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Hypertension and ethnic group: not as plain as black or white

Onyebuchi E Okosieme   (10 April 2006)

a possible role for eplerenone in hypertension-related atrial fibrillation

oscar,m jolobe   (11 April 2006)

Hypertension and ethnic groups: not so black and white

Charles Agyemang, Raj Bhopal, Bruce and John Usher Professor of Public Health, Public Health Sciences Section, Division of Community Health Sciences, University of Edinburgh, Teviot Place, Edinburgh EH89AG   (22 April 2006)

Vitamin D - causal connection?

Helga M. Rhein   (22 April 2006)

Down with types of 'essential' hypertension

Kennedy Cruickshank   (22 April 2006)

Disappointed

Frances Akinwunmi   (24 April 2006)

Hypertension and ethnic group – a coat of many colours

Therese Tillin, Alun Hughes, Nish Chaturvedi   (26 April 2006)

Hypertension and ethnic group: story incomplete

Sam Wystan Mhlongo, Mbokazi AJ   (26 April 2006)

The right therapeutic outcome for wrong reasons?

Michael S. Myslobodsky, MD, D.Sc.   (29 April 2006)

Hypertension and ethnic group: not as plain as black or white 10 April 2006
Onyebuchi E Okosieme, Specialist Registrar Centre for Endocrine and Diabetes Science, School of Medicine, Cardiff University, Cardiff CF14 4XN, Send response to journal: Re: Hypertension and ethnic group: not as plain as black or white	Brown makes a case for making treatment choices in patients with hypertension based on ethnicity (1). However, it is unclear if his use of the term ethnicity refers to skin pigmentation or common ancestry. The latter would certainly be difficult to accurately determine from the clinical encounter while the usefulness of the former would depend on the homogeneity of biological characteristics within the ethnic group. For black people, such homogeneity remains to be proven. The black population is highly heterogeneous, both within a genetic and geographical context. Most of the available knowledge on the pathophysiological profile in black patients with hypertension is based on the well-researched North American black population (2). African Americans are mostly descended from West, Central and South East African ancestors with whom they may share genetic traits. However, they may not necessarily share the same heritage with Africans from other parts of the continent. Recent African migrant populations in the United Kingdom and North America form a different group with rapidly evolving social and cultural characteristics. In Africans living in Africa, there is wide ethnic and cultural diversity. To date these populations have not been adequately studied and their pathophysiological profiles remain poorly characterised. As doctors, we cherish clinical guidelines for the feeling of security they add to our practice. However, guidelines based on our patient’s pigmentation may give a false sense of security. Physicians in Africa, Europe and North America will increasingly be confronted by black patients with hypertension from diverse backgrounds. It will be presumptuous to apply the data obtained from North American blacks to all black populations and until enough information is available, we must exercise caution in recommending treatment choices based on ethnicity. References: (1) Brown MJ. Hypertension and ethnic group. BMJ. 2006; 332:833-6. (2) Nesbitt SD. Hypertension in black patients: special issues and considerations. Curr Hypertens Rep. 2005; 7:244-8. Competing interests: None declared
a possible role for eplerenone in hypertension-related atrial fibrillation 11 April 2006
oscar,m jolobe, retired geriatrician 1 The Lodge, 842 Wilmslow Road, Didsbury m20 2RN Send response to journal: Re: a possible role for eplerenone in hypertension-related atrial fibrillation	Notwithstanding the fact that the preferred option for blacks is the CD antihypertensive drug regime comprising calcium channel blockers and diuretics, respectively(1), adjunctive treatment which reduces the risk of hypertension-related atrial fibrillation(AF) also needs to be considered. On meta analysis, angiotensin converting enzyme (ACE) inhibitors, as well as angiotensin receptor blockers (ARBs), have this effect(2), validated, in the latter instance, in a prospective study using losartan as the ARB agent(3). The focus must now be on the blockade of those components of the renin-angiotensin-aldosterone system which are "race neutral". Promising results come from a study comprising at least 409 patients, including subgroups in whom 15-25% of the subjects were blacks. In that study a blood pressure lowering effect attributable to the aldosterone blocker eplerenone was documented in whites as well as blacks(4). In a smaller study in which patient subgroups were characterised by a 4-6% content of blacks, the adjunctive use of eplerenone enhanced the antihypertensive effect of ACE inhibitors and ARB's, respectively(5). Even