When Homosapiens between 5-12,000 years ago committed to a more sedentary life practice with agriculture and animal farming, the Neolithic Period, the species underwent a major metabolic change and adjustment, that set the template for a nutrition that increasingly consumed more carbohydrate, fewer macro and micro-items, protein and fibre. Wheat, barley, maize, rye and rice seed grains were variously incorporated into nutrition slowly, after grinding and added to water for gruel and later beer. These were ‘whole grains’ and starches were released and spilled for consumption, we know as flour. Inspite of being whole grains, metabolic and structural skeletal changes arose in homosapiens.
For the first time we as a species had to contend with more carbohydrate daily than we had ever. Carbohydrate as hunter gatherers came from fibrous plants, seeds, berries, leaves, nuts, that required a different digestion process, as the starch had to first be released and converted to glucose in the gut. The process was protracted and more complicated, one which we had functioned with for at least 5-7 million years, that had its origins arguably in the first species with an elementary gut, such as the termite that consumes wood fibre!!
Not only was more carbohydrate consumed now, the ratio to fats, protein and fibre changed. This has been evidenced by Eaton and Cordain, studying hunter gatherer groups. Prior to that, histologic, biochemical and atomic studies with analysis, have confirmed the nutrition changes and revealed metabolic changes, features, consistent with the consequences of this nutrition. Height, bone length, pelvis and cranium size decreased. These phenotypic and atomic chemical changes I would argue are the genesis of our current degenerative diseases: manifesting as over weight, obesity, diabetes, hypertension, atheromatous vascular disease. Could we include Alzheimer’s disease and endothelial cancers?The changes, the above features, were absent in the skeletons of hunter gatherers, who did not change their nutrition, prior to this Neolithic period.
The changes could be described as clinically consistent with a form of malnutrition. Its commonly demonstrated in vast populations of the non-affluent world. At this time in our evolution, the Neolithic Period, infection flourished with proximity and I contend less robust immunity with malnutrition and poor protein consumption. Animal exposure was less of a contributor.
With time mechanical, industrial and scientific changes led to the removal of the outer casing of these seeds such, that only a carbohydrate flour remained. Processing this product with sucrose sugar later was the basis of the processed food industry, that is arguably the second largest industry on the planet, just behind the ‘Medical’ industry. Can you see a link there?
So a digestive system that had functioned similarly dealing with the type of food structure housing the carbohydrate, arguably for as long as herbivores, then omnivores had been on the planet, much more than 5-7 million years, had to adjust in the blink of an eyelid, in evolutionary time. Pancreatic cells increasingly had to respond more often and excessively to the carbohydrate load with insulin synthesis and release. The carbohydrate load and excess insulin, made insulin receptors less sensitive, as did factors from parked glucose as triglycerides in adipose tissues.The fat cells became an endocrine organ and initiated and maintained chronic inflammation.
The excess glucose from the carbohydrate is converted to fatty acids in the liver, measured as triglycerides in the blood and it provides low density lipoprotein as a small dense oxidised particle seen in atheroma lesions. No, saturated fat and cholesterol are not responsible. Yudkin, a UK physician demonstrated that in early 1960’s, but few accepted it.
Atheroma has been shown in a collection of arteries by MRI scanning of mummies over 3000 years old in Egypt. The area known as Egypt today was the ‘wheat bowl’ arguably of the world 3-4000 years ago. It had a thriving beer brewing culture also. This evidence of Atheroma is the oldest we have to date and it was found in arguably the area of major CHO consumption, not saturated fat and cholesterol.We have evidence ,I and others have postulated that an infective agent, like a virus infection in childhood, may initiate vascular lesions that do not develop, if the later nutrition does not facilitate it.
OWOB was recognised by very early chroniclers BC and subsequently and this feature was described in literature and recorded in art, sculpture and later photography. Its prevalence was limited but women knew how to deal with it by reducing CHO. An acceptable study in the USA in 1900 showed OWOB was near 1%! Its now 65-70%.
