from lipogenesis from carbs. maybe sat fat in your blood is a problem but a result of eating carbs!
I wander why none of the professional bloggers like yourself, stefan, eads haven't picked up on this study. The rest of the results of this study are very significant but not real surprise for the low carb fans.
would love to hear your opinion on these findings

Stephan Guyenet said...

Wow, I had never actually seen those graphs before... shocking!

The carb association was striking as well. Thanks for posting.

Dr. B G said...


Did I tell you I quit too? (then I had one niggly one about a coupla wks ago? TERRIBLE)

It the best habit to quit(over and over). j/k!!! Quit, it's the best thing one can do for their health. And to stay alive for their family and friends. And fave bloggers :)


Dr. B G said...


I'm still trying to understand all the desaturases and membrane signalling thingies that go on with fatty acids. I think carbs generate TGs which are then stored as toxic WAT white adipose -- in liver, lipomas, pancreas, gallbladder, thyroid, pineal, pituitary, hypothalamus, etc which eventually attract the repair (immune) system and get calcified.

Volek doesn't touch upon PPAR-delta but these are our nutrient sensors and increase our ability to metabolize the preferred energy fuel, fatty acids. Omega-3 co-exists with high quality protein and saturated and monounsat fatty acid dietary sources (eg meat, fish, crustaceans, fowl, eggs). It makes sense these all sense and subsequently activate their own metabolism. Thank you the link. Another stunningly quiet solution to the current obesity and diabetes epidemic. Love Volek.


Dr. B G said...


Shocking isn't it? The carb intake wasn't that low 47%. You reviewed the UCSF trial on the paleo hunter-gatherer diet, remember? The diet was ~ 50% carbs and they also had relatively impressive lipoprotein and insulin control results.

PUFAs are scary. They really screw our lipid bilayers and the subsequent cellular signalling of ALL our hormones -- f*cks up the brain too. Thyroid has it's own signalling system in the brain (their own T4 and deiodinases) and corn oil has been shown to potently shut off ATPases in response to thyroid.

Effect of membrane fatty acid composition on the action of thyroid hormones on (Ca2+ + Mg2+)-adenosine triphosphatase from rat erythrocyte.
Galo MG, Uñates LE, Farías RN.
J Biol Chem. 1981 Jul 25;256(14):7113-4.

steve said...

out of curiosity, are you an MD, or Phd is Pharmacy? Interesting studies nd observations

Dr. B G said...


I have a doctorate in pharmacy. For my bachelors, I was trained as a nutritionist at Cal Berkeley, which I often didn't tell friends because I ate high fat foods & 'cr*p'.


steve said...

i did notice that the study referred to woman and not men. In fact the editorial seemed to highlight this, and said it appears that reducing LDL in men more important. What about eating large amounts of sat fat as it has to do with prostate health?
What about your diet? How much saturated fat do you consume in a day, and in what forms: red meat, eggs, fish, poultry.dairy. Thanks!

Dr. B G said...

Hey Steve,

Small LDL causes CAD for both men and women. Dr. Eades (proteinpower.com) has a good blog on that. We 'track' small LDL and DR. Davis goal is ~ 60-180 nmol/L on NMR or VAP, for regression.

About a 1/3 of the women were on HRT or ERT. After menopause, women are like men in terms of heart disease risk, and in fact it estimated 2-3 x worse. If/when plaque develops, instead of focal points like men, atherosclerosis is more systemic and widespread. This is why women have non-distinct, vague, anginal symptoms (back ache, shortness of breath, 'heartburn', anxiety, etc) not the crushing L-sided chest pain that men have.

Women also have higher rates of mortality compared to men b/c of underdiagnosis of ER idiot physicians. CAD kills more women than breast cancer but gets no real discussion in the media.

Crowe FL et al 2008 Am J Clin Nutr found no association betw saturated fat and prostate cancer risk. Hyperinsulinemia causes prostatitis and prostate CA (and breast CA as well).

DCF (the Xfit I luv) recently found a ranch out in Paso Robles, ?Crenshaw Ranch I think. I just bought a 1/4 grass-fed cow and we've been really enjoying it. It tastes just FANTASTIC all seared or stir fried in coconut oil (mine is semi-refined I believe from Omega Nutrition, scentless).

I estimate about 18% sat fat so about 40g daily from beef, eggs, coconut oil, pork (from the asian market like 99 ranch), free range chicken (from Costco, TJ's or Whole WALLET), and fatty fish (hamachi, etc and fish eggs 2-3x/wk). I do cream and halfnhalf still, otherwise I'm trying to do minimal dairy. Does that help? My insulin is high right now that's why the Trigs were up (synthetic progestin excess, low grade tooth infection -- but just got it pulled).


steve said...

Thank you; yes, indeed helpful. hard to get "natural" type food- free range chicken, eggs,etc when you work in an offie all day. Can do for brkfast/dinner unless have to have dinner out.

i do not believe the Japanese sat fat intake is anywhere near yours, but their non veggie carb intake is on the low side. i believe the jury is still out on the issue of how much sat fat is prudent, even in the face of low carb eating. Lo carb should be the way to go, nevertheless. Your husband and kids are at least eating healty and hopefully appreciative! Regards,

donny said...

I was reading a paper I found about glycogen storage disease. It mentioned that while people with the disorder (at least one form of it, anyways) produced more saturated fat through di nov lipogenesis than usual. So their levels of saturated fat in serum were much higher than is considered ideal. "Paradoxically," they didn't suffer from artherosclerosis. Chronic hypoglycemia was also cited. The abstract below fits in well;


We report a 60-year-old Japanese patient with glycogen storage disease type 1a (GSD1a) who was thoroughly evaluated for risk factors of atherosclerosis. As often observed in patients with GSD1a, this patient has multiple risk factors for atherosclerosis including hyperlipidemia, hypertension, glucose intolerance with insulin resistance, and chronic kidney disease. However, she lacked clinically evident atherosclerosis as generally observed in GSD1a patients. Unexpectedly, this patient had marked hyperadiponectinemia (27.6 μg/mL; reference range, 4.1-18.9 μg/mL) with increase in the ratio of high–molecular weight to total adiponectin. Although the reason for the hyperadiponectinemia was not clear, at least it seemed to protect against enhanced atherosclerogenesis otherwise promoted by a battery of risk factors. Although further studies are needed, hyperadiponectinemia in addition to hypoinsulinemia might explain at least in part the lack of evident atherosclerosis in patients with GSD1a.
High adiponectin of course usually means high HDl. Hypoinsulinemia sort of jumps off the page, too. We even have the possibility of saturated fat causing endothelial "dysfunction" in the form of high blood pressure, as in some studies, without having the end result of artherosclerosis as suggested in those same studies.

jimpurdy1943@yahoo.com said...

The part about smoking makes me doubt the whole study. I have known too many smokers, including my wife, who died because their lungs were destroyed by smoking. If smokers did better than non-smokers, I suspect there was some other factor which mitigated the smoking.

Stephan Guyenet said...


Good point, the lowest quartile of CHO wasn't that low at 47%. Basically the result says not to eat more than 50% CHO (assuming it's reflecting causality). It would be interesting to see what would happen at even less CHO.

I can't wait until someone does a study on low-carb diets with true mortality/CHD endpoints. I'm amazed their hasn't been one yet. There's probably a lot of resistance to it.

Thanks for the thyroid reference. Omega-6 also shuts down the main heat-generating ATPase in the liver.