Hu FB Research Articles

THE NEED FOR OPTIMUM NUTRITIONAL STRATEGIES FOR CARDIOVASCULAR HEALTH IN PAKISTANI POPULATION

THE NEED FOR OPTIMUM NUTRITIONAL STRATEGIES FOR CARDIOVASCULAR HEALTH IN PAKISTANI POPULATION

Salivary pH, dental caries and Body Mass Index (BMI) in the middle school students in Eastern Makassar

Objective: This study aimed to assess the association of salivary pH, dental caries and body mass index (BMI) in middle school students in eastern MakassarMaterial and Methods: This study included 60 middle school students from two schools in eastern Makassar. Data were collected by filling out a questionnaire, weight and height measurement, dental examination, and saliva collection. Body mass index was calculated by dividing weight and height in kg/m2, saliva was collected by draining method, and salivary pH was measured with Saliva-Check Buffer (GC Japan). Decay Missing Filled-Teeth (DMF-T) indexes are used to assess dental caries. Statistical analysis was performed by chi-square and ANOVA with a significance of 0.05.Results: This study showed that overweight and obesity are more prevalent in female students than male students. Salivary pH in underweight students and overweight and obese students were lower compared to normal BMI students, while DMF-T score in underweight, overweight, and obese students were higher than the normal BMI students.Conclusion: It can be concluded that BMI have a significant association with salivary pH and DMF-T score.1. Wang L, Zhou B, Zhao Z, et al. Body-mass index and obesity in urban and rural China: findings from consecutive nationally representative surveys during 2004–18. Lancet 2021;398: 53-63.2. Garrouste-Orgeas M, Troché G, Azoulay E, et al. Body mass index. Intensive Care Med 2004;30: 437-443.3. Barlian B, Azhari, Pramanik F. Correlation between mandibular trabeculae bone density on panoramic radiograph and body mass index of men aged 5-35 years old. J Dentomaxillofac Sci 2018;3: 166-168.4. Bellagambi FG, Lomonaco T, Salvo P, et al. Saliva sampling: Methods and devices. An overview. TrAC-Trends Anal Chem 2020;124: 115781.5. Zalewska A, Kossakowska A, Taranta-Janusz K,et al. Dysfunction of salivary glands, disturbances in salivary antioxidants and increased oxidative damage in saliva of overweight and obese adolescents. J Clin Med 2020;9: 548.6. Mosca AC, Stieger M, Neyraud E, et al. How are macronutrient intake, BMI, ethnicity, age, and gender related to the composition of unstimulated saliva? A case study. J Texture Stud 2019;50: 53-61.7. Pannunzio E, Amancio OMS, Vitalle MSDS, et al. Analysis of the stimulated whole saliva in overweight and obese school children. Rev Assoc Méd Bras 2010;56: 32-36.8. Primasari A, Hulu KP. Dryness of the oral cavity in the salivary status of overweight women. J Homeop Nat Med 2019;5: 50-53.9. Al-Hussaini A, Bashir MS, Khormi M, et al. Overweight and obesity among Saudi children and adolescents: Where do we stand today?. Saudi J Gastroenterol 2019;25: 229.10. Hruby A, Hu FB. The epidemiology of obesity: A big picture. Pharmaco Economics 2015;33: 673-689. 11. Alshihri AA, Rogers HJ, Alqahtani MA, et al. Association between dental caries and obesity in children and young people: A Narrative Review. Int J Dent 2019;2019: 1-8. 12. Groth SW, Morrison-Beedy D. Obesity risk in urban adolescent girls: nutritional intentions and health behavior correlates. J NY State Nurses Assoc 2011;42: 15-28.13. Baliga S, Muglikar S, Kale R. Salivary pH: A diagnostic biomarker. J Indian Soc Periodontol 2013;17: 461.14. Anamaria B, Eugen B, Daniela E, et al. Interrelation between salivary pH, buffer capacity and dental caries in underweight, normal weight and overweight children. Revista de Chimie 2017;68: 1353-1356.

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

China's Belt and Road Initiative from a global health perspective.

China's Belt and Road Initiative from a global health perspective.

U-Shaped Association between Plasma Manganese Levels and Type 2 Diabetes.

