SATURATED FAT and CHOLESTEROL CONSUMPTION DOES NOT CAUSE INDIGENOUS CORONARY HEART DISEASE or METABOLIC DISEASE.
In 1992 I had the opportunity to spend twelve months at Cairns base Hospital, to escape several years of being ‘Corporate Managed’ by a group of drongos in NZ, who knew nothing about medicine. This was another ‘Corporate’ fashion statement, effected by the gullible politicians, with as usual, no acceptable evidence to medicine it had any value, and it did not for patients or staff either. It transferred power and control to the ‘elite’, which has nothing to do with talent, skill, knowledge or standards.They had the usual Corporate commercial slogans, like we are here to ‘share’the management of hospitals and clients with you’. Really! They were so generous, as we did not ask them. If I told my patients that, they would dress and leave if conscious!!There would be a collection of patients in pyjamas at the lifts!!
My clinical experience with Indigenous patients at Cairns, Yarrahba, Rockhampton, Bidgerdii and Woorabinda, left me in no doubt that saturated fat and cholesterol consumption played no part in their CHD and DM. A dietic review easily revealed that. I would try to discuss it, but there was a ‘silence’ about the issue, or statements that they ate ‘junk’ food or they had an ethnic defect. Really informed and scientific! Indigenous central obesity, hypertension and smoking were not in dispute as risk factors, no different to the risk factors of the caucasian population. So what was responsible for the extent and prematurity of CHD, where inspite of very limited Indigenous disease data in NT and WA until 1984, Indigenous Australians had a stated life expectancy 22 years less than the Australian caucasian population in 1984! I spoke with the chief ‘Health’ statistician in Canberra in 1995 and he candidly said he could not supply me with the list of data for Indigenous Australians I requested and there were no ‘national’ figures! Where was the UN, Unesco,the World Health Organisation?Where was Australian Medicine?
I was surprised to find in the preparation of my book Stone Agers in the Wrong Lane and Nomad Physician, there was a goodly sprinkling of Australian doctors and other researchers, looking at Indigenous disease issues from the 1930’s. It seemed quickly established that adoption of caucasian life practices played an important part. As recent as 1966, autopsy studies of Australian Indigenous in SA, revealed at worst, minor CHD! It was at this time CHD mortality in the US reached its peak! This change included nutrition which initially was below the radar, compared with smoking, booze and OWOB.The convention then was if you became OWOB, you were eating excessively. If the Aboriginal had CHD, saturated fat and cholesterol was responsible. In none of the studies was there convincing evidence for that. If so, where did it come from? When you are poor, in a state of poverty, relying on a meagre benefit, you cannot afford all the cuts of beef, lamb, pig, chicken, turkey,fish, cheese, milk, butter, yoghurt and cream. You adopt the swagman’s sustenance, flour, water, tea , matches and a billy can, metaphorically. This was reflected in their lipid profiles in the studies I mentioned looking at DM and the CQ study I completed with Tom Lynch. Their excess DM did not arise from saturated fat and cholesterol!!
The early Indigenous studies generally traced the prevalence of DM and its complications, finding hyperglycemia, insulin resistance, and abnormal glucose tolerance with measurements of blood pressure, ecg recordings, BMI’s, anthropometric measurements and a lipid profile either of total cholesterol, or more recently the same with LDL, HDL and TG’s. These studies repeatedly showed the indices of DM as the neurological, cardiovascular and renal complications galloped through the Indigenous people. Cute small studies by O’Dea demonstrating the reversal of DM and its complications in a small cohort of Indigenous men over seven weeks, by being left in the ‘bush’, to consume ‘bush tucker’, was seminal!
My review of this quite large group of studies simply demonstrated that adoption of the introduced Colonial life practice, from the hunter gatherer state, with an extensive documented consumption of plant, fruit, berry and animal items, a form of assimilation, was responsible for the diseases of CHD, central abdominal obesity, diabetes and renal disease. Colonial doctors in Africa observed, documented and published this data largely in the late 19th century and early 20th century. The US had similar experiences with their Indigenous people. US academic medicine showed no interest. But why was this Indigenous Australian population perishing so early and extensively?
