Background Image
Table of Contents Table of Contents
Previous Page  46 / 74 Next Page
Information
Show Menu
Previous Page 46 / 74 Next Page
Page Background

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 2, March/April 2019

112

AFRICA

et al

. Acute cardiovascular and sympathetic effects on nicotine replase-

ment therapy.

Hypertension

2006;

47

(6): 1162–1167.

13. Tarvainen MP, Niskanen JP, Lipponen JA, Ranta-Aho PO, Karjalainen

PA. Kubios HRV – Heart rate variability analysis software.

Comput

Methods Programs Biomed

2014;

113

(1): 210–220.

14. Rajendra AU, Joseph P, Kannathal N, Lim CM, Suri J. Heart rate vari-

ability: A review.

Med Biol Eng Comput

2007;

44

(12): 1031–1051.

15. Task force of The European Society of Cardiology and The North

American Society of Pacing and Electrophysiology. Heart rate variabil-

ity. Standards of measurement, physiological interpretation and clinical

use.

Circulation

1996;

93

: 1043–1065.

16. Voss A, Schulz S, Schroeder R, Baumert M, Caminal P. Methods

derived from nonlinear dynamics for analyzing heart rate variability.

Philos Trans A Math Phys Eng Sci

2009;

367

(1887): 277–296.

17. Minami J, Ishimitsu T, Matsuoka H. Effects of smoking cessation

on blood pressure and heart rate variability in habitual smokers.

Hypertension

1999;

33

(1 Pt 2): 586–590.

18. Thayer HF, Sollers JJ 3rd, Ruiz-Padial E, Vila J. Estimating respiratory

frequency from autoregressive spectral analysis of heart period.

IEEE

Eng Med Biol Mag

2002;

21

(4): 41–45.

19. Ferrer E, Peinado VI, Castaneda J, Prieto-Lloret J, Olea E, Gonzalez-

Martin MC,

et al

. Effects of cigarette smoke and hypoxia on pulmonary

circulation in the guinea pig.

Eur Respir J

2011;

38

(3): 617–627.

20. Moudgil R, Michelakis ED, Archer SL. Hypoxic pulmonary vasocon-

striction.

J Appl Physiol

2005;

98

(1): 390–403.

21. Brewer GJ, Sing CF, Eaton JW, Weil JV, Brewer LF, Grover RF. Effects

on hemoglobin oxygen affinity of smoking in residents of intermediate

altitude.

J Lab Clin Med

1974;

84

(2): 191–205.

22. Freitas J. Tobacco influence on carboxyhemoglobin, oxihemoglobin

dissociation and erythrocyte filtration.

Acta Med Port

1983;

4

: 73–75.

23. West JB. The physiologic basis of high-altitude diseases.

Ann Intern Med

2004;

141

(10): 789–800.

24. Wu TY, Ding SQ, Liu JL, Jia JH, Chai ZC, Dai RC,

et al

. Smoking,

acute mountain sickness and altitude acclimatisation: a cohort study.

Thorax

2012;

67

(10): 914–919

25. Imai K, Sato H, Hori M, Kusuoka H, Ozaki H, Yokoyama H,

et al

.

Vagally mediated heart rate recovery after exercise is accelerated in

athletes but blunted in patients with chronic heart failure.

J Am Coll

Cardiol

1994;

24

(6): 1529–1535.

26. Burtscher M, Szubski C, Faulhaber M. Prediction of susceptibility to

AMS in simulated altitude.

Sleep Breath

2008;

12

(2): 103–108.

Evolving evidence about diet and health

Nutritional research initially focused almost entirely on

conditions of nutritional deficiencies (e.g. scurvy, beriberi,

pellagra). By the 1950s, with the increase in coronary heart

disease in high-income countries, attention shifted to a range

of so-called diet–heart hypotheses.

These included the putative and harmful effects of fats

(especially saturated fats) and the protective effects of the

so-called Mediterranean diet to explain why individuals in

the USA, northern Europe and the UK were more prone to

coronary heart disease, whereas those in European countries

around the Mediterranean (or Japan) seemed to have lower

risks.

Some of the initial studies were enormously influential

while undergoing limited scrutiny as to the rigor of their

methods. The lack of replication of these early claims should

have prompted caution and re-examination of whether fats

(especially saturated fats) were indeed harmful.

More recently, studies using standardised questionnaires,

careful documentation of outcomes with common

definitions, and contemporary statistical approaches to

minimise confounding have generated a substantial body

of evidence that challenges the conventional thinking that

fats are harmful. Also, some populations (such as the US

population) changed their diets from one relatively high in

fats to one with increased carbohydrate intake. This change

paralleled the increased incidence of obesity and diabetes.

The focus of nutritional research has recently shifted

to the potential harms of carbohydrates. Indeed, higher

carbohydrate intake can have more adverse effects on key

atherogenic lipoproteins (e.g. increase the apolipoprotein

B-to-apolipoprotein A1 ratio) than can any natural fats.

Additionally, in short-term trials, extreme carbohydrate

restriction led to greater short-term weight loss and lower

glucose concentrations compared with diets with higher

amounts of carbohydrate.

Robust data from observational studies support a harmful

effect of refined, high-glycaemic-load carbohydrates on

mortality. The realisation that cardiovascular disease is a

global epidemic, with most cases occurring in developing

countries, has also stimulated studies involving multiple

countries at different economic levels.

Last year, the Prospective Urban Rural Epidemiology

(PURE) study of 135 335 individuals from 18 countries in

five continents showed that a diet high in carbohydrates

(more than approximately 60% of energy) but not high in

saturated fats, was associated with higher risk of death.

However, in PURE, even the group with the highest level of

fats (i.e. quintile 5; mean total fat intake 35% of energy, and

saturated fat intake 13% of energy) was not as high as the

average in studies from Finland (37 and 20%, respectively),

Scotland (37 and 17%, respectively), or the USA (38 and

16%, respectively), done in the 1960s and 1970s.

Therefore, a marked reduction in fat intake in several

countries might have occurred over the past few decades

in several countries. It is not clear that further reductions

in dietary fat intake will lead to reductions in incidence of

disease.

continued on page 119…