more encouraging is the prospective study of 168 subjects (including 55 blacks) with low- renin hypertension in whom eplerenone proved to had better antihypertensive efficacy than losartan(6). These studies are sufficiently encouraging to prompt a prospective study to evaluate the role of aldosterone blockade in reducing the risk of hypertension-related AF in low renin hypertension irrespective of race. References (1) Brown M Hypertension and ethnic group BMJ 2006:332:833-6 (2) Madrid A., Peng J., Zamora J et al The role of angiotensin receptor blockers and/or angiotensin converting enzyme inhibitors in the prevention of atrial fibrillation in patients with cardiovascular diseases Pacing Clin Electrophysiol 2004:27:1405-10 (3) Watchell K., Lehto M., Gerdts E et al Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenolol J Am Coll Cardiol 2005:45:712-9 (4) Weinbereger MH., Roniker B., Krause SL., Weiss RJ Eplerenone, a selective aldosterone blocker, in mild to moderate hypertension Am J Hypertens 2002:15:709-16 (5) Krum H., Nolly H., Workman D et al Efficacy of eplerenone added to renin-angiotensin blockade in hypertensive patients Hypertension 2002:40:117-23 (6) Weinbereger MH., White WB., Ruilope L-M et al Effects of eplerenone versus losartan in patients with low-renin hypertension Am Heart J 2005:150:426-33 Competing interests: None declared
Hypertension and ethnic groups: not so black and white 22 April 2006
Charles Agyemang, Associate Researcher Department of Social Medicine, Academic Medical Centre, 1100 DD, Amsterdam, The Netherlands, Raj Bhopal, Bruce and John Usher Professor of Public Health, Public Health Sciences Section, Division of Community Health Sciences, University of Edinburgh, Teviot Place, Edinburgh EH89AG Send response to journal: Re: Hypertension and ethnic groups: not so black and white	Dear Editor Brown’s article makes a case for making treatment choices in patients with hypertension based on ethnicity.[1] There are several issues in his paper that need attention that oversimplify a complex matter. Brown does not recognise the important heterogeneity within the African, Asian and European descent populations. This has resulted in misleading conclusions.[2,3] Brown claimed that ‘black’ people tend to develop hypertension at an earlier age than ‘white’ people. This assertion may be applicable in the USA but not in the UK and other countries. Agyemang and Bhopal’s review showed similar blood pressure levels among African and European descent children in the UK.[4] Their review on African descent adults also showed similar blood pressure levels and similar hypertension rates in the younger age groups but higher rates in the population in older age groups of 35 years and above.[5] Indeed their findings in the UK contrast with the higher BP levels and hypertension rates reported among African Americans at all ages in the USA. However, this is not surprising since there are substantial differences in culture, eating habits, geographical locations and migration experience between African American and other African descent populations in western countries,[2] all of which are important determinants of hypertension. One pressing question in the UK is: What are the causes of the rapid rise in blood pressure in African descent population after the 35 years and above? Answering this question is crucial and will require a cohort study. Hypertension is not only a ‘black’ peoples’ disease as is often portrayed. On the world stage, blood pressure levels and hypertension rates are much lower in sub-Saharan Africa than in other world regions.[7] Although easily forgotten, less than half a century ago, ancestral African populations living traditional lives showed a lower mean blood pressure with little or no increase with increasing age, and a low prevalence of hypertension.[8] Hypertension rate reported among African Americans is also not abnormally high when compared with rates reported among other populations in the western countries. Cooper and others [9] found a huge variation in prevalence of hypertension among European and African descent groups globally. The hypertension rate in African Americans (44.0%) was not abnormally high when viewed internationally. Contrary to expectations, the prevalence of hypertension was lower amongst the White people in USA (26.8%) and Canada (27.4%) as compared to European countries, ranging from 38.4% in Sweden to 55.3% in Germany. These data indicate that inferences from population surveys done in certain geographical areas in a particular social context may not be applicable as logical benchmarks for other areas. It is worth emphasising that the awareness, treatment, and control of hypertension in North America are far better than those reported in most Europe countries.[10] The rates reported in African Americans are also far better than those reported among all ethnic groups in the UK.