Prevention 2014: Nutrition and Dyslipidemias

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Ralph L. LaForge, MS

1st Annual Duke Preventive Cardiology Symposium
Saturday, April 26, 2014
The overall goal of this activity is to review the latest advancements in the management of lipids in clinical practice, including the new American Heart Association and American College of Cardiology guidelines on lipids announced in November 2013. Topics include learning about evaluation and treatment options in lipids and lipoprotein disorders, as well as focusing on new prevention guidelines, physical activity, nutrition, drug therapies, advanced lipoprotein testing, special patient populations, and new technologies for lifestyle management.

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  • AHA/ACC: The nutrition evidence review date range was 1998 to 2009 (17 studies, 28 articles)Rationale: This recommendation is based largely on studies of the DASH dietary pattern (DASH and DASH-Sodium), which provided the highest quality evidence for a dietary pattern causing improvements in BP and lipid profiles(see ES3-ES9). The LDL-C lowering effect has been demonstrated in men and women, African Americans and non-African Americans, and in adults of all ages (ES6). The evidence suggests that the effects of the recommended dietary pattern persist as long as the pattern is consumed. The caloric (energy) intake should be appropriate for the individual – e.g., restricted for those attempting weight loss. Patients also should be encouraged to adapt the recommended dietary pattern to their personal and cultural preferences. Materials are available to assist patients in achieving the recommended dietary pattern at different calorie levels (see below). The 2010 U.S. Department of Health and Human Services Dietary Guidelines for American recommend the USDA food pattern and the DASH eating plan (49). Overall, the recommended dietary pattern is consistent with the American Heart Association diet(50) and the USDA Food Pattern. (49) The USDA Food Pattern offers lacto-ovo vegetarian and vegan adaptations. Therefore, this recommendation is consistent with other national guidelines. Clinicians should be familiar with the recommendations, advise their patients to adopt them, and provide easy access to information (see below). Dietary planning and nutritional counseling is often facilitated by referral to a nutrition professional.
  • Trans fats (or trans fatty acids) are created in an industrial process that adds hydrogen to liquid vegetable oils to make them more solid.  Another name for trans fats is “partially hydrogenated oils."  Look for them on the ingredient list on food packages.Hydrogenation of an unsaturated fatty acid refers to the addition of hydrogen atoms to the acid, causing double bonds to become single ones, as carbon atoms acquire new hydrogen partners (to maintain four bonds per carbon atom). Full hydrogenation results in a molecule containing the maximum amount of hydrogen (in other words, the conversion of an unsaturated fatty acid into a saturated one). Partial hydrogenation results in the addition of hydrogen atoms at some of the empty positions, with a corresponding reduction in the number of double bonds. Typical commercial hydrogenation is partial in order to obtain amalleable mixture of fats that is solid at room temperature, but melts upon baking (or consumption).
  • Nov. 7, 2013 - The U.S. Food and Drug Administration announced its preliminary determination that partially hydrogenated oils (PHOs), the primary dietary source of artificial trans fat in processed foods, are not “generally recognized as safe” for use in food. The FDA’s preliminary determination is based on available scientific evidence and the findings of expert scientific panels.  The agency has opened a 60-day comment period on this preliminary determination to collect additional data and to gain input on the time potentially needed for food manufacturers to reformulate products that currently contain artificial trans fat should this determination be finalized. “While consumption of potentially harmful artificial trans fat has declined over the last two decades in the United States, current intake remains a significant public health concern,” said FDA Commissioner Margaret A. Hamburg, M.D. “The FDA’s action today is an important step toward protecting more Americans from the potential dangers oftrans fat. Further reduction in the amount of trans fat in the American diet could prevent an additional 20,000 heart attacks and 7,000 deaths from heart disease each year – a critical step in the protection of Americans’ health.” Consumption of trans fat raises low-density lipoprotein (LDL), or “bad” cholesterol, increasing the risk of coronary heart disease. The independent Institute of Medicine (IOM)has concluded that trans fat provides no known health benefit and that there is no safe level of consumption of artificial trans fat. Additionally, the IOM recommends that consumption of trans fat should be as low as possible while consuming a nutritionally adequate diet. In recent years, many food manufacturers and retailers have voluntarily decreased trans fat levels in many foods and products they sell. Trans fat can be found in some processed foods, such as certain desserts, microwave popcorn products, frozen pizzas, margarines and coffee creamers. Numerous retailers and manufacturers have already demonstrated that many of these products can be made without trans fat.   Thanks to these efforts, along with public education, the consumption of trans fat in American diets has been significantly reduced. Since trans fat content information began appearing in the Nutrition Facts label of foods in 2006, trans fat intake among American consumers has declined from 4.6 grams per day in 2003 to about 1 gram per day in 2012. “One of the FDA’s core regulatory functions is ensuring that food, including all substances added to food, is safe,” said Michael Taylor, the FDA’s deputy commissioner for foods and veterinary medicine. “Food manufacturers have voluntarily decreased trans fat levels in many foods in recent years, but a substantial number of products still contain partially hydrogenated oils, which are the major source of trans fat in processed food.” Following a review of the submitted comments, if the FDA finalizes its preliminary determination, PHOs would be considered “food additives” and could not be used in food unless authorized by regulation. If such a determination were made, the agency would provide adequate time for producers to reformulate products in order to minimize market disruption. The FDA’s preliminary determination is only with regard to PHOs and does not affect trans fat that naturally occurs in small amounts in certain meat and dairy products.  
  • NHANES is conducted by the National Center for Health Statistics (NCHS) at the Centers for Disease Control and Prevention. It uses a stratified, multistage probability sampling design, which enables samples to represent the US civilian noninstitutionalized population.13 Data are collected at their homes and mobile examination centers (MECs). Among adults in NHANES during the 1999-2010 period, the unweighted response rate for the household interview was 74.8%; that for the MEC examination was 70.8%.15This study included data from individuals 20 years or olderAmong statin users, caloric intake in the 2009-2010 period was 9.6% higher (95% CI, 1.8-18.1; P = .02) than that in the 1999-2000 period. In contrast, no significant change was observed among nonusers during the same study period. Statin users also consumed significantly less fat in the 1999-2000 period (71.7 vs 81.2 g/d; P = .003). Fat intake increased 14.4% among statin users (95% CI, 3.8-26.1; P = .007) while not changing significantly among nonusers. Also, BMI increased more among statin users (+1.3) than among nonusers (+0.4) in the adjusted model (P = .02).Conclusions and Relevance  Caloric and fat intake have increased among statin users over time, which was not true for nonusers. The increase in BMI was faster for statin users than for nonusers. Efforts aimed at dietary control among statin users may be becoming less intensive. The importance of dietary composition may need to be reemphasized for statin users.Although the paper is limited by its cross-sectional design, Sugiyama and colleagues state that it is reasonable to conclude the average American treated with statins is eating more calories and more fat than the average American taking statins was doing a decade ago. At present, they can only speculate as to the reasons for this."One possibility is that statin use may have undermined the perceived need to follow dietary recommendations. Patients who recognized that their LDL-cholesterol levels were lowered drastically by statins may have lost the incentive to pursue dietary modifications," write the researchers. "Physicians might have contributed to this process by shifting the focus of consultations from diet to statin regimen adherence once statin treatment had begun."Putting the Findings Into PerspectiveDr Mahesh Patel (Duke University School of Medicine, Durham, NC), who was not affiliated with the study, said the new analysis is interesting because it explores something that is rarely studied in medicine, that being the interaction between medication and lifestyle habits. However, he is cautious about making firm conclusions based on the data."It is tempting to conclude that patients prescribed statins adopted a more liberal diet than the individuals who were not taking the drugs, but the study only reflects population averages" and does not track the same patients over the 10-year period, he told heartwire .DrSekarKathiresan (Massachusetts General Hospital Heart Center, Boston) agreed with the need for caution. The analysis, which is based on a somewhat "sexy hypothesis," tends to fit with people's preconceived notions about the ill effects of medication use. The lament often heard is that people will simply abandon moderation when it comes to diet because they are now being treated with a statin."The flaw is that this is a nonrandomized, observational study, and the statin use might simply be marking a subset of patients who ate more over a 10-year period," Kathiresan told heartwire .
  • N=87 trials
  • From: Mozaffarian et al’s (2010) review and meta-analysis of randomized controlled trials showed that replacement of SFAwith PUFA was associated with lower predicted CHD risk (RR 0.91, 95% CI 0.8720.95), based on changes in thetotal-C/HDL-C ratio; (Fig. 6)Effects on CHD risk of consuming PUFA, carbohydrate, or MUFA in place of SFA. Predicted effects were determined bychanges in the TC/HDL-C ratio in short-term trials (eg, each 5% energy of PUFA replacing SFA lowers TC/HDL-C ratio by 0.16) coupledwith observed associations between the TC/HDL-C ratio and CHD outcomes in middle-aged adults. Evidence for effects of dietary changeson actual CHD events came from the meta-analysis of eight randomized controlled trials for PUFA replacing SFA and from the Women’sHealth Initiative randomized controlled trial for carbohydrate replacing SFA. Evidence for observed relationships of usual dietary habitswith CHD events was from a pooled analysis of 11 prospective cohort studies. RCT, randomized controlled trials; RR, relative risk;TC, total cholesterol; WHI, Women’s Health Initiative. Permission to reuse figure granted by PLoS Medicine
  • These nuts include hazelnuts (or filberts), macadamia nuts, pecans, almonds, pistachios and cashews.