In Stone Ages in the Wrong Lane I have graphed since 1900 the consumption of natural foods species, with micronutrients, saturated fat, protein and they have all fallen since WWII in the US. Similarly trans fats, an extensive range of chemicals in food and packaging, vegetable oils, sucrose sugar, fructose sugar, high fructose corn syrup, alcohol, tobacco and all processed foods have increased markedly since WWII and particularly since 1980. I have labelled the time prior to WWII as the period of ‘nutrition deprivation’ and post, the period of ‘nutrition decadence’.
I did the same for the degenerative diseases and found their prevalence increased significantly after WWII and markedly after 1980. Lustig suggests this later increase was due to fructose via corn syrup, that is parked directly in adipose tissue. Corn syrup entered the processed food market in the 1980’s and sucrose use fell!!
Symptomatic CHD was recognised as angina in the mid late 19th century in Europe, due to partial coronary artery obstruction. Heart attack, coronary artery occlusion was first described in the early 1900’s in Europe and in 1928 in the US. The prevalence and mortality from the same in the US climbed to a peak in the late 1960’s-70”s then drifted downwards but has arguably returned to the peak figures. At no time has the prevalence of CHD faltered, just the mortality. Why? There has been a significant change in the way CHD now presents, with much less complete occlusion to partial occlusion that responds better to treatment, with a better prognosis. This is a patho-biological change that may be due to a general decrease in smoking in the affluent world. Or is CHD being detected and treated more effectively, earlier? Smoking is increasing in the non-affluent world, focusing on pro-bono product to children.
The simplistic concept that the consumption of cholesterol, determined the blood levels that in turn produced arterial lesions of atheroma was based on very poor biological concepts and science, that I have covered in my series of blogs on coronary artery disease. Atheroma,Atheromatous vascular disease, CHD are metabolic diseases where CHO nutrition overload effects excess fat(fatty acid) accumulation, insulin levels, insulin resistance, the production of hormone like factors that are responsible for a low grade systemic inflammation. The excess glucose from CHO consumption is partly converted to fatty acids in the liver who then find their way into adipose(fat) tissue and some is converted to small dense often oxidised LDL, that is found in atheroma lesions. Consumed saturated fat and cholesterol will elevate HDL and another type of LDL, that consists of large fluffy begnin LDL, that has nothing to do with atheromas.
Why does small dense LDL enter the vessel wall?Often LDL levels are normal or marginally elevated in CHD, as we found in our Aboriginal study. At this stage cardiology has no clear explanation for this, other than the small dense often oxidised LDL particles offer a large number and density of particles to physically enter the artery lining, which is likely inflammed.
Another potential hypothesis of artery entry I have proffered in other blogs. It is established now that the very early lesions of endothelial lumps, fatty streaks, fibrous plaques from fetus to adolescent, are a biological template for increasingly complicated atheroma lesions. The Nigerian study showed that if individuals do not have life practices and CHO laden nutrition, with these early lesions, they do not develope CHD, the early lesions do not evolve to obstructive or unstable atheroma. I have postulated these early lesions may be due to the Herpes virus, Cytomegalovirus, who appears to have the most consistent association with CHD.
I believe there is enough evidence to consider arterial atheroma, as CHD, peripheral and cerobrovascular disease, a two perhaps three stage disease in its evolution.Stage one is at the fetal, neonate stage with endothelial, elastic and smooth muscle changes. Viral infection such as Cytomegalovirus could be responsible or act as a pathogen that sites these lesions. Stage two.These lesions evolve, develope, become inflammed and accumulate small dense oxidised LDL who arrives as an ambulance!. This lesion may be an infected, inflammed lesion with accumulating lipid and as such has healing and collagen tissue present. Stage three. The lesion is now unstable and an infection such as a winter virus can increase inflammation and burst the lesion, that then initiates clot and obstruction variously.This can occur several times, followed by healing. Stage two can be avoided, influenced by avoiding the established RF’s. Its where the community needs to be.This is a hypothesis. Consumming animal saturated fat and cholesterol plays no part. That is a fact!!
I cover this in a Post on Indigenous coronary heart disease.