[11] Agyemang and Bhopal also showed that the common perception that blood pressure and prevalence of hypertension in South Asians are comparatively high is unreliable - the picture is complex.[6] The review showed a geographical variation between London (comparatively high blood pressure in South Asians) and the rest of the UK (comparatively low or similar blood pressure). There is also stark heterogeneity within the South Asian groups, with slightly higher blood pressure in Indians, slightly lower blood pressure in Pakistanis, and much lower blood pressure in Bangladeshis. Perhaps, the questions we should be asking are how do we improve hypertension awareness, treatment and control in all ethnic groups in Europe to match those reported in North America, and how do we harness the heterogeneity within and between ethnic groups to improve our understanding of high blood pressure?. 1. Brown MJ. Hypertension and ethnic group. BMJ 2006;332(7545):833-6. 2. Agyemang C, Bhopal R, Bruijnzeels M. Negro, Black, Black African, African Caribbean, African American or what? Labelling African origin populations in the health arena in the 21st century. J Epidemiol Community Health. 2005;59(12):1014-8. 3. Bhopal R. Glossary of terms relating to ethnicity and race: for reflection and debate. J Epidemiol Community Health 2004;58:441-5. 4. Agyemang C, Bhopal R, Bruijnzeels M. Do variations in blood pressures of South Asian, African and Chinese descent children reflect those of the adult populations in the UK? A review of cross-sectional data. J Hum Hypertens. 2004;18(4):229-37. 5. Agyemang C, Bhopal R. Is the blood pressure of people from African origin adults in the UK higher or lower than that in European origin white people? A review of cross-sectional data. J Hum Hypertens. 2003 ;17(8):523 -34. 6. Agyemang C, Bhopal RS. Is the blood pressure of South Asian adults in the UK higher or lower than that in European white adults? A review of cross-sectional data. J Hum Hypertens 2002;16:739-51. 7. Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet 2005; 365: 217–223. 8. Shaper AG, Wright DH, Kyobe J: Blood pressure and body build in three nomadic tribes of northern Kenya. East Afr Med J 1969,46:273-81. 9. Wolf-Maier K, Cooper RS, Kramer H, Banegas JR, Giampaoli S, Joffres MR, Poulter N, Primatesta P, Stegmayr B, Thamm M. Hypertension treatment and control in five European countries, Canada, and the United States. Hypertension 2004;43:10-7. 10. Cooper RS, Wolf-Maier K, Luke A, Adeyemo A, Banegas JR, Forrester T, Giampaoli S, Joffres M, Kastarinen M, Primatesta P, Stegmayr B, Thamm M. An international comparative study of blood pressure in populations of European vs. African descent. BMC Med 2005;3:2. 11. Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988–2000. JAMA. 2003; 290: 199–206 Competing interests: None declared
Vitamin D - causal connection? 22 April 2006
Helga M. Rhein, General Practitioner Sighthill Health Centre, Edinburgh, Calder Road EH11 4AU Send response to journal: Re: Vitamin D - causal connection?	Could the lack of Vitamin D play a role in the aetiology of hypertension in black and asian people? (1) In the U.K. it is thought that as many as 94% of otherwise healthy South Asian adults suffer of Vitamin D deficiency. (1) Have the references in Morris Brown's article (2) been examined for lattitude of location of studied populations? I suspect that black or asian people have a higher prevalence of hypertension when they live in areas of relatively low sun exposure with resulting low intra-dermal Vitamin D production, like U.K. or U.S., as opposed to areas of high sun exposure with high intra-dermal Vitamin D production, like Africa or South Asia. Helga Rhein References: (1) Drug and Therapeutic Bulletin, Vol44, No 4, April 2006, Primary vitamin D deficiency in adults (2) BMJ, Vol 332, 8 April 2006, Morris J Brown: Hypertension and ethnic group Competing interests: None declared
Down with types of 'essential' hypertension 22 April 2006
Kennedy Cruickshank, Professor of Cardiovascular Medicine & Clinical Epidemiology Manchester University & Royal Infirmary M13 9NT Send response to journal: Re: Down with types of 'essential' hypertension	Dear Sir Morris Brown’s provocative resume of ethnicity & hypertension (BMJ April 8th) resurrects issues from the Platt-Pickering debate of the 1960s (1). He sides with the Platt (monogenic?) camp, which lost. Morris’ A (no longer B) C, D strategy for treating high blood pressure (‘hypertension’) based on initials of the major classes of effective antihypertensive drugs (2) has been hugely influential in developing clear guidelines. It has helped primary care achieve greatly improved levels of treatment and control of hypertension in the last 3 years. Redirecting this purely pragmatic approach for treatment into ‘classifying’ hypertension as type 1 or 2 and to link this simplistically to yet another candidate