Stampfer MJ Research Articles

Cardiovascular Harm From Egg Yolk and Meat: More Than Just Cholesterol and Saturated Fat.

Cardiovascular Harm From Egg Yolk and Meat: More Than Just Cholesterol and Saturated Fat.

FRIED FOOD AND POSSIBLE HEALTH HAZARDS

FRIED FOOD AND POSSIBLE HEALTH HAZARDS

Aspirin and Delayed Chemoprevention of Colorectal Cancer.

Featured articles: Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC. Aspirin use and the risk for colorectal cancer and adenoma in male health professionals. Ann Intern Med 1994;121:241–6.2 Giovannucci E, Egan KM, Hunter DJ, Stampfer MJ, Colditz GA, Willett WC, Speizer FE. Aspirin and the risk of colorectal cancer in women. N Engl J Med 1995;333:609–14.3 In the 1980s, emerging epidemiologic evidence suggested that risk of colorectal cancer was lower in aspirin users. This finding drew interest from researchers. The Physicians' Health Study was a randomized, double-blinded, placebo-controlled trial of aspirin (325 mg taken every other day) and β-carotene. The trial was terminated in 1988 after 4.7 years because of a significant reduction in myocardial infarction in aspirin users. The investigators resourcefully used the data to consider aspirin use in relation to colorectal cancer risk. They published in 1993 that aspirin did not reduce colorectal cancer incidence during 5 years of randomized treatment and follow-up evaluation (1). This disappointing result …

Menopausal Hormone Therapy and Cardiovascular Disease: Unraveling the Role of Age and Time Since Menopause Onset.

Featured Article: Stampfer MJ, Colditz GA, Willett WC, Manson JE, Rosner B, Speizer FE, Hennekens CH. Postmenopausal estrogen therapy and cardiovascular disease: ten-year follow-up from the Nurses' Health Study. N Engl J Med 1991;325:756–2.3 A quarter century has elapsed since the publication of the article featured here, itself an extension of a 1985 paper on the same topic. These findings of a marked lowering of coronary heart disease (CHD)4 stimulated the Women's Health Initiative (WHI) trial. CHD is uncommon at menopause, so to increase statistical power, the WHI enrolled older women (range 50–79 years). However, the estrogen-progestin (1) and the estrogen-only trials were terminated early because of risk (2). The divergence of the trial and observational findings generated intense discussion that has not fully abated. A knee-jerk reaction was that observational studies were flawed, and one could only believe data from trials. A more reasoned reaction was to explore possible reasons. One explanation …

Sophisticated sleep improves our brains: Our advanced cognitive and social skills might derive from the evolution of improved sleep quality; today, sleep therapy could help with mental health issues and learning.

In the past decades, sleep researchers have been quietly accumulating knowledge about the physiology of sleep. Without any real health application for this knowledge, however, the public and the press have slept blissfully through most of their breakthroughs. Yet, recent findings about the evolution of sleep in humans and the effects of sleep disruption on human health seem to have finally woken the public up. A recent paper from David Samson and Charles Nunn, evolutionary anthropologists from Duke University in the USA, puts forward the hypothesis that humans have evolved more efficient sleep patterns than other primates and that this is because “[e]arly humans experienced selective pressure to fulfill sleep needs in the shortest time possible” [1]. This efficient slumber, the authors argue, might have contributed to setting our ancestors on the evolutionary path toward human civilization. The New York Times , among other newspapers, covered the publication, which follows in the wake of research indicating that human sleep patterns have stayed largely stable during the course of human evolution, from hunter‐gatherers to modern city dwellers [2]. Both of these insights provide evolutionary context for the health impact of too little sleep, with both epidemiological and clinical research showing that sleep disruption has a negative effect on health and well‐being. More recently, however, there is evidence that sleep has distinctly positive therapeutic potential to treat a variety of phobias and other psychotic conditions. The evolutionary study that attracted media attention raises interesting questions about the co‐evolution of sleep and human cognitive faculties. Samson and Nunn suggest that sleep became subject to strong selective pressures—“including increased predation risk […] threats from intergroup conflict, and benefits arising from increased social interaction” [1]—when our ancestors moved down from the trees and onto the savannah. As a result, …