  • Background: Guidelines advocate changes in fatty acid consumption to promote cardiovascular health.Purpose: To summarize evidence about associations between fatty acids and coronary disease.Data Sources: MEDLINE, Science Citation Index, and Cochrane Central Register of Controlled Trials through July 2013.Study Selection: Prospective, observational studies and randomized, controlled trials.Data Extraction: Investigators extracted data about study characteristics and assessed study biases.Data Synthesis: There were 32 observational studies (530 525 participants) of fatty acids from dietary intake; 17 observational studies (25 721 participants) of fatty acid biomarkers; and 27 randomized, controlled trials (103 052 participants) of fatty acid supplementation. In observational studies, relative risks for coronary disease were 1.02 (95% CI, 0.97 to 1.07) for saturated, 0.99 (CI, 0.89 to 1.09) for monounsaturated, 0.93 (CI, 0.84 to 1.02) for long-chain ω-3 polyunsaturated, 1.01 (CI, 0.96 to 1.07) for ω-6 polyunsaturated, and 1.16 (CI, 1.06 to 1.27) for trans fatty acids when the top and bottom thirds of baseline dietary fatty acid intake were compared. Corresponding estimates for circulating fatty acids were 1.06 (CI, 0.86 to 1.30), 1.06 (CI, 0.97 to 1.17), 0.84 (CI, 0.63 to 1.11), 0.94 (CI, 0.84 to 1.06), and 1.05 (CI, 0.76 to 1.44), respectively. There was heterogeneity of the associations among individual circulating fatty acids and coronary disease. In randomized, controlled trials, relative risks for coronary disease were 0.97 (CI, 0.69 to 1.36) for α-linolenic, 0.94 (CI, 0.86 to 1.03) for long-chain ω-3 polyunsaturated, and 0.89 (CI, 0.71 to 1.12) for ω-6 polyunsaturated fatty acid supplementations.Limitation: Potential biases from preferential publication and selective reporting.Conclusion: Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.Primary Funding Source: British Heart Foundation, Medical Research Council, Cambridge National Institute for Health Research Biomedical Research Centre, and Gates Cambridge.CAMBRIDGE, UK — A meta-analysis has revived the debate over best dietary recommendations for cardiovascular health; specifically, whether there's an evidence base supporting the traditional message to consume foods rich in long-chain omega-3 and omega-6 polyunsaturated fatty acids (PUFA) and avoid those laden with saturated fats [1]. But questions about the report emerged even before its online publication today."We found essentially null associations between total saturated fatty acids [SFA] and coronary risk," in studies looking at dietary fat intake and those focusing on circulating fatty-acid levels, according to the authors, led by Dr Rajiv Chowdhury (University of Cambridge, UK). Nor were there significant associations between CV risk and dietary intake of long-chain omega-3 and omega-6 polyunsaturated fatty acids. Other findings suggested that dietary supplements containing those fatty acids don't significantly reduce coronary risk.The group's meta-analysis of over 70 reports, including prospective cohort studies and randomized trials, will be published March 18, 2014, in the Annals of Internal Medicine."Our findings do not support cardiovascular guidelines that promote high consumption of long-chain omega-3 and omega-6 and polyunsaturated fatty acids and suggest reduced consumption of total saturated fatty acids," they write.The analysis shows "no strong evidence" to justify those cardiovascular guidelines, "especially for saturated fat," senior author DrEmanuele Di Angelantonio (University of Cambridge) told heartwire . So there's a need for further trials to explore the issue, he said, to determine just what the recommendations should be.But the meta-analysis has already been questioned. In an email exchange with heartwire , Dr Eric B Rimm (Harvard School of Public Health, Boston, MA) said, "My colleagues were quite surprised at the findings. We uncovered a serious mistake in their review of PUFA that likely will change the results substantially." And the parts of the meta-analysis focusing on PUFA didn't summarize the relevant studies correctly, according to Rimm, who added that "the results are in serious question."Moreover, the group's conclusion about saturated fat "has little context, because it likely represents the result of when you exchange saturated fat in your diet for refined grain. Thus, saturated fat is no better or worse than eating white bread. We have known that for decades, so [it] is not new."Rimm said he and his colleagues have contacted the report's authors about their issues with the analysis.Also contacted by heartwire , Dr Alice H Lichtenstein (Tufts University, Boston, MA) replied by email, "the majority of the evidence suggests that replacing saturated fat with polyunsaturated fat reduces heart disease risk, whereas replacing saturated fat with carbohydrate does not. This new study only assessed one factor, an indicator of dietary fat, and not the whole picture, making the conclusions questionable."Regarding assertions of errors in the report, Di Angelantonio said, "We recently spotted some minor mistakes in some of the data that will not in any way affect the main results of the study." He confirmed that another group contacted him and his coauthors about "some other minor mistake," adding, "we are making an erratum that will be sent to [Annals of Internal Medicine] in the next 24 hours, so there will be an updated version. But it's unlikely that the main conclusions will change."As for the analysis itself, it covered 45 prospective observational studies and 27 randomized controlled trials looking at dietary PUFA intake, levels of circulating PUFA, and intake of fatty-acid dietary supplements in populations throughout the most of the world.
  • Natural sources[edit]Monounsaturated fats are found in natural foods such as red meat, whole milk products, nuts and high fat fruits such as olives and avocados. Olive oil is about 75% monounsaturated fat. The high oleic variety sunflower oil contains as much as 85% monounsaturated fat. Canola oil and Cashews are both about 58% monounsaturated fat. Tallow (beef fat) is about 50% monounsaturated fat and lard is about 40% monounsaturated fat. Other sources include macadamia nut oil, grapeseed oil, groundnut oil (peanut oil), sesame oil, corn oil, popcorn, whole grain wheat, cereal, oatmeal,safflower oil, almond oil, sunflower oil, hemp oil, tea-oil Camellia, and avocado oil.Rudel LL, Parks KS, Sawyer JK. Compared with dietary monounsaturated and saturated fat, polyunsaturated fat protects African greenmonkeys from coronary artery atherosclerosis. ArteriosclerThrombVasc Biol. 1995;15:2101–2110.
  • Oleic acid is a fatty acid that occurs naturally in various animal and vegetable fats and oils. In chemical terms, oleic acid is classified as a monounsaturated omega-9 fatty acid, abbreviated with a lipid number of 18:1 cis-9. It has the formula CH3(CH2)7CH=CH(CH2)7COOH.[2] The term "oleic" means related to, or derived from, oil or olive, the oil that is predominantly composed of oleic acid. Oleic acid is a common monounsaturated fat in human diet. Monounsaturated fat consumption has been associated with decreased low-density lipoprotein (LDL) cholesterol, and possibly increased high-density lipoprotein (HDL) cholesterol.[20] However, its ability to raise HDL is still debated.Olive oil: Extra virgin is the highest quality and most expensive olive oil classification. It should have no defects and a flavor of fresh olives.In chemical terms extra virgin olive oil is described as having a free acidity, expressed as oleic acid, of not more than 0.8 grams per 100 grams and a peroxide value of less than 20 milliequivalent O2. It must be produced entirely by mechanical means without the use of any solvents, and under temperatures that will not degrade the oil (less than 86°F, 30°C).In order for an oil to qualify as “extra virgin” the oil must also pass both an official chemical test in a laboratory and a sensory evaluation by a trained tasting panel recognized by the International Olive Council.  The olive oil must be found to be free from defects while exhibiting some fruitiness.
  • Yokoyama M et.al. Lancet April 2007Associated with a significant reduction in deaths from cardiac causes but had no effect on arrhythmias or all-cause mortality
  • METHODSIn this double-blind, placebo-controlled clinical trial, we enrolled a cohort of patients who were followed by a network of 860 general practitioners in Italy. Eligible patients were men and women with multiple cardiovascular risk factors or atherosclerotic vascular disease but not myocardial infarction. Patients were randomlyassigned to n−3 fatty acids (1 g daily) or placebo (olive oil). The initially specified primary end point was the cumulative rate of death, nonfatal myocardial infarction,and nonfatal stroke. At 1 year, after the event rate was found to be lower than anticipated, the primary end point was revised as time to death from cardiovascularcauses or admission to the hospital for cardiovascular causes.CONCLUSIONSIn a large general-practice cohort of patients with multiple cardiovascular risk factors, daily treatment with n−3 fatty acids did not reduce cardiovascular mortality andmorbidity.
