Supports Chapter 21: Diseases of the heart and blood vessels
An interesting study has just been published which looks at a wide range of possible variables in the formation of the arterial lesions thought to cause heart attacks. The interesting part is that, although all the traditional ‘risk factors’ for heart disease such as cholesterol, HDL, LDL were considered, the factor that really stood out was none of these. It was blood glucose levels – from a ‘healthy’ carbohydrate-based diet, perhaps?
This study is open access so anyone can read the full paper online.
Nunes JPL, Silva JC (2009) Systemic Correlates of Angiographic Coronary Artery Disease. PLoS ONE 4(1): e4322. doi:10.1371/journal.pone.0004322
Abstract
Coronary angiography allows a direct evaluation of coronary anatomy.
The aim of the present investigation was to search for correlations between the magnitude of coronary artery disease, as assessed by angiography, and a number of systemic parameters.
A group of 116 patients (80 male, 36 female) with coronary heart disease diagnosed by angiography, aged 62.0610.5 years, was the subject of an observational study.
Correlation and linear regression analysis using coronary artery disease burden (CADB - sum of the percentage of the luminal stenosis encountered in all the lesions of the coronary arterial trees) as dependent variable, and age, sex, plasma calcium, phosphorus, magnesium, glucose, HDL cholesterol, LDL cholesterol, triglycerides, uric acid, estimated glomerular filtration rate and body mass index as independent variables, were carried out.
Significant correlation values versus CADB were seen with age (r 0.19, p 0.04), uric acid (r 0.18, p 0.048) and fasting plasma glucose (r 0.33, p,0.001). Linear regression analysis, yielding a global significance level of 0.002, showed a significant value for glucose (p 0.018) and for sex (0.008).
In conclusion, among several systemic parameters studied, plasma glucose was found to be correlated to coronary artery atherosclerosis lesions.
3 comments:
IMO the lipids are a marker for hyperinsulinemia. Would have been useful if they'd looked more at postprandial glucose which often goes south well before the fasting levels are affected - and which is obviously controllable by reducing carb input per meal.
Well before reaching the rather high diagnostic criterion for "diabetes" you may be controlling your BG by overproducing insulin postprandially, worsened by insulin resistance. By the time diabetes is diagnosed maybe 50% of the pancreatic beta cells have died. That's a time when intervention could have prevented further disintegration
Hi Trinkwasser
You are quite right about postprandial insulin production. I had hoped to put a graph on this blog illustrating the postprandial glucose and insulin response in obese adolescents (but couldn't work out how to do it!)
What is shows is that, in response to a normal glucose tolerance test, where a healthy person's glucose would rise steeply to a high level and then fall as insulin is produced (there is an example on my Website), in an obese adolescent, with insulin resistance, the initial glucose rise is very small as that person's insulin response is so dramatic. This must put a strain on the pancreas.
And, as Type-1 diabetes is becoming much more common, particularly in the US, it could well be that continuing high glucose loads fuelled by the high-carb, 'healthy eating' message, is damaging these kids' pancreases and creating Type-1 diabetics from otherwise healthy kids.
Not just obese adolescents, don't forget some 20% of Type 2s are skinny - like me, and other family members who show insulin resistance despite being slim fit and active. Unfortunately I can't get the others off their "healthy" diets despite showing them how much my BG and lipids are improved.
IMO I have probably never had a proper Phase 1 insulin response since early childhood, but my Phase 2 is still quite strong, though often delayed, which gives a pattern of a high spike immediately after eating, followed by a rapid drop (reactive hypoglycemia when the insulin output also fails to shut down). This may also be due to IR in the receptors.
I suspect the basis is genetic (runs through one specific line of the family, going back generations) but the genes are triggered by the diet. They were probably useful in the past, for rapidly stashing fat to fuel a food shortage or a migration, but never get shut down in times of continuous plenty.
The Government seems to believe that some 30% of the population *will* become diabetic, but doesn't seem to see that connection - nor that to the rapidly rising rates of obesity, not to mention other cardiovascular diseases, since they are insisting on pushing carbs and low fat on everyone. Or perhaps they are trying to eliminate us from the gene pool?
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