Effect of screening and lifestyle counselling on incidence of ischaemic heart disease in general population: Inter99 randomised trial
BMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g3617 (Published 09 June 2014) Cite this as: BMJ 2014;348:g3617
All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
In a previous discussion in BMJ of 25th June 2014 I discussed how and why I changed my diet to treat angina in 1997, and would now like to present some background information for that decision.
When I was nineteen years old I was a gymnastic instructor and decided to apply for scholarships in leadership training in a course called Group Work at the South Australian Institute of Technology. I was offered one from the state government, a second from the federal government, and a third from the National Fitness Council of Australia, and accepted one, and completed the course in four years part time.
The course involved various subjects, and the topics included sociology and population studies, and I have maintained my interest in them since. The Institute of Technology later merged with the University of South Australia who notified me that I was therefore an alumni of Uni SA.
When I developed angina in 1997 I already had a reasonable knowledge of the history of medicine and society, particularly in relation to developments since the industrial revolution in food production and distribution technology which resulted in changes from the consumption of natural foods to processed foods which are mixed with a variety of ingredients such as salts, sugars, and fats etc. which each influence health in various ways.
Consequently when I read a book about the Pritikin diet and noticed that the native tribespeople of Africa had no heart disease, and when I saw studies of various groups in modern societies, and that those who ate vegetarian diets had the least heart disease and the longest life expectancy, I recognised why that was so, and became a vegetarian myself.
The angina pain ceased to be a problem after six months.
However, my gymnastic experience also gave me some insight into the aspect of exercise.
I have included an essay on that topic as an attachment for those who may be interested.
Competing interests: No competing interests
The Inter99 randomised trial [1] investigated the effects of systematic screening for risk factors for ischemic heart disease (IHD), followed by repeated lifestyle counselling, on the 10 year development of IHD at a population level. 11,708 people were allocated in the intervention group and 52,4% accepted the invitation; the control group was not invited to screening.
After five years the intervention group, with individual counselling, delivery of written material and, for patients at high risk, group based counselling, showed a significant effect on lifestyle. In fact there was a substantial reduction in the prevalence of smoking, improved dietary habits (significantly greater decrease in saturated fat intake and significant increase in the unsaturated/saturated fat ratio and fish intake), sustained physical activity (among men), and a decrease in binge drinking, a significant improvement in self reported mental health and sustained self reported physical health [1]. These published data indicate that the counselling was able to promote beneficial changes at the individual level, at least for some time.
Nevertheless, the outcome results were disappointing: no significant difference emerged in the primary end point (HR for IHD 1.03, 95% CI 0.94-1.13), or in the secondary end points (stroke 0.98, 0.87-1.11; combined end point 1.01, 0.93-1.09; total mortality 1.00, 0.91-1.09). Even in Model 3, adjusted for age, sex, education, ethnicity, cohabitation, and comorbidity, no difference was apparent. The analysis of the whole intervention group, including a subgroup of 1,308 people randomly allocated to a low intensity, less comprehensive lifestyle intervention (Appendix 1), was at least as much disappointing, with a HR for total mortality 1.01 (0.93-1.10) at 10 year follow-up.
The authors’ hypotheses to explain these bad results are: 1) primary care physicians are already able to identify patients at high risk and to intervene when needed; 2) obtaining an effect at the population level is difficult if the participation rate is low; 3) people who drop out from the programmes have often the less healthy lifestyle, and are the people who potentially could benefit most; 4) only a small proportion of those who participate are able to change to a healthier lifestyle, and those who succeed in lifestyle changes have difficulties in maintaining them over the long term, resulting in further dilution of a possible effect of the intervention.
All these reasons can explain the absence of any significant benefit, but another reason may have operate in an opposite direction, causing a small tendency to a damage.