Outcome of a public consultation on the Draft Scientific Opinion of the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) on Dietary Reference Values for folate

Outcome of a public consultation on the Draft Scientific Opinion of the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) on Dietary Reference Values for folate

Petar Alaupovic

Petar Alaupovic, an internationally renowned biochemist and lipidologist, died on January 30, 2014, in Oklahoma City at the age of 91 years. Dr Alaupovic was a founder of the modern field of lipoproteins whose ideas continue to have an impact on its development. He performed research and taught at Oklahoma Medical Research Foundation since 1960. In 1964, Dr Alaupovic, known to his colleagues as Dr A or Pierre, proposed a revolutionary new classification system for lipoproteins. Until that time, the classification of lipoproteins focused on the physical properties of lipoproteins, emphasizing the lipid component and the size of the lipoprotein particle. However, Dr Alaupovic considered the protein part to have great biological importance that directed every step in the metabolism of lipoproteins and determined their effects on atherosclerosis. When he began his research on lipoproteins, there were considered to be just 2 apolipoproteins, apolipoprotein B and apolipoprotein A. Using immunologic and protein chemistry techniques, he isolated and characterized several additional apolipoproteins associated with lipoproteins. He proposed the ABC nomenclature for apolipoproteins, which initially included apolipoproteins A-I, A-II, B, C-I, C-II, C-III, D, and E. Most important to the subsequent progress in the field of lipoprotein, he subdivided the major lipoprotein classes, apolipoprotein A-I …

Association of HLA-DRB1*15 and HLA-DQB1* 06 with SLE in Saudis

BACKGROUND AND OBJECTIVESSystemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by humoral autoimmunity. The etiology of SLE is thought to be multifactorial including environmental, hormonal, and genetic factors. The human leukocyte antigen (HLA) has extensively been associated with the susceptibility to SLE; however, the association is heterogeneous among different ethnic groups. The aim of this study was to determine the association of HLA-A, HLA-B, HLA-DRB1, and HLA-DQB1 with SLE susceptibility in the Saudi population.DESIGN AND SETTINGSA total of 86 consecutive SLE patients attending the rheumatology clinic at King Abdulaziz Medical City, Riyadh, were recruited for this study.METHODSHLA types were determined by the polymerase chain reaction sequence-specific oligonucleotide (PCR-SSP) method in 86 patients and 356 control subjects.RESULTSThe following HLA alleles were found to be positively associated with SLE: HLA-A*29 (OR=2.70; 95% CI=1.03–7.08; P=.0035), HLA-B*51 (OR=1.81; 95% CI=1.17–2.79; P=.0066), HLA-DRB1*15 (OR=1.45; 95% CI=0.98–2.29; P=.063), and HLA-DQB1*06 (OR=1.67; 95% CI=1.19–2.36; P=.0032), whereas HLA-DRB1*16 was negatively associated with the disease (OR=0.18; 95% CI=0.02–1.3; P=.055). HLA-DRB1*15 haplotypes were significantly associated with SLE (OR=2.01, 95% CI=1.20–3.68, P=.008); this was mainly due to the HLA-DRB1* 15-DQB1*06 association.CONCLUSIONSOur data suggest an association between MHC class I and class II (HLA-A*29, HLA-B*51, HLA-DRB1*15, and HLA-DQB1*06) and susceptibility to SLE in the Saudi population. HLA-DRB1*15-DQB1*06 haplotype showed the highest risk factor for the disease that is similar to what was seen in the African American patients, suggesting shared susceptibility genetic factors among these ethnic groups.

