Carbohydrates and heart disease

Atherogenic dyslipidemia is a lipoprotein profile that predisposes one to cardiovascular disease. Grundy (1997) characterizes it by four markers: 1) a borderline high-risk LDL cholesterol (130 to 159 mg/dL), 2) moderately raised (often high normal) triglycerides (greater than 150 mg/dL), 3) small LDL particles, and 4) low HDL cholesterol (less than 40 mg/dL for men and 50 mg/dL for women). The third marker is due to data indicating that not all LDL particles are atherogenic; a preponderance of small, dense LDL particles (known as a pattern B phenotype) is associated with increased coronary artery disease (Austin et al., 1988). The presence of atherogenic dyslipidemia itself is a marker for metabolic syndrome.

Source:

Ronald Krauss and colleagues have convincingly shown that changes in carbohydrate intake profoundly affects LDL phenotypes (reviewed in Krauss, 2001). The figure below is a nice summary of the basic observation that restricting carbohydrates reduces the incidence of the atherogenic LDL particle pattern. Note especially the apparent continuity of the effect, and the fact that the carbohydrates are not even severely restricted (certainly nowhere near the levels required to induce ketosis). If you have a half hour to spare, you can catch a recent webcast talk by Krauss summarizing the Pathophysiology of Atherogenic Dyslipidemia.

Source: Krauss, 2001

If you want to full scoop on recent research on the relationship between carbohydrates and dyslipidemia and metabolic syndrome, definitely take the time to check out this review article from Jeff Volek and colleagues (it's technically still in press, but you can grab the galley proofs online). It covers a lot of ground, and is well worth the effort.

Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome.

Volek JS, Fernandez ML, Feinman RD, Phinney SD.

Department of Kinesiology, University of Connecticut

Abstract: Abnormal fatty acid metabolism and dyslipidemia play an intimate role in the pathogenesis of metabolic syndrome and cardiovascular diseases. The availability of glucose and insulin predominate as upstream regulatory elements that operate through a collection of transcription factors to partition lipids toward anabolic pathways. The unraveling of the details of these cellular events has proceeded rapidly, but their physiologic relevance to lifestyle modification has been largely ignored. Here we highlight the role of dietary input, specifically carbohydrate intake, in the mechanism of metabolic regulation germane to metabolic syndrome. The key principle is that carbohydrate, directly or indirectly through the effect of insulin, controls the disposition of excess dietary nutrients. Dietary carbohydrate modulates lipolysis, lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels. Several of these processes are the subject of intense investigation at the cellular level. We see the need to integrate these cellular mechanisms with results from low-carbohydrate diet trials that have shown reduced cardiovascular risk through improvement in hepatic, intravascular, and peripheral processing of lipoproteins, alterations in fatty acid composition, and reductions in other cardiovascular risk factors, notably inflammation. From the current state of the literature, however, low-carbohydrate diets are grounded in basic metabolic principles and the data suggest that some form of carbohydrate restriction is a candidate to be the preferred dietary strategy for cardiovascular health beyond weight regulation.

PMID: 18396172

From the archives of Science magazine

A remarkable confluence of interests:The second article is a classic by D. MacKay.

Is the omega-6:omega-3 ratio of beef relevant?

Although it's still debatable what the optimal dietary ratio of omega-6 to omega-3 fatty acids is, there's good evidence that the contemporary dietary intake of polyunsaturated fatty acids has over time become heavily skewed towards a higher intake of omega-6 than omega-3 fatty acids (Cordain et al., 2005; Simopoulos, 2002). The current US diet is estimated to have a omega-6:omega-3 ratio between 10:1 to 12:1, while Cordain and colleagues estimate a ratio of between 2:1 and 3:1 for a traditional hunter-gatherer diet. There is growing consensus that reducing the omega-6:omega-3 dietary ratio may reduce the morbidity and mortality associated with a wide range of metabolic disorders.

This is all well and good, but ratios can be misleading and it's important to keep in mind the absolute mass of fatty acids consumed (Mozaffarian & Rimm, 2006; Wijendran & Hayes 2004). Case in point: one of the purported benefits of grass-fed beef is that grass-fed beef has a better omega-6:omega-3 ratio than grain-fed beef. This is also one of the reasons that wild-caught salmon is recommended over farm-raised salmon. What do the actual data look like? The table below shows the fatty acid profiles of the aforementioned meats.