The hypothesis could be some degree of overtreatment and iatrogenesis in the intervention group. In fact, while people in the control group and their general practitioners (GPs) had no knowledge of an ongoing intervention, in the intervention group the people classified at high risk were informed of their elevated values, as were their GPs. The authors state that 60% of people in the intervention group were classified at high risk, but for some of them this was a likely overclassification, on the ground of current cardiovascular risk calculators, provided that the participants were only 30-60 years at randomisation. The clinical response of the GPs was probably a pharmacological treatment of their LDL cholesterol, blood pressure, glycated haemoglobin, and so on, according to the targets of the current guidelines, exposing some patients early to harmful treatments, or to overtreatment, in attempting to reach overly strict targets. Two meta-analyses [2,3] showed that intensive glucose-lowering treatment (mean glycated haemoglobin [HbA1c] 6.7% vs about 7.5%) was associated with a trend towards increased all-cause mortality (by 2-4% or more) and cardiovascular mortality (by 11%, or by 58% after exclusion of trials with a Jadad score of ≤3 [2]). Indeed in the screening group of the ADDITION-Cambridge trial [4] the incidence of deaths was, in tendency, greater than in the control group in all-cause (hazard ratio 1.06), cardiovascular-related (1.02), cancer-related (1.08), other causes (1.10), and even diabetes-related mortality (1.26). The explanations for the lack of significant differences in the screening group (dilution, contamination, etc.) were inconsistent with the data, which show a tendency towards a worse performance, more consistent with possible arms of overtreatment or too intensive therapies [5].
Another meta-analysis shows that blood pressure targets of less than 130/80 mm Hg are associated with a trend towards increased all-cause mortality compared with targets of >130-135 mm Hg, despite the authors’ claims to the contrary [6]. Indeed the 2013 ESC-ESH Hypertension Guidelines [7], taking at last note of the evidence, elevated the treatment goals to <140/90 mm Hg for all adult patients, including those with ≥3 risk factors, organ damage, or patients with diabetes or cardiovascular or chronic kidney disease, for whom previous targets were <130/80 mm Hg, and even less for proteinuric patients.
Finally, the latest CTT Collaborators’ meta-analysis data [8] show that, for patients with a 5-year risk of major vascular events at baseline of less than 5%, the relative risk of any death with statins was not 0.91 as stated by the authors, but about 1.02 (there were 195 vascular and non-vascular deaths in 12,358 participants on statins and 193 in 12,432 participants in the control groups) [9].
The hypothesis of a iatrogenic damage for some people is in keep also with the even worse results showed by women (Appendix 3): in Model 3 HR for IHD 1.09 (0.93-1.27), IHD + stroke 1.08 (0.95-1.22), total death 1.04 (0.90-1.20). In fact it is well known that adult women have a lower cardiovascular and all-cause mortality risk than men of the same age, and overtreating women can expose some of them to a net damage, in the absence of any compensatory benefit.
References
[1] Jorgensen T, Jacobsen RK, Toft U, Aadahl M, Glumer C, Pisinger C. Effect of screening and lifestyle counselling on incidence of ischaemic heart disease in general population: Inter99 randomised trial. BMJ 2014;348:g3617.
[2] Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M, Lafont S, Bergeonneau C, Kassaï B, et al. Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: meta-analysis of randomised controlled trials. BMJ 2011; 343: d4169.
[3] Hemmingsen B, Lund SS, Gluud C, Vaag A, Almdal T, et al. Intensive glycaemic control for patients with type 2 diabetes: systematic review with meta-analysis and trial sequential analysis of randomised clinical trials. BMJ 2011; 343: d6898.
[4] Simmons RK, Echouff o-Tceugui JB, Sharp SJ, Sargeant LA, Williams KM, et al. Screening for type 2 diabetes and population mortality over 10 years (ADDITION-Cambridge): a cluster-randomised controlled trial. Lancet 2012; 380:1741-48.
[5] Donzelli A. Screening for type 2 diabetes and population mortality over 10 years. Lancet 2012; 381:902-3.
[6] Lv J, Neal B, Ehteshami P, Ninomiya T, Woodward M, et al. Effects of intensive blood pressure lowering on cardiovascular and renal outcomes: a systematic review and meta-analysis. PLoS Med 2012; 9: e1001293.
[7] Mancia G, Fagard R, Narkiewicz K, Redon G, Zanchetti A, Bohm M, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension. J Hypertens 2013; 31:1281-1357.
[8] Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL
cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of
individual data from 27 randomised trials. Lancet 2012; 380: 581–90.