Exercise: important for prevention and treatment of disease

British Journal of Hospital MedicineVol. 72, No. 4 EditorialExercise: important for prevention and treatment of diseaseMike LoosemoreMike LoosemoreSearch for more papers by this authorMike LoosemorePublished Online:16 Aug 2013https://doi.org/10.12968/hmed.2011.72.4.186AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Department of Health (2004) At least five a week: Evidence on the impact of physical activity and its relationship to health. A report from the Chief Medical Officer. Department of Health, London Google ScholarDunn A, Trivedi MH, Kampert JB, Clark CG, Chambliss HO (2005) Exercise treatment for depression: efficacy and dose response. Am J Prev Med 28(1): 1–8 Crossref, Medline, Google ScholarHu FB, Meir J, Stampfer MJ et al. (2000) Physical activity and risk of stroke in women. JAMA 283(22): 2961–7 Crossref, Medline, Google ScholarSwedish National Institute of Public Health (2010) Physical Activity in the Prevention and Treatment of Disease. Professional Associations for Physical Activity, Sweden Google ScholarWei M, Gibbons LW, Kampert JB, Nichaman MZ, Blair SN (2000) Low cardiorespiratory fitness and physical inactivity as predictors of mortality in men with type 2 diabetes. Ann Intern Med 132(8): 605–11 Crossref, Medline, Google Scholar FiguresReferencesRelatedDetailsCited byThe importance of exercise for patients with kidney diseaseAngela Lumsdon26 November 2014 | Journal of Renal Nursing, Vol. 6, No. 6EXERCISE IN KIDNEY DISEASE AND DIABETES: TIME FOR ACTION14 February 2012 | Journal of Renal Care, Vol. 38 1 April 2011Volume 72Issue 4ISSN (print): 1750-8460ISSN (online): 1759-7390 Metrics History Published online 16 August 2013 Published in print 1 April 2011 Information© MA Healthcare LimitedPDF download

Could Direct Inhibition of Inflammation Be the “Next Big Thing” in Treating Atherosclerosis?

The treatment of atherosclerosis during the past 2 decades has been focused on reductions in atherogenic lipids, such as low-density lipoprotein cholesterol, and, more recently, has moved toward attempting to increase high-density lipoprotein cholesterol. However, another major component of atherosclerosis is inflammation. Although long recognized in the laboratory, clinical investigators1 have more recently measured high-sensitivity C-reactive protein (hsCRP) in large clinical trials and linked higher levels with increased risk of mortality and cardiovascular events. This has led to intense interest in inflammation as a target for treatment, with the possibility that it could be the “next big thing” in managing atherosclerosis. See accompanying article on page 2256 With this information as a backdrop, the model of vascular injury used by Sarov-Blat et al2 allows initial testing of the effects of a novel antiinflammatory agent in patients with atherosclerosis. The paradigm of coronary stenting, leading to vascular injury and resulting in an inflammatory response that signals neointimal proliferation, and subsequent in-stent restenosis share many similar features of the inflammatory cascade that propagates atherosclerosis.3,4 Such extracellular stimuli are relayed to coordinated cellular responses through intracellular phosphorylation cascades, such as the mitogen-activated protein kinase (MAPK) pathways.5 So far, 4 classes of mammalian MAPK have been identified: extracellular signal–regulated kinases, c-jun N-terminal kinase or stress-activated protein kinase, extracellular signal–regulated kinase/big MAP kinase 1, and the p38 MAPKs.6 In their study, Sarov-Blat et al turn their attention to the inhibition of p38 MAPK using a newly developed agent to attenuate the inflammatory stimulus generated …

Establishing a Clinical Basis for hsCRP in the Prevention and Treatment of Cardiovascular Disease

Featured Articles: Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973–9.1 Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000;342:836–43.2 In the early 1990s, the concept that inflammation was an integral component of atherothrombosis was highly controversial and based almost entirely on bench observations (1). However, pioneering translational studies by Attilio Maseri, Brad Berk, Lewis Kuller, and others found that among smokers or those with acute or chronic ischemia, inflammatory biomarkers including C-reactive protein (CRP)3 were indicative of high vascular risk. Because concentrations of CRP and other acute-phase reactants increase after ischemia and are directly related to smoking, however, studies in these populations could not exclude the likelihood that increases in CRP were a result rather than a precedent for disease. The 2 articles highlighted here both dealt with the ability of inflammatory biomarkers in general, and high-sensitivity CRP (hsCRP) in particular, to predict vascular risk in otherwise healthy asymptomatic men and women—a relevant clinical issue, as half of all heart attacks and strokes occur among those with average or even low concentrations of cholesterol. The first paper derived from a large NIH-funded primary prevention trial comparing low-dose aspirin to placebo that was being conducted among 22 000 initially healthy American men by my epidemiologic mentor, Charles Hennekens. Working …

