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.
Competing interests:
No competing interests
22 April 2006
Kennedy Cruickshank
Professor of Cardiovascular Medicine & Clinical Epidemiology
Rapid Response:
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.
Competing interests: No competing interests