[9] Donzelli A. Statins for people at low risk of cardiovascular disease. Lancet 2012; 380:1814-15.
The views expressed are his own and do not represent the views of his Organization.
I declare that I have no conflicts of interest.
Competing interests: No competing interests
Dear Editor
Professor MM Singh asks for data on changes in practices related to smoking, alcohol intake, dietary practices including intake of saturated fats, physical activity etc. Changes in lifestyle after five years have been extensively described earlier (references 15-20). We compared self-reported changes in lifestyle in the intervention group with those in a random sample of the control group, who answered a questionnaire. As no one in the control group was invited to the research centre, we do not have lipid markers in the control group participants, so this comparison cannot be made. We did not invite the control group to the clinic in order to avoid a spill over effect of the intervention, as seen in e.g. the MRFIT study. The aim of the Inter99 was not to describe which influence lifestyle changes and changes in blood lipids had on incidence of ischaemic heart disease, but to analyse whether screening and repeated life style counselling had any effect on incidence of the disease on a population level. There can be many reasons for the lack of effect. One – which was discussed in the paper – was that people from the lower social classes, with the unhealthiest lifestyle and the highest risk of ischaemic heart disease were under-represented among attendees. Other explanations could be that the changes obtained (ref 15-20) were too small and occurred in too few participants to affect the incidence of ischaemic heart disease (see comment from Dr. Tyron) or that many participants returned to their usual unhealthy lifestyle habits after the five year intervention period. The latter question is being analysed presently. It is important to remember that a general health check in a large unselected general population sample is entirely different from small scale interventions among few motivated people. Due to the randomisation procedure we have no reason to suspect major differences between the intervention group and the control group as regard the other factors responsible for ischaemic heart diseases as mentioned by Professor Singh.
Tyron speculates whether the changes in life style were big enough to induce a change in ischaemic heart disease, and as mentioned in the answer to Professor Singh this could be one of the explanations. Furthermore, those from the lower social classes that did not turn up might be at higher risk, which will dilute the effect on the population level. The example Tyron mentions with tobacco reduction is very illustrative – high relative changes can become small in absolute terms and can again become even smaller when non-response is taken into account. This clearly indicates that high risk strategy is not feasible on a population level, which was clearly demonstrated in the Inter99 study. We therefore do not agree with Tyron that we cannot draw firm conclusion from the Inter99 study. As all the former population-based studies have shown similar results, we believe it is safe to conclude that general health checks are not the way forward. But we do agree with Tyron that we should use all the tools that are available in combatting ischaemic heart diseases and other non-communicable diseases. Here we will argue that the structure of society (including regulation, taxation, subsidies, bans etc.) is the primary tool. This should be combined with information and individually aimed strategies. Furthermore we need to be careful to invite industries to advise health authorities in public health matters. Industries have a great interest in supporting that the individual has the full responsibility, a “blame the victims” strategy (smokers, obese people etc.). It is of great concern that general health checks are now performed in UK, Australia and Russia in spite of clear indications that they do not work. In UK a number of food industries (e.g. McDonalds, PepsiCo) were invited to advise the health authorities (J Wise BMJ 2010;341:1132). This is very problematic indeed and should be avoided, as these industries’ primary interest is to increase their market shares.
Professor M. Kopp asks for questionnaires developed to assess life style, motivation to change life style and health behaviour. These data are published in references 15-20. Furthermore, the full Danish versions of the questionnaires are available on our web site, www.Inter99.dk
Professor DS Sheriff argues that prevention is better than cure. We fully agree with Professor Sheriff, and every health professional should of course continue giving opportunistic advice on healthy lifestyle to their patients, as there is evidence of the effect, at least on smoking. However, our study clearly indicates that the way forward is not general health checks on a population level. A lot of literature, referred to in the Inter99 article, shows that structural changes in society have this preventive effect.
