The NEW Track Your Plaque Diet: Part 3
Special Issues
Lipoprotein(a)
Summary:
* Liberal fat intakesome saturated fats from eggs, meats (non-cured and processed), dairy; monounsaturated; fish oil
* Completely avoid hydrogenated, "trans," fats
* Wheat and cornstarch reduction or elimination
Scientific Summary of the Lp(a) experience
(adapted from Unique Strategies for Lipoprotein(a) Reduction)
Low-carbohydrate diets may reduce Lp(a) modestly. A carefully conducted University of Connecticut study in 29 overweight men showed that a diet of 13% carbohydrate, 60% fat (no controlled proportions of saturated, polyunsaturated, etc.), 27% protein, without restriction in calories resulted in an average of 11% reduction in Lp(a). Interestingly, the average weight loss was 16.5 lbs over the three-month period (Wood RJ et al, 2006).
On the other hand, fat restriction (low-fat, high-carbohydrate diet) raises Lp(a), as demonstrated by another study in 37 healthy women in which Lp(a) increased 7–9% by reducing total fat intake from 36% of calories to 31%, achieved by reducing saturated fat (Silaste M et al 2004). Another study in 140 men showed a similar effect (Shin MJ et al 2007).
With regards to fat composition of the diet, omega-3 fatty acids from fish oil capsules and eating fish (see above) have the potential for both reducing Lp(a) levels, as well as suppressing production of the most undesirable small apo(a) portion of the Lp(a) molecule. Saturated fats also reduce Lp(a). Saturated fat effects show great variation among different individuals, ranging from 5% to 30% lower Lp(a) with diet unrestricted in saturated fat. Interestingly, the stearic acid component of saturated fats stands out as the factor that raises Lp(a), unlike other saturated fatty acids palmitic, lauric, and myristic fatty acids, which do not (Müller H et al 2003; Sanders TAB et al 1997). Stearic acid is especially plentiful in the saturated fat from chocolate (43% of total fat) and red meats (14%). (There are no studies specifically examining the effects of dark chocolate or cocoa on Lp(a).) Nonetheless, the net effect of saturated fat is Lp(a) reduction.
Trans fatty acids (hydrogenated fats) raise Lp(a), generally around 5%, though some people show much greater increases (Clevidence BA et al 1997; Mensink RP et al 1992). Although monounsaturated fats (e.g, canola, olive) may be desirable from an insulin-sensitizing standpoint, they may also raise Lp(a) by 10–12% (Vessby B et al 2002). From a fat composition viewpoint, a diet rich in omega-3 fatty acids and saturated fats, and low in hydrogenated trans-fats and perhaps monounsaturates, is therefore most beneficial for Lp(a) reduction.
Weight loss may result in modest reduction of Lp(a) in obese or overweight people. In one small French experience in 62 overweight people, participants with Lp(a) >20 mg/dl experienced 17.6% reduction in Lp(a) with weight loss of approximately 15 lbs over 6 weeks, achieved through calorie restriction (Kiortsis DN et al 2001). ??
Soy protein
Soy protein, while exerting a modest LDL-reducing effect, may also increase Lp(a) 15-20%, while the dairy protein, casein, may reduce Lp(a) (Nilausen K 1999; Teede HJ et al 2001). However, these observations have not been consistent; one small study in females suggested no Lp(a) effect (Merz-Demlow BE et al 2000), another larger study in 130 participants receiving 30 grams soy protein also showed no effect (Tonstad S et al 2002).??
Alcohol
Alcohol, i.e., ethanol provided by alcoholic beverages, reduces Lp(a) in a dose-dependent manner: the more you drink, the more Lp(a) is reduced, up to 57% reduction, an observation confirmed in a number of studies (Fontana P et al 1999; Välimeli M et al 1991; Marth E et al). Unlike the apo(a)-size effects of omega-3 fatty acids, alcohol did not exert any beneficial effect on apo(a) profile, despite the reduction in Lp(a), according to one very well-conducted study (Fontana P et al 1999). Conversely, withdrawal of alcohol from chronic users triggers a rebound of Lp(a), an effect also confirmed in several studies (Huang CM et al 1992). ??Although deeply-pigmented red wines are suspected to provide benefits over and above their alcohol content (presumably due to flavonoid content), no such specific relationship with Lp(a) has been identified.
Of course, there are other effects of alcohol to consider, including beneficial rises in HDL at low quantities (up to two servings a day), but increasingly adverse effects, including increased triglycerides and blood pressure (more than four drinks per day), with greater amounts.
