Archive for June, 2011

Olive Oil and Fish Oil Update

Sunday, June 26, 2011 // Uncategorized

Here is something from the journal Neurology via Journal Watch on stroke reduction by the use of olive oil.

Olive Oil Use Associated with Lower Stroke Risk
Regular use of olive oil confers a lower risk for ischemic stroke, according to a French cohort study reported in Neurology.
Olive oil use was gauged by dietary recall at baseline in some 7600 subjects followed for a median of 5 years. All participants were aged 65 or older; a subgroup of 1200 underwent baseline measurement of plasma fatty acids.
Compared with nonusers, there was a 41% lower risk for stroke among intensive users of olive oil — i.e., using the oil in dressings as well as for cooking. Similarly, plasma oleic acid levels among the tested subgroup roughly paralleled olive oil intake and an accompanying lower stroke risk.
Editorialists agree with the authors that oleic acid is only an indirect — and as yet unvalidated — measure of olive oil use.

Here is the abstract from the article.

  • Article

Olive oil consumption, plasma oleic acid, and stroke incidence

The Three-City Study

  1. C. Samieri, PhD,
  2. C. Féart, PhD,
  3. C. Proust-Lima, PhD,
  4. E. Peuchant, MD, PhD,
  5. C. Tzourio, MD, PhD,
  6. C. Stapf, MD,
  7. C. Berr, MD, PhD and
  8. P. Barberger-Gateau, MD, PhD

+ Author Affiliations


  1. From the Research Center INSERM, U897, Department of Nutritional Epidemiology (C. Samieri, C.F., P.B.-G.), Bordeaux; Research Center INSERM, U897, Department of Biostatistics (C.P.-L.), Bordeaux; University Victor Segalen Bordeaux 2 (C. Samieri, C.F., C.P.-L., P.B.-G.), ISPED, Bordeaux; INSERM (E.P.), U876, Bordeaux; CHU de Bordeaux (E.P.), Hôpital Saint-André, Department of Biochemistry, Bordeaux; INSERM (C.T.), U708, Neuroepidemiology Unit, University Pierre et Marie Curie Paris VI, Paris; Department of Neurology (C.T., C. Stapf), Hôpital Lariboisière, APHP, Paris; University Diderot Paris VII (C. Stapf), Paris; INSERM (C.B.), U1061, University Montpellier 1, Montpellier; and CHU Montpellier (C.B.), CMRR Languedoc Roussillon, Montpellier, France.
  • Address correspondence and reprint requests to Dr. Cécilia Samieri, Equipe Epidémiologie de la Nutrition et des Comportements Alimentaires, INSERM, U897, Université Bordeaux 2, ISPED case 11, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France [email protected]
  • Abstract

    Objective:To determine whether high olive oil consumption, and high plasma oleic acid as an indirect biological marker of olive oil intake, are associated with lower incidence of stroke in older subjects.

    Methods:Among participants from the Three-City Study with no history of stroke at baseline, we examined the association between olive oil consumption (main sample, n = 7,625) or plasma oleic acid (secondary sample, n = 1,245) and incidence of stroke (median follow-up 5.25 years), ascertained according to a diagnosis validated by an expert committee.

    Results:In the main sample, 148 incident strokes occurred. After adjustment for sociodemographic and dietary variables, physical activity, body mass index, and risk factors for stroke, a lower incidence for stroke with higher olive oil use was observed (p for trend = 0.02). Compared to those who never used olive oil, those with intensive use had a 41% (95% confidence interval 6%–63%, p= 0.03) lower risk of stroke. In the secondary sample, 27 incident strokes occurred. After full adjustment, higher plasma oleic acid was associated with lower stroke incidence (pfor trend = 0.03). Compared to those in the first tertile, participants in the third tertile of plasma oleic acid had a 73% (95% confidence interval 10%–92%, p = 0.03) reduction of stroke risk.

    Conclusions: These results suggest a protective role for high olive oil consumption on the risk of stroke in older subjects.

  • Received September 27, 2010.
  • Accepted January 19, 2011.
  • Copyright © 2011 by AAN Enterprises, Inc.
  •  

    The following is the conclusion of a review article in last weeks New England Journal of Medicine entitled” N-3 Fatty Acids and Cardiovascular Disease” :

    Conclusions

    On the basis of currently available evidence, the American Heart Association (AHA) has recommended94that all adults eat fish (particularly fatty fish) at least twice a week, as well as vegetables containing plant-derived n–3 fatty acids (ALA). The AHA also suggests that patients with documented coronary heart disease consume approximately 1 g of EPA and DHA (combined) per day, from oily fish or fish-oil capsules (after consultation with a physician). The AHA recommendations also state that EPA–DHA supplements may be useful in patients with severe hypertriglyceridemia (>500 mg of triglycerides per deciliter [5.6 mmol per liter]), for whom effective doses are higher: 2 to 4 g of EPA–DHA per day to lower triglyceride levels by 20% to 40%. The AHA advises caution with respect to contaminants and notes that many species of fish are low in methylmercury95and that fish-oil supplements are free of methylmercury.

    The n–3 fatty acids continue to attract interest as a possible addition to available lifestyle measures and medications for the prevention of cardiovascular disease, but important gaps in knowledge remain. Data are lacking from clinical and mechanistic studies of the putative benefits of n–3 fatty acids for both primary and secondary

    For those who want more information, here is the entire article:

    Review Article

    Drug Therapy

    n–3 Fatty Acids in Cardiovascular Disease

    Raffaele De Caterina, M.D., Ph.D.

    N Engl J Med 2011; 364:2439-2450June 23, 2011

    Article

    Cardiovascular disease is the leading cause of death worldwide, and preventive approaches, particularly achievable dietary changes, have major public health implications. An increased dietary intake of n–3 (polyunsaturated) fatty acids is one such dietary approach. This review discusses advances since the topic was last reviewed in the Journal 1 and highlights current gaps in knowledge.

    Historical Perspective

    In response to anecdotal reports of a low prevalence of coronary heart disease among Greenland Eskimos (Inuits), Bang and Dyerberg undertook six expeditions to Greenland starting in the late 1960s. They confirmed a very low incidence of myocardial infarction and reported an antiatherogenic blood lipid pattern, as well as markedly reduced platelet reactivity, in this population as compared with Danish controls.2,3 These findings were attributed to the Inuit diet, which was composed mainly of seal and whale and was extremely rich in marine n–3 fatty acids. The prevalence of inflammatory and immune diseases among the Inuits was also reported to be very low.4 In a seminal article in 1978, Dyerberg and colleagues presented the hypothesis that marine n–3 fatty acids might provide protection against atherosclerosis and thrombosis,5 and they began research on the potential effects of n–3 fatty acids in the prevention and treatment of vascular disease.

    Biosynthesis of Essential Polyunsaturated Fatty Acids

    Polyunsaturated fatty acids, organic acids that naturally contain more than one double bond in the aliphatic chain, are named according to the number (>1), position, and configuration of such double bonds, which also largely determine their physical and biologic properties. Biologically relevant families of polyunsaturated fatty acids are the n–6 and the n–3 fatty acids (Figure 1Figure 1Chemical Structure and Pathway of Conversion of Linoleic and Alpha-Linolenic Acid (ALA) into Longer Derivatives (Long-Chain, or Highly Unsaturated Polyunsaturated Fatty Acids).). Mammals lack enzymes to insert the double bond in the n–6 or n–3 position; therefore, linoleic acid and alpha-linolenic acid (ALA), as well as some of their elongation products, are essential nutrients for mammals; the lack of these nutrients leads to a syndrome of deficiency of essential fatty acids.6,7 In humans, this deficiency is usually characterized by desquamative rashes and hyperkeratotic dermatoses.8 Current estimates of the minimum requirements for n–6 and n–3 fatty acids in adults are 1.0% and 0.2% of daily energy intake, respectively,9 with acceptable (but not necessarily ideal) macronutrient distribution ranges for eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) of 0.25 to 2.0 g per day.10

    Plant tissues and oils are good sources of linoleic acid and ALA. Photosynthesizing plants are especially rich in ALA, accounting for up to 55% of the fatty acids present in green vegetables. However, green vegetables generally contribute little to the optimal intake of ALA in humans, as compared with certain plant oils such as soybean, flaxseed, linseed, and rapeseed (canola) oils, as well as walnuts. Mammalian cells cannot synthesize linoleic acid and ALA, though limited (1 to 5%)11 conversion to longer-chain polyunsaturated fatty acids occurs through further desaturation and elongation. Linoleic acid can ultimately be converted to arachidonic acid (20:4 n–6) and, through the same series of enzymes, ALA can be converted to EPA (20:5 n–3). The further conversion of EPA to DHA (22:6 n–3) involves a complex series of additional reactions,12 but the conversion is very limited11 (Figure 1). DHA accumulates in all tissues, including the heart and the vessel wall, but it particularly accumulates in the nervous system and the retina, where it serves important physiological functions.