Samuel Finniken refers to an article from 1987 reaching very much the same conclusions as Inter99. A Cochrane review from 2012 summarised the evidence so far including articles published even earlier (ref 36 in the article). In 1986 Norwegian researchers (ref 3 in the article) showed an effect of screening and health counselling in a selected group of young Norwegian men. This led to an introduction of general health check of all 40 year old Norwegians without any assessment of the effect on population level. Later the Norwegian study has been criticised for not showing a significant effect (Ebrahim). The summary of all reports is in accordance with the Inter99 results. In spite of this more countries perform a general health check of the population – why?
Competing interests: No competing interests
I was aware that many people make New Year’s resolutions to lose weight by various means such as changing diet or starting an exercise program but sooner or later most of them have given up and and within a year almost all of them have regained any weight that they initially lost, and some are even heavier.
Consequently, in 1997, when I was diagnosed with angina, and learned that Nathan Pritikin had cured his heart disease with a vegetarian diet, I decided to try that method myself, and knew that I would need to be serious and strict about it.
I also needed a practical way of proceeding and I found that heart disease was common in modern civilised society and non-existent in native vegetarian tribespeople of the nineteenth century, and that the major difference was that modern foods are generally packaged in boxes, bottles, and cans, and contain increased percentages of sugars, fats, oils, salts, flavourings, and preservatives which affect the blood to cause the build up of cholesterol on artery walls.
I therefore placed a rubbish bin in my kitchen and opened my refrigerator and cupboards and removed all of the packets, bottles, and cans, and soon replaced them all with fresh fruit, vegetables, nuts, berries, and grains.
After a few weeks I found that the new diet was less tasty, and more boring, so I needed to offset that aspect by developing the idea that “it was better to be a live vegetarian than a dead junk food eater”.
As more time went by I gradually determined more palatable ways of combining the fruit and vegetables in soups, salads, and stews, and by the sixth month the angina symptoms had gradually eased away and I was able to stop taking medication.
Many things have happened since then which would be too complicated to explain briefly, but needless to stay I am still alive seventeen years later and I present this report to show the value of the knowledge of general population trends.
Competing interests: No competing interests
Sir,
Whilst reading this interesting and relevant piece of research, I was stuck by the parallels with another article I stumbled upon recently. Published in the BMJ in 1987, a simple audit done in a single general practice, concluded that case finding for diabetes and hypertension through a screening programme was not effective (1).
Much has changed since then, not least the diagnostic criteria for these common conditions. In 1987 the authors used glycosylated haemoglobin levels of over 10% in the diagnosis of diabetes, and diastolic blood pressures of over 100 mmHg for a diagnosis of hypertension. These values seem absurd in comparison to the ones we use today. However, when considering the results of Inter99 (2), the concluding remark in the 1978 article probably remains equally valid and applicable today as it did then:
“Opportunistic case finding by family doctors therefore remains probably the most feasible and cost effective measure in the community for the foreseeable future”
Perhaps not much has changed after all?
References:
1. Fairley R. How effective is case finding at detecting diabetes and hypertension in the community? Br Med J (Clin Res Ed). 1987;294(6581):1202.
2. Torben Jørgensen, Rikke Kart Jacobsen, Ulla Toft, Mette Aadahl, Charlotte Glümer, Charlotta Pisinger. Effect of screening and lifestyle counselling on incidence of ischaemic heart disease in general population: Inter99 randomised trial. BMJ. 2014;348. doi: 10.1136/bmj.g3617.
Competing interests: No competing interests
The present large scale study on screening and lifestyle counselling showed no significant reduction in the incidence of ischemic heart disease in the intervention group as compared to the control group over a decade of follow-up. The repeated counselling sessions in the study group were mainly related to smoking, diet, and physical activity and these too were individualized according to risk of developing ischaemic heart disease (IHD).
Although the researchers have shown that the counsellors were trained and very reliable, the study does not provide information on the changes in practices related to smoking, alcohol intake, dietary practices including intake of saturated fats, physical activity, etc. Information on this aspect would be useful in understanding the incidence of IHD in the study population. Implicating IHD incidence solely on the effect of counselling is inappropriate since several factors are responsible for the occurrence of IHD viz. family history, type A personality, treatment of co-morbid conditions such as hypertension, diabetes, etc. Non-modifiable factors (age, sex, genetic predisposition, etc.) cannot be changed with counselling.