gene surely is retrogressive. High blood pressure is a continuum along which hypertension is again pragmatically defined as the level of blood pressure above which treatment does more good than harm. Hypertension is not a ‘type’ and anyway ‘type 2’ likely evolved from sub-clinical ‘type 1’ a decade or two earlier in the life course. His analogy with diabetes merely underlines the poverty of understanding for the aetiology of ‘type 2’ diabetes. Elsewhere, Pickering wrote that perhaps the most difficult notion to teach doctors or medical students was ‘…to count beyond 2 – that people have a disease or do not, albuminuria (microalbuminuria?) or not, ‘hypertension’ or not’. Let’s not go back to these dichotomies, least of all for understanding the origins of high blood pressure in African-origin populations. Rising blood pressure starts early in everyone, in some faster than others (3). The problem for the gene lobby is that its efforts to find repeatable linkage of candidate genes to phenotype have almost universally failed to date. Perhaps that is because we ignore at our peril basic concepts of integrated physiology, after all the product of gene function, and homeostasis and its disturbances. Down with discrete ‘types’. Yours Kennedy Cruickshank Professor of Cardiovascular Medicine & Clinical Epidemiology Manchester University & Royal Infirmary M13 9NT Manchester. References: 1. Swales JD (Editor). Platt versus Pickering: a debate on the basis of hypertension. Keynes Press. BMA, London 1985. 2. Brown MJ, Cruickshank JK, Dominiczak AF, MacGregor GA, Poulter NR, Russell GI, Thom S, Williams B; Executive Committee, British Hypertension Society. Better blood pressure control: how to combine drugs. J Hum Hypert 2003; 17: 81-6. 3. Cruickshank JK, F Mzayek F, Liu L, Kieltyka L, Sherwin R, Webber LS, Srinavasan SR, Berenson GS. Origins of the ‘black/ white’ difference in blood pressure: roles of birth weight, postnatal growth, early blood pressure and adolescent body size: The Bogalusa Heart Study. Circulation 2005; 111: 1932-37. Competing interests: JKC works with MB for the British Hypertension Society, and has done so in this field for his medical career.
Disappointed 24 April 2006
Frances Akinwunmi, Cover Interface Pharmacist Homerton Hospital E9 6SR Send response to journal: Re: Disappointed	I am disappointed at the inclusion of an 18th century engraving of black slaves to illustrate that ‘survival of the fittest’ slaves may have impacted on the high incidence of hypertension in blacks in the western world today. I found it lacking in both sensitivity and taste and wonder if it was entirely necessary. Competing interests: None declared
Hypertension and ethnic group – a coat of many colours 26 April 2006
Therese Tillin, Research Fellow International Centre for Circulatory Health, Imperial College at St Mary's, London W2 1PG, Alun Hughes, Nish Chaturvedi Send response to journal: Re: Hypertension and ethnic group – a coat of many colours	We agree with Morris Brown (1) that there is a paucity of evidence regarding pathogenesis and efficacy of treatment of hypertension in different ethnic groups. However, there are aspects of his epidemiological review that are incomplete -notably consideration of blood pressure and prevalence of hypertension in migrants to the UK of Indo-Asian descent. The National Health Survey for England demonstrates that all Indo-Asian ethnic subgroups in the UK have lower blood pressures than the general population, and that blood pressures are particularly low in people of Bangladeshi origin (2). The origins of the increased risk of hypertension in people of black African descent remain unclear. Although widely quoted, the claim that the greater blood pressures observed in people of black African descent in the US are partly attributable to survival selection based on the ability to conserve salt during slave transportation (1) is based on weak evidence and has been heavily criticised (3). Finally, whilst black Americans with hypertension are more likely to have low renin (4), there is considerable overlap in values between black and white Americans and ethnicity cannot be used to predict renin status (4). A recent meta-analysis (5) indicated that black and white people had similar responses to all categories of anti-hypertensive medications and that there was more variation in responses to treatment within groups of hypertensive black African and white Americans than between them,. Thus, we would question that there is any ‘…certainty of a difference in type of hypertension and drug response…’(1) in black people. Studies of ethnic group differences in risk factors and hypertension phenotypes are important in aiding understanding of pathogenesis, but in our view, treatment strategies should be tailored to the individual rather than their ethnic group. Yours Therese Tillin, Research Fellow Alun Hughes, Professor of Clinical Pharmacology Nish Chaturvedi, Professor of Clinical Epidemiology International Centre for Circulatory health Imperial College at St Mary's, London W2 1PG Reference List (1) Brown MJ. Hypertension and ethnic group. BMJ 2006; 332(7545):833 -836. (2) Health Survey for England 2004: Health of Ethnic Minorities - Full Report. The Information Centre. 