    EPA and DHA enter the food chain through marine phytoplankton, and they pass through fish and marine mammals — seals, walruses, and whales — which are the main components of the Eskimo diet. In Western diets, the main source of EPA and DHA intake is fish, especially oily fish (e.g., mackerel, trout, salmon, herring, and sardines). Fish-oil preparations contain variable amounts of n–3 fatty acids in the form of triglycerides, ethyl esters, or free fatty acids.

    Transgenic animals that express the fat-1 gene from the worm Caenorhabditis elegans have been raised. This gene encodes an n–3 fatty acyl desaturase catalyzing the conversion of 18- and 20-carbon n–6 substrates into n–3 fatty acids. A supplementation approach with the use of meat from these transgenic animals might permit a marked enrichment of mammalian cells with n–3 fatty acids beyond that which is possible through dietary approaches, with obvious clinical implications.13,14

    Metabolism and Mechanisms of Action

    Polyunsaturated fatty acids modulate local signaling and structure, primarily after esterification (prevalently in the sn-2 position) in glycerophospholipids and incorporation into cell membranes (see the Supplementary Appendix, available with the full text of this article at NEJM.org). There are three broad categories of biologic effects: those mediated by the release of bioactive mediators, direct effects on ion channels that modulate a number of events (e.g., arrhythmogenesis), and other direct effects on membranes that require incorporation into cell phospholipids.

    The n–3 fatty acids can be released through the actions of phospholipase A2, induced by a variety of stimuli, and are converted through both orthodox and novel pathways to signaling molecules. The orthodox pathways involve reactions catalyzed by cyclooxygenases and lipoxygenases to biologically active eicosanoids, including prostaglandins, thromboxanes, and leukotrienes (Figure 2Figure 2“Orthodox Pathways” of Polyunsaturated Fatty Acid Metabolism.). Thromboxanes and leukotrienes derived from n–3 fatty acids are in general much less potent local mediators than the corresponding n–6 fatty acid derivatives in orthodox pathways. The n–3 fatty acids are also converted to biologically active epoxides, alcohols, diols, and ketones through recently discovered new pathways (Figure 3Figure 3Novel Pathways of Polyunsaturated Fatty Acid Metabolism.). A number of local mediators, discovered as a result of elucidating such new pathways, are potent (in the nanomolar range) and stereoselective, with antiinflammatory actions and actions prompting the resolution of inflammation, and they are produced during this resolution phase of inflammation through transcellular biosynthetic routes (i.e., the product of one cell is transformed by neighboring cells). Thus, these compounds are termed “resolution-phase interaction products” (resolvins)16,17 (Figure 3). In addition, unsaturated fatty acids, through nitration, can generate nitro-fatty acids that globally suppress inflammation at micromolar concentrations18 (Figure 3).

    In low micromolar concentrations, n–3 fatty acids have direct effects without undergoing metabolism. Some direct effects, such as antiarrhythmic effects, occur rapidly,19 without incorporation of n–3 fatty acids into the cell membranes. These free fatty acids cause steric interference with sodium, potassium, and calcium channels; this blocking mechanism is distinct from that of other known classes of antiarrhythmic agents.20 Conversely, incorporation into cell membranes is required for slow-onset and long-acting direct antiinflammatory, antiatherogenic effects, modulating the expression of endothelial proinflammatory, proatherogenic genes (genomic effects).21,22 The incorporation of fatty acids appears to alter the properties of lipid rafts and caveolae, contributing to membrane fluidity. Thus, hormone-receptor binding and the function of membrane-associated proteins are affected.23,24 In turn, this incorporation has been associated with decreased generation of intracellular reactive oxygen species and a consequent diminished activation of redox-sensitive transcription factors, such as the nuclear factor-κB system, modifying the expression of proinflammatory, proatherogenic genes.22,25 There is evidence that n–3 fatty acids signal through G-protein–coupled receptor 120, modulating inflammatory and insulin-sensitizing effects that occur in monocytes and macrophages.26

    Through one or more of the above mechanisms, n–3 fatty acids may affect several intermediate determinants of cardiovascular risk. At doses of 3 g per day or more, these substances generally reduce hypertriglyceridemia in humans27,28 without changing cholesterol levels substantially.29 The n–3 fatty acids are also associated with decreased levels of markers and mediators of inflammation such as the cytokines interleukin-1β and tumor necrosis factor α.30,31 Studies have shown that increased intake of n–3 fatty acids is associated with a small reduction in blood pressure (approximately 2 to 3 mm Hg systolic and 1 to 2 mm Hg diastolic)32 and with a reduction in the resting heart rate (approximately 3 beats per minute).33 Other studies suggest that the intake of n–3 fatty acids is associated with improved cardiac diastolic filling,33 modulation of autonomic function (thus increasing heart-rate variability),34 and increased baroreceptor control,35 which in turn reduce the risk of fatal arrhythmias. Some data suggest that n–3 fatty acids improve insulin sensitivity36 and mildly inhibit platelet function,37,38 though the overall effects on hemostasis appear to be modest. Despite a mild increase in the bleeding time, clinically important bleeding, originally described in Eskimos,4 has not been substantiated in other groups.39,40 A short course of n–3 fatty acid supplementation has been reported to improve endothelial function41 and to reduce features of inflammatory atherosclerotic plaque.42

    Animal Models

    Experimental studies in animal models fall broadly into two categories: studies exploring the progression of vascular disease or thrombosis, and studies of antiarrhythmic effects. In several animal models, n–3 fatty acids improved endothelial function and diminished atheromas, but such results are inconsistent, probably reflecting differences in the species used and the study design.43

    In Langendorff preparations of perfused rabbit heart44 and in feeding experiments in rats45 and monkeys,46 n–3 fatty acids were associated with an increased arrhythmogenic threshold. In a canine model of sudden death due to exercise-induced ventricular fibrillation, the intravenous infusion of an emulsion of n–3 fatty acid concentrate47 or isolated EPA, DHA, or ALA plus serum albumin48 prevented ventricular fibrillation (see the Supplementary Appendix).

    Epidemiologic Studies

    In 25 studies involving a total of 280,000 participants, there was an inverse association between fish consumption and morbidity or mortality from coronary heart disease.49,50 The first epidemiologic observations in Greenland Inuits51,52 (with an estimated mean n–3 fatty acid intake of up to about 15 g per day52) suggested that a nutritional factor was associated with cardiovascular protection. This observation was subsequently confirmed in natives of Northern Canada and Alaska who were living traditionally,4,5,53,54 and in Japanese,55 Western, and Chinese populations49,56,57 (Table 1 in the Supplementary Appendix). Blood levels of n–3 fatty acids also appear to correlate inversely with death from cardiovascular causes58,59 and total mortality.60

    Clinical Trials

    Secondary Prevention of Cardiovascular Disease

    In the Diet and Reinfarction Trial,60,61 a total of 2033 male survivors of myocardial infarction were randomly assigned in a open-label fashion to receive or not receive one of the following three dietary recommendations: a reduction in fat intake with an increase in the ratio of polyunsaturated fatty acids to saturated fat, an increase in the intake of cereal fiber, and an increase in the intake of oily fish (200 to 400 g per week, providing an additional 500 to 800 mg of n–3 fatty acids per day). Participants who declined to eat fish were allowed to take fish-oil capsules (900 mg of EPA–DHA per day). There was a 29% reduction in the rate of death from any cause over a 2-year period in the group of persons who received advice on increasing fish consumption.61,62 This study was novel in showing that dietary advice and subsequent changes in fish intake might influence mortality, but the dietary intervention was complex, the study design was unavoidably open-label, and the study lacked power to detect a true difference in mortality between the two groups.