The outcome of counselling in terms of changes in other risk factors including lipid profile should have been correlated with the incidence of IHD as well. These parameters would indicate whether these risk factors have been reduced over time or no changes have taken place and these factors can be put in the model for risk factor analysis for incidence of IHD. This will help in understanding the factors responsible for IHD despite competent counselling.
Competing interests: No competing interests
Dear Editor,
First we would like to commend Torben Jørgensen and colleagues on over a decade of work on the Inter99 Trial. They have made significant contributions over these years to key public health questions. However, we would like to remind readers of the challenges in drawing firm conclusions from the results of the Inter99 Trial. Over the last three decades, the prevalence of ischaemic heart disease has been falling in many countries around the world, including Denmark.(1) In addition, many of the risk factors leading to such diseases (including tobacco use, though excluding body mass index) have also been in decline.(1) This is a great victory for public health, but in light of national efforts that have altered prevalence, drawing conclusions about the impact of specific initiatives is challenging.
When looking at the impact of the Inter99 intervention on risk factor prevalence, previous publications indicated a strong impact on tobacco use, but less so on other risk factors.(2-7) Even the impact on tobacco use may not be as significant as the results initially indicate, considering a 9.1% differential in five-year abstinence of daily smokers results in only a 1.8% reduction in smoking prevalence (assuming a 20% smoking prevalence). Given the general decline in smoking prevalence in Denmark over this time, it is hard to separate the effects of personal interventions and national efforts.
Lifestyle counselling interventions alone have actually been shown to be relatively weak; the US Preventive Services Task Force does not recommend behavioural counselling in a primary care setting as it has concluded that the health benefits are small.(8) Furthermore, while the American Heart Association recommends a complex framework for population-wide cardiovascular risk behaviour change, including multiple interventions at all levels from governments down to schools and worksites, it notably excludes behavioural counselling.(9)
We agree with Jørgensen and colleagues’ comments on the importance of environmental change, and that “people face major barriers to making healthy choices and powerful pressures to adopt unhealthy ones”. Many of these barriers have been highlighted in Nicholas Freudenberg’s book Lethal but Legal.(10) Experience of 25 years in Finland (11) has shown the efficacy of a combination of environmental and regulatory change with effective high- risk interventions. However, we do not agree with the authors that “the way towards a healthier population is, to a greater extent, the responsibility of politicians and health administrators”. Instead, we propose utilising all of the tools available, guided by many of the principles of behavioural economics, for effective behaviour change.(12) Relying on rational responses of individuals to interventions, as many traditional behaviour change models do, ignores many of the irrational behavioural responses of the individuals, which must be considered in any behaviour change programme.(13) We have seen great successes in sustainable healthy behaviour change through the use of behavioural economics principles.(14, 15) It is essential to consider the full spectrum of evidence-based interventions and use tried and proven behavioural economic principles to design comprehensive programmes alongside government intervention.
References
1. Data from the Institute for Health Metrics and Evaluation Data Visualisations. Available at http://www.healthdata.org/
2. Pisinger C, Glümer C, Toft U, von Huth Smith L, Aadahl M, Borch-Johnsen K, et al. High risk strategy in smoking cessation is feasible on a population-based level: the Inter99 study. Prev Med 2008;46:579-84.
3. Toft U, Kristoffersen L, Ladelund S, Ovesen L, Lau C, Borch-Johnsen K, et al. The impact of a population-based multi-factorial lifestyle intervention on changes in long-term dietary habits: the Inter99 study. Prev Med 2008;47:378-83.
4. Smith LV, Ladelund S, Borch-Johnsen K, Jørgensen T. A randomized multifactorial intervention study for prevention of ischaemic heart disease (Inter99): the long-term effect on physical activity. Scand J Public Health 2008;36:380-8.
5. Aadahl M, von Huth Smith L, Toft U, Pisinger C, Jørgensen T. Does a population-based multifactorial lifestyle intervention increase social inequality in physical activity? Br J Sport Med 2011;45:209-15.
6. Toft U, Pisinger C, Aadahl M, Lau C, Linneberg A, Ladelund S, et al. The impact of a population-based multi-factorial lifestyle intervention on alcohol intake: the Inter99 study. Prev Med 2009;49:115-21.