  • The median duration of follow-up was 5.0 years (interquartile range, 4.0 to 5.5).The primary end point, a composite of death from cardiovascular causes orhospital admission for cardiovascular causes, occurred in 1478 patients(11.8%), including 733 of 6239 patients who received n−3 fatty acids(11.7%) and 745 of 6266 who received placebo (11.9%).
  • In the prespecified subgroup analyses, the only significant interaction was between the efficacy of n−3 fatty acids and sex. The eventrate for the primary outcome was lower among women than among men, with a significantly lower rate of events among those whoreceived n−3 fatty acids than among those who received placebo. Horizontal lines indicate 95% confidence intervals, which were calculatedby means of a Cox proportional-hazards model.
  • DISCUSSIONThe Risk and Prevention Study tested the hypothesis that n−3 fatty acids, which have been shown to be beneficial in patients who have had a myocardial infarction (in the GruppoItaliano per lo Studio dellaSopravvivenzanell'InfartoMiocardico [GISSI]–Prevenzione study2) or heart failure (in the GISSI Heart Failure [GISSI-HF] study3), would be effective in reducing cardiovascular risk among patients who were treated according to the standard of care and who had multiple cardiovascular risk factors or atherosclerotic disease but no previous myocardial infarction.Although the reasons for the discrepancy between the null results of our study and the results of the GISSI–Prevenzione and GISSI-HF trials2,3 remains to be determined, a possible explanation can be hypothesized. The beneficial effect of n−3 fatty acids in those two trials was due to a reduction in sudden deaths from cardiac causes. It is conceivable that the effects of n−3 fatty acids become manifest primarily in patients who are particularly prone to ventricular arrhythmic events (e.g., those with a myocardial scar or left ventricular dysfunction). Our trial had extremely limited power to detect a reduction in sudden deaths from cardiac causes or arrhythmic events. The safety profile of n−3 fatty acids in this population of older persons who are already receiving many treatments for chronic disease could be of interest for their use in patient populations that are more prone to fatal and nonfatal arrhythmic events.2,3,13GruppoItaliano per lo Studio dellaSopravvivenzanell'InfartomiocardicoDietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet1999;354:447-455[Erratum, Lancet 2001;357:642, 2007;369:106.]11324 patients surviving recent (less than or equal to 3 months) myocardial infarction were randomly assigned supplements of n-3 PUFA (Ig daily, n=2836), vitamin E (300 mg daily, n=2830), both (n=2830), or none (control, n=2828) for 3.5 years. The primary combined efficacy endpoint was death, non-fatal myocardial infarction, and stroke. Intention-to-treat analyses were done according to a factorial design (two-way) and by treatment group (four-way). Findings Treatment with n-3 PUFA, but not vitamin E, significantly lowered the risk of the primary endpoint (relative risk decrease 10% [95% CI 1-18] by two-way analysis, 15% [2-26] by four-way analysis). Benefit was attributable to a decrease in the risk of death (14% [3-24] two-way, 20% [6-33] four-way) and cardiovascular death (17% [3-29] two-way, 30% [13-44] four-way). The effect of the combined treatment was similar to that for n-3 PUFA for the primary endpoint (14% [1-26]) and for fatal events (20% [5-33]). Interpretation Dietary supplementation with n-3 PUFA led to a clinically important and satistically significant benefit. Vitamin E had no benefit. Its effects on fatal cardiovascular events require further exploration.
  • 98% of fish oil ingested from whole fish is in triglyceride form, but ethyl esters are becoming increasingly popular within the supplement industry.Evidence has also suggested that compared with ethyl ester, supplementation of omega-3 fatty acids as triglycerides results in a 50% increase in plasma levels of free fatty acids Dietary fish oil (triglycerides) is digested in the small intestine by the emulsifying action of bile salts and the hydrolytic activity of pancreatic lipase1,5. The hydrolysis of a TG molecule produces two free fatty acids (FFA) and a monoglyceride (one fatty acid combined to glycerol)1,5. These metabolic products are then absorbed by intestinal enterocytes and reassembled again as TGs1,5. Carrier molecules called chylomicrons then transport the TGs into the lymphatic channel and finally into the blood6The digestion of EEs is slightly different due to the lack of a glycerol backbone1.  Glycerol has three hydroxyl groups One of the causative factors for the poor bioavailability of EE is a much greater resistance to digestive enzymes. Eg. pancreatic lipaseThe ethanol in EE form MUST be filtered through the liver. As we have just discussed, when ethyl esters are consumed, they are processed in the liver, where the ethanol is drawn off, and the body must then rebuild the resulting free fatty acids back into a triglyceride. Any form of alcohol filtering through the liver runs the risk of side effects. In the small intestine it is again the pancreatic lipase that hydrolyzes the fatty acids from the ethanol backbone, however; the fatty acid-ethanol bond is up to 50 times more resistant to pancreatic lipase as compared to hydrolysis of TGs7,8. The EEs that get hydrolyzed produce FFA plus ethanol. The FFA’s are taken up by the enterocytes and must be reconverted to TGs to be transported in the blood1. The TG form of fish oil contains its own monoglyceride substrate; whereas EE fish oils, coupled to ethanol, do not. EE must therefore obtain a glycerol substrate from another source. Without a glycerol or monoglyceride substrate TG re-synthesis is delayed, suggesting that transport to the blood is more efficient in natural TG fish oils in comparison to EEs. Ethyl ester fish oils are less stable, and readily oxidizeOmega-3 fatty acids in the form of EEs are much less stable than those in the natural TG form and readily oxidize. The oxidation kinetics of DHA as an EE or as a TG was assessed by measuring the concentration of oxygen found in the head space of a reaction vessel with both TG and EE forms17. The EE form of DHA was more reactive, and quickly oxidized, demonstrating that EEs are far less stable and can more readily produce harmful oxidation products17Triglyceride Form:none• Almost all Clinical evidence showing omega-3 benefits relate to fish consumption. Fish are in a TG form. There are no ethyl ester fish in nature. humans must consume fish oil in the same form as the fish to receive the maximum benefits.• ethyl esters have been in the human food chain approximately 20 years.• Triglyceride fatty acids have been eaten safely, and for great benefit, for an estimated 600 million years. NEthyl Esters vs. TriglyceridesThe chemical structure in which the omega–3 fatty acids are delivered can play an important role in their absorption. Recent data have demonstrated that omega–3 fatty acids delivered in a triglyceride form may result in greater plasma levels and a higher omega–3 index compared with omega–3 fatty acids delivered in the form of ethyl esters.
  • Epanova contains EPA and DHA in their free fatty acid form at a total concentration of 50-60% EPA and 15-25% DHA BACKGROUND: plasma levels are less influenced by food than for ethyl ester forms.OBJECTIVE: The aim was to evaluate the safety and lipid-altering efficacy in subjects with severehypertriglyceridemia of an investigational pharmaceutical omega-3 free fatty acid (OM3-FFA) containingeicosapentaenoic acid and docosahexaenoic acid.METHODS: This was a multinational, double-blind, randomized, out-patient study. Men and womenwith triglycerides (TGs) $500 mg/dL, but ,2000 mg/dL, took control (olive oil [OO] 4 g/d; n 5 99),OM3-FFA 2 g/d (plus OO 2 g/d; n 5 100), OM3-FFA 3 g/d (plus OO 1 g/d; n 5 101), or OM3-FFA4 g/d (n 5 99) capsules for 12 weeks in combination with the National Cholesterol Education ProgramTherapeutic Lifestyle Changes diet.RESULTS: Fasting serum TGs changed from baseline by 225.9% (P,.01 vs OO),225.5% (P,.01vs OO), and 230.9% (P , .001 vs OO) with 2, 3, and 4 g/d OM3-FFA, respectively, compared with24.3% with OO. Non-high-density lipoprotein cholesterol (non-HDL-C), total cholesterol-to-HDLCratio, very low-density lipoprotein cholesterol, remnant-like particle cholesterol, apolipoproteinCIII, lipoprotein-associated phospholipase A2, and arachidonic acid were significantly lowered (P ,.05 at each OM3-FFA dosage vs OO); and plasma eicosapentaenoic acid and docosahexaenoic acidwere significantly elevated (P , .001 at each OM3-FFA dosage vs OO). With OM3-FFA 2 and 4 g/d(but not 3 g/d), low-density lipoprotein cholesterol was significantly increased compared with OO(P , .05 vs OO). High-sensitivity C-reactive protein responses with OM3-FFA did not differ significantlyfrom the OO response at any dosage. Fewer subjects reported any adverse event with OO vsOM3-FFA, but frequencies across dosage groups were similar. Discontinuation due to adverse event, primarilygastrointestinal, ranged from 5% to 7% across OM3-FFA dosage groups vs 0% for OOThe increase in LDL-C with 2 and 4 g/d OM3-FFA vs OO was not accompanied by a significant increase in ApoB concentration at any dosage, and non-HDL-C, VLDL-C,and RLP-C levels were significantly reduced in all OM3-FFA groups compared with the OO group
  • Mary Wojczynski study: Background: Postprandial lipemia (PPL) is likely a risk factor for cardiovascular disease but these changes have notbeen well described and characterized in a large cohort. We assessed acute changes in the size and concentrationof total and subclasses of LDL, HDL, and VLDL particles in response to a high-fat meal. Participants (n = 1048) fromthe Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) Study who ingested a high-fat meal wereincluded in this analysis. Lipids were measured at 0 hr (fasting), 3.5 hr, and 6 hr after a standardized fat meal.Particle size distributions were determined using nuclear magnetic resonance spectroscopy. Analyses were stratifiedby baseline triglycerides (normal vs. elevated) and gender. The effect of PPL on changes in lipoprotein subclasseswas assessed using repeated measures ANOVA.Results: Postprandially, LDL-C, HDL-C, VLDL-C, and triglycerides increased regardless of baseline triglyceride status,with the largest increases in VLDL-C and TG; however, those with elevated triglycerides demonstrated largermagnitude of response. Total LDL particle number decreased over the 6-hour time interval, mostly from a decreasein the number of small LDL particles. Similarly, total VLDL particle number decreased due to reductions in mediumand small VLDL particles. Large VLDL particles and chylomicrons demonstrated the largest increase inconcentration. HDL particles demonstrated minimal overall changes in total particle number.Conclusions: We have characterized the changes in LDL and VLDL particle number, and their subclass patternsfollowing a high-fat meal.