Background:Manganese is both an essential element and a known toxicant, and it plays important roles in many mechanisms in relation to type 2 diabetes (T2D). However, epidemiological studies of this relationship are rare.Objective:We investigated the association between plasma manganese and newly diagnosed T2D as well as whether the association could be modified by manganese superoxide dismutase (MnSOD) polymorphisms.Methods:We conducted a case–control study of 3,228 participants in China: 1,614 T2D patients and 1,614 controls. Concentrations of plasma magnesium were measured, and all participants were genotyped for the MnSOD Val16Ala polymorphism (rs4880).Results:A U-shaped association was observed between plasma manganese and T2D, with increased odds ratios (ORs) in relation to either low or high plasma manganese levels. Compared with the middle tertile, the multivariate-adjusted ORs [95% confidence intervals (CIs)] of T2D associated with the lowest tertile and the highest tertile of plasma manganese were 1.89 (1.53, 2.33) and 1.56 (1.23, 1.97), respectively. In spline analysis, the U-shaped association was consistently indicated, with the lowest odds of T2D at the plasma manganese concentration of 4.95 μg/L. Minor allele frequencies (C allele) of the MnSOD Val16Ala polymorphism (rs4880) in the normal glucose tolerance (NGT) and the T2D groups were 13.57% and 14.50%, respectively. The MnSOD rs4880 polymorphism was not associated with T2D, and no interaction was found between plasma manganese and the MnSOD rs4880 polymorphism in relation to T2D.Conclusions:Our results suggested a U-shaped association between plasma manganese and T2D; both low and high levels of plasma manganese were associated with higher odds of newly diagnosed T2D. The U-shaped association was not modified by the MnSOD rs4880 polymorphism.Citation:Shan Z, Chen S, Sun T, Luo C, Guo Y, Yu X, Yang W, Hu FB, Liu L. 2016. U-shaped association between plasma manganese levels and type 2 diabetes. Environ Health Perspect 124:1876–1881; http://dx.doi.org/10.1289/EHP176

Urgent Care Needs Among Nonurgent Visits to the Emergency Department.

Urgent Care Needs Among Nonurgent Visits to the Emergency Department.

Genome-Wide Analysis of DNA Methylation and Cigarette Smoking in a Chinese Population.

Background:Smoking is a risk factor for many human diseases. DNA methylation has been related to smoking, but genome-wide methylation data for smoking in Chinese populations is limited.Objectives:We aimed to investigate epigenome-wide methylation in relation to smoking in a Chinese population.Methods:We measured the methylation levels at > 485,000 CpG sites (CpGs) in DNA from leukocytes using a methylation array and conducted a genome-wide meta-analysis of DNA methylation and smoking in a total of 596 Chinese participants. We further evaluated the associations of smoking-related CpGs with internal polycyclic aromatic hydrocarbon (PAH) biomarkers and their correlations with the expression of corresponding genes.Results:We identified 318 CpGs whose methylation levels were associated with smoking at a genome-wide significance level (false discovery rate < 0.05), among which 161 CpGs annotated to 123 genes were not associated with smoking in recent studies of Europeans and African Americans. Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs was significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAH biomarker for smoking.Conclusion:We identified DNA methylation markers associated with smoking in a Chinese population, including some markers that were also correlated with gene expression. Exposure to naphthalene, a byproduct of tobacco smoke, may contribute to smoking-related methylation.Citation:Zhu X, Li J, Deng S, Yu K, Liu X, Deng Q, Sun H, Zhang X, He M, Guo H, Chen W, Yuan J, Zhang B, Kuang D, He X, Bai Y, Han X, Liu B, Li X, Yang L, Jiang H, Zhang Y, Hu J, Cheng L, Luo X, Mei W, Zhou Z, Sun S, Zhang L, Liu C, Guo Y, Zhang Z, Hu FB, Liang L, Wu T. 2016. Genome-wide analysis of DNA methylation and cigarette smoking in Chinese. Environ Health Perspect 124:966–973; http://dx.doi.org/10.1289/ehp.1509834

Smoking harms

Practice NursingVol. 26, No. 10 EditorialSmoking harmsKelly DavisKelly DavisSearch for more papers by this authorKelly DavisPublished Online:30 Sep 2015https://doi.org/10.12968/pnur.2015.26.10.473AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References Morris S (2015) Is Britain ready for outdoor smoking bans? The Guardian. www.theguardian.com/society/2015/jul/22/outdoor-smoking-ban-britain (accessed 22 September 2015) Google ScholarPan A, Wang Y, Talaei M, Hu FB, Wu T (2015) Relation of active, passive, and quitting smoking with incident type 2 diabetes: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. doi: https://doi.org/10.1016/S2213-8587(15)00316-2 Crossref, Google ScholarPublic Health England (2015) Guidance: Smoking and quitting in England. http://tinyurl.com/ok8q59d (accessed 22 September 2015) Google Scholar FiguresReferencesRelatedDetails 2 October 2015Volume 26Issue 10ISSN (print): 0964-9271ISSN (online): 2052-2940 Metrics History Published online 30 September 2015 Published in print 2 October 2015 Information© MA Healthcare LimitedPDF download