    The Gruppo Italiano per lo Studio della Soprawivenza nell’Infarto Miocardico (GISSI)-Prevenzione trial29 randomly assigned 11,324 survivors of recent myocardial infarction (within the previous 3 months) to receive n–3 polyunsaturated fatty acids (1 g per day, in 2836 patients), vitamin E (300 mg per day, in 2830 patients), both (in 2830 patients), or neither (in 2828 patients [the control group]) for 3.5 years. No placebos were used in the study. Among the patients who received n–3 fatty acids alone, as compared with the control group, there was a 15% reduction in the composite primary end point of death, nonfatal myocardial infarction, or nonfatal stroke (P<0.02), with a 20% reduction in the rate of death from any cause (P<0.01) and a 45% reduction in the rate of sudden death, an end point adjudicated by a committee whose members were unaware of the group assignments (P<0.001), whereas the incidence of myocardial infarction was not significantly reduced. Vitamin E provided no additional benefit.29 Survival curves diverged early after randomization. Total mortality was significantly reduced after only 3 months of treatment (relative risk, 0.59), and the rate of sudden death after only 4 months (relative risk, 0.47).63 However, the study was open-label and had a high dropout rate (>25%), limiting its generalizability.

    Burr et al.64 reported on a trial involving 3114 male patients of general practitioners in south Wales. These patients, who were younger than 70 years of age and had angina pectoris, were randomly assigned to four groups that received different advice about food. The first group was advised to consume two portions of oily fish each week or three fish-oil capsules daily. The second group was advised to consume more fruits, vegetables, and oats. The third group received both recommendations, and the fourth group received no specific dietary advice. After 3 to 9 years, there was no reduction in mortality in the groups of patients who received dietary advice on increasing fish consumption. Furthermore, no other effects were attributable to advice regarding fruit. Contrary to the prespecified hypothesis, the risk of death from cardiac causes was higher among patients who were advised to consume oily fish than among those who were not so advised (adjusted hazard ratio, 1.26; 95% confidence interval [CI], 1.00 to 1.58; P=0.047), and the risk of sudden death from cardiac causes was even greater (1.54; 95% CI, 1.06 to 2.23; P=0.02). The apparent excess risk occurred largely in the subgroup of patients who received fish-oil capsules. There was no evidence that this excess risk was due to interactions with other medications that the participants were receiving.64 However, there were several problems during the conduct of this trial, including the inability to check long-term adherence to the assigned treatments and between-group differences in changes in concomitant medications and health behaviors.65

    In the Japan Eicosapentaenoic Acid (EPA) Lipid Intervention Study (JELIS; ClinicalTrials.gov number, NCT00231738),66 the long-term use of pure EPA was tested in an open-label trial for efficacy in the prevention of major coronary events in Japanese patients with hypercholesterolemia. A total of 18,645 patients with total cholesterol levels of 252 mg per deciliter or higher (≥6.5 mmol per liter) were randomly assigned to receive either 1800 mg of EPA per day with statins (9326 patients) or statins alone (9319 patients). The primary end point was a major coronary event, defined as sudden death from cardiac causes, fatal or nonfatal myocardial infarction, unstable angina pectoris, angioplasty, stenting, or coronary-artery bypass grafting; these outcomes were adjudicated by investigators who were unaware of the group assignments. At a mean follow-up of 4.6 years, the primary end point occurred in 262 patients in the EPA group (2.8%) and in 324 patients in the control group (3.5%) — a 19% relative reduction in major coronary events (P=0.01).66 There was also a significant reduction in stroke.67 The level of low-density lipoprotein cholesterol after treatment decreased similarly in both groups and thus was not a major factor in the observed effect. Nonfatal coronary events were also significantly reduced in the EPA group, but sudden death from cardiac causes and death from coronary causes were not. The reduction in events associated with EPA was similar in patients with and those without a history of coronary artery disease, but it was significant only in the former group, with a very low number needed to treat (19).68 The JELIS study showed the efficacy of EPA in a population that did not have high cholesterol levels but did have other risk factors, including elevated triglyceride levels, low levels of high-density lipoprotein cholesterol, and impaired glucose tolerance. The lack of an effect on the incidence of sudden death probably reflects the high background n–3 fatty acid intake in the Japanese population.

    The GISSI Heart Failure Study (GISSI-HF, NCT00336336)69 was a randomized, double-blind, placebo-controlled trial testing whether fish oil could reduce morbidity and mortality in a large population of patients with symptomatic chronic heart failure (New York Heart Association class II, III, or IV) of any cause who were considered to be at high risk for sudden cardiac death and were receiving standard treatment. Patients were randomly assigned to receive n–3 fatty acids at a dose of 1 g per day (in 3494 patients) or placebo (in 3481 patients) and were followed for a median of 3.9 years. In a secondary analysis, patients were also randomly assigned, in an open-label design, to receive either rosuvastatin at a dose of 20 mg per day or placebo. The primary end points were the time to death and a composite of the time to death or admission to the hospital for cardiovascular reasons. A total of 955 patients in the fish-oil group died from any cause, as compared with 1014 patients in the placebo group (27% vs. 29%; adjusted hazard ratio, 0.91; 95.5% CI, 0.83 to 1.00; P=0.04). A total of 1981 patients in the fish-oil group (57%) and 2053 patients in the placebo group (59%) died or were admitted to the hospital for cardiovascular reasons (adjusted hazard ratio, 0.92; 99% CI, 0.85 to 1.00; P=0.009). On the basis of the results, 56 patients would need to be treated for a median of 3.9 years to avoid 1 death, and 44 would need to be treated to avoid 1 death or admission to the hospital for cardiovascular reasons.69 Thus, the GISSI-HF trial confirmed the reduction in mortality seen in the GISSI-Prevenzione trial, although the extent of the reduction was smaller. However, no other pharmacologic agent tested in contemporary trials has been shown to reduce mortality among patients with symptomatic chronic heart failure. Indeed, the rosuvastatin-versus-placebo comparison in the GISSI-HF study did not show the efficacy of statin therapy.

    The recent randomized, double-blind, multicenter Alpha Omega trial70 included 4837 patients with previous myocardial infarction (median elapsed time, 3.7 years). The patients were 60 to 80 years of age, and 78% were men. They received one of four trial margarines: a margarine supplemented with a combination of EPA and DHA (with a targeted additional daily intake of 400 mg of EPA–DHA — a dose less than half that used in the GISSI-Prevenzione and GISSI-HF trials), a margarine supplemented with ALA (targeted additional daily intake of 2 g of ALA), a margarine supplemented with EPA–DHA and ALA, or a placebo margarine. The primary end point was the rate of major fatal and nonfatal cardiovascular events and cardiac interventions. Data were analyzed according to the intention-to-treat principle. In patients who received the EPA–DHA supplement, plasma levels of EPA and DHA increased (by much less than the levels obtained in the GISSI-Prevenzione trial). Levels of EPA, but not of DHA, also increased in the ALA group, suggesting some conversion of ALA to EPA. A major cardiovascular event occurred in 671 patients (13.9%) during the follow-up period. Neither EPA–DHA nor ALA reduced the primary end point (hazard ratio with EPA–DHA, 1.01; 95% CI, 0.87 to 1.17; P=0.93; hazard ratio with ALA, 0.91; 95% CI, 0.78 to 1.05; P=0.20). In a prespecified subgroup analysis involving female participants, ALA, as compared with placebo and EPA–DHA alone, was associated with a reduction in the rate of major cardiovascular events that did not achieve significance (hazard ratio, 0.73; 95% CI, 0.51 to 1.03; P=0.07). The adverse-event rates did not differ significantly among the study groups.70 The outcome of the EPA–DHA supplementation in this study is difficult to interpret because the supplementation dose was small and its effects might have been obscured by the larger amount of ALA administered in half the groups in the comparison. In this instance, the factorial design of the study was inappropriate for the two nonindependent study drugs tested. Furthermore, the study was underpowered to detect differences between each of the four study groups.