  • Lipid-Lowering Therapy Does Not Affect the Postprandial Drop in High Density Lipoprotein-Cholesterol (HDL-c) Plasma Levels in Obese Men With Metabolic Syndrome: A Randomized Double Blind Crossover TrialGideon R. Hajer; Geesje M. Dallinga-Thie; Leonie C. van Vark-van der Zee; Jobien K. Olijhoek; Frank L. J. VisserenClinEndocrinol.  2008;69(6):870-877.  ©2008 Blackwell PublishingPosted 12/26/2008Summary and IntroductionSummaryIntroduction: The postprandial lipid metabolism in metabolic syndrome patients is disturbed and may add to the increased cardiovascular risk in these patients. It is not known whether postprandial high density lipoprotein-cholesterol (HDL-c) metabolism is also affected and whether this can be influenced by statin and/or ezetimibe treatment.Methods: Prospective, randomized, double blind, crossover trial comparing simvastatin 80 mg with simvastatin/ezetimibe 10 mg/10 mg treatment for 6 weeks on postprandial HDL-c metabolism in 15, nonsmoking, male, obese metabolic syndrome patients (Adult Treatment Panel III, ATPIII). Only study medication was allowed. HDL-c concentrations, cholesteryl ester transfer (CET), CET protein (CETP) mass and adiponectin were measured before and after oral fat loading. ClinicalTrials.gov NCT00189085.Results: Plasma HDL-c levels remained stable during continuous fasting following an overnight fast. Pre-fat load HDL-c concentrations without treatment, after simvastatin and simvastatin/ezetimibe treatment were 1.15 ± 0.04, 1.16 ± 0.05 and 1.11 ± 0.04 mmol/l. Fat load induced a 11% drop in HDL-c plasma levels; 1.02 ± 0.05 mmol/l (P < 0.001) which was not affected by either therapy. Triglyceride levels during fat load were similar after both treatments. Total CET increased from 9.73 ± 0.70 to 12.20 ± 0.67 nmol/ml/h (P = 0.004). Four hours after fat loading CETP mass was increased while adiponectin levels were decreased, irrespective of treatment.Discussion:HDL-c levels decrease as CET increases after fat loading in obese metabolic syndrome patients. This is not influenced by either simvastatin or simvastatin/ezetimibe treatment. After fat loading, CETP mass and CET increased, and adiponectin decreased pointing towards a potential role for intra-abdominal fat. Decreased postprandial HDL-c levels may contribute to the increased cardiovascular risk in metabolic syndrome patients on top of already low HDL-c levels.It has been shown that HDL becomes enriched with TG, leading to increased removal of HDL from the plasma,thereby decreasing HDL-C [17]
  • From the Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy (G Annuzzi, LB, GC, AM, G Anniballi, MV, CV, PC,GDC, FP, GR, and AAR), and the Institute of Food Science, National , Avellino, ItalyThe main dietary sources of polyphenols were decaffeinated green tea, decaffeinated coffee, dark chocolate, blueberry jam, artichokes, onions, spinach, rocket, andextra-virgin olive oilBackground: The postprandial triglyceride-rich lipoprotein (TRL)concentration is a recognized independent cardiovascular diseaserisk factor. Diet is the natural approach for these postprandial alterations.Dietary polyphenols and long chain n23 polyunsaturatedfatty acids (LCn3s) are associated with a lower cardiovascular diseaserisk.Objective: This randomized controlled study evaluated, in personswith a high risk of cardiovascular disease, the effects of diets naturallyrich in polyphenols and/or marine LCn3s on plasma TRLsand urinary 8-isoprostane concentrations, a biomarker of oxidativestress.Design: According to a 2 3 2 factorial design, 86 overweight/obeseindividuals with a large waist circumference and any other componentof the metabolic syndrome were randomly assigned to an isoenergeticdiet 1) poor in LCn3s and polyphenols, 2) rich in LCn3s,3) rich in polyphenols, or 4) rich in LCn3s and polyphenols. Thediets were similar in all other components. Before and after the8-wk intervention, fasting and postmeal TRLs and 8-isoprostaneconcentrations in 24-h urine samples were measured.Results: Dietary adherence was good in all participants. Polyphenolssignificantly reduced fasting triglyceride concentrations (2-factorANOVA) in plasma (P = 0.023) and large very-low-density lipoproteins(VLDLs) (P = 0.016) and postprandial triglyceride total areaunder the curve in plasma (P = 0.041) and large VLDLs (P = 0.004).LCn3s reduced postprandial chylomicron cholesterol and VLDLapolipoprotein B-48. The concentrations of urinary 8-isoprostanedecreased significantly with the polyphenol-rich diets. Lipoproteinchanges induced by the intervention significantly correlated withchanges in 8-isoprostane.Conclusions: Diets naturally rich in polyphenols positively influencefasting and postprandial TRLs and reduce oxidative stress.Marine LCn3s reduce TRLs of exogenous origin. Through theireffects on postprandial lipemia and oxidative stress, polyphenolsmay favorably affect cardiovascular disease risk.ProceduresAt baseline and after the 8-wk intervention, body weight,height, and waist circumference were measured according tostandardized procedures (21). After a 12-h overnight fast, theparticipants consumed a 1000-kcal test meal composed of rice,butter, parmesan cheese, bresaola, and white bread, with intakesof olive oil, extra-virgin olive oil, salmon, and decaffeinatedgreen tea differing in order to obtain a similar composition as theassigned diet (see Supplemental Table 3 under “Supplementaldata” in the online issue). Before and 2, 4, and 6 h after the meal,blood samples were collected for the measurement of plasmaconcentrations of cholesterol and triglycerides and triglyceriderichlipoproteins (TRLs) (chylomicrons and large VLDLs), andapolipoprotein B-48 (apo B-48) in large VLDLs. In addition,24-h urine samples were collected on the day after the test meal,to measure 8-isoprostane concentrations, after adequately trainingthe study participants on proper collection and storage proceduresFor isoprostane analysis, after collection, 10-mL urine sampleswere centrifuged for 5 min (3000 rpm, at 48C). After removal ofthe sediment, they were fractionated into 500-mL aliquots withthe addition of 0.005% butylatedhydroxytoluene in ethanol andstored at 2808C. Immediately before the assay, one aliquot wasthawed in ice, centrifuged, and diluted 10 times. Concentrationsof 8-isoprostane were measured in triplicate with a Cayman8-isoprostane enzyme immunoassay kit, performed manually,and read through with DiaSorinEtiStar Spectrophotometry.Concentrations are expressed as ng isoprostanes released in 24h. The interassay CV was 14.3%, and the intraassay CV was8.2%. All evaluations were performed before and after the 8-wkintervention by personnel who were blind to the assignment.Fasting lipids and lipoproteinsThe 8-wk interventions with polyphenols, LCn3s, or theircombination, appeared to decrease fasting plasma triglyceridescompared with the control diet (Table 3). By 2-factor ANOVA,only the effect of polyphenols was statistically significant (P =0.023); no significant effects for LCn3s or their interaction werefound. Fasting total and LDL-cholesterol concentrations werenot significantly affected by the dietary interventions. Polyphenolssignificantly decreased fasting concentrations of triglycerideand cholesterol in large VLDL and HDL fractions; nosignificant effects for LCn3s or their interaction were found.