Flaxseed and almonds
Ground flaxseed (2 tbsp/day) and raw almonds (1/4 cup/day) achieves Lp(a) reductions of approximately 7% (Jenkins DJ et al 2002). Both foods not only reduce Lp(a), but also reduce LDL and may partly counteract the small LDL particle size tendency through their blood sugar-reducing effect.
Diabetes, pre-diabetes, and "hyper-metabolic syndrome" (including Apo E2 and E4)
This special pattern can be recognized by having any of the following features:
* HDL is 50 mg/dl or less
* Small LDL >30% of total LDL
* Triglycerides 100 mg/dl or greater
* Blood sugar (fasting) is greater than 100 mg/dl or one or two hour after-eating is >120 mg/dl
* C-reactive protein is greater than 1 mg/l
despite normal body weight or BMI.
In other words, while most people develop these characteristics when overweight, there is an important group of people who develop these features even with what appears to be normal body weight. We call this "hypermetabolic syndrome," while others call it "normal weight obesity."
Say, for example, that you are a 5 foot 9 inch male weighing 165 lbs (BMI 24.4) yet show blood sugar of 110 mg/dl, HDL of 41 mg/dl, triglycerides 150 mg/dl: you may fall in this category. This means that your tendency towards abnormal insulin responses (i.e., insulin resistance and/or excessive insulin surges) is exaggerated compared to other people.
One important subgroup prone to hypermetabolic syndrome are people with the Apo E2 or Apo E4 gene characteristic (E2/E3, E3/E4, or E2/E4 with one "dose" of each gene, or E2/E2 or E4/E4 with two "doses" of the gene; apoE3/E3 is the "normal" form).
The standard Track Your Plaque approach for metabolic control is applied in this situation, but intensified. Like standard metabolic syndrome, hypermetabolic syndrome is worsened by conventional diets and the standard wisdom of "eat a balanced diet," eat "heart healthy" whole grains, and low-fat diets.
While the same principles articulated in the New Track Your Plaque Diet: Part II apply, people with extreme metabolic syndrome need to be even more strict. This means:
* Absolute elimination of wheat and cornstarch?since these foods trigger surges in blood sugar greater than table sugar
* Minimal sweets (dark chocolates with >70% cocoa are a safe haven)
* Minimal non-wheat carbohydrates?minimal white and red potatoes, minimal rices (except wild); little or no non-wheat alternatives such as quinoa, sorghum, bulghur, rye, barley. Oats are also a problem area and should be oat bran only, not oatmeal, though even oat bran can raise blood sugar and insulin substantially: small quantities, infrequently. Flaxseed is safe, since it contains no digestible carbohydrates.
* Healthy oils should be included in every meal.
This eating style facilitates achieving true ideal weight, which may be a BMI <25, perhaps as low as 19-23.
Apo E2 and E4
Data suggest that people with the apo E4 characteristic experience greater risk for coronary events and have higher total and LDL cholesterol than the E3 or E2 patterns. Total and LDL cholesterol reductions are also greater in people with apo E4 when saturated fat and cholesterol are reduced in the diet. However, much of the data are limited, in that some studies only report total cholesterol (and thereby clouded by effects that might work through HDL and triglycerides, as well as LDL) and few observations on LDL particle size have been made.
There are also some observations that suggest that people with apo E4 may respond more vigorously to statin drugs, with greater reductions than in people with apo E3 or apo E2 (Maitland-van der Zee AH et al 2006). Some data suggest that apo E4 increases potential for metabolic syndrome (Sima A et al 2007).
Although difficult to tease from the literature, our experience has been that apo E2 heightens insulin resistance much more so than the other apo E forms. These people tend to fall more commonly in our hypermetabolic syndrome category.
Regardless of whether apo E2 or E4 are present or not, our lipid targets remain the same. Likewise, management of features of the metabolic syndrome remains unchanged; knowing that the E2 or E4 patterns underlie the tendency simply provides some "reassurance" that there is indeed a genetic basis for it.
Should you have one or two "doses" of apo E4, it may be helpful to more strictly limit saturated fat compared to other people if LDL cholesterol (or apoprotein B or LDL particle number) remain above your target level. Perhaps a statin drug should be considered more seriously for high LDL cholesterol values, as well.
Diabetes
The New Track Your Plaque Diet clearly differs in many fundamental ways from the standard diabetic diet taught in diabetes education classes and advocated by the American Diabetes Association (ADA).