Association of Urinary Concentrations of Bisphenol A and Phthalate Metabolites with Risk of Type 2 Diabetes: A Prospective Investigation in the Nurses’ Health Study (NHS) and NHSII Cohorts

Background: Prospective evidence regarding associations for exposures to bisphenol A (BPA) and phthalates with type 2 diabetes (T2D) is lacking.Objective: We prospectively examined urinary concentrations of BPA and phthalate metabolites with T2D risk.Methods: We measured BPA and eight major phthalate metabolites among 971 incident T2D case–control pairs from the Nurses’ Health Study (NHS) (mean age, 65.6 years) and NHSII (mean age, 45.6 years).Results: In the NHSII, BPA levels were not associated with incident T2D in multivariate-adjusted analysis until body mass index was adjusted: odds ratio (OR) comparing extreme BPA quartiles increased from 1.40 (95% CI: 0.91, 2.15) to 2.08 (95% CI: 1.17, 3.69; ptrend = 0.02) with such an adjustment. In contrast, BPA concentrations were not associated with T2D in the NHS (OR = 0.81; 95% CI: 0.48, 1.38; ptrend = 0.45). Likewise, urinary concentrations of total phthalate metabolites were associated with T2D in the NHSII (OR comparing extreme quartiles = 2.14; 95% CI: 1.19, 3.85; ptrend = 0.02), but not in the NHS (OR = 0.87; 95% CI: 0.49, 1.53; ptrend = 0.29). Summed metabolites of butyl phthalates or di-(2-ethylhexyl) phthalates were significantly associated with T2D only in the NHSII; ORs comparing extreme quartiles were 3.16 (95% CI: 1.68, 5.95; ptrend = 0.0002) and 1.91 (95% CI: 1.04, 3.49; ptrend = 0.20), respectively.Conclusions: These results suggest that BPA and phthalate exposures may be associated with the risk of T2D among middle-aged, but not older, women. The divergent findings between the two cohorts might be explained by menopausal status or simply by chance. Clearly, these results need to be interpreted with caution and should be replicated in future studies, ideally with multiple urine samples collected prospectively to improve the measurement of these exposures with short half-lives.Citation: Sun Q, Cornelis MC, Townsend MK, Tobias DK, Eliassen AH, Franke AA, Hauser R, Hu FB. 2014. Association of urinary concentrations of bisphenol A and phthalate metabolites with risk of type 2 diabetes: a prospective investigation in the Nurses’ Health Study (NHS) and NHSII Cohorts. Environ Health Perspect 122:616–623; http://dx.doi.org/10.1289/ehp.1307201

Is Plasma Pentadecanoic Acid a Reasonable Biomarker of Dairy Consumption?

Despite advances in biomedical research and clinical medicine, the burden of cardiovascular disease (CVD) remains extremely high.[1][1] This underscores the importance of primary prevention and the search for novel therapeutic strategies. Modifiable lifestyle factors, including dietary habits, play

FTO genotype and 2-year change in body composition and fat distribution in response to weight-loss diets: the POUNDS LOST trial. Diabetes 2012;61:3005–3011

Zhang X, Qi Q, Zhang C, Hu FB, Sacks FM, Qi L. FTO genotype and 2-year change in body composition and fat distribution in response to weight-loss diets: the POUNDS LOST trial. Diabetes 2012;61:3005–3011 In the print version of the article listed above, there was an omission of authors and their institutional affiliations. The POUNDS LOST study, on which this project was based, was jointly conducted by the Harvard School of Public Health in Boston, Massachusetts, …

Review: Interventions to reduce or modify dietary fat reduce cardiovascular events

