Friday, March 11, 2011

Saturated with Fear

              As of January 31st 2011, the 2010 Dietary Guidelines were released by the Department of Agriculture (USDA) and the Department of Health and Human Services (HHS). The Dietary Guidelines for Americans has been published every 5 years since 1980, each time being updated with new recommendations on foods to limit or increase. One of the prevailing aspects of recommendation is to reduce saturated fat intake, due to its affect on cholesterol levels. This is in accordance with something called “The Lipid Hypothesis”. It’s modern view was developed in 1951 and proposed a connection between saturated fats and cholesterol in the blood and the development of heart disease (CHD). Since its proposal and the subsequent emergence of heart disease as a major cause of death in the US the Lipid Hypothesis has become the backbone of dietary advice, especially when it comes to dietary fat. There are many different types of cholesterol carrier molecules that exist in the body, the most well known being HDL and LDL. Cholesterol is always cholesterol, but the type of protein carrying it (HDL,LDL, or VLDL) can result in positive or negative interactions in the body. There are however other contributors to CHD, such as the ratio of HDL (“good” cholesterol) to LDL (“bad” cholesterol) and inflammation. (1, 6-8) The Dietary guidelines do not specifically recommend that you replace saturated fat with omega 3s. Therefore saturated fats are expected to be replaced with various unsaturated fats from vegetables sources. However saturated fats may not be positively associated with the risk of heart disease. (2) There is research that shows that the avoidance of most polyunsaturated fat (particuarly the omega 6 variety), the un-avoidance of saturated fats and increasing omega 3 intake can be protective of heart health.

             First, let’s review what affect the two dietary fats in question have on total cholesterol, HDL, and LDL. Saturated fats increase total cholesterol, HDL, and LDL. However, the type of LDL they raise is the "large puffy" somewhat benign kind that is not the atherogenic "small dense" LDL. The end result is higher total cholesterol, but a better ratio of “good” cholesterol to “bad”. Polyunsaturated fats have the effect of decreasing total cholesterol, HDL, and LDL. Both HDL and LDL are lowered in equal amounts. In summary, saturated fat will lead to an increase in total cholesterol, but a more favorable HDL:LDL ratio.(18-21) Polyunsaturated fat will lead to a decrease in total cholesterol, but no change in the HDL:LDL ratio. So now you might be thinking “saturated fat increases total cholesterol, that’s no good!”; However total cholesterol has not shown to be a reliable predictor of CHD risk when compared to the HDL:LDL ratio. (3-5)

Recently a rich source of saturated fat, coconut, has emerged as a new health food and dairy replacement for those lactose-intolerant. Coconut oil consists of a whopping 92% saturated fat! However as much of the marketing of coconut is sure to note, it contains 47.5% Lauric Acid, a “special” type of saturated fat that is used almost immediately by the body for energy and has antimicrobial and antibacterial properties. In fact it has actually been shown to decrease triglycerides (another important marker for CHD) and LDL; while increasing HDL. (9,10)

When we take a look at many of the other sources of saturated fat such as butter, whole milk, Cheese and red meat that are pasture fed (grass fed) we see an increase in fat soluble vitamins such as Vitamin A and E, CLA (a beneficial type of trans fat), omega 3 content, B vitamins and minerals, and lower total fat. (16,17)

             Controlling the amount of omega 3s and omega 6s in your diet can help reduce risk for a variety of diseases. (11-13) Both Omega 3 and Omega 6 fatty acids are types of polyunsaturated fats. Most sources of polyunsaturated fats are heavily skewed towards omega 6s.  By consuming saturated fats rather than polyunsaturated fats from plant sources you are not making any negative changes to the omega 3: omega 6 ratio in your diet. A typical American diet has a ratio of omega6:omega 3 of somewhere around 18:1. This imbalance in omega 6 fatty acids to omega 3s increases the development of many chronic diseases including cardiovascular disease and can increase risk of death from CHD. In the prevention of cardiovascular disease, a ratio of 4:1 was associated with a 70% decrease in total mortality, and an even lower ratio was needed to see changes in other diseases and cancers.(14,15) Omega 3s must come from somewhere though, and if you cut out sources of mostly polyunsaturated fat then you are also cutting out sources of omega 3s. However, the only considerable dietary sources of omega 3s that are not even higher in omega 6s are seafood, flax seed, Algae oil, and Chia/Salba seed.

  • By increasing omega 3 intake from wild fish, pasture raised beef, game meat, and vegetarian sources such as Algae, flax, and Chia seed you are helping to lower the omega 6: omega 3 ratio.

  • -A lower omega 6: omega 3 ratio that is closer to ~4:1 will help reduce inflammation and the risk of many chronic diseases.

  • -By consuming saturated fats you are increasing the HDL:dense LDL ratio , which Is protective, and a better predictor of risk than total cholesterol.

  • -If eating rich sources of saturated fat, look for the grass-fed variety.

  • -All natural vitamin rich sources of saturated fat that have been used for centuries include: Pastured Butter, Lard, and coconut oil or milk.

  • -By consuming polyunsaturated fats you are decreasing “good” and “bad” cholesterol.

  • Sources of high omega 6 fats and low omega 3s include: Most sources of fat from vegetables, seeds, and nuts. Olive Oil, Canola Oil, Avocado, and Macadamia Nuts are all low in total polyunsaturated fat because of their high monounsaturated fat content, but still have very skewed Omega 6:Omega 3 ratios.



