Conventional accepted RFs for CHD have never completely explained the prevalence of CHD in affluent populations. When the same RFs are measured in non-affluent and Indigenoust populations, they are present but do not explain the extent and consequences of CHD, that manifest as major reductions in life expectancy. Are there other contributing factors responsible for the increased prevalence and mortality?After all the majority of research is done in affluent caucasian populations. The list of RFs have remained unchanged for near 50-60 years: smoking, serum cholesterol, hypertension, DM, and treatment for these conditions may well be responsible for the reduction in annual CVD mortality but not prevalence. For a long time cardiology was not sure where OWOB fitted and so linked it to DM. The dogma from the USA was to reduce animal fat and cholesterol in the diet to help avoid CHD. If you have read other posts in my blog or numerous publications, including my Stone Agers in the Wrong Lane, this concept was entirely false and never proven to be the case. It was arguably the largest ‘con’ ever in medicine.Could this falsehood be playing a part in the caucasian, Indigenous CHD prevalence and the discrepancy in the caucasian RFs?
Providing cardiology services to the Indigenous in Northern Australia in the early 1990’s it was apparent to me they were not consuming animal fat or cholesterol in any quantity at all and I had a dietitian confirm that at Woorabinda.The animal sources of saturated fat and cholesterol due to cost, were rarely available to them on a benefit and too much of that was spent on tobacco and alcohol! Its difficult to consume large quantities of saturated fat in an average diet and more so on a benefit!!Total cholesterol, LDL levels did not reflect the extent of CHD morbidity and mortality in this cohort, who had at that time a life expectancy estimated at 20 years less than caucasians. If their CHD was due to cholesterol and LDL I would expect these two indices to be significantly elevated and frequently so. They were not!!! Triglycerides were commonly raised and the ‘good’ cholesterol, HDL was low!! We recognise these features now as CHO, Atherogenic Dyslipidemia, but not then. Because pre-diabetes, DM was common amongst the Indigenous, this dyslipidemia appeared to accompany them. At one time it was known as the Diabetic Dyslipidemia!!
In the early 1990’s features of the German PROCAM study were finding their way into the literature, looking at cardiology RFs in German men. There was one cohort of non-diabetic men with the triglyceride, HDL features and CHD. This was what I was witnessing in the Indigenous patients. What would German men and Indigenous in Australia have, or be experiencing, to share this lipid feature?
For me as a cardiologist, clinically involved with the Indigenous Australian, there were inconsistencies in the origin of their CHD, which was premature and extensive. The official dogma from the US and most ‘health’ bodies was that saturated fat and cholesterol was the dietary contributor to CHD and they would raise your serum cholesterol and LDL. Well the Indigenous cohort I was observing and clinically managing were not consuming saturated fat and cholesterol hardly and consistent with that, elevated cholesterol and LDL was not a feature of their lipid profile. Oops! But the elevation of TG’s and low HDL was a very common feature in their lipid profile. Could they be playing a part in Indigenous CHD? Up until the PROCAM data these indices had not convincingly been linked to CHD, although a low HDL was often seen in CHD.
The TG/HDL ratio was used by Endocrinologists as a measure of insulin resistance, seen in DM and Metabolic syndrome. DM prevelance in Indigenous Australian studies ranged between 10-15 %, but the TG/HDL feature was much more common. 80-90% of DM patients die of CHD. How much did smoking, OWOB, hypertension and the Metabolic Syndrome contribute to Indigenous CHD?
If cholesterol was to play any part in CHD, what type was it and where did it come from?It became apparent that CHO excess consumption was responsible for IR(insulin res) raised TG’s and lowered HDL. So animal fat and consumed cholesterol played no part. So if you had CHD, raised TG/HDL ratio and near normal, normal cholesterol and LDL, where did the LDL found in the artery lesions arise?
We now know the LDL that enters the artery is a small dense often oxidised variety that arises from the TG’s!!! So consumed saturated fat and cholesterol do not contribute to small dense LDL but can produce a large fluffy variety that does not enter the artery wall. Measuring smLDL is more available now and counting the number of LDL particles indicates the extent of CHD. At this stage, TG/HDL, with sdLDL is arguably our best indicator of CHD.
Method. Woorabinda and Bidgerdii Aboriginal medical centres in Central Queensland provided 803 adult participants.Dr.Tom Lynch provided all laboratory data pro bono. Hb, WBC, U/electrolytes, creatinine, glucose, LFT’s, lipid profile(cholesterol, LDL, HDL,TG) CMV antibody, and microalbuminuria. Weight, hip/waist was measured.