7. Pisinger C, Toft U, Aadahl M, Glümer C, Jørgensen T. The relationship between lifestyle and self-reported health in a general population: the Inter99 study. Prev Med 2009;49:418-23.
8. Moyer VA; U.S. Preventive Services Task Force. Behavioral counseling interventions to promote a healthful diet and physical activity for cardiovascular disease prevention in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2012 Sep 4;157(5):367-71.
9. Pearson TA, Palaniappan LP, Artinian NT, Carthenon MR, Criqui MH, Daniels SR, et al. American Heart Association Guide for Improving Cardiovascular Health at the Community Level, 2013 Update: A Scientific Statement for Public Health Practitioners, Healthcare Providers, and Health Policy Makers. Circulation. 2013;127:1730-1753.
10. Freudenberg N. Lethal but Legal: Corporation, Consumption, and Protecting Public Health. OUP USA 24 April 2014.
11. Puska P. Successful prevention of non-communicable diseases: 25 year experiences with North Karelia Project in Finland. Public Health Medicine 2002; 4(1):5-7.
12. The Behavioral Foundations of Public Policy. Edited by Eldar Shafir. Princeton University Press 2012.
13. Ariely D. Predictably Irrational: The Hidden Forces that Shape our Decisions. HarperCollins 2009.
14. Patel DN, Nossel C, Alexander E, Yach D. Innovative Business Approaches for Incenting Health Promotion in Sub-Saharan Africa: Progress and Persisting Challenges. Progress in Cardiovascular Diseases 2013: 356-362.
15. Volpp KG, Troxel AB, Pauly MV, Glick HA, Puig A, Asch DA, et al. A randomized, controlled trial of financial incentives for smoking cessation. N Engl J Med 2009;360(7):699–709.
Competing interests: K. Tryon and D. Yach are paid employees of the Vitality Institute, part of Discovery Holdings SA. The company has a material interest in lowering health risks among its members through workplace programs
Reading this very important and comprehensive trial I wondered why authors have not used questionnaires developed to assess lifestyle, motivation to change lifestyle and health behaviour. Questionnaire material used in earlier population health surveys would have allowed more comparisons of the presented data and might have been a more valid instrument to document life-style changes in the different study groups. From a methodological point of view, results regarding the prediction from the physical sreening measurements seem trustworthy, but it seems likely, that reported life-style changes in the counselling group of the INTER99 randomised trial were influenced by under- or overreporting and therefore, do not entirely reflect 'real changes' in health behaviour.
Competing interests: No competing interests
Obesity and obesity related metabolic disorders including insulin resistant states are one of the leading causes of IHD. Biomarkers or risk factor assessment can be easy in a homogeneous population which has a scientific data base and medical facilities to intervene or treat or counsel the patient.
It is suggested that for every 4 kg/m2 increase in BMI, the risk for IHD is calculated to be a 52% increase. These data add evidence to support a causal link between increased BMI and IHD risk, though the mechanism may ultimately be through intermediate factors like hypertension, dyslipidemia, and type 2 diabetes.
Therefore prevention is better than cure may be the policy one could adopt and educate by creating awareness regarding heart attacks.
Børge G. Nordestgaard et al .The Effect of Elevated Body Mass Index on Ischemic Heart Disease Risk: Causal Estimates from a Mendelian Randomisation Approach . PLoS Med 9(5): e1001212. doi:10.1371/journal.pmed.1001212
Competing interests: No competing interests
The Family Diet and Heart Disease
When I was young our family’s main meal was the Sunday roast.
My mother would cook some beef in the oven and then pour the fat from the tray into a container where it was left to cool and go hard and white as lard.
Sometimes she would melt some lard and spread it onto toast and give it to us as toast and dripping, and tell us that our grandmother used to eat it during the depression and the war.
Sometimes she would add Vegemite which was advertised as containing vitamin B which was good for health.
She would also combine some cooked potato with milk and a large lump of butter to make mashed potato, and add roast pumpkin, and cooked cauliflower or cabbage to the meal.
She would then serve jelly and ice cream as desert.