When taking these points into account, it seems logical that limiting sources of high omega 6s, increasing omega 3s, and consuming nutrient dense sources of saturated fat would be quite heart healthy. But let us remember that you are never eating just saturated fat or polyunsaturated fat. Each comes in its own delicious vehicle delivered straight to your taste buds along with many other beneficial anti-oxidants, vitamins, minerals and other phytonutrients. Demonizing or worshiping any particular constituent of food is a flawed way of looking at the confusing world of nutrition.



References

1) Wang Z, Nakayama T. Inflammation, a link between obesity and cardiovascular disease. Mediators Inflamm. 2010;2010:535918. Epub 2010 Aug 5.

2) Siri-Tarino PW, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46. Epub 2010 Jan 13.

3) von Schacky C. Cardiovascular disease prevention and treatment. Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):193-8. Epub 2009 Jun 10

4) Volk MG. An examination of the evidence supporting the association of dietary cholesterol and saturated fats with serum cholesterol and development of coronary heart disease. Altern Med Rev. 2007 Sep;12(3):228-45. .
5) Stehbens WE. Science, atherosclerosis and the "age of unreason": a review. Integr Physiol Behav Sci. 1993 Oct-Dec;28(4):388-95.
6) Kimura T, et al. . Low-density lipoprotein-cholesterol/high-density lipoprotein-cholesterol ratio predicts lipid-rich coronary plaque in patients with coronary artery disease--integrated-backscatter intravascular ultrasound study. Circ J. 2010 Jul;74(7):1392-8. Epub 2010 May 18.
7) Fernandez ML, Webb D. The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk. J Am Coll Nutr. 2008 Feb;27(1):1-5.
8) Ballantyne CM, Hoogeveen RC. Role of lipid and lipoprotein profiles in risk assessment and therapy. Am Heart J. 2003 Aug;146(2):227-33.
9) Kochikuzhyil BM, et al. Effect of saturated fatty acid-rich dietary vegetable oils on lipid profile, antioxidant enzymes and glucose tolerance in diabetic rats. Indian J Pharmacol. 2010 Jun;42(3):142-5.
10) Nevin KG, Rajamohan T. Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem. 2004 Sep;37(9):830-5.
11)  von Schacky C. Cardiovascular disease prevention and treatment. ) Prostaglandins Leukot Essent Fatty Acids. 2009 Aug-Sep;81(2-3):193-8. Epub 2009 Jun 10.
12) Breslow JL. n-3 fatty acids and cardiovascular disease. Am J Clin Nutr. 2006 Jun;83(6 Suppl):1477S-1482S.
13) von Schacky C. Omega-3 fatty acids and cardiovascular disease. Curr Opin Clin Nutr Metab Care. 2007 Mar;10(2):129-35.
14) Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med (Maywood). 2008 Jun;233(6):674-88. Epub 2008 Apr 11.
15) Simopoulos AP. The omega-6/omega-3 fatty acid ratio, genetic variation, and cardiovascular disease. Asia Pac J Clin Nutr. 2008;17 Suppl 1:131-4.

16) S.K. Duckett et al, Journal of Animal Science, (published online) June 2009, “Effects of winter stocker growth rate and finishing system on: III. Tissue proximate, fatty acid, vitamin and cholesterol content.”
17) Duckett, S. K., D. G. Wagner, et al. (1993). "Effects of time on feed on beef nutrient composition." J Anim Sci   71(8): 2079-88.
18) Francisco J. Sánchez-Muniz. Dietary Fat Saturation Affects Apolipoprotein AII Levels and HDL Composition in Postmenopausal Women. The American Society for Nutritional Sciences J. Nutr. 132:50-54, 2002
19) Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb 1992 Aug;12(8):911-9
20) Maria Teresa Montoya, et al. Fatty acid saturation of the diet and plasma lipid concentrations, lipoprotein particle concentrations, and cholesterol efflux capacity1,2,3. American Journal of Clinical Nutrition, Vol. 75, No. 3, 484-491, March 2002
21) Hayek T, et al. Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates and decreasing the fractional catabolic rates of HDL cholesterol ester and apolipoprotein (Apo) A-I. Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice. J Clin Invest. 1993 Apr;91(4):1665-71.

Thursday, February 24, 2011

Intoduction

A diary, a place to rant, a place to discuss, to learn and to journal my own training in the hopes to get stupid fast. I have a lot to say about sports nutrition, and training - whether it be on the bike or in the weight room.

So who am I? I'm a cyclist who has recently found a love for track cycling, and who coincidentally has always loved weight lifting. Luckily, these two go pretty well together; at least more so than road cycling. I'm a Nutrition major at Colorado State University, where I ride for the rag-tag collegiate sports club team that we have. I just joined Big Ring Cycles U-25 Developmental Team... the first real cycling team I've ever been on.

I only started riding when I moved to Colorado, which was January '09. Before that I was just lifting weights, and even FARTHER before that in High School I was a track and field middle distance runner and pole vaulter.

My racing goals are to excel in the match sprints, Kilo, and criterium racing. I still love weight lifting, so I have some 1RM squat goals as well ; 400lbs. Currently I can back squat 350lbs, and front squat ~245lbs. I'd like to get my fronts up to a 300lbs as well.

With that short introduction, I am off to get some work done in the gym and in the books.