Polyphenols and Cholesterol Efflux

Despite strong evidence for an inverse association between high-density lipoprotein cholesterol (HDL-C) levels and cardiovascular risk,1 successful therapeutic strategies to target HDL have remained elusive. A recent Phase III clinical trial failed to show clinical benefit with the cholesteryl ester transfer protein inhibitor torcetrapib despite markedly increased HDL-C levels.2,3 This outcome reinforced a growing consensus that measurement of HDL-C alone may be an incomplete surrogate for the in vivo functionality of HDL and the clinical efficacy of targeting HDL. The careful mechanistic assessment of HDL function has thus emerged as a potential way forward.4 Macrophage reverse cholesterol transport (RCT), the process by which cholesterol is transported from macrophage “foam” cells to the liver for ultimate fecal excretion, has been postulated to play a major role in HDL-mediated atheroprotection.5 Indeed, quantitative measures of macrophage RCT are more strongly associated with atherosclerosis than plasma HDL-C concentrations in mice.6 The first critical step of macrophage RCT involves efflux of cellular cholesterol to circulating HDL particles. Research in recent years has documented a specific role for the macrophage transporters ATP-binding cassette subfamilies A1 and G1 (ABCA1 and ABCG1) in cholesterol efflux (see the Figure). These findings have stimulated efforts to target the macrophage at the cellular level as a means of enhancing overall RCT. For example, pharmacological agonism of the liver X receptor (LXR) upregulates both ABCA1 and ABCG1 expression,7,8 promotes macrophage cholesterol efflux ex vivo and RCT in vivo, …

Leapfrogging Data

Properly designed and conducted randomized controlled clinical trials (RCTs) are the premier tool for both testing mechanistic hypotheses and critically ascertaining the risks and benefits of a therapy or strategy for clinical care. The sample size of a trial is mainly a function of the rates of its primary objectives and the presumed influence of the intervention. Trials focusing on a primary outcome variable that can be readily quantified in each subject, such as blood pressure or plasma cholesterol levels, require substantially fewer participants and shorter durations to determine whether their predefined measurement is altered compared with a morbidity and mortality trial. Trials designed to determine whether clinical prognosis is altered by an intervention depend on the proportion of patients experiencing the predefined adverse clinical event(s) and often require 100s-fold–greater patient-time exposures to test their primary hypothesis and provide even modest information about safety. These resource-intense morbidity and mortality trials are generally only performed when information from observational studies as well as smaller mechanistic and surrogate- outcomes RCTs are so highly supportive of a favorable outcome that they justify the effort. Despite this understandable stacking of the cards with the best available information, many of the morbidity and mortality trials conducted to test for a potential favorable impact of an intervention conclude by not supporting the prestudy hypothesis-generating data.1 The lessons in humility offered by these neutral or negative outcomes trials underscore the importance of obtaining crucial risk–benefit data before widespread adoption of even an apparently favorable therapy.2 Articles pp 2506 and 2515 For rational therapeutic decision making, we would ideally like to have both a framework of reliable mechanistic information and robust clinical outcomes and safety data. Sometimes major clinical outcomes trials are designed with a complement of embedded ancillary trials to generate a more complete picture …

Dietary n-3 Polyunsaturated Fatty Acids Enhance Hormone Ablation Therapy in Androgen-Dependent Prostate Cancer