Our approach of reducing processed carbohydrates, especially those made with wheat and cornstarch, is completely outside standard advice. While the ADA in a recent policy statement grudgingly suggested that a low-carbohydrate diet might be beneficial, they qualified it by warning that if it is undertaken for a short time of no more than a few months because of uncertain long-term effects.
We disagree. If low-carbohydrate is equated with an Atkins'- like approach of unrestrained meat eating, cured and processed meats, indiscriminate fat take, along with elimination of carbohydrates, then we agree: This style of eating is nothing more than a weight loss strategy, not an eating style for long-term overall health, including in diabetics.
However, it is hard to imagine that a diet that actually eliminates diabetes for many diabetics or, at least, yields enormous gains in sugar control sufficient to eliminate insulin in type II diabetics or reduce medication need significantly can be unhealthy in any way. And that is precisely what happens in the eating style advocated in the New Track Your Plaque Diet: Diabetics enjoy either far better sugar control, or reverse diabetes altogether. It makes no sense whatsoever to caution against a diet that is curative.
We find the ADA caution over uncertain long-term effects untenable. The low-carbohydrate diet advocated in the Track Your Plaque program is nothing like the Atkins' program, nor is it truly no-carb in that plentiful vegetables, nuts, and some unprocessed carbohydrate sources (e.g., beans, wild rice, mushrooms, fruit) are encouraged.
Nonetheless, any diabetic, type I or type II, will need to watch blood sugars closely during the first few weeks of incorporating the Track Your Plaque diet program. In type I, in particular, in which insulin injections are used, the transition from the standard ADA diet to the Track Your Plaque diet should be gradual to ensure smooth transition without the danger of excessive hypoglycemia (low blood sugar). Some type I diabetics will need to increase complex carbohydrate intake (e.g., beans, peas, some grains) over that advocated in the Track Your Plaque diet to prevent the lows that can occur. Of course, this should be carefully monitored by your doctor.
Type II diabetics generally have an easier time transitioning to the Track Your Plaque style of eating. However, low blood sugars remain a risk during the transition period and close blood sugar monitoring is essential. It remains important to avoid the excessive lows of blood sugar during the transition phase.
Gout
At some levels, the New Track Your Plaque Diet and the conventional diet designed to avoid gout attacks can clash.
For instance, our reliance on lean meats and not restricting inclusion of alcohol (as long consumption is light to moderate) can increase purine intake and thereby increase blood levels of uric acid, the factor that crystallizes in joints, triggering attacks of gout.
However, newer thinking on uric acid and gout suggest that the Track Your Plaque diet and gout are not as incompatible as they first appear.
If you have gout and have been instructed on diet, there are several issues to be aware of based on the newest clinical observations:
* Fructose intake, e.g., processed foods such as low-fat or non-fat salad dressings, fruit drinks, beer, breads, etc. increase uric acid levels and gout attacks significantly (Choi HK et al 2008). These foods should be avoided.
* Coffee drinkers have lower blood levels of uric acid than non-coffee drinks (Choi HK et al 2007). Teas appear to have no effect. Thus, coffee may exert a modest protective effect.
* Sugar-sweetened soft drinks increase uric acid and should be avoided. This is not true for artificially-sweetened soft drinks (Choi HK et al 2008).
* While beer and "hard" liquor raise uric acid levels, wine does not (Choi HK et al 2004).
* Vitamin C, 500 mg per day, is associated with lower uric acid levels (Gao X et al 2008).
Nuts (raw) likely exert little or no effect on uric acid levels.
People with gout are routinely instructed to limit meat and seafood due to high purine intake; this has been confirmed and will need to be taken into consideration in your Track Your Plaque program.
Yet another factor to consider is whether or not your doctor has prescribed the drug allopurinol; people who take allopurinol are afforded more leeway in diet, as this effectively blocks production of uric acid from purines in the diet.
There are other issues to consider in the patient with gout, e.g., kidney function, acidity vs. alkalinity, etc. that are best addressed by your primary care doctor or rheumatologist.
References
Lipoprotein(a)
Clevidence BA, Judd JT, Schaefer EJ et al. Plasma lipoprotein(a) levels in men and women consuming diets enriched in saturated, cis-, or trans-monounsaturated fatty acids. Arterioscler Thromb Vasc Biol 1997 Sept; 17(9):1657–1661.
Herrmann W, Biermann J, Kostner GM. Comparison of effects of N-3 to N-6 fatty acids on serum level of lipoprotein(a) in patients with coronary artery disease. Am J Cardiol 1995 Sep 1;76(7):459–462.