    Other studies, each involving fewer than 600 patients, have addressed the use of n–3 fatty acids to prevent restenosis after coronary angioplasty, atrial fibrillation, or other clinical conditions, with mortality as the end point. The results are inconclusive, because these studies together accounted for less than 4% of all deaths reported in trials of n–3 fatty acids.71-80

    Prevention of Arrhythmias in Patients with Implantable Cardioverter−Defibrillators

    Since several studies showed that n–3 fatty acids reduce the rates of death from cardiac causes and sudden death, the hypothesis that n–3 fatty acids work largely by preventing life-threatening cardiac arrhythmias gained increasing attention.47,81,82 Three double-blind, randomized, placebo-controlled intervention studies involving patients with implantable cardioverter–defibrillators investigated the direct effects of fish oil on ventricular tachyarrhythmias77,79,80; none convincingly showed that supplementation with n–3 polyunsaturated fatty acids prevented discharges from implantable cardioverter–defibrillators. However, a meta-analysis of these three trials (involving a total of 1148 patients)83 suggested that patients with underlying coronary artery disease, in whom triggered ectopic beats and prolonged action potentials are predominant proarrhythmogenic mechanisms, might benefit, whereas patients with heart failure, in whom arrhythmias are mostly caused by reentry, might not. These studies were small, and the hypothesized relative risk reduction, 20% at best, would require several thousand patients in order to be conclusive.

    Small, mostly uncontrolled studies have shown that fish oil may be useful in reducing the incidence of supraventricular arrhythmias, including atrial fibrillation.84

    Comparisons of EPA, DHA, and ALA

    The favorable effects of fish oils were originally attributed primarily to EPA. However, more DHA than EPA accumulates in the body, and DHA has broadly similar biologic effects. Only in the past 10 years have sufficient quantities of purified EPA or DHA become available for controlled trials, and these trials suggest some differential properties (see the Supplementary Appendix). Only one large trial66 selectively administered EPA. Some studies have suggested that ALA may have biologic properties that are independent of its conversion to EPA and DHA,44,48,85 although this is controversial.86

    Background Diet and Ratio of n–6 to n–3 Fatty Acids

    Western diets are low in n–3 fatty acids but have high amounts of n–6 fatty acids, such as those in poultry, meat, and most vegetable oils, as compared with early human diets.87 Some investigators have speculated that larger amounts of n–6 fatty acids, such as those in today’s Western diets, may promote many diseases of modern life, including cardiovascular disease. Therefore, it has been hypothesized that lowering the intake of n–6 polyunsaturated fatty acids (decreasing the ratio of n–6 to n–3 fatty acids, no matter how it is defined) would have favorable effects.88 This idea has been disputed, since epidemiologic studies in Western populations have generally shown that the intake of n–6 fatty acids has a favorable inverse relationship with morbidity and mortality from cardiovascular causes,86,89 although the effect is weaker than that seen with n–3 fatty acids. Small studies involving varying intakes of dietary polyunsaturated fatty acids (mostly n–6 polyunsaturated fatty acids) showed that the intake paralleled reciprocal changes in saturated fatty acids.90 Randomized, controlled trials have not provided clear evidence that dietary intake of foods rich in pure n–6 fatty acids reduces the risk of coronary heart disease.91 Data from randomized, controlled trials are lacking to test the hypothesis that a selective lowering of the intake of n–6 fatty acids, without altering the intake of saturated or n–3 fatty acids, will be beneficial.

    Much less controversial is the possibility that, given the existence of quite different background n–3 fatty acid intakes, one can expect varying outcomes from studies involving different populations that received similar amounts of n–3 fatty acids. For example, studies of an increased intake of n–3 fatty acids showed an association with a reduction in the risk of sudden death in Western populations,29 but this has not been seen in the Japanese population,66 which has a much higher dietary intake of fish and a very low baseline rate of sudden death.

    Fish Contaminants and Counterbalanced Effects of n–3 Fatty Acids

    Although contaminants in pharmaceutical preparations of fish oil can be controlled easily, this is not true of contaminants in seafood. The presence of such contaminants, especially mercury, has direct implications for dietary recommendations at the population level.92 If long-term mercury exposure were to increase cardiovascular risk, the relevant question for recommendations regarding fish consumption would be the balance of the relative harm and benefits. Most current epidemiologic evidence suggests that the benefits of fish consumption outweigh the harm.93

    Conclusions

    On the basis of currently available evidence, the American Heart Association (AHA) has recommended94 that all adults eat fish (particularly fatty fish) at least twice a week, as well as vegetables containing plant-derived n–3 fatty acids (ALA). The AHA also suggests that patients with documented coronary heart disease consume approximately 1 g of EPA and DHA (combined) per day, from oily fish or fish-oil capsules (after consultation with a physician). The AHA recommendations also state that EPA–DHA supplements may be useful in patients with severe hypertriglyceridemia (>500 mg of triglycerides per deciliter [5.6 mmol per liter]), for whom effective doses are higher: 2 to 4 g of EPA–DHA per day to lower triglyceride levels by 20% to 40%. The AHA advises caution with respect to contaminants and notes that many species of fish are low in methylmercury95 and that fish-oil supplements are free of methylmercury.

    The n–3 fatty acids continue to attract interest as a possible addition to available lifestyle measures and medications for the prevention of cardiovascular disease, but important gaps in knowledge remain. Data are lacking from clinical and mechanistic studies of the putative benefits of n–3 fatty acids for both primary and secondary prevention.

    Disclosure forms provided by the author are available with the full text of this article at NEJM.org.

    I thank Charles N. Serhan, Roberto Marchioli, Claudio Galli, and Marika Massaro for helpful comments on an earlier version of the manuscript.

    Source Information

    From the Institute of Cardiology and the Center of Excellence on Aging, Gabriele d’Annunzio University, Chieti; and the Gabriele Monasterio Foundation, Pisa — both in Italy.

    Address reprint requests to Dr. De Caterina at the Institute of Cardiology, Gabriele d’Annunzio University–Chieti, c/o Ospedale SS. Annunziata, Via dei Vestini, 66013, Chieti, Italy, or at [email protected].

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    Breast Implants Are Temporary

    Saturday, June 25, 2011 // Uncategorized

    The following is from Journal Watch and goes over their safety, but also the fact that they should not be considered a forever device.  It is followed by the FDA’s press release.

    FDA: Silicone Breast Implants Not ‘Lifetime Devices’
    Silicone breast implants are not “lifetime devices,” the FDA said on Wednesday, noting that 20% of women who receive the implants for augmentation — and potentially half who receive them for reconstruction — will need to have them removed within 10 years.
    The agency examined data from postapproval studies and from its own adverse event reporting system, and also conducted a literature review. It found that capsular contracture, reoperation, and implant removal were the most frequent adverse outcomes with silicone implants. Other common adverse events included implant rupture, wrinkling, asymmetry, scarring, pain, and infection. The longer the women had implants, the more likely they were to have complications.
    The implants did not appear to cause breast cancer, reproductive problems, or connective tissue disease, although the FDA stressed that the data are preliminary.

    FDA NEWS RELEASE

     
    For Immediate Release: June 22, 2011
    Media Inquiries: Erica Jefferson, 301-796-4988, [email protected]
    Consumer Inquiries: 888-INFO-FDA
     
    FDA provides updated safety data on silicone gel-filled breast implants
    Agency highlights information women should know when considering implants
     
    The U.S. Food and Drug Administration released a report today updating the clinical and scientific information for silicone gel-filled breast implants, including preliminary safety data from studies conducted by the manufacturers as a condition of their November 2006 approval.
     
    While the report confirms that silicone gel-filled breast implants are safe and effective when used as intended, women should fully understand the risks prior to considering silicone gel-filled breast implants for breast augmentation or reconstruction.
     
    Based on the report, women should know:
    • Breast implants are not lifetime devices. The longer a woman has silicone gel-filled breast implants, the more likely she is to experience complications. One in 5 patients who received implants for breast augmentation will need them removed within 10 years of implantation. For patients who received implants for breast reconstruction, as many as 1 in 2 will require removal 10 years after implantation.
    • The most frequently observed complications and outcomes are capsular contracture (hardening of the area around the implant), reoperation (additional surgeries) and implant removal. Other common complications include implant rupture, wrinkling, asymmetry, scarring, pain, and infection.
    • The complications that existed for women receiving breast implants at the time of approval are similar to the complications observed today.
    • Preliminary data do not indicate that silicone gel-filled breast implants cause breast cancer, reproductive problems or connective tissue disease, such as rheumatoid arthritis.  However, in order to rule out these and other rare complications, studies would need to enroll more women and be longer than those conducted thus far.
    The report includes preliminary safety data from post-approval studies conducted by each of the two breast implant manufacturers (Allergan and Mentor), a summary and analysis of adverse events received over the years by the FDA, and a comprehensive review and analysis of recent scientific publications that discuss the safety and effectiveness of silicone gel-filled breast implants. FDA approved silicone gel-filled breast implants in November 2006 for breast augmentation in women over age 22 and for breast reconstruction in all women.
     