Hormone ablation therapy typically causes regression of prostate cancer and represents an important means of treating this disease, particularly after metastasis. However, hormone therapy inevitably loses its effectiveness as tumors become androgen-independent, and this conversion often leads to death because of subsequent poor responses to other forms of treatment. Because environmental factors, such as diet, have been strongly linked to prostate cancer, we examined the affects of dietary polyunsaturated fatty acids (PUFAs; at 1.5 wt%) on growth of androgen-dependent (CWR22) and androgen-independent (CWR22R) human prostatic cancer xenografts, the acute response of CWR22 tumors to ablation therapy, and their progression to androgen independence. Significant diet-induced changes in tumor n-3 or n-6 PUFA content had no affect on CWR22 or CWR22R tumors growing with or without androgen support, respectively. However, dietary changes that increased tumor eicosapentaenoic acid and linoleic acid content enhanced responses to ablation therapy, measured by cancer cell apoptosis and mitosis. In addition, relapse to androgen-independent growth (measured by renewed increases in tumor volume and serum prostate-specific antigen after ablation) positively correlated with tumor arachidonic acid content. There was no correlation between expression of 15-lipoxygenase isozymes or their products and tumor growth or responses to ablation. In conclusion, dietary n-3 PUFA may enhance the response of prostate cancer to ablation therapy and retard progression to androgen-independent growth by altering tumor PUFA content.

Pregnancy Is an Essential Spontaneous Screening Stress Test for the Risk of Early Stroke in Women