  • Our 2014 Physician Lifestyle Report provides a revealing look at physicians' personal lives, including dietary habits, use of alternative treatments for their own health, and level of happiness at work and at home. This comprehensive report, with new questions and insights this year, represents data from more than 30,000 US physicians.
  • Adherence to a Mediterranean Diet and Survival in a Greek PopulationAntonia Trichopoulou, M.D., Tina Costacou, Ph.D., Christina Bamia, Ph.D., and DimitriosTrichopoulos, M.D. Univ. of AthensN Engl J Med 2003; 348:2599-2608June 26, 2003Methods: We conducted a population-based, prospective investigation involving 22,043 adultsin Greece who completed an extensive, validated, food-frequency questionnaire at baseLine. A higher degree ofadherence to the Mediterranean diet was associated with a reduction in total mortalityAlso Walter Willet quote (above).Ecologic evidence suggesting beneficial health effects of the Mediterranean diet has emerged from the classic studies of Keys.Trichopoulou et al. have quantified adherence to the Mediterranean diet in terms of a ninepointscale. This group and others have used minor variants of this scale and have reported inverseassociations between the score and total mortality among elderly persons in small studies, eachincluding fewer than 400 subjects.
  • Dr. Estruch at the Department of Internal Medicine, Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain, or at restruch@clinic.ub.es,Participants in the control group also received dietary training at the baseline visit andcompleted the 14-item dietary screener used to assess baseline adherence to the Mediterraneandiet. Thereafter, during the first 3 years of the trial, they received a leaflet explaining the lowfatdiet (Table S2 in the Supplementary Appendix) on a yearly basis. However, the realizationthat the more infrequent visit schedule and less intense support for the control group might belimitations of the trial prompted us to amend the protocol in October 2006. Thereafter, participantsassigned to the control diet receivedpersonalized advice and were invited to groupsessions with the same frequency and intensityas those in the Mediterranean-diet groups,
  • AHA/ACC: The evidence review date range was 1998 to 2009
  • In chemical terms extra virgin olive oil is described as having a free acidity, expressed as oleic acid, of not more than 0.8 grams per 100 grams and a peroxide value of less than 20 milliequivalent O2. Oleic acid is a fatty acid that occurs naturally in various animal and vegetable fats and oils. It is an odorless, colourless oil, although commercial samples may be yellowish. In chemical terms, oleic acid is classified as a monounsaturated omega-9 fatty acid,In order for an oil to qualify as “extra virgin” the oil must also pass both an official chemical test in a laboratory and a sensory evaluation by a trained tasting panel recognized by the International Olive Council.  The olive oil must be found to be free from defects while exhibiting some fruitiness.Tree nuts include almonds, Brazil nuts, cashews, chestnuts, filberts/hazelnuts, macadamia nuts, pecans, pistachios, and walnuts.
  • Olive oil is composed mainly of the mixed triglyceride esters of oleic acid and palmitic acid and of other fatty acids, along with traces of squalene (up to 0.7%) and sterols (about 0.2% phytosteroland tocosterols). The composition varies by cultivar, region, altitude, time of harvest, and extraction process.Oleic acid is a fatty acid that occurs naturally in various animal and vegetable fats and oils. It is an odorless, colourless oil, although commercial samples may be yellowish. In chemical terms, oleic acid is classified as a monounsaturatedomega-9 fatty acid
  • The IOC currently has 17 state members plus the European Union. These states account for over 98 per cent of the world's olive production. The following states of the IOC are below (the year of the state's first ratification of one of the Agreements is included; an asterisk indicates that the state was a founding member of the IOOC): Albania (2009) Algeria (1963) Argentina (2009) European Union*[1] Croatia (1999) Egypt (1964) Iran (2004) Iraq (2008) Israel* (1958) Jordan (2002) Lebanon (1973) Libya* (1956) Montenegro (2007) Morocco (1958) Syria (1997) Tunisia* (1956) Turkey (2010) Uruguay (2013)
  • Report: Most Imported Extra Virgin Olive Oils Aren’t Extra Virgin: In a recent report, 69 percent of imported olive oil samples and 10 percent of California olive oil samples labeled as extra virgin failed to meet the IOC/USDA standards for extra virgin olive oil. Read more…International Olive Council Standards for Olive OilTrue extra-virgin olive oil (EVOO) is extracted from olives using only pressure, a process known as cold pressing.Some of the main antioxidants are the anti-inflammatory oleocanthal, as well asoleuropein, a substance that protects LDL cholesterol from oxidation (4, 5).Extra virgin olive oil phenols down-regulate lipid synthesis in primary-cultured rat-hepatocytes. J NutrBiochem. 2014Kevin Maki’s study:Among the 54 healthy men and women in the feeding study, consumption of foods made with corn oil resulted in significantly lower levels of LDL (bad) cholesterol and total cholesterol than the same foods made with extra virgin olive oil. Corn oil lowered LDL cholesterol by 10.9 percent compared to extra virgin olive oil's 3.5 percent reduction1,2, and total cholesterol decreased by 8.2 percent with corn oil compared to 1.8 percent for extra virgin olive oilCoconut oil contains a large proportion of lauric acid—a saturated fat that raises blood cholesterol levels by increasing the amount of high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol. This may create a more favourable blood cholesterol profile, although it is unclear whether coconut oil may promote atherosclerosis through other pathways.[30] Because much of the saturated fat of coconut oil is in the form of lauric acid, coconut oil may be a better alternative to partially hydrogenated vegetable oil when solid fats are required.[31] In addition, virgin coconut oil (VCO) is composed mainly of medium-chain triglycerides,[32] which may not carry the same risks as other saturated fats.[31][33]
  • Olive oil is on average 10% linoleic acid (an omega-6 oil) and less than 1% linolenic acid (an omega-3 oil), therefore the ratio is 10:1 on average.Fat and Olive Oil - Olive oil is widely known to be high in monounsaturated (good) fatSpain produces 43.8% of world production of olive oil.[13] 75% of Spain's production comes from the region of Andalucía, particularly within Jaén province, although other regions also produce excellent oil. Although Italy is a net importer of olive oil, it still accounts for 21.5% of the world's production. Greece accounts for 12.1% of world production and Syria for 6.1%, as third and fourth largest producers in the World. Portugal accounts for 5% and its main export market is Brazil. Morocco is the world's sixth largest producer.[14]
  • Objective: To assess the efficacy of Mediterranean diets for the primary prevention of diabetes in the Prevención con DietaMediterránea trial, from October 2003 to December 2010 (median follow-up, 4.1 years).Design: Subgroup analysis of a multicenter, randomized trial. (Current Controlled Trials: ISRCTN35739639) Setting: Primary care centers in Spain.A Mediterranean diet supplemented with extra-virgin olive oil (EVOO) cut the risk for developing type 2 diabetes by about a third among adults at high risk for cardiovascular disease (CVD) compared with a low-fat diet, a new analysis finds.The results, from the subgroup of subjects in the Spanish cardiovascular prevention study Prevencion con DietaMediterránea (PREDIMED) who did not have diabetes at baseline, were published January 6 in the Annals of Internal Medicine by Jordi Salas-Salvado, MD, PhD, from UniversitatRoviraiVirgili, Reus, Spain, and colleagues."The PREDIMED trial provides strong evidence that long-term adherence to a Mediterranean diet supplemented with EVOO without energy restrictions…results in a substantial reduction in the risk for type 2 diabetes among older persons with high cardiovascular risk," Dr. Salas-Salvado and colleagues write.The Mediterranean diet is high in fat (30% to 40% of total calories) from vegetable sources such as olive oil and nuts and relatively low in dairy products. The diet also commonly includes sauces with tomato, onions, garlic, and spices and moderate wine consumption."Of note, this dietary pattern is palatable and has a high potential for long-term sustainability, with obvious public-health implications for primary prevention of diabetes," the investigators write.Commenting on the study for Medscape Medical News, William S. Yancy Jr, MD, associate professor of medicine at Duke University Medical Center, Durham, North Carolina, said that the findings demonstrate overall