    As a condition of approval, the FDA required each of the two companies to conduct six post-approval studies to characterize the long-term performance and safety of the devices.
     
    Both manufacturers have communicated to the FDA the difficulties in following women who have received silicone gel-filled breast implants. The FDA is working with Allergan and Mentor to address those challenges and increase patient participation and follow-up.
     
    “The FDA will continue to monitor and collect safety and performance information on silicone gel-filled breast implants, but it is important that women with breast implants see their health care providers if they experience any symptoms,” Jeffrey Shuren, M.D., J.D., director of FDA’s Center for Devices and Radiological Health. “Women who have enrolled in studies should continue to participate so that we may better understand the long-term performance of these implants and identify any potential problems.”
     
    The FDA is holding an expert advisory panel in the next few months to discuss how post-approval studies on breast implants can be more effective.
      
    At this time, the FDA is recommending that health care professionals and women who have silicone gel-filled breast implants do the following:
    • Follow up. Women should continue to routinely follow up with their health care professionals. This includes getting routine MRIs to detect silent rupture.
    • Be aware. Breast implants are not lifetime devices. Breast implants are associated with significant local complications and outcomes, including capsular contracture, reoperation, removal, and implant rupture. Some women also experience breast pain, wrinkling, asymmetry, scarring and infection.
    • Pay attention to changes. Women should notify their health care professionals if they develop any unusual symptoms. All serious side effects should be reported to the breast implant manufacturer and Medwatch, the FDA’s safety information and adverse event reporting program. Report online1 or by calling 800-332-1088.
    • Stay in touch. If a woman has enrolled in a manufacturer-sponsored post-approval study, she should continue to participate. These studies are the best way to collect information about the long-term rates of complications.
    The report is part of the FDA’s ongoing effort to ensure that women who have or who may be considering silicone gel-filled breast implants are informed of all possible complications and outcomes. As an additional step, the agency has redesigned its website2 to include comprehensive information on silicone gel-filled and saline-filled breast implants.
     
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    Diet, Lifestyle and Weight Gain

    Thursday, June 23, 2011 // Uncategorized

    Here is a summary of the article in yesterday’s New England Journal followed by the abstract from Journal.  It shows the impact that consumption of some food groups and some activity have on weight gain over the years.

    Long-Term Weight Gain Independently Mediated by Dietary and Lifestyle Factors
    Several specific changes in diet and lifestyle can independently contribute to long-term weight gain, according to a New England Journal of Medicine study.
    Researchers followed some 120,000 nonobese U.S. health professionals, evaluating self-reported changes in diet, lifestyle, and weight every 4 years. (All subjects were followed for at least 12 years; most were followed for 20.) The average weight gain was 3.4 lb for each 4-year period.
    Dietary factors leading to the most weight gain included increased consumption of potatoes, sugar-sweetened beverages, and meats. Weight loss was associated with increased consumption of vegetables, whole grains, fruits, nuts, and yogurt.
    Increased physical activity (as opposed to absolute levels of activity) was also associated with weight loss. For its part, smoking cessation led to weight gain in the short term but had a smaller long-term effect.

     

    Original Article

    Changes in Diet and Lifestyle and Long-Term Weight Gain in Women and Men

    Dariush Mozaffarian, M.D., Dr.P.H., Tao Hao, M.P.H., Eric B. Rimm, Sc.D., Walter C. Willett, M.D., Dr.P.H., and Frank B. Hu, M.D., Ph.D.

    N Engl J Med 2011; 364:2392-2404June 23, 2011

    Background

    Specific dietary and other lifestyle behaviors may affect the success of the straightforward-sounding strategy “eat less and exercise more” for preventing long-term weight gain.

    Methods

    We performed prospective investigations involving three separate cohorts that included 120,877 U.S. women and men who were free of chronic diseases and not obese at baseline, with follow-up periods from 1986 to 2006, 1991 to 2003, and 1986 to 2006. The relationships between changes in lifestyle factors and weight change were evaluated at 4-year intervals, with multivariable adjustments made for age, baseline body-mass index for each period, and all lifestyle factors simultaneously. Cohort-specific and sex-specific results were similar and were pooled with the use of an inverse-variance–weighted meta-analysis.

    Results

    Within each 4-year period, participants gained an average of 3.35 lb (5th to 95th percentile, −4.1 to 12.4). On the basis of increased daily servings of individual dietary components, 4-year weight change was most strongly associated with the intake of potato chips (1.69 lb), potatoes (1.28 lb), sugar-sweetened beverages (1.00 lb), unprocessed red meats (0.95 lb), and processed meats (0.93 lb) and was inversely associated with the intake of vegetables (−0.22 lb), whole grains (−0.37 lb), fruits (−0.49 lb), nuts (−0.57 lb), and yogurt (−0.82 lb) (P≤0.005 for each comparison). Aggregate dietary changes were associated with substantial differences in weight change (3.93 lb across quintiles of dietary change). Other lifestyle factors were also independently associated with weight change (P<0.001), including physical activity (−1.76 lb across quintiles); alcohol use (0.41 lb per drink per day), smoking (new quitters, 5.17 lb; former smokers, 0.14 lb), sleep (more weight gain with <6 or >8 hours of sleep), and television watching (0.31 lb per hour per day).

    Conclusions

    Specific dietary and lifestyle factors are independently associated with long-term weight gain, with a substantial aggregate effect and implications for strategies to prevent obesity. (Funded by the National Institutes of Health and others.)

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    Multivitamin Mayhem

    Wednesday, June 22, 2011 // Uncategorized

    My late father said that Americans have the most expensive urine in the world.  The implication is that water soluble vitamins are not stored in the body,but  are excreted in the urine.  My stance is that health doesn’t come in a pill.  There is little evidence that supplements prevent disease.  Most people take them for insurance.  The nutrients that are most important are the ones that are in food.  The following is a fairly well  balanced article on the subject of vitamin supplements  from The Wall Street journal which carries a lot of good general articles on health.

    The Wall Street Journal

    Multivitamins: So Many Types, So Many Labels

    • By MELINDA BECK

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    Your mother made you take them. Many doctors agree. Even the Flintstones seem to endorse them. But do you really need a multivitamin?

    How do you know if you need a multivitamin? And how do you choose which one? Melinda Beck explains.

    The answer is … probably not, although much depends on your age, gender, diet and health. One thing is certain: A one-size-fits-all multivitamin can’t precisely meet everyone’s needs. People over 50 need extra vitamin B-12, but not as much iron as many multivitamins contain. Children who take adult multivitamins may be getting too much vitamin A. And many women need a separate supplement to get extra calcium, since it’s too bulky to fit into a multivitamin.

    No wonder the vitamin aisle is so confusing, as manufacturers tailor products for different population segments. One-A-Day brand alone offers 14 versions, from Men’s 50+ Advantage to Vitacrave Gummies for kids

    Reading labels can lead to even more confusion. Recommended Dietary Allowances (RDA) for vitamins and minerals, which are set by the independent Institute of Medicine, differ by an individual’s age and gender. But for convenience, the Food and Drug Administration requires dietary supplements to list a single Daily Value, usually the highest needed.

    For some people, that’s too high: The RDA for iron, for example, is 8 milligrams for men and postmenopausal women. But the Daily Value on supplement labels is 18 milligrams, the amount recommended for women of childbearing age. What’s more, the Daily Values haven’t been updated since 1968, even though the institute’s recommendations for some vitamins and minerals have changed.

    “In some cases, they are wildly off,” says Paul Coates, director of the National Institute of Health’s Office of Dietary Supplements. An FDA spokeswoman said the agency is considering revisions.

    There is no standard multivitamin formula. The term applies to any combination of vitamins and minerals in any strength, as long as they are listed on the label.

    The label may not even exactly match what’s in the bottle. ConsumerLab, a supplement-testing company, reported last week that 10 of 38 multivitamin brands tested contained either more or less of some ingredients than the label indicated.

    And price was no predictor of quality. Some multivitamins selling for less than 10 cents a day performed better on the tests than those selling for 50 cents or more.

