Dyslipidaemia and hypertension co-exist in the same way as nettles and dock leaves grow in the same beds. Whereas nitrogen-rich soil provides a friendly environment for the latter, obesity is the substrate for the two cardiovascular risk factors.
The link between obesity, morbidity and mortality has been known since the days of Hippocrates. The great Persian physician Ibn Sina wrote volumes on the hazards of obesity 1,000 years ago.
More recently in 1988 Gerald Reaven, had a ‘Eureka’ moment, and subsequently presented the concept of the metabolic syndrome at that year’s American Diabetes Association Banting Lecture.
He formally linked the conditions together, blaming hyperinsulinaemia, amongst other physiological mechanisms.
Since then elements and criteria of the syndrome have been refined: the most recent, the International Diabetes Federation definition, cites abdominal obesity as the only ‘must have’ factor for eligibility.
The original description of the syndrome was a major step forward, ensuring that clinicians did not consider individual elements in isolation, but as co-conspirators towards CVD. However, the passage of time has attenuated the relevance of the metabolic syndrome; it is past its sell-by date.
Rick factors for CVD
It was once a stimulus to improve the whole spectrum of risk factors, but now the link between BP, lipids and glucose is so deeply ingrained that it is second nature to consider them together.
Furthermore, with enhanced recognition of the science behind obesity, and the breadth of the damage wrought by visceral fat, the tight definition of the ‘syndrome’ is too restrictive. Journals are full of the dangers of lipotoxicity; the sinister effects of ectopic fat in the liver, muscles, heart, pancreas and even brain.
It is too simplistic to restrict attention to the four basic areas of BP, cholesterol, sugar and obesity, whereby conditions such as polycystic ovary syndrome and obstructive sleep apnoea are deemed ‘second class’ by their omission.
The leading cause of death worldwide is cardiovascular disease: dyslipidaemia is the main risk factor, but obesity is a major independent factor, and is also indirectly responsible for raised lipids, and a highly atherogenic lipid profile characterised by small dense LDL particles.
Interheart showed that deranged lipids, measured by ApoB:ApoA1 ratio is the pre-eminent risk factor for MI, with smoking, hypertension and abdominal obesity close behind.
Weight loss
Abdominal obesity and weight gain are the strongest predictors of early atherosclerosis in apparently healthy adults.1 Around 38% of patients who have a BMI >27 have hypercholesterolaemia,2 and Framingham revealed that for every 10% weight gain, cholesterol increases by 12mg/dl.
Dyslipidaemia develops progressively as BMI increases from 21kg/m2, which, alongside the change in nature and density of LDL particles, ultimately increases the risk of coronary heart disease by a factor of around 3.6.3
Beneficial weight loss describes a weight loss of 10kg inducing a reduction in total cholesterol of only 0.25mmol/L, around 5%,4 whereas the National Cholesterol Education Programme reports that every 3kg of diet-induced weight lost increases HDL by 1mg/dl. Gains are only clinically relevant when weight loss is maintained.5
Blood pressure
High BP multiplies the risk induced by dyslipidaemia. The risk of becoming hypertensive during a lifetime exceeds 90% for someone in a developed country.6 The likelihood of hypertension is around fivefold greater in obese individuals than among those of normal weight.
Two thirds of cases are linked to excess weight,7 and cross-sectional population surveys suggest that over 85% of hypertension exists in individuals with BMI values above 25kg/m2.8 A large 10-year prospective study reported that individuals who subsequently developed hypertension were more obese and had higher insulin and triglyceride levels, compared with those who remained normotensive.9
Reducing weight benefits BP; a meta-analysis as long ago as 1988 showed a reduction in systolic BP and diastolic BP of 2.4 and 1.5mmHg per kilogram loss. 10
Diet
Poor diet leads to obesity, whilst independently raising BP. Dietary fats raise systolic and diastolic BP as well as lipids, as demonstrated in the DASH trials.11 Energy-dense diets rich in fats and refined sugars promote weight gain,12 and high sugar intakes can increase BP by 6.9mmHg (systolic) and 5.3mmHg (diastolic).13
Conversely, high fruit and vegetable intake lowers BP, the effect being equivalent to a reasonably potent antihypertensive drug.
Obesity causes dyslipidaemia, hypertension and dysglycaemia. Weight loss is effective in improving all of them, and should be prioritised alongside pharmacotherapy as a logical approach to reducing weight-related cardiovascular risk.
CLICK HERE TO VIEW OUR HEALTHY CHOLESTEROL RESOURCE CENTRE
Dr Haslam is a GP in Hertfordshire, physician in obesity medicine at Luton & Dunstable Hospital, and chair of the National Obesity Forum.
References
1. Stamatelopoulos KS, Lekakis JP, Vamvakou G. The relative impact of different measures of adiposity on markers of early atherosclerosis, International Journal of Cardiology 2007; 119: 139-46.
2. Xenical Pro. Data on file (Ref. 038-014), Genentech USA, Inc., South San Francisco, CA 94080-4990.
3. Wannamethee SG, Shaper AG, Durrington PN, Perry IJ. Hypertension, serum insulin, obesity and the metabolic syndrome. J Hum Hypertens 1998; 12: 735–41.
4. Avenell A , Broom J, Brown TJ, et al. Systematic review of the long term effects and economic consequences of treatments for obesity and implications for health improvements. Health Technol Assess 2004; 8: 1–182.
5. National Heart, Lung and Blood Institute. Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). www.nhlbi.nih.gov/guidelines/cholesterol
6. Hypertension: uncontrolled and conquering the world. Lancet 2007; 370: 539.
7. Kastarinen MJ, Nissinen AM, Vartiainen EA, et al. Blood pressure levels and obesity trends in hypertensive and normotensive Finnish population from 1982 to 1997. J Hypertens 2000; 18: 255–62.
8. Cassano PA, Segal MR, Vokonas PS, Weiss ST. Body fat distribution, blood pressure, and hypertension: a prospective cohort study of men in the normative aging study. Ann Epidemiol 1990; 1: 33–48.
9. Skarfors ET, Lithell HO, Selinus I. Risk factors for the development of hypertension: a 10-year longitudinal study in middle-aged men. J Hypertension 1991; 9: 217-23.
10. Staessen J, Fagard R, Amery A. The relationship between body weight
and blood pressure. J Hum Hypertens. 1988; 2: 207–17.
11. Appel LJ, Moore TG, Obarzanek R, et al. A clinical trial of effects of dietary patterns on blood pressure. N Engl J Med 1997; 336: 1117–24.
12. Drewnowski A. Energy density palatability and satiety: implications for weight control. Nutr Rev 1998; 56: 347–53.
13. Raben A, Vasilaras TH, Moller AC, Astrup A. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. Am J Clin Nutr 2002; 76: 721–29.