ACP Journal Club17 January 2012Review: Interventions to reduce or modify dietary fat reduce cardiovascular eventsScott Kahan, MD, MPH, Yoni Freedhoff, MDScott Kahan, MD, MPHJohns Hopkins Weight Management Center, Baltimore, Maryland, USA (S.K.)Search for more papers by this author, Yoni Freedhoff, MDUniversity of Ottawa, Ottawa, Ontario, Canada (Y.F.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-156-2-201201170-02005 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationHooper L, Summerbell CD, Thompson R, et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev. 2011;(7):CD002137. https://pubmed.ncbi.nlm.nih.gov/21735388Clinical Impact RatingsGIM/FP/GP: References1 World Health Organization. Prevention of Cardiovascular Disease: Guidelines for assessment and management of cardiovascular risk. Geneva. World Health Organization. 2007. Google Scholar2 He FJ, MacGregor GA. Comment: Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials. Lancet. 2011;378:380-2. [PMID: 21803192] Google Scholar3 Hu FB, Manson JE, Willett WC. Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr. 2001;20:5-19. [PMID: 11293467] Google Scholar4 Shai I, Schwarzfuchs D, Henkin Y, et al; Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008;359:229-41. [PMID: 18635428] Google Scholar5 Mozaffarian D, Appel LJ, Van Horn L. Components of a cardioprotective diet: new insights. Circulation. 2011;123:2870-91. [PMID: 21690503] Google Scholar6 Wansink B, Chandon P. Can “low fat” nutrition labels lead to obesity? Journal of Marketing Research. 2006;43:605-17. Google Scholar Author, Article, and Disclosure InformationAuthors: Scott Kahan, MD, MPH; Yoni Freedhoff, MDAffiliations: Johns Hopkins Weight Management Center, Baltimore, Maryland, USA (S.K.)University of Ottawa, Ottawa, Ontario, Canada (Y.F.)This article was published at Annals.org on 3 January 2012. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoReview: Interventions to reduce dietary salt do not reduce mortality or morbidity Scott Kahan and Yoni Freedhoff Metrics 17 January 2012Volume 156, Issue 2Page: JC1-5KeywordsDietFatsFoodHeart failureMortalityMyocardial infarctionOilsProteinsSaltsSodium ePublished: 17 January 2012 Issue Published: 17 January 2012 Copyright & PermissionsCopyright © 2012 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...

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, …

Prediction Models That Include Genetic Data

Can alternative modeling approaches that integrate genetic data help to improve the prediction of risk for common diseases? In this issue of Circulation: Cardiovascular Genetics , Stengard et al1 set out to answer this question with regard to several genetic variations of the APOE gene and risk for ischemic heart disease (IHD). In their study, they included 3686 women and 2772 men with no medical history of IHD from the Copenhagen City Heart Study and sought to correlate IHD events to risk factors such as abnormal lipid levels, hypertension, diabetes, smoking history, and various APOE genotype data during a mean of 6.5 years of follow-up. Article see p 22 The traditional statistical approach to this analysis would be to use Cox proportional hazard modeling to map the hazard of developing IHD to a linear combination of significant risk factors. Stengard et al adopted an interesting alternative procedure that is consistent with the intuition that risk factors may have different effects in subjects with different unmeasured exposures (for example different genetic backgrounds and/or other unknown variables). Therefore, rather than looking for the risk factors that have a homogeneous effect on the hazard for IHD, the authors used the rule induction algorithm PRIM to discover subgroups of subjects with varying combinations of phenotypic risk factors for IHD and APOE alleles e2, e3, and e4. They then used the PRIM again to further segregate these subgroups according to additional genotypes in …

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

We are what we eat

![][1] The old adage that pregnant women eat for two might be more true than ever before in the light of recent research into diet and the control of gene expression. The link between the diet of pregnant women—and, to some extent, men—during pre‐conception and the health of the fetus has been viewed mostly in terms of major risk factors such as smoking or substance abuse. However, epidemiological and molecular research is revealing a more complex and subtle picture of how a pregnant woman's eating behaviour influences the expression of her own—and possibly her fetus's—genes, and thus the long‐term health of her children. “Type II diabetes, heart disease due to obesity, insulin resistance, and hypertension are the diseases most strongly associated with maternal diet during pregnancy,” said Karen Lillycrop, who specializes in perinatal nutrition at the University of Southampton in the UK. In addition, there is growing evidence that dietary effects, which can alter the expression and control of genes, might even have been a driving force for human evolution. A recent study revealed that the greatest divergence between the genomes of humans and chimpanzees is found among genes that control metabolism and are closely associated with diet (Somel et al , 2008). The mechanisms that allow the genome to interact with environmental factors, such as diet, are epigenetic changes—a concept first proposed by the British biologist Conrad Waddington (1905–1975) in 1942 to describe the interplay between genes and the environment in determining the phenotype of an organism. Further research since Waddington's time has shown that epigenetic changes not only take place during embryonic development, but also throughout the lifetime of an organism. The same mechanisms—notably DNA methylation and histone modification—have a role in the acquisition and maintenance of epigenetic changes induced by dietary or other environmental factors. In fact, they … [1]: /embed/graphic-1.gif

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

Stroke in Diabetic Patients: Is It Really a Macrovascular Complication?

To the Editor: We have read with interest the article by Wilcox et al,1 in which they demonstrated the positive effect of pioglitazone on stroke recurrence in patients with type 2 diabetes mellitus (DM). However, we would like to stress a particular concern regarding a basic concept in the difficult question of DM and stroke. In this study, as in other previous studies, stroke is considered a macrovascular event in diabetic patients, but is …

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 …