benefit for the Mediterranean diet, but not necessarily in comparison with a true low-fat diet."These results are fairly convincing that the Mediterranean diet prevents the onset of diabetes compared with a usual diet," he observed, noting that the "low-fat" diet used in the study was actually closer to a "usual diet" because adherence to the low-fat diet in the study's control arm wasn't good."The Mediterranean diet may ultimately be found to be healthier than a low-fat diet, but this study did not effectively test that," said Dr. Yancy, whose research focus is obesity and nutrition.Nonetheless, he believes the study lends support to a Mediterranean diet prescription. "It may not be definitive, but it is a very reasonable recommendation, because we are not aware of any harms from the Mediterranean diet — except maybe cost or lack of familiarity/convenience to Americans — and there is a growing body of evidence showing its benefits," he told Medscape Medical News.Diabetes Risk Cut By a ThirdThe larger PREDIMED study enrolled 7447 men and women aged 55 to 80 years who did not have CVD at baseline but were at risk for it. They were randomized to 1 of 3 diets: a Mediterranean diet supplemented with either EVOO (50 mL/d) or mixed nuts (30 g/d) or a control diet with advice to reduce intake of all types of fat. Subjects were not calorie-restricted and were given no instructions regarding physical activity.The main PREDIMED findings, published in February 2013, showed that both Mediterranean diets cut the CVD event risk by as much as 30% compared with the controls at 4.8 years of follow-up. And preliminary results from 1 of the 11 PREDIMED centers suggested that the Mediterranean diet also reduced the incidence of type 2 diabetes, based on 55 incident cases.The current report includes the substudy population of 3541 who did not have diabetes at baseline and had available information during follow-up.Over a median of 4.1 years' follow-up, adherence was better with the Mediterranean diet/supplemental foods compared with the low-fat–advice group, as assessed by questionnaire and biomarker measurement in a random subset.A total of 273 participants developed diabetes, including 6.9% of the Mediterranean-diet/EVOO group, 7.4% of the Mediterranean-diet/mixed-nuts, group, and 8.8% of controls on the low-fat diet. After adjustment for potential confounders, hazard ratios for diabetes among those on the Mediterranean compared with low-fat diet were a significant 0.60 with EVOO supplementation and a nonsignificant 0.81 with added mixed nuts.When the 2 Mediterranean diet groups were combined, there was a significant overall approximate 30% risk reduction for type 2 diabetes compared with the controls. These results were consistent when examined by subgroups of sex, age, comorbidities, smoking status, CVD family history, and adiposity."Many Healthy Foods"The beneficial CVD effects of the Mediterranean diet are believed to be due to its inclusion of ingredients containing various minerals, polyphenols, and other phytochemicals that combat oxidative stress, inflammation, and insulin resistance, Dr. Salas-Salvado and colleagues note.Regarding the diet's effect on diabetes risk in particular, Dr. Yancy pointed out that carbohydrates are the main drivers of blood sugar level, and "the Mediterranean diet is typically lower in carbohydrates than usual diets or low-fat diets. It is also a lower glycemic-load diet."It's not clear why the Mediterranean diet supplemented with mixed nuts failed to show a significant diabetes reduction benefit. The authors and Dr. Yancy suggest that this could be due to chance.Or, Dr. Yancy speculated, "Another reason may be that the foods that one eats with olive oil are better for preventing diabetes than those one eats with nuts. Or the higher monounsaturated-fat intake of the EVOO is more important than the polyunsaturated fatty acids from the nuts."Nonetheless, he told Medscape Medical News, "It helps that both Mediterranean diet arms led to reduced diabetes rates, ie, both arms were in the same direction… Diet changes can be quite powerful for improving health, and a Mediterranean diet emphasizes many healthy foods based on prior clinical trials and epidemiological studies."The study was funded by the funding agency for biomedical research of the Spanish government, Instituto de Salud Carlos III, through grants provided to research networks specifically developed for the trial. The FundaciónPatrimonioComunalOlivarero and Hojiblanca, California Walnut Commission, Borges, and Morella Nuts donated the olive oil, walnuts, almonds, and hazelnuts, respectively, used in the study. Dr. Salas-Salvado has received research funding from the International Nut Council; is a nonpaid member of the scientific advisory board of the International Nut Council; has received fees from InstitutoDanone as a member of the scientific committee and from Danone as a consultant; has received fees from Nuts for Life and Eroski Distributors for lectures; and fees for consulting from Font VellaLanjaron. His institution has received grants from the Nut and Dried Fruit Foundation and Eroski Distributors. Disclosures for the coauthors are listed here. Dr. Yancy has reported no relevant financial relationships.
  • Scarce data are available on the effect of the traditional Mediterranean diet (TMD) on heart failure biomarkers. We assessed the effect of TMD on biomarkers related to heart failure in a high cardiovascular disease risk population.Participants were assigned to a low-fat diet (control, n = 310) or one of two TMDs [TMD + virgin olive oil (VOO) or TMD + nuts]. Depending on group assignment, participants received free provision of extra-virgin olive oil, mixed nuts, or small non-food gifts. After : Individuals at high risk of cardiovascular disease (CVD) who improved their diet toward a TMD pattern reduced their N-terminal pro-brain natriuretic peptide compared with those assigned to a low-fat diet. The same was found for in vivo oxidized low-density lipoprotein and lipoprotein(a) plasma concentrations after the TMD + VOO diet. From our results TMD could be a useful tool to mitigate against risk factors for heart failure. Changes in lipoprotein(a) after TMD + VOO were less than those in the control group (P = 0.046) in which an increase (P = 0.035) was observed. No changes were observed in urinary albumin or albumin/creatinine ratio.From our results TMD could modify markers of heart failure towards a more protective mode
  • BACKGROUND:The Mediterranean and Dietary Approaches to Stop Hypertension (DASH) diets are characterized by higher intake of fruit, vegetables, whole grains, and unsaturated fatty acids. All of these foods and nutrients may affect cholesterol, inflammation, the development of atherosclerosis, and, therefore, risk of cardiac death.
  • Tree nuts and peanuts:Tree nuts include almonds, Brazilnuts, cashews, chestnuts, filberts/hazelnuts, macadamia nuts, pecans, pistachios, and walnuts. 
  • Alaska Native Tribal Health ConsortiumThe Store Outside Your Door project is a Wellness and Prevention initiative to promote the knowledge and use of traditional foods and traditional ways.Traditional Foods, Contemporary ChefTraditional Foods, Contemporary Chef is a webisode series highlighting traditional foods from around the state. Each webisode takes you out to harvest from “the Store Outside Your Door” then into the kitchen to learn how to prepare a delicious and nutritious traditional dish with a contemporary twist.Beautiful Aqpik berries (aka Salmonberry, Cloudberry). These were picked just outside of Point Hope several years ago. YUMMM.
  • Action steps:Complete a Domestic Physical Activity History Form [PDF - 44KB] on the patient before assigning specific household or yard chores to the circuit.Complete the Household Circuit Form [PDF - 37KB] by coupling two or more household, yard or community activities spaced with 1- or 2-minute rest break periods.The duration of each activity or chore depends on the time requirement of the chore/activity but is generally between 5-15 minutes.In the beginning two or three activities will be sufficient; however as the participant's stamina and fitness improve each circuit should increase to include six to ten diverse activities.Always start and end the circuit with activity that requires a low-level physical effort, e.g., easy stretching or slow walking and then add activities in an order that requires increasing effort.The total time for the circuit should be between 20-90 minutes depending on the health status and fitness of the participant.The total energy expenditure (kcal) will be dependent on the total duration, average intensity or work load of the circuit activities and the body mass of the participant.Refer to the Ainsworth's Compendium of Activities which compares hundreds of domestic activities by their relative energy expenditure (in METs).