HomeStrokeVol. 39, No. 8Pregnancy Is an Essential Spontaneous Screening Stress Test for the Risk of Early Stroke in Women Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBPregnancy Is an Essential Spontaneous Screening Stress Test for the Risk of Early Stroke in Women Lionel Carbillon Lionel CarbillonLionel Carbillon Department of Obstetrics and Gynaecology, Assistance Publique Hopitaux de Paris, Hopital Jean Verdier, University of Paris 13, Paris, France Search for more papers by this author Originally published26 Jun 2008https://doi.org/10.1161/STROKEAHA.107.514190Stroke. 2008;39:e138Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 26, 2008: Previous Version 1 To the Editor:Boden-Albala et al1 evaluated the effect of the metabolic syndrome on stroke risk in a 3298 stroke-free community residents prospectively followed-up for a mean of 6.4 years. They observed that this risk was greater among women (hazard ratios=2.0; 95% CI, 1.3 to 3.1) than men (hazard ratios=1.1; 95% CI, 0.6 to 1.9). However, like others,2,3 they did not analyze the course of the pregnancies during the meantime in these women.However, pregnancy may be considered an essential metabolic and vascular spontaneous screeening stress test for early stroke and coronary heart disease in women,4 and the metabolic syndrome is a possible underlying mechanism common to cardiovascular disease and pre-eclampsia.5Ray et al6 assessed the risk of premature cerebrovascular, coronary, or peripheral artery disease over a 14-year period. They showed that this risk was higher after pre-eclampsia with placental dysfunction, and that the future risk of cardiovascular disease in these women was higher when they presented with the features of the metabolic syndrome. Their study supported that the future risk of cardiovascular disease was highest in women who had pre-eclampsia in combination with poor fetal growth. Smith et al7 also demonstrated from a population-based study that the subsequent maternal risk of ischemic heart disease during a 15- to 19-year follow-up was associated with pre-eclampsia.Thus, further studies that aim to assess the risk factors of stroke in women should collect detailed data on the pregnancy course and outcomes. Indeed, after a placentally complicated pregnancy, women are at increased risk of later cerebrovascular and cardiovascular complications. The onset of the metabolic syndrome during pregnancies subsequently complicated by pre-eclampsia could define the highest-risk group. In these women, the postpartum is a favorable period for a cardiovascular and metabolic check, counseling, and may afford women the opportunity to take action through diet and lifestyle.1 Boden-Albala B, Sacco RL, Lee HS. Metabolic Syndrome and Ischemic Stroke Risk. Northern Manhattan Study. Stroke. 2008; 39: 30–35.LinkGoogle Scholar2 Daviglus ML, Stamler J, Pirzada A Yan LL, Garside DB, Liu K, Wang R, Dyer AR, Lloyd-Jones DM, Greenland P. Favorable cardiovascular risk profile in young women and long-term risk of cardiovascular and all-cause mortality. JAMA. 2004; 292: 1588–1592.CrossrefMedlineGoogle Scholar3 Stampfer MJ, Hu FB, Manson JE, Rimm EB, Willett WC. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 2000; 343: 16–22.CrossrefMedlineGoogle Scholar4 Newstead J, von Dadelszen P, Magee LA. Preeclampsia and future cardiovascular risk. Expert Rev Cardiovasc Ther. 2007; 5: 283–294.CrossrefMedlineGoogle Scholar5 Harskamp RE, Zeeman GG. Preeclampsia: at risk for remote cardiovascular disease. Am J Med Sci. 2007; 334: 291–295.CrossrefMedlineGoogle Scholar6 Ray JG, Vermeulen MJ, Schull MJ, Redelmeier DA. Cardiovascular health after maternal placental syndromes (CHAMPS): population-based retrospective cohort study. Lancet. 2005; 366: 1797–1803.CrossrefMedlineGoogle Scholar7 Smith GC, Pell JP, Walsh D. Pregnancy complications and maternal risk of ischaemic heart disease: a retrospective cohort study of 129,290 births. Lancet. 2001; 357: 2002–2006.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Valdés G (2022) Focus on today’s evidence while keeping an eye on the future: lessons derived from hypertension in women, Journal of Human Hypertension, 10.1038/s41371-021-00652-y, 36:10, (882-886), Online publication date: 1-Oct-2022. Wang Y, Mínguez-Alarcón L, Gaskins A, Missmer S, Rich-Edwards J, Manson J, Pan A and Chavarro J (2021) Association of spontaneous abortion with all cause and cause specific premature mortality: prospective cohort study, BMJ, 10.1136/bmj.n530, (n530) Eliseev E, Doroshenko D, Averkov O, Konysheva O, Kamchatnov P and Zubarev A (2017) Difficulties in the diagnosis of stroke in pregnant women, Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova, 10.17116/jnevro20171173220-25, 117:3. Vyp. 2, (20), . Akhvlediani K, Logutova L, Travkina A, Petrukhin V, Vlasov P, Lubnin A, Melnikov A and Budykina T (2015) Ischemic stroke and pregnancy, Rossiiskii vestnik akushera-ginekologa, 10.17116/rosakush201515665-71, 15:6, (65), . August 2008Vol 39, Issue 8 Advertisement Article InformationMetrics https://doi.org/10.1161/STROKEAHA.107.514190PMID: 18583559 Originally publishedJune 26, 2008 PDF download Advertisement

Weight Loss and Blood Pressure Control (Pro)

Overweight is an increasingly prevalent condition throughout the world. Current estimates, which are probably conservative, indicate that at least 500 000 000 people worldwide are overweight as defined by a body mass index (BMI) of between 25.0 and 29.9 and an additional 250 000 000 are obese with a BMI of 30.0 or higher.1 In the United States, recent data indicate that as much as 66% of the adult population is overweight or obese.2 Overweight and obesity are established risk factors for cardiovascular disease (CVD), stroke, noninsulin dependent diabetes (NIDDM), certain cancers, and numerous other disorders.3,4,5,6,7 It is also a risk factor for hypertension.8 Hypertension, defined as a systolic blood pressure in excess of 140 mm Hg or a diastolic blood pressure higher than 90 mm Hg, is also a globally increasing public health concern. Roughly 1 billion individuals worldwide are estimated to exhibit clinically significant elevated blood pressure with about 50 million of those residing in the United States.8 Hypertension, in turn, is associated with increased risk for CVD, stroke, renal disease, and all-cause mortality.9,10,11,12 The JNC VII report defines Stage 1 hypertension as blood pressure levels between 140 and 159 mm Hg systolic and 90 and 99 diastolic. Additionally, the report establishes a category of Prehypertension (Systolic blood pressure between 120 and 140 mm Hg or diastolic between 80 and 89 mm Hg). These 2 blood pressure classifications are deemed to be appropriate primary targets for lifestyle modification interventions, including weight loss. Higher levels of blood pressure, or stage 1 hypertension that is maintained over a long period, should be addressed primarily with medications or other physician directed treatments. There is a positive relationship between overweight or obesity and blood pressure and risk for hypertension. As early as the 1920s, a significant …