2006. (3) Kaufman JS, Hall SA. The slavery hypertension hypothesis: dissemination and appeal of a modern race theory. Epidemiology 2003; 14(1):111-118. (4) Alderman MH, Cohen HW, Sealey JE, Laragh JH. Plasma renin activity levels in hypertensive persons: their wide range and lack of suppression in diabetic and in most elderly patients. Am J Hypertens 2004; 17(1):1-7. (5) Sehgal AR. Overlap between whites and blacks in response to antihypertensive drugs. Hypertension 2004; 43(3):566-572. Competing interests: Alun Hughes is Secretary to the British Hypertension Society and has received sponsorship in the past from pharmaceutical companies. Nish Chaturvedi currently receives fees for steering committee work and trial funding from AstraZeneca and Takeda
Hypertension and ethnic group: story incomplete 26 April 2006
Sam Wystan Mhlongo, Head of Department & Chief Specialist University of Limpopo, Family Medicine & PHC, Mbokazi AJ Send response to journal: Re: Hypertension and ethnic group: story incomplete	In his otherwise interesting article under the title: “Hypertension and ethnic group” BMJ Vol 332, 8 April 2006 page 833, we have found it very interesting and to some degree informative regarding the care of patients. However, we take issue with the author for appearing to ignore relevant issues. He must know that the vast majority of published studies on this subject has focused on African Americans and African Caribbeans as indeed his references show 1. A sensitive issue that has not been addressed is what is meant by ethnicity. In the article, it is quite clear that the question of genes is hypothesized. Phenotypically, black Africans in Africa may look like African Americans and African Caribbeans, but genetically both African Americans and African Caribbeans are of mixed ancestry much more than their brothers and sisters in the continent of Africa. This fact is beyond dispute and is accepted by all social anthropologists. Under the circumstances, one may postulate that hypertension may not be the same amongst Africans in Africa and those in the diaspora, i.e. African Caribbeans, African Americans and African Latinos. This article has ignored this fact and one is left with the idea that all black ethnic groups are homogenous. With regard to the management of hypertension in whatever ethnic group, the question of compliance and culture has not been addressed. Nicky Britten and other researchers have shown that when it comes to compliance, social class has little or no bearing but culture and ethnicity do. Mhlongo2 and Morgan3 at The United Medical and Dental Schools of Guys and St. Thomas Hospitals have demonstrated this fact. It is not clear from this article whether or not these “plasma rennin” hypertensives were compliant with their medication. It is also not clear as to whether or not they were also self medicating since it does not appear as if they were strictly followed. References: 1. Grell GAC. Management of Hypertension in the Caribbean: the Jamaican perspective. From Ethnic Factors in Health and Disease: Edited by JK Cruickshank and DG Beevers 1989, published by Wright. 2. Mhlongo SWP. Lay beliefs and responses concerning hypertension and its management in two culturally distinct groups. SA Family Practice, 2002, 25(2):16-21. 3. Morgan Myfawny and Watkins CJ. Managing Hypertension: beliefs and responses to medication among cultural groups. (Sociology of health & Illness: Vol 10 No. 41988 ISS 0141, 1989) Competing interests: None declared
The right therapeutic outcome for wrong reasons? 29 April 2006
Michael S. Myslobodsky, MD, D.Sc., Professor Howard University, Washington, DC 20059 Send response to journal: Re: The right therapeutic outcome for wrong reasons?	The right result therapeutic outcome for wrong reasons. Dear Sir, A higher prevalence of hypertension in Black people was attributed recently [1] to the sodium “thrifty” alleles that are more likely to be selected in a hot, low-salt environment. This evolutionary driver, known as the “slavery hypothesis for hypertension” and referred to Curtin[2] is presumably further aggravated by the transatlantic slave trade that has made additional demand on survival of the gene-bearers. We are led to believe that in an environment where saltshakers are within the handgrip, hypertension would prevail in the ancestry of people forcibly brought from Africa to the shore of the New World. The study may seem to provides support for the hypothesis ex-juvantibus, i.e., in a better response to calcium blockers and diuretics in black people with type 2 hypertension as opposed to the effects of angiotensin converting enzyme inhibitors and angiotensin blockers.