  • Prevention 2014: Nutrition and Dyslipidemias

    1. 1. Dietary Recommendations for CHD and Dyslipidemia Ralph LaForge, MS, CLS, FNLA Consulting Faculty Division of Endocrinology, Metabolism and Nutrition Duke University Medical Center Durham, NC rlaforge@nc.rr.com
    2. 2. Agenda 2013 ACC/AHA and IAS dietary and dyslipidemia guideline micro overview Dietary fatty acids and lipid/lipoprotein response Post-prandial lipemia and atherogenic lipoprotein exposure 2014 Physician Dietary Pattern Report Evidence-based dietary patterns and cardiometabolic risk – evidence from PREDIMED
    3. 3. http://www.athero.org/IASPositionPaper.asp http://www.lipid.org www.heart.org/HEARTORG/Conditions/Understanding-the-New- Prevention-Guidelines AHA/ACC Lifestyle Guidelines National Lipid Association’s Lifestyle and Dyslipidemia Recommendations May, 2014
    4. 4. AHA/ACC Lifestyle Guidelines: LDL–C - Advise adults who would benefit from LDL–C lowering to:
    5. 5. There is strong evidence that the reductions in LDL–C were achieved when consuming dietary patterns in which saturated fat intake was reduced from 14% to 15% of calories to 5% to 6%. Reducing saturated fat intake lowers both LDL–C and HDL–C. 2013 AHA/ACC Dietary Guidelines
    6. 6. Dietary Therapy LDL-C Reduction Rx Reduce intake of saturated fatty acids to < 7% of total calories Lower intake of trans fatty acids to <1% of total calories
    7. 7. Other Dietary Therapy • Maintain relatively high intakes of fruits, vegetables, and fiber • Replace excess saturated fatty acids with either complex, fiber-rich carbohydrates (with emphasis on whole grains) or monosaturated/polysaturated fatty acids • Consume fish rich in n-3 fatty acids • Other cardioprotective foods include nuts, seeds and vegetable oils
    8. 8. KEY POINT The latest International, NLA and ACC/AHA lifestyle guidelines are mostly in agreement as to appropriate dietary management of dyslipidemia and both recommend Mediterranean and DASH dietary patterns. The ACC/AHA evidence review is more dated (1996-2009)
    9. 9. NHANES survey 1999 through 2010. N=27, 886 US adults (non-randomized observational study)  Statin users were consuming an extra 192 kcal per day in 2009–2010 than they were in 1999–2000, and this could have contributed to the increase in BMI, which was the equivalent of a 3- to 5-kg weight gain JAMA Intern Med. Published online April 24, 2014 UCLA/Tokyo/Harvard
    10. 10. N = review of 87 trials
    11. 11. CHD Events and Polyunsaturated Fat Intake (polys replacing sat fats) 19%
    12. 12. • Decades of clinical studies in humans have demonstrated that modification of the fatty acid content of can affect the lipoprotein/lipid profile. • For example, LDL-C increases when carbohydrate in the diet is replaced with either trans-fatty acids or SFAs. • Conversely, LDL-C is reduced when carbohydrates are replaced with MUFAs or PUFAs, although the effect is more pronounced with PUFA. • HDL-C is reduced by the addition of transfatty acids to the diet, but replacement of carbohydrate with SFAs, MUFAs, or PUFAs will increase HDL-C, with MUFA having an intermediate effect between those of SFA and PUFA. • The total-C/HDL-C ratio is raised by trans-fatty acid intake but there is a relatively neutral effect with SFAs because they increase both total-C and HDL-C. Baum S, Kris-Etherton P et.al. JCL 2012 Some Fat Facts
    13. 13. Baum S, Kris-Etherton P et.al. JCL 2012 Pooled analysis of 11 prospective cohort studies REPLACEMNET TRIALS  
    14. 14. for
    15. 15. R. La Forge/2012 1 scone = 140 - 500 calories 5-10 minutes to consume = 1.4 – 5 mile walk 25 – 90 minutes
    16. 16. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis Chowdhury R et.al. Annals Int. Med. 2014 (Cambridge UK, BHR) Relative Risk (95% CI) for Coronary Events, Top vs Bottom Third of Total Dietary Fatty Acid Intake Levels in Prospective Cohort Studies* *32 studies, 530,525 participants, mean follow-up 5–23 years. All adjusted for age, sex, smoking, diabetes, and blood pressure, and other influences on CV risk. Conclusion: Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.
    17. 17. Caution About Excessive Dietary MUFAs (at least in animal studies) • Studies in African Green Monkeys – Diets 35% total energy as fat – Those fed MUFA developed equivalent CAD as those fed saturated fat despite lower LDL-C than those on saturated fat • Saw enrichment of cholesteryl oleate in plasma cholesteryl esters that correlated with coronary cholesterol ester concentration • Promotes aortic atherosclerosis in transgenic mice Rudel LL, et al. J Clin Invest. 1997;100:74-83.
    18. 18. KEY POINT When evaluating diet studies one must carefully consider which foods and nutrients are substituted for those that are displaced. With regard to MUFA, specifically oleic acid— one element of a Mediterranean diet, substantial evidence was presented for favorable effects on CVD risk markers and a suggestion of benefit from some observational studies. Considering some of the conflicting findings it may be best to reduce all sources of fat - save n3 FA
    19. 19. Fish Oil – Omega 3fa Stories and Conundrums Circa 2014
    20. 20. Fish Oil & Arrhythmias and Mortality Yokoyama M et.al. Lancet , 2007 Leon
    21. 21. N Engl J Med 2013;368:1800-8. - Patients were randomly assigned to n−3 fatty acids (1 g daily) or placebo (olive oil). - Men and women with multiple CV risk factors or atherosclerotic vascular disease who had not had a myocardial infarction. N= ~12,500 860 general practitioners in Italy
    22. 22. Kaplan–Meier Curves for Death or First Hospitalization Due to Cardiovascular Cause. RPSCG 2013
    23. 23. Effect of n−3 Polyunsaturated Fatty Acids on the Risk of Death or First Hospitalization Due to Cardiovascular Cause, According to Prespecified Subgroups. RPSCG 2013
    24. 24. CONCLUSIONS from the RPCSG In a large general-practice cohort of patients with multiple cardiovascular risk factors, daily treatment with n−3 fatty acids did not reduce cardiovascular mortality and morbidity RPSCG 2013
    25. 25. Although the reasons for the discrepancy between the RCSPG and the 1999 GISSI trial remains to be determined, a possible explanation can be hypothesized: The beneficial effect of n−3 fatty acids in those two trials was due to a reduction in sudden deaths from cardiac causes. It is conceivable that the effects of n−3 fatty acids become manifest primarily in patients who are particularly prone to ventricular arrhythmic events (e.g., those with a MI scar or LV dysfunction). RPSCG 2013
    26. 26. Omega 3 fatty acid supplements Ethel esters (Vascepa, Lovaza) vs Free fatty acids (e.g., Epanova) EVOLVE trial (30% TG  Davidson et.al. 2014)
    27. 27. Largest double-blind, randomized, controlled investigation of a lipid-altering drug in patients with severe hypertriglyceridemia, a novel formulation that contained free fatty acid forms of both EPA and DHA produced significant lowering of TGs and non-HDL-C concentrations at 2-, 3-, and 4-g/d dosages (25-30% TG ) N=400, TG ~700 mg/dL, 12 wks
    28. 28. KEY POINT N3 fatty acids have numerous utilities depending on for whom and how much n3 is ingested. Higher doses (≥3g/day) reduce TG Smaller doses may reduce CVD risk
    29. 29. Postprandial Lipemia and Atherogenic Lipoproteins
    30. 30. Postprandial Response 250 200 150 100 50 0 -50 Schaefer EA Am J Clin Nut 2002;75:191 TG % change from fasting N=88 Variability in Plasma TG Response to Fatty Meal (2 sausages, 2 eggs, 2 muffins @ McD)
    31. 31. Postprandial Lipemia (TG) Issues Acute response to high fat meal • TG time/area under the curve is greater with T2D, visceral ob, & MetSyn • Decreased arterial endothelial function • Decreased HDL-C response • Increased IDL- VLDL remnant exposure Napolitano 2013 Nakajima, 2012 Wojczynski, 2011 Giannattasio, 2005 Wang, 2011 Hajer, 2008 Kris-Etherton, 2007 Nestel, 2001 Whitman, 1998 Zhang, 1998 2-10 hrs low fat meal
    32. 32. CM CMr IDL VLDL VLDLr LPL LPL Arterial Endothelial Cells Postprandial Atherogenic Lipoprotein Interactions with lipoprotein lipase (LPL) arterial wall
    33. 33. Endothelial inflammation correlates with subject triglycerides and waist size after a high-fat meal Ying I. Wang et.al. Am J Physiol Heart Circ Physiol. Mar 2011; 300(3): H784–H791. UC Davis Role of macrophage activation in the lipid metabolism of postprandial triacylglycerol-rich lipoproteins. Napolitano M et.al. Exp Biol Med.2013 Jan;238(1):98-110 The characteristics of remnant lipoproteins in the fasting and postprandial plasma Nakajima K lin Chim Acta.2012 Jul 11;413(13-14):1077-86. Oxidized type IV hypertriglyceridemic VLDL-remnants cause greater macrophage cholesteryl ester accumulation than oxidized LDL Whitman SC Lipid Res. 1998 May;39(5):1008-20. Univ. W. Ontario Post –prandial remnant lipids impair arterial compliance Nestel PJ et.al. JACC 2001;37:1929 High fat meal effect on LDL, HDL, and VLDL particle size and number (GOLDN) Wojczynski M et.al. Lipids in Health and Disease 2011;10:181 U of AL Select post-prandial TG Issues