Impaired Fetal Growth, Cardiovascular Disease, and the Need to Move on

The final step in the acceptance of a new medical hypothesis is often the approval of significant funding to investigate it. In the case of developmental programming (ie, the notion that the in utero environment determines susceptibility to many diseases later in life), this has recently come in the form of support by the US Congress for the National Children’s Study, a $3 billion project to follow the impact of environmental factors before, during, and after pregnancy on disease manifestation in some 100 000 children up to the age of 25 years.1 This initiative will, no doubt, yield a wealth of correlative data and identify many new factors potentially affecting developmental programming. Article p 405 Much of the concept underlying the National Children’s Study stems from the pioneering work of Barker and colleagues,2 whose epidemiological observation of increased cardiovascular risk in children with low birth weight has spurred a large number of retrospective studies during the past 30 years. Despite some conflicting results, most of these studies support the notion that reduced birth weight is indeed associated with increased hypertension, diabetes mellitus, and cardiovascular disease. However, the strong correlation between birth weight and duration of gestation, plus the fact that a short gestation also may be associated with cardiovascular risk,3 poses the question to what extent low birth weight is truly responsible. In this issue of Circulation , an article by Kaijser and coworkers4 at the Karolinska Institute in Stockholm provides a convincing answer. By scanning 250 000 records of birth at 4 major delivery units in Sweden between 1925 and 1949, they identified a cohort of 6437 subjects, which included 2937 children born preterm (<37 weeks of gestation) and 2181 with a birth weight <2000 g for girls or <2100 g for boys. During the …

Exercise and cardiovascular risk reduction: time to update the rationale for exercise?

although it is generally accepted that the promotion of exercise accords with clinical best practice, the anecdotal experience of many primary care physicians, cardiologists, and exercise physiologists is that, even when exercise prescriptions are adhered to, risk factors often fail to demonstrate

Alcohol, wine, and vascular diseases: an abundance of paradoxes

the “french paradox” is usually defined as a low rate of coronary artery disease (CAD) in France despite high prevalence of the usual CAD risk traits. In 1819 Dr. Samuel Black, an Irish physician interested in angina pectoris and perceptive about epidemiologic aspects, wrote what is probably the

Diet and Primordial Prevention of Cardiovascular Disease in Children and Adolescents

It is now clear that the process of atherosclerosis begins in childhood. A series of pathology studies, starting with autopsy examination of young soldiers killed in combat in the Korean War1 and the war in Vietnam2 to more recent studies such as the Pathobiologic Determinants of Atherosclerosis in Youth (PDAY) study3 and the Bogalusa study,4,5 have demonstrated that fatty streaks in the aorta and coronary arteries develop early in life and that even the more advanced and more concerning fibrous plaques are present in a proportion of adolescents and young adults. The PDAY and Bogalusa studies also have demonstrated that the traditional risk factors such as high body mass index, high blood pressure, and dyslipidemia are strongly associated with the presence and extent of arterial lesions.3,4 The Bogalusa cohort also has demonstrated that the presence of multiple risk factors is associated with an even higher risk for atherosclerotic lesions.5 Article p 1032 It is also well known that atherosclerotic cardiovascular disease is the most common cause of death in developed countries.6 Not uncommonly, the first clinical episode related to atherosclerosis is sudden cardiac death.7 Taken together, these data argue very strongly for the prevention of atherosclerosis and for prevention efforts to begin early in life. This might best be labeled primordial prevention because it is aimed at the prevention of development of risk factors in the first place. However, pediatric prevention of cardiovascular …