[1] That may well appear as the right result for wrong reasons. The longevity of the “slavery hypothesis” even when dressed up genetically is hardly warranted. Actually, Curtin[2] protested the premise s mistaken on all counts. More recently, it was branded as an “old pseudoscientific canard.”[3] The possibility that ethnic differences in hypertension are associated with pre- or perinatal programming of obesity, salt sensitivity, nephron number and vascular anatomy makes the “slavery hypothesis” unnecessary on still another count. In the Windkessel model of the pulsatile/continuous hemodynamics (Windkessel stands for air chamber in its early German incarnations), the need to accommodate peripheral resistance in multiple bodily segments of the vascular network (within the kidney, muscle, or brain) is known to be particularly complex. [4] Somewhat complicating the simplicity of the Poiseuille's law, the resistance of the microcirculatory network and blood pressure is expected to go up when and to the extent, the networks of smaller arteriolar branches and capillaries will be impoverished, a condition known as rarefaction. In premature infants and/or those with lower birth weight, rarefaction may be a common factor of in utero programming of hypertension.[5] In a model of vascular programming based on prenatal maternal protein restriction it was found that diverse anatomical topography of microvascular rarefaction appears early during the neonatal period, in association with decreased angiogenesis.[6] Although the precise role of the rennin-angiotensin system in the programming of hypertension has yet to be elucidated, the responsibility of characteristics from the intrauterine period, through infancy and childhood, including an inverse relation of birth weight to blood pressure becomes increasingly credible.[7] In the United States, blacks have a greater prevalence of low birth weight than whites,[8-10] suggesting that the higher prevalence of hypertension among in that ethnic group may be related to fetal programming.[11] Finally, Ward et al.[12] reported a strong inverse relationship between cardiovascular reactivity (a reduction in the systolic and the diastolic response to stress) and size at birth in women. Since psychological stressors are recognized as a catalyst of sustained hypertension this first finding in humans may herald the need to redirect in the future the focus of preventive measures from socio- cultural and psychosomatic variables to those intended to control prematurity and low birthweight. Michael S Myslobodsky, MD, D.Sc. Professor Howard University, 2441 6str. NW Washington, DC 20059 Competing interests: None declared References 1. Brown MJ: Hypertension and ethnic group. BMJ 2006, 332:833-836. 2. Curtin PD: The slavery hypothesis for hypertension among African Americans: the historical evidence. Am J Public Health 1992, 82:1681-1686. 3. Kaufman JS: No More "Slavery Hypothesis" Yarns. Psychosom Med 2001, 63:324-325. 4. Safar ME, Boudier HS: Vascular Development, Pulse Pressure, and the Mechanisms of Hypertension. Hypertension %R 101161/01HYP00001679928087626 2005, 46(1):205-209. 5. Chapman N, Mohamudally A, Cerutti A, Stanton A, Sayer AA, Cooper C, Barker D, Rauf A, Evans J, Wormald R et al: Retinal vascular network architecture in low-birth-weight men. J Hypertens 1997, 15(12):1449-1453. 6. Pladys P, Sennlaub F, Brault S, Checchin D, Lahaie I, Le NLO, Bibeau K, Cambonie G, Abran D, Brochu M et al: Microvascular rarefaction and decreased angiogenesis in rats with fetal programming of hypertension associated with exposure to a low-protein diet in utero. Am J Physiol Regul Integr Comp Physiol %R 101152/ajpregu000312005 2005, 289(6):R1580- 1588. 7. Lawlor DA, Smith GD: Early life determinants of adult blood pressure. Curr Opin Nephrol Hypertens 2005, 14(3):259-264. 8. Hulman S, Kushner H, Katz S, Falkner B: Can cardiovascular risk be predicted by newborn, childhood, and adolescent body size? An examination of longitudinal data in urban African Americans. J Pediatr 1998, 132(1):90 -97. 9. Foster HW, Wu L, Bracken MB, Semenya K, Thomas J: Intergenerational effects of high socioeconomic status on low birthweight and preterm birth in African Americans. Journal of the National Medical Association 2000, 92(5):213-221. 10. Ruijter I, Miller JM: Evaluation of low birthweight in African Americans. Journal of the National Medical Association 1999, 91(12):663- 667. 11. Forrester T: Historic and early life origins of hypertension in Africans. J Nutr 2004, 134(1):211-216. 12. Ward AM, Moore VM, Steptoe A, Cockington RA, Robinson JS, Phillips DI: Size at birth and cardiovascular responses to psychological stressors: evidence for prenatal programming in women. J Hypertens 2004, 22(12):2295- 2301. Competing interests: None declared