    34. 34. (a) HDL-c baseline-corrected concentrations after an overnight fast, with and without 100g fat load and after oral fat loading with and without treatment. (b) Total cholesteryl ester transfer (mean ± SEM) after oral fat load without treatment. Hajer JCEN,2008 Postprandial HDL-C Response to Fat Load
    35. 35. Diets naturally rich in polyphenols improve fasting and postprandial dyslipidemia and reduce oxidative stress: a randomized controlled trial Annuzzi et.al. Am J Clin Nutr 2014;99:463–71. Naples Randomly assigned to one of the following nutritional isoenergetic interventions for 8 wk: 1) control diet, low in LCn3s and polyphenols; 2) diet rich in LCn3s* and low in polyphenols; 3) diet rich in polyphenols and low in LCn3s; or 4) diet rich in LCn3s and polyphenols.  Diets naturally rich in polyphenols positively influence fasting and postprandial TRLs (20-30%). * decaffeinated green tea, dark chocolate, blueberry jam, artichokes, onions, spinach, rocket, and extra-virgin olive oil
    36. 36. Top 25 Riches Food Sources of Polyphenols (per serving) Black Elderberry Black Chokeberry Blackcurrant Highbush blueberry Globe artichoke heads Coffee, filtered Lowbush Blueberry Sweet Cherry Strawberry Blackberry Plum Red Raspberry Flaxseed Meal Dark Chocolate Chestnut Black Tea Green Tea Pure Apple Juice Apple Whole Grain Rye Bread Hazelnut red wine Soy Yogurt Cocoa Powder Pure Pomegranate Juice
    37. 37. Hours after high fat meal (100g) 0 2 4 6 8 400 300 200 100 TG mg/dL Preprandial Exercise and Postprandial Lipemia e.g., 400-500 kcal ex 6-12 hrs prior to fat meal Trombold 2013 Hashimoto 2013 Ho 2011 Mestek 2011 Farah 2010 Smith 2004 Petitt 2003 Thomas 2000 Zhang 1998
    38. 38. KEY POINT Excess post-prandial TG particularly after high fat (i.e., 50- 100+g) meals contribute to elevated postprandial and long resident times of TGRL’s which are atherogenic. This is concerning - considering the choice of calories of many Americans and that perhaps as many spend more than half of the wakeful day in a post absorptive state. It is not necessary to measure PPTG/TGRL but rather assess and modify dietary behavior particularly in insulin resistant, metabolic syndrome, and type 2 diabetes patients Sufficient pre-prandial physical activity should also be considered prior to high-fat meals
    39. 39. MedScape 2/2014 Popular Diets: What Docs Eat, 2014 Physician Lifestyle Report February 19, 2014 N=30,000
    40. 40. Scherer 2014
    41. 41. Tradi t i onal Medi t erranean di et ary pat t ern: Char act er i zed by a hi gh i nt ake of : veget abl es l egumes f rui t s and nut s cereal s ol i ve oi l f i sh nut s l ow i nt ake of : sat urat ed f at dai ry product s (l ow t o moderat e) meat and poul t ry r egul ar but moder at e i nt ake of : et hanol , pri mari l y i n t he f orm of wi ne and general l y duri ng meal s. Ant oni a Tr i chopoul ou, NEJM 2003 (MDS)
    42. 42. N Engl J Med 2013; 368:1279-1290
    43. 43. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet: The PREDIMED trial  Participants (n = 7447) at high CVD risk with no CVD were randomly assigned to follow one of three diet interventions:  Mediterranean diet supplemented with extra-virgin olive oil (1 L/week)  Mediterranean diet supplemented with mixed nuts (30 g/d; 15 g walnuts; 7.5 g almonds; 7.5 g hazelnuts)  Control diet (advice to reduce dietary fat)  Participants received quarterly individual and group education sessions and, depending on treatment, free extra-virgin olive oil or mixed nuts.  The primary end point was the rate of major cardiovascular events (myocardial infarction, stroke, or death from cardiovascular causes).  The trial was stopped after a median follow-up of 4.8 years rather than continuing for 6 years, as planned. Estruch, R. et al. N Engl J Med. 2013;368:1279-1290.
    44. 44. Food Recommendations for the Mediterranean Diet Groups and the Control Diet Group Estruch, R. et al. N Engl J Med. 2013;368:1279-1290. Mediterranean Diet MeDiet + EVOO MeDiet + Nuts (1L/week) (30 g/d) Low Fat Diet (Control) Olive Oil Low Fat Dairy Tree Nuts & Peanuts Bread, Potatoes, Pasta, Rice Fresh Fruits Fresh Fruits Vegetables Vegetables Fish (fatty) & Seafood Lean Fish & Seafood Legumes Sofrito White Meat Wine w/ Meals
    45. 45. Olive Oil
    46. 46. IOC - Madrid
    47. 47. EXTRA VIRGIN criteria:  Oleic acid, of not more than 0.8 grams per 100 grams and a peroxide value of less than 20 milliequivalent O2.  It must be produced entirely by mechanical means without the use of any solvents, and under temperatures that will not degrade the oil (less than 86°F, 30°C).
    48. 48. Difference Between MeDiet + EVOO and MeDiet +Nuts Estruch, R. et al. N Engl J Med. 2013;368:1279-1290. MeDiet + EVOO MeDiet + Nuts EVOO (1L/week) Walnuts 15 g/d Almonds 7.5 g/d Hazelnuts 7.5 g/d
    49. 49. PREDIMED Trial: The Incidence of Acute Myocardial Infarction, Stroke, and Death from Cardiovascular Causes by Treatment Estruch, R. et al. N Engl J Med. 2013;368:1279-1290. 30% RRR
    50. 50. Estimates of Incidence of the Significant Separate Component (Stroke) of the Primary Endpoint Estruch, R. et al. N Engl J Med. 2013;368:1279-1290. 34-49% RRR
    51. 51. Prevention of Diabetes With Mediterranean Diets: A Subgroup Analysis of a Randomized Trial: Predimed Substudy Jordi Salas-Salvadó et.al. Annals of Int. Med., Jan 6 2014 3541 patients aged 55 to 80 years at high CV risk. 4.1 yr f/u Intervention: Mediterranean diet supplemented with extra-virgin olive oil (EVOO), Mediterranean diet supplemented with nuts, or a control diet (advice on a low-fat diet). No intervention to increase physical activity or lose weight was included. Measurements: Incidence of new-onset type 2 diabetes mellitus (prespecified secondary outcome). Results: Multivariate-adjusted hazard ratios were 0.60 for the Mediterranean diet supplemented with EVOO and 0.82 for the Mediterranean diet supplemented with nuts compared with the control diet. ~30% RRR Conclusion: A Mediterranean diet enriched with EVOO but without energy restrictions reduced diabetes risk among persons with high cardiovascular risk.
    52. 52. Effect of the Mediterranean diet on heart failure biomarkers: a randomized sample from the PREDIMED trial. Fitó M,, Estruch R, Salas-Salvadó Jet.al. Eur J Heart Fail.2014 Feb 24 METHODS AND RESULTS: A total of 930 subjects at high cardiovascular risk (420 men and 510 women) were recruited in the framework of a multicentre, randomized, controlled, parallel-group clinical trial directed at testing the efficacy of the TMD on the primary prevention of cardiovascular disease (The PREDIMED Study). 1 year of intervention, both TMDs: - decreased plasma N-terminal pro-brain natriuretic peptide, vs. control group (P < 0.05). - Oxidized LDL-C decreased in both TMD groups (P < 0.05), the decrease in TMD + VOO group reaching significance vs. changes in control group (P = 0.003). CONCLUSIONS:. From our results TMD could modify markers of heart failure towards a more protective mode
    53. 53. Mediterranean and Dietary Approaches to Stop Hypertension dietary patterns and risk of sudden cardiac death in postmenopausal women. Bertoia ML et.al Am J Clin Nutr.2014 Feb;99(2):344-51. WHI Examine the association between the Mediterranean and DASH dietary patterns and risk of sudden cardiac death (SCD) in women. Prospective cohort of 93,122 postmenopausal women enrolled in the Women's Health Initiative for an average of 10.5 y. Women completed a FFQ during f/u. We scored their diets according to how closely the reported diet resembled each dietary pattern. SCD was defined as death that occurred within 1 h of symptom onset. RESULTS: A higher Mediterranean diet score was associated with lower risk of SCD (HR: 0.64) when women in the highest quintile were compared with women in the lowest quintile after adjustment for age, total energy, race, income, smoking, and physical activity. After adjustment for potential mediators, the association was similar (HR: 0.67). A higher DASH diet score was not associated with risk of SCD. However, sodium intake, which is a crucial component of the DASH dietary pattern, was not well characterized by the FFQ.
    54. 54. KEY POINT A Mediterranean dietary pattern is perhaps the most evidenced-based dietary recommendation to reduce cardiometabolic risk. Olive oil and nut enhancement may bring more significant CMR reduction EAT MORE EAT LESS veget abl es l egumes f r ui t s and nut s cer eal s ol i ve oi l f i sh MODERATE I NTAKE: et hanol , e.g., wi ne and gener al l y dur i ng meal s. sat ur at ed f at dai r y pr oduct s (l ow t o moder at e) meat and poul t r y
    55. 55. Overlap in new dietary guideline agreement – nothing really new Fatty acids and CVD – substitutions not additions The reality of postprandial lipemic responses to HFM Provider dietary habits need to improve Mediterranean dietary patterns appear to be the most evidence-based (DASH not to be forgotton) SUMMARY POINTS
    56. 56. ANHC & Eastern Aleutian Tribes The rapid increase in CHD and diabetes prevalence in Alaskan Natives 1990 - 2003 - 2008
    57. 57. http://www.anthctoday.org/storeoutside/ https://www.facebook.com/StoreOutside Alaska Native Tribal Health Consortium

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