From a cardiologists perspective, in retrospect, several interesting features were present. Rarely did total cholesterol and serum LDL levels exceed the normal range, in a cohort that was ‘riddled’ with CHD!We observed this managing patients with ‘heart’ attacks’ in CCU’s! This cohort was not consuming excess saturated fat and cholesterol. Similar studies amongst the First Americans in the US, revealed near identical results, BUT still the Lipid Hypothesis trucked on. Why?Castelli, head of the Framingham Heart Study stated in 1992 that saturated fat and cholesterol was not responsible for CHD and I heard him repeat it in Auckland at a NZ Cardiac meeting!! That was an enigma for me! Yes, DM was common in Indigenous Australians, between12-15% compared with3-5% in caucasions, but this level could not account for the extent of CHD. From my perspective there was nothing revealed in this large number of Australian Indigenous studies to link consumption of saturated fat, cholesterol with blood levels or the clinical extent of CHD. I had graduated from an academic institution that had demonstrated in studies, that the hunter-gatherer’s of a collection of Pacific Islands had no evidence of CHD or its risk factors, consuming higher levels of saturated fat than in affluent nations, and they had no CHO or sugar in their diet!! Keys and US medicine ignored the results of TIMS and other Indigenous studies in Africa and the USA.
Looking at the Lipid Hypothesis history, it was hard to know whether Keys was just ignorant, without a medical perspective as a nutritionist or whether his personality prevented him from wavering from his faulty dogma. The same Island cohort on migrating to NZ within six months were expressing risk factor abnormalities and reduced their saturated fat, while overdosing on processed CHO and sugar! It was like conducting a laboratory study. Like the French Lyon Study and the Procam study later, American medicine ignored these studies essentially.
A feature of all the Indigenous Australian DM studies when they were measured, was the elevation of TG and the depression of HDL. Historically HDL was considered the ‘good’ cholesterol and demonstrated to be associated with the absence of CHD. The status of TG initially for some time was unclear and some-what ignored with respect to CHD. With time amongst those with DM, elevated TG and depressed HDL became a feature and described as DM Dyslipidemia and later CHO Dyslipidemia. In 1994 the German Procam study drew attention to the association of CHD and this lipid abnormality, in a study cohort who were not diabetic.Again slowly the Americans conceded that this ratio of TG and HDL may play an additional part in CHD, but total cholesterol and LDL still held centre stage. BUT, you did not raise TG and depress HDL by eating saturated fat and cholesterol, you needed to ‘overdose’ on processed CHO, sugar and vegetable oils.! All was quiet again.
By this time the cholesterol carrier proteins Apo A and Apo B were closely studied and still are. LDL was found not to be one entity but two and possibly more. If you were able to raise the serum LDL with excess saturated fat consumption, the HDL levels increased too and the LDL increase was due to large fluffy collections, particles, that are deemed harmless. This data says it is fine to eat saturated fat as far as CHD is concerned. So why is LDL associated with CHD? Well this LDL type, is primarily a small dense often oxidised particle that is sourced from TG’s!! The TG’s arise from CHO overdose. This takes us back to the early 1960’s when Yudkin was ignored in the US, when he showed CHO was responsible for CHD and demonstated this to Key’s on reviewing the 7 Countries data. This damming, critical fact was essentially ignored in the US until now. The consequences in morbidity and mortality are staggering.