    The Council for Responsible Nutrition, a trade group that represents most multivitamin and other supplement makers, says, “It concerns us anytime ConsumerLab says we don’t meet label claims,” says CRN’s chief executive and president. Steven Mister. “But there is nothing in the report that suggests that consumers are getting levels that will do them harm.”

    Are multivitamins even necessary? The dietary supplement industry likens them to nutritional insurance—filling in gaps when people don’t eat perfectly balanced meals.

    That rationale has helped make multivitamins, introduced in the 1940s, the best-selling dietary supplement, with more than $4.8 billion in sales in 2008, according to Nutrition Business Journal. A third of American adults take them regularly. Use is particularly high among women, children, physicians, the elderly and people with high incomes, low body-mass indexes and healthy eating habits, according to government surveys.

    Given those traits and demographics, people most likely to benefit from multivitamins—due to unhealthy habits—also are least likely to take them. Conversely, because people who take multivitamins tend to have other healthy habits, it’s difficult to prove what effect multivitamins have, if any, in overall health.

    Looking at randomized controlled trials, the gold standard for determining cause-and-effect, a NIH panel in 2007 concluded that “the present evidence is insufficient to recommend either for or against the use of [multivitamins and minerals] by the American public to prevent chronic disease.” A 2003 U.S. Preventive Services Task Force report found insufficient evidence either for or against taking multivitamins to prevent cancer or cardiovascular disease.

    The dietary-supplement trade group says observational studies have shown benefits, including a lower risk of cataracts and colon cancer, and fewer colds.

    Such studies, though, can’t determine cause and effect, only association. And several large observational trials have come to opposite conclusions.

    A study in the American Journal of Epidemiology this year that followed 182,000 people in Hawaii and California for 11 years found no association between multivitamin use and deaths from cancer, cardiovascular disease or any cause.

    Compared with over-the-counter and prescription drugs, dietary supplements are lightly regulated. Makers don’t need to demonstrate that they are safe or effective. But there are limits to what they can claim. Ads that use terms such as “support” breast health or mental alertness must note that such statements haven’t been evaluated by the FDA and that the product isn’t intended to diagnose, treat, cure or prevent any disease.

    Still, a scientific consensus has emerged that some groups of people do require more of certain nutrients than they are likely to get from food. Women who might become pregnant should get an additional 400 micrograms a day of folic acid, to reduce the risk of serious neurological issues in a fetus that may occur even before a woman knows she is pregnant.

    People over age 50 should get the recommended 2.4 micrograms of vitamin B-12 from supplements or fortified foods because they become less able to absorb it from food as they age. Vegetarians and vegans also need extra B-12.

    Infants who are being breastfed should get 400 International Units (IUs) a day of supplement vitamin D until they are weaned. In fact, most Americans need 600 IUs per day, according to a 2010 report from the Institute of Medicine. People who get minimal sun exposure and don’t consume much salmon or milk also should supplement their Vitamin D.

    On the other hand, some people may get too much of certain nutrients, depending on their age and health, particularly if they use the current Daily Values listed on labels as a guide. For example, 100% of the current Daily Value for vitamin A is 5,000 IUs—which is over the Institute of Medicine’s safe upper limit of 2,000 IUs for children and far beyond the RDA for children ages 1 through 3 of just 1,000 IUs. Excess vitamin A can cause headaches, hair loss, visual disturbances and a possibly increased risk of osteoporosis. And smokers should avoid taking extra beta carotene, which has been linked to increased risk of lung cancer.

    The consumer-advocacy group Center for Science in the Public Interest has asked the FDA to require warning labels on multivitamins and other supplements for some of these conditions.

    Officials at the dietary-supplement trade group say evidence of the need for such warnings is scant, and the upper limit for vitamins is still safe. “That’s not to say that if you cross that threshold, you will have a fatal condition,” says Duffy MacKay, a naturopathic doctor and CRN vice president.

    Given all the complexities, it pays to discuss individual needs with a doctor, dietitian or other health professional. Some people may find the à la carte approach works best. Others may like the extra “insurance” provided by a multivitamin targeted to their age and sex.

    Dr. Coates, of the NIH, says based on the best evidence, “If you are taking multivitamins, there is no reason to stop, and if you are not taking them, there is no reason to start. You are unlikely to harm yourself, whatever you’re doing.”

    Write to Melinda Beck at [email protected]

    Copyright 2011 Dow Jones & Company, Inc. All Rights Reserved

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    Blood Pressure Meds and Cancer/Sports Drinks/Tai Chi

    Monday, June 13, 2011 // Uncategorized

    Here is a trio of recent newsworthy articles from Journal Watch.

    There has been some concern in some recent studies about a possible link between a class of blood pressure medications and cancer.  ARB’s or Angiotensin Receptor Blockers are a well tolerated class of medications which are usually used as a substitute for patients who cannot tolerate another class of blood pressure medication, ACE inhibitors ( Angiotensin Converting Enzyme). due to side effects.  This recent statement by the FDA absolves ARB’s.

    FDA: ARBs Don’t Cause Cancer
    The FDA has absolved angiotensin-receptor blockers of suspicions that they can cause cancer.
    The agency analyzed 31 randomized trials comprising some 150,000 patients after a somewhat smaller meta-analysis published in the Lancet Oncology in June 2010 showed a modestly increased risk.
    The FDA announced that “any concern about a relationship between ARB use and development of cancer has been resolved” by its analysis.
    FDA Drug Safety Communication: http://www.fda.gov/Drugs/DrugSafety/ucm257516.htm

    Pediatricians Should Ask About Patients’ Use of Sports and Energy Drinks
    Caffeine-containing “energy” drinks should never be used by children and adolescents, and carbohydrate-rich “sports” drinks should be restricted or avoided completely, according to an American Academy of Pediatrics report in Pediatrics.
    On reviewing recent literature, an AAP committee concludes the following:
    At annual visits, clinicians should ask about patients’ use of sports (high-carbohydrate) and energy (high-caffeine) drinks, taking the opportunity to explain the differences between the two and the dangers they pose.
    Plain water, not commercial drinks, is the best source of hydration.
    Young athletes participating in vigorous, prolonged activities should be discouraged from using sports drinks outside of those activities because of their high caloric content.
    Energy drinks should never be consumed in this age group because of their high stimulant content.
    Low-fat milk is a good substitute for drinks purporting to replenish amino acids in muscle recovery.

    For Which Conditions Is Tai Chi Effective?
    Systematic review finds benefit only for falls prevention and psychological health.
    Tai chi, a gentle exercise program that emphasizes controlled breathing and relaxation, has been evaluated as a potential therapy for many diseases and chronic conditions, but results are inconsistent (JW Gen Med May 3 2011 and JW Gen Med Aug 19 2010). Several recent systematic reviews have been conducted to resolve these inconsistencies, and this study is a “review of the reviews.” After a search of the English, Chinese, and Korean medical literature, researchers identified 35 systematic reviews of tai chi; at least 11 reviews were conducted by one of the authors of this meta-review.
    The 35 reviews addressed the value of tai chi in more than 15 diseases and chronic conditions, including cancer, Parkinson disease, rheumatoid arthritis, and cardiovascular disease. Of the four reviews that addressed falls prevention, three showed positive benefit, and one was equivocal. Of the five reviews that addressed psychological health, four were positive, and one was equivocal. The remaining reviews showed no consistent benefit for any other condition.
    Comment: Given the nature of tai chi — which is gentle, rhythmic, and nonspecific — its lack of specific benefit for metabolic and cardiovascular conditions is not surprising. However, its benefits in preventing falls and improving psychological health are clear, and it can be recommended for these specific purposes, especially in older people.
    — Thomas L. Schwenk, MD
    Published in Journal Watch General Medicine May 26, 2011
    Citation(s):
    Lee MS and Ernst E. Systematic reviews of t’ai chi: An overview. Br J Sports Med 2011 May 16; [e-pub ahead of print]. (http://dx.doi.org/10.1136/bjsm.2010.080622)

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    The Latest Weight Loss App

    Sunday, June 12, 2011 // Uncategorized

    • The Wall Street Journal

    I’ve written that there seems to be an Iphone  app for everything.  There are many that count calories.  This is the first that I’ve heard of that will estimate the calories of your meal. 