We had a large back yard with a chook yard at the far end and a dozen or more fruit trees in the mid yard, and once a year she would collect the fruit and cut each item in half to remove the seeds and then put the fruit into a fowlers jam making container about 2 feet high and 2 feet in diameter. When it was half full of fruit she would pour in sugar until it formed a large triangular mound to the top, and then add fluid and then boil it to become jam.
She would then pour it into large jars with air tight seals on the lids, and store them in the cupboard to be used throughout the year for jam sandwiches.
She also baked sponge cakes in two pieces and put them together with layers of jam and cream in between and icing on top.
She would also make us fritz and sauce sandwiches, sometimes with tomato or lettuce, to take to school and on other occasions give us lunch money which I used to buy fish and chips or chico rolls.
Health education at that time was virtually non-existent.
As my mother got older she gained excessive weight and developed heart problems and died at about the age of fifty.
I recall her saying often that she had worked hard all day and was rewarding herself with a little treat which was chocolates, jam and cream on toast, or cake filled with jam and cream.
My father smoked cigarettes all day, and drank alcohol as soon as the finished work and went to the hotel or RSL club.
When he was 57 he had pain in his leg which was diagnosed as a blood clot, and told to retire and give up smoking and drinking or he would have a heart attack and die.
He kept smoking and drinking so I asked him why and he said that his entire social life involved smoking and drinking with his mates, and if he gave that up he wouldn’t have a life worth living.
He said that he hoped that he died quick and didn’t have to linger for years in a nursing home like his mate Nobby.
Sometimes he invited me to the club to play table tennis, and when he hit the ball with force his face would go bright red, so I told him to slow down or he might burst a blood vessel in his brain, but he ignored me and kept playing that way.
One day I received a phone call to say that he had just died of a heart attack, and with some additional conversations I was able to conclude what happened.
He had just finished a game of table tennis, and had a cigarette in his mouth, and an empty beer glass in his hand and was heading for the bar to fill it again when he dropped to the floor.
He was still alive when the ambulance arrived five minutes later but was dead on arrival at the hospital, and I thought that he was lucky to die the way he wanted to.
When my brother was in his late 30s I noticed that he was using a spray ventilator to assist his breathing so I asked him if he had asthma, and he said he didn’t, but was using the spray because of a heart problem.
He was always smoking cigarettes and drinking copious quantities of cola, so I asked him why he smoked when he knew it was a cause of lung cancer, and he said because it made him feel relaxed.
He died of a heart attack when he was 41 years old.
I developed heart problems when I was 47.
I then read a book about the Pritikin diet which reported that native tribespeople of Africa in the nineteenth century had no signs of heart disease, but 50% of people aged over fifty in modern Western societies had heart disease by the age of fifty.
I became a vegetarian immediately and have made some modifications to my diet since, but am still alive 19 years later.
My conclusion is that many factors contribute to heart disease but diet is the main one, and the easiest to control, but it does require self discipline.
I also note that my mother and father and brother were essentially fatalists insofar as they accepted whatever happened to them without doing much to remove the cause or change.
However many years ago I decided to be the master of my own destiny, insofar as if ever I developed a problem it was my own responsibility to identify the cause and do something about it.
Of course life would be a lot easier if I just accepted what happened and did nothing about it, but to typify my approach I coined the phrase in my CD about how I survived heart disease . . . “it is better to be a live vegetarian than a dead junk food eater”.
References:
Banfield Max Allan, 2014 (June 25th), The value of population studies in determining the cause and treatment of disease, BMJ 2014;348:g3617,(Online Rapid Responses), Actual page of response is http://www.bmj.com/content/348/bmj.g3617/rr/703395
Banfield Max Allan, 2015 (Jan 18th), Angina and its relation to diagnosis, diet, exercise, and cure, The British Medical Journal (Online Rapid Responses), Cite this as: BMJ 2014;348:g3617, Actual page, http://www.bmj.com/content/348/bmj.g3617/rr
Attachment page; Angina and its relation to diagnosis, exercise, and cure, http://static.www.bmj.com/sites/default/files/response_attachments/2015/...
Competing interests: No competing interests