In the early 1990’s working in Central Queensland with many Indigenous patients, I realised saturated fat and cholesterol consumption was minor and not playing a part in their extensive CHD.This observation was the genisis of the CQ Indigenous Cardiac Risk Factor Study. What really was responsible? The German Procam data had just been published and the lipid profile of their patients with CHD was synonomous with my experience amongst Indigenous patients. A new interest in the part the Herpes group of viruses may be playing in atheroma lesions and CHD in the US emerged; now access to the aorta, carotid and coronary arteries, made lesion biopsies simpler. Cytomegalovirus(CMV) I felt was the front runner, on the evidence we had and its behaviour in transplant coronary artery atheroma. Chronic inflammation and insulin resistance emerged at this time associated with CHD. New interest arose in the association of microalbuminuria and CHD, and efforts to explain this two organ link produced new studies.Looking for features that may explain the disparity in CHD mortality for Indigenous Australians, I looked for evidence of TG/HDL lipid abnormality, insulin resistance, inflammation, CMV past infection, with microalbuminuria as well as the list of conventional measurable risk factors.
I spent time with the elders of Woorabinda and Bidgerdii and obtained their consent and support. The CQ University Ethics Committee gave approval after the Rockhampton Hospital Ethics Committee turned it down twice!! I must say all consultants at Rockhampton Hospital agreed to refer Indigenous patients and were not members of the Ethics Committee!!
Professor John Neutze, Professor John Scott and Professor Norman Sharpe from the Department of Cardiology, Auckland Medical School supported the study concept and offered helpful reviews and suggestions. Dr. Tom Lynch generously provided pro bono, all the laboratory work for 875 participants. The ‘health’ teams at Woorabinda and Bidgerdii were vital for the collection of data.Liz Young was our key Indigenous support.
The study was completed in 1997 and presented in part or complete at cardiology meetings, physician and general practice meetings in Australia and New Zealand.At this time and subsequently, the Lipid Hypothesis, the consumption of saturated animal fat and cholesterol, drowned the debate on the origins of CHD. The US journal, Circulation was interested in the concepts, made suggestions that would have cost us out of the park. Our results attracted little interest in cardiology. In the last decade, the mood has changed and evidence based challenges and reassessment of past studies has sunk the lipid hypothesis.Our study demonstrated that the CHO, Atherogenic Dyslipidemia present in 376 adults in the study was the the dominant lipid abnormality due to the ‘overdosing’ of processed CHO and sugar, not animal saturated fat and cholesterol. We drug treated all the afflicted patients for three months. The contribution of cytomegalovirus has a way to go: infection studies on the early lesions of fatty streak and and fibrous plaque could help.
I have after twenty years, retrieved some presentation data below, because the significance of Cytomegalovirus in atheroma has become more probable and a vaccine closer to acceptance, for other reasons. Cardiology(most) now accepts, that Carbohydrate Dyslipidemia, Atherogenic Dyslipidemia, where the ratio of TG/HDL is elevated due to ‘overdosing’ on CHO and sugar and fructose, is the basis of arterial atheroma, responsible for small dense LDL present in arterial lesions. Carbohydrate Dyslipidemia was clearly demonstrated at near 50% of adults in this QLD., study with the Metabolic Syndrome. I treated 396 adults from the study with this lipid abnormality with fibrate, provided free of charge by the drug company and had Queensland Health deny this population the services of a dietitian to help eliminate processed CHO and sugars from their diet, not saturated fat and cholesterol.They refused to continue the fibrate medication also. We felt a better name for them was Queensland Unhealthy.
I believe this CQ Aboriginal CV Study (1996-7) has data of value, twenty years later. In particular it demonstrated the major extent of the Atherogenic Dyslipidemia, CHO Dyslipidemia that was decimating, and largely responsible, (with tobacco) for the extent of the morbidity and mortality in this Indigenous cohort. Twenty years ago, inspite of my emphasis when presenting the data at meetings, that this cohort of Indigenous Australians riddled with CHD, did not have the conventially accepted cholesterol levels to support it, the lipid hypothesis survived. Triglycerides and HDL abnormalities due to CHO overdosing were the culprits. It also showed once again, too often where Government institutions are not helpful for disease.
This data provides a treatment program from childhood, to help avoid CHD, our leading killer, in Aboriginal and Caucasions. Incidently it will have impact on OWOB, DM, MS and arguably other pathologies, AD and some cancers.