    A Picture Is Worth 1,000 Calories

    How does the addictive Meal Snap app know what you ate? A little magic and then some

    By KATHLEEN SQUIRES

    Compulsive eating, I get. But compulsive food photography? If you’re one of those people who tweets and posts your meals on Facebook, I’ve always considered you a bit of a nut.

    Koren Shadmi for The Wall Street JournalSnap a photo of a dish; the app will identify it and calculate the calorie count within seconds.

    MEAL SNAP

    MEAL SNAP

    It wasn’t until I found Meal Snap, a $3 iPhone app created by Daily Burn, Inc., that I gained some insight into the food photo phenomenon. It’s an astounding tool: Snap a photo of a dish; the app will identify it and calculate the calorie count within seconds. But exactly how does it know I’m eating a chicken potpie? Though the creators chalk it up to “magic,” I presumed there had to be someone in Bangalore peeking at my snapshots. I asked Daily Burn’s CEO, Andy Smith, if this was the case. Smith’s answer was vague: “It is a combination of people and some advanced algorithms built on top of our database of 400,000 foods.”

    Aha! But who are these “people”? Daily Burn wouldn’t elaborate, but technology expert Scott Steinberg, CEO of TechSavvy Global, speculates that they are likely “Mechanical Turks.” Says Mr. Steinberg: “Mechanical Turk, Amazon.com’s freelancing platform, puts up ads saying something like ‘For two to five cents, can you identify the food that is in this image?'” Interesting. So it may turn out that there are those even more obsessive than food photo fetishists—folks who figure out what others are eating for pennies a pop.

    Make Those Photos Drool-Worthy

    3 essential tricks to irresistible food shots

    1. Head for the Sun. If you know you’re going to be shooting your meal (covertly and politely, of course) try to get a window seat. “Natural light that’s filtered through glass is always best,” says Penny de los Santos, a contributing photographer for Saveur.

    2. Kill the Flash. If it’s dark and you’re shooting with a phone, your flash will make the most gourmet meal look like cafeteria food. Ms. de Los Santos recommends a dinner companion illuminate the dish with a candle, a flashlight app or multiple phones. It’s geeky, but it works.

    3. Get the Big Picture.Everyone wants to shoot juices oozing out of a burger, but if you get too close it becomes abstract. For good composition, Ms. de Los Santos says to pull back and give the subject a little space. Food you can identify is always more appetizing.

    With 50,000 downloads since its April launch, Meal Snap already has a cult following, myself included. But while most probably use it as an easy way to keep a meal journal and track their caloric intake, it was more of a game to me—I simply wanted to outsmart these “Turks.”

    Starting easy, I snapped a Big Mac. The app immediately recognized it and returned the calorie range as 396-594. McDonald’s lists it at 540. Close enough. Then I tried to stump it with ethnic food. The mechanical Turk, not from Bangalore but apparently of Cajun heritage, identified Indian dal as “shrimp étouffée, 445-667 calories.” When a key lime pie returned “milk peas, 67-100 calories,” I thought, what are “milk peas” and exactly what part of Mechanical Turkey is this person from?

    Feeling a little sorry for this Turk, I helped him out by submitting an optional caption for my next meal of rabbit roulade with cheese-stuffed squash blossom. A swift response gave a tight range of 239-258 calories, deemed correct by CalorieKing.com. One last trick, a plate of dog biscuits, fetched: “Whoops! Not food!”

    Meal Snap can be a useful, if sometimes unreliable, diet tracker. But for me, it’s a sport, an entertainment and more importantly, proof that technology is really only as good as the “magicians” behind it.

    Read more: http://online.wsj.com/article/SB10001424052702304432304576369983237942502.html#ixzz1P5pFmUA3

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    Ovarian Cancer Screening Update

    Sunday, June 12, 2011 // Uncategorized

    Unfortunately, there is no good screening test or combination of screening tests  for ovarian cancer as this latest study concludes.  This is a summary from the ACP Observer:

    Screening may not decrease ovarian cancer mortality rates, study finds

    Screening for ovarian cancer with CA-125 tests and transvaginal ultrasound may not reduce mortality rates, a new study suggests.

    To determine the effect of ovarian cancer screening on mortality, researchers from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening trial randomly assigned women to an intervention group (screening with CA-125 and transvaginal ultrasound at baseline, annual transvaginal ultrasound for three additional years, and annual CA-125 for five additional years) or a usual care group (usual medical care with no annual screening). The study was conducted at 10 U.S. screening centers from November 1993 to July 2001. The primary outcome measure was death from ovarian cancer, and secondary outcome measures were incidence of ovarian cancer and complications of screening and diagnostic tests. The study was published early online June 4 by the Journal of the American Medical Association.

    Study participants ranged in age from 55 to 74 years at study entry and were followed for a median of 12.4 years (range, 10.9 to 13.0 years). Overall, 39,105 women were assigned to the intervention group and 39,111 were assigned to the usual care group. Two hundred twelve women in the intervention group and 176 in the usual care group were diagnosed with ovarian cancer (5.7 per 10,000 person-years and 4.7 per 100,000 person-years, respectively; rate ratio [RR], 1.21; 95% CI, 0.99 to 1.48), and 118 and 100 women, respectively, died of the disease (3.1 per 10,000 person-years vs. 2.6 per 10,000 person-years; RR for mortality, 1.18; 95% CI, 0.82 to 1.71).

    A total of 3,285 women in the intervention group had false-positive results on screening; of these, 1,080 had surgical follow-up, and of these, 163 had one or more serious complications, defined as infection, direct surgical complications, cardiovascular or pulmonary complications, or other. In the usual care group, 2,914 women died of causes other than ovarian, colorectal and lung cancer versus 2,924 women in the intervention group (76.2 per 10,000 person-years vs. 76.6 per 10,000 person-years; RR, 1.01; 95% CI, 0.96 to 1.06).

    The authors acknowledged that their study did not collect data on all aspects of treatment, such as type of systemic therapy. They also noted that although the study was powered to detect a mortality reduction of 35%, smaller effect sizes could also be considered worthwhile from a public health perspective, and that the screening tests studied might be more useful if different cutoffs were used to define positive results. However, they concluded that in the U.S., the screening strategy used in the PLCO trial “does not reduce disease-specific mortality in women at average risk for ovarian cancer but does increase invasive medical procedures and associated harms.”

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    Is Raising HDL a Good Idea?

    Sunday, June 5, 2011 // Uncategorized

    Once upon a time there was cholesterol.  Higher levels were associated with a higher risk of  heart attacks.  Then cholesterol was broken down into LDL (low density lipoprotein) and HDL (high density lipoprotein).  Elevated amounts of LDL and lower levels of HDL were found to be risk factors.  Statins such as Lipitor, Crestor and Zocor lower LDL levels and reduce the risk of heart attacks.  Their ability to raise HDL is less pronounced.  Lipitor in higher doses may lower HDL cholesterol.  Niacin has been promoted as one of the most potent agents at raising HDL cholesterol, though it is trickier to take than statins due to it’s side effects.   If we can lower LDL and raise HDL then patients should do better, right?  Not necessarily according to this recent study.

    From Journal Watch:

    Trial of Niacin to Increase HDL in High-Risk Patients Stopped Early After Showing No Benefit
    A major government study has been stopped early because it showed no benefit to raising HDL levels with niacin in patients at high risk for cardiovascular events, the National Heart, Lung, and Blood Institute announced Thursday.
    In the AIM-HIGH trial, the rate of MI, stroke, hospitalization for acute coronary syndrome, or revascularization among some 3400 patients did not differ between a group taking statin plus high-dose niacin and one taking statin plus placebo during 32 months’ follow-up. All patients had well-controlled LDL levels at entry, but had low HDL levels and high triglycerides.
    Asked to comment, Dr. Harlan Krumholz of Journal Watch Cardiology wrote: “This study reinforces that medications that change a risk factor do not necessarily change patient risk. Niacin, fibrates, and ezetimibe have so far failed to show that they improve patient outcomes in patients on statins. Be on guard for claims that are based only on how an intervention affects a risk factor — we need studies that show us the effect of these drugs on outcomes that patients experience.”