A few things to note. First, the total PUFA content of grass and grain-fed beef is pretty low. Second, grass-fed beef only contains marginally more omega-3 fatty acids than grain-fed beef. This, together with a marginally lower omega-6 content results in a slightly lower omega-6:omega-3 ratio for grass-fed beef. In addition, the two samples of grain-fed beef are very similar in most respects, but one sample has an omega-6:omega-3 ratio of >17 while the other is <5. Does that mean one is healthier to eat than the other? Not in any meaningful way, looking at the ratio alone is misleading since it conceals the fact that this difference is due to a mere 30 mg of omega-3 fatty acids. To get a sense of how small that is, recall that current recommendations for daily omega-3 intake are over 2000 mg (ALA+EPA+DHA). The absolute amount of omega-3 fatty acids derived from beef is just too small, regardless of whether it is grass or grain-fed. A one pound steak only has between 70-225 mg of omega-3 fatty acids (most of which isn't the more beneficial marine omega-3s, EPA and DHA). Compare this to the amount of omega-3s you get from either wild-caught or farmed salmon. So while it's true that the omega-6:omega-3 ratios are lower for grass-fed beef, a look at the absolute masses of the separate fatty acid classes suggests that this isn't really practically relevant.

Now don't get me wrong, there are many other benefits of grass-fed beef. If money weren't a constraint, I would eat it all the time. However, I don't think that the omega-3 content of beef should be a factor when deciding whether to buy grass-fed over grain-fed. If you want to improve your omega-6:omega-3 dietary ratio, you would do better to eat more seafood and reduce your intake of vegetable oils.

Get fat!

Good fats of course, those being ω-3 fatty acids (a type of polyunsaturated fatty acid [PUFA], another being the ω-6 fatty acids; these are also referred to as n-3 and n-6 fatty acids). Members of these families are derived from the essential fatty acids linoleate (LA) and α-linolenate (LNA). Strictly speaking, these two are the only essential fatty acids (required through diet), although that term is often extended to the entire family of PUFAs (Cunnane, 2003). The ω-3 and ω-6 fatty acids are critical for a host of bodily functions, which you can read about in reviews by Das (2006) and Wijendran and Hayes (2004). Very roughly speaking ω-6 fatty acids are pro-inflammatory whereas ω-3 fatty acids are anti-inflammatory. More specifically, the ω-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are antithrombotic and antiarryhthmic, and dietary intake of these fatty acids is associated with reduced risk of death from cardiovascular disease.

Source: Mozaffarian and Rimm 2006.

Although current evidence indicates that the relative dietary ratios of ω-3 and ω-6 fatty acids is a indicator for overall health (Wijendran and Hayes 2004; Simopoulos, 2002), the mechanisms by which EPA and DHA reduce the risk of cardiac mortality remain unclear. The assumption is that direct incorporation of these fatty acids into the myocardium of the heart underlies their health benefits. That dietary intake directly modulates myocardial phospholipid profile was recently documented by Metcalf et al. (2007). The authors examined the atrial tissue of people undergoing elective cardiac surgery following varying durations of dietary supplementation with fish oil (6 g EPA+DHA/day, for 7-60 days). They found that fish oil supplementation increased the amount of EPA and DHA in the cell membranes of both atrial tissue as well as red blood cells.


It has been proposed that the cardioprotective effects of EPA and DHA result from replacement of arachidonic acid (AA) in cardiac membranes. AA is a precursor of a wide array of eicosanoids (Funk, 2001). These compounds promote inflammatory responses, platelet aggregation, and vasoconstriction. Although these are essential metabolic functions, excess AA-derived eicosanoids can promote atherosclerotic disease and thrombosis.

Source: Calder 2006.

Metcalf et al. also showed that dietary fish oil supplementation reduced atrial AA concentrations, consistent with the idea that part of the benefit of EPA and DHA may be due to the reduction in AA-derived pro-inflammatory factors.


These phosphospholipid adaptations in atrial tissue may thus underlie the cardioprotective effects of dietary fish oil. In support of this, the timescale and magnitude of these changes is broadly consistent with the observation that the protective effects of ω-3 fatty acid supplementation begin early, but reach significance only after about three months.

Source: Marchioli et al. 2002.

Also of note is the fact that supplementing with flaxseed oil (high in ALA) did not result in any changes in ω-3 fatty acid concentrations. This is likely due to the fact that dietary ALA is converted to EPA and DHA at extremely low rates (Plourde & Cunnane 2007), which is consistent with suggestions that ALA supplementation is not cardioprotective (Matthan et al. 2005; Wang et al. 2006).

Nut fats

In case you were wondering about the fat profile of nuts (I was cause I just ate 600 calories of cashews):

Source

Fat profiles of cooking oils

Ran out of olive oil today, and before downing some canola oil (2 tbsp ~240 calories), I found a couple of nice charts illustrating the fat profiles of lots of cooking oils:

Includes some more exotic oils:

A different view in terms of absolute value:

To the future:
A very informative post on cooking oils here.