Jenkins DJ, Kendall CW, Marchie A, Parker TL, Connelly PW, Qian W, Haight JS, Faulkner D, Vidgen E, Lapsley KG, Spiller GA. Dose response of almonds on coronary heart disease risk factors: blood lipids, oxidized low-density lipoproteins, lipoprotein(a), homocysteine, and pulmonary nitric oxide: a randomized, controlled, crossover trial. Circulation 2002;106:1327–1332.
Marcovina SM, Kennedy H, Bittolo Bon G et al. Fish intake, independent of apo(a) size, accounts for lower plasma lipoprotein(a) levels in Bantu fishermen of Tanzania: The Lugalawa Study. Arterioscler Thromb Vasc Biol 1999 May;19(5):1250–1256.
Mensink RP, Zock PL, Katan MB, Hornstra G. Effect of dietary cis and trans fatty acids on serum lipoprotein(a) levels in humans. J Lipid Res 1992 Oct;33(10):1493–1501.
Merz-Demlow BE, Duncan AM, Wangen KE, Xu X, Carr TP, Phipps WR, Kurzer MS. Soy isoflavones improve plasma lipids in normocholesterolemic, premenopausal women. Am J Clin Nutr 2000; 71: 1462–1469.
Nilausen K, Meinerrz H. Lipoprotein (a) and dietary proteins: casein lowers lipoprotein (a) concentrations as compared with soy protein. Am J Clin Nutr 1999;69:419–425.
Sanders TAB, Oakley FR, Miller GJ et al. Influence of n-6 versus n-3 polyunsaturated fatty acids in diets low in saturated fatty acids on plasma lipoproteins and hemostatic factors. Arterioscl Thrombo Vasc Biol 1997;17:3449–3460.
Shin MJ, Blanche PJ, Rawlings RS, Fernstrom HS, Krauss RM. Increased plasma concentrations of lipoprotein(a) during a low-fat, high-carbohydrate diet are associated with increased plasma concentrations of apolipoprotein C-III bound to apolipoprotein B-containing lipoproteins. Am J Clin Nutr 2007 Jun;85(6):1527–1532.
Teede HJ, Dalais FS, Kotsopoulos D et al. Dietary soy has both beneficial and potentially adverse cardiovascular effects: a placebo-controlled study in men and postmenopausal women. J Clin Endocrinol Metab 2001 Jul;86(7):3053?3060.
Tonstad, S, Smerud K, Hoie L. A comparison of the effects of 2 doses of soy protein or casein on serum lipids, serum lipoproteins, and plasma total homocysteine in hypercholesterolemic subjects. Am J Clin Nutr 2002 Jul;76(1):78–84.
Välimeli M, Laithinen K, Ylikahri C, Ehnholm C, Jauhiainen M, Bard JM, Fruchart JC, Taskinen MR. The effect of moderate alcohol intake on serum apolipoprotein A-I-containing lipoproteins and lipoprotein(a). Metabolism 1991;40:1168–1172.
Apoprotein E
Bennett AM, Angelantonio EG et al. Association of Apolipoprotein E Genotypes With Lipid Levels and Coronary Risk. JAMA 2007;298:1300-1311.
Maitland-van der Zee AH, Jukema JW et al. Apolipoprotein-E polymorphism and response to pravastatin in men with coronary artery disease (REGRESS). Acta Cardiol 2006 Jun;61(3):327-31.
Olivieri O, Martinelli N et al. ApoE epsilon2/epsilon3/epsilon4 polymorphism, ApoC-III/ApoE ratio and metabolic syndrome. Clin Exp 2007 Dec;7(4):164-72.
Sima A, Iordan A et al. Apolipoprotein E polymorphism--a risk factor for metabolic syndrome. Clin Chem Lab Med 2007;45(9):1149-53.
Gout
Choi HK, Curhan G. Coffee, tea, and caffeine consumption and serum uric acid levels: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2007 Jun 15;57(5):816-21.
Choi HK, Curhan G. Beer, liquor, and wine consumption and serum uric acid level: the Third National Health and Nutrition Exmination Survey. Arthritis Rheum 2004 Dec 15;51(6):1023-29.
Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. Brit Med J 2008;336:309-312 (9 February), doi:10.1136/bmj.39449.819271.BE (published 31 January 2008)
Choi JW, Ford ES, Gao X, Choi HK. Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum 2008 Jan 15;59(1):10916.
Choi HK, Liu S, Curhan G. Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid. Arthritis Rheum 2005 Jan;52(1):283-289.
Gao X, Curhan G et al. Vitamin C intake and serum uric acid concentration in men. J Rheum 2008 Sep;35(9):1853-58. |