    For those who want more information here is the news release from the NIH:

    Embargoed for Release
    Thursday, May 26, 2011
    11 a.m. EDT

    Contact:
    NHLBI Communications Office
    301-496-4236

    NIH stops clinical trial on combination cholesterol treatment

    Lack of efficacy in reducing cardiovascular events prompts decision

    The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health has stopped a clinical trial studying a blood lipid treatment 18 months earlier than planned. The trial found that adding high dose, extended-release niacin to statin treatment in people with heart and vascular disease, did not reduce the risk of cardiovascular events, including heart attacks and stroke.

    Participants were selected for AIM-HIGH because they were at risk for cardiovascular events despite well-controlled low-density lipoprotein (LDL or bad cholesterol). Their increased risk was due to a history of cardiovascular disease and a combination of low high-density lipoprotein (HDL or good cholesterol) and high triglycerides, another form of fat in the blood. Low HDL and elevated triglycerides are associated with an increased risk of cardiovascular events. While lowering LDL decreases the risk of cardiovascular events, it has not been shown that raising HDL similarly reduces the risk of cardiovascular events.

    During the study’s 32 months of follow-up, participants who took high dose, extended-release niacin and statin treatment had increased HDL cholesterol and lowered triglyceride levels compared to participants who took a statin alone. However, the combination treatment did not reduce fatal or non-fatal heart attacks, strokes, hospitalizations for acute coronary syndrome, or revascularization procedures to improve blood flow in the arteries of the heart and brain.

    “Seeking new and improved ways to manage cholesterol levels is vital in the battle against cardiovascular disease,” said Susan B. Shurin, M.D., acting director of the NHLBI. “”This study sought to confirm earlier and smaller studies. Although we did not see the expected clinical benefit, we have answered an important scientific question about treatment for cardiovascular disease. We thank the research volunteers whose participation is key in advancing our knowledge in this critical public health area, and the dedicated investigators who conducted the study.”

    The AIM-HIGH trial, which stands for Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health, enrolled 3,414 participants in the United States and Canada with a history of cardiovascular disease who were taking a statin drug to keep their LDL cholesterol low. Study participants also had low HDL cholesterol and high triglycerides, which meant that they were at significant risk of experiencing future cardiovascular events. Niacin, also known as Vitamin B3, has long been known to raise HDL and lower triglycerides. Eligible participants were randomly assigned to either high dose, extended-release niacin (Niaspan) in gradually increasing doses up to 2,000 mg per day (1,718 people) or a placebo treatment (1,696 people). All participants were prescribed simvastatin (Zocor), and 515 participants were given a second LDL cholesterol-lowering drug, ezetimibe (Zetia), in order to maintain LDL cholesterol levels at the target range between 40-80 mg/dL.

    The NHLBI funded the AIM-HIGH study with additional support from Abbott Laboratories, a pharmaceutical company based in Abbott Park, Ill. Abbott also provided Niaspan and Merck Pharmaceuticals, based in Whitehouse Station, N.J., provided Zocor. All drugs used in the study were approved for marketing in the United States and Canada and have been on the market for many years.

    Researchers began recruiting participants in early 2006. The study was scheduled to finish in 2012. The average age of the participants was 64 years. Pre-existing medical conditions included coronary artery disease (92 percent); metabolic syndrome, which is a cluster of risk factors for heart disease (81 percent); high blood pressure (71 percent); and diabetes (34 percent). More than half of participants reported having a heart attack prior to entering the study.

    The rationale for the AIM-HIGH study was based in part on a large number of observational studies that consistently showed that low HDL cholesterol increases the risk of cardiovascular events in men and women, independent of high LDL cholesterol. In addition, previous small clinical studies showed that relatively high residual cardiovascular risk exists among patients with cardiovascular disease, low HDL cholesterol, and high triglycerides despite intensive management of LDL cholesterol.

    However, efforts to find HDL-raising treatments that actually reduce this residual risk have thus far proved disappointing. Fenofibrate, an HDL-raising drug, failed to reduce the rate of cardiovascular events in patients with diabetes in the Action to Control Cardiovascular Risk in Diabetes (ACCORD trial) despite favorable effects on HDL and triglycerides. Another HDL-raising drug, torcetrapib, actually increased the rate of cardiovascular events in the Investigation of Lipid Level Management to Understand its Impact in Atherosclerotic Events (ILLUMINATE) trial despite lowering LDL and triglycerides and raising HDL levels, as intended.

    Earlier studies of niacin had shown more favorable results. Unlike AIM-HIGH, the earlier studies were not designed specifically to evaluate the impact of raising HDL on the risk of cardiovascular events while maintaining excellent LDL control. Several other trials testing this hypothesis, including a large international trial of high dose, extended-release niacin, are still ongoing.

    As is customary in clinical trials, the NHLBI established an independent data and safety monitoring board (DSMB) to monitor trial progress and participant safety. At a regularly scheduled meeting on April 25, 2011, the study’s DSMB concluded that high dose, extended-release niacin offered no benefits beyond statin therapy alone in reducing cardiovascular-related complications in this trial. The rate of clinical events was the same in both treatment groups, and there was no evidence that this would change by continuing the trial. For this reason, the DSMB recommended that the NHLBI end the study.

    The DSMB also noted a small and unexplained increase in ischemic stroke rates in the high dose, extended-release niacin group. This contributed to the NHLBI acting director’s decision to stop the trial before its planned conclusion. During the 32-month follow-up period, there were 28 strokes (1.6 percent) reported during the trial among participants taking high dose, extended-release niacin versus 12 strokes (0.7 percent) reported in the control group. Nine of the 28 strokes in the niacin group occurred in participants who had discontinued the drug at least two months and up to four years before their stroke. Previous studies do not suggest that stroke is a potential complication of niacin, and it remains unclear whether this trend in AIM-HIGH arose by chance, was related to niacin administration or some other issue.

    All AIM-HIGH study participants have been informed of the results and will be scheduled for clinic visits within the next 2.5 months. Participants will be followed for an additional 12 to 18 months.

    “Patients who were not in the AIM-HIGH trial should not stop taking high dose, extended-release niacin without talking to their doctor first,” said Shurin.

    “The lack of effect on cardiovascular events is unexpected and a striking contrast to the results of previous trials and observational studies,” said Jeffrey Probstfield, M.D., AIM-HIGH co-principal investigator and professor of medicine and epidemiology at the University of Washington, Seattle. “The AIM-HIGH findings do not support the trial’s hypothesis that, in the population studied, adding extended-release niacin to simvastatin in participants with well-controlled LDL cholesterol can provide additional clinical benefit.”

    “The results from AIM-HIGH should not be extrapolated to apply to potentially higher-risk patients such as those with acute heart attack or acute coronary syndromes, or in patients whose LDL cholesterol is not as well-controlled as those in AIM-HIGH,” said William E. Boden, M.D., AIM-HIGH co-principal investigator and professor of medicine and preventive medicine at the University at Buffalo, N.Y.

    The niacin tested in the study is a proprietary formulation used in doses of 500-2,000 milligrams (mg), manufactured by Abbott Laboratories and approved and regulated by the U.S. Food and Drug Administration. Low doses of niacin, typically 20 to 100 mg, can be found in multivitamin formulations available without a prescription. The FDA regulates the use of high doses of niacin (over 500 mg), which is approved by prescription for helping treat low HDL cholesterol and/or high triglycerides. At prescription-level doses, some people experience flushing. The extended-release formulation of niacin tested in AIM-HIGH was intended to help reduce the likelihood of flushing.

    An estimated 1 in 7 Americans has high blood cholesterol. It is a major risk factor for cardiovascular disease, which kills 800,000 Americans a year. Cholesterol can build up in the walls of arteries and cause them to narrow, a condition known as atherosclerosis.

    “As we continue to search for new approaches to treating cholesterol problems, it is important to remember the value of existing treatments. The key to treating high cholesterol so patients can reduce their risk of cardiovascular disease is to lower the level of LDL cholesterol, through well-established drug treatments such as statins and lifestyle changes,” said Patrice Desvigne-Nickens, M.D., NHLBI project officer for the AIM-HIGH trial.

    The AIM-HIGH investigators will now focus on completing data collection and analysis. The preliminary outcomes of the study are expected to be reported at scientific meetings in the fall of 2011.

    Find more information about this clinical trial (NCT00120289) at www.clinicaltrials.gov.

    These patients had elevated cholesterol tiglycerides along with HDL.  Do thes results apply to those without that triad?  That remains to be seen.  for now, I will be more cautious about recommending Niacin which can raise blood gluocse and uric acid levels.

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