The Neolithic period of homosapiens time on this planet has provided us with evidence that we as a species underwent anatomical structural changes at this time that would have arisen only with significant metabolic changes that we can observe in bone changes and anatomical mineral measurements. These variations, changes can be compared with the skeletons of pre-Neolithic ancestors and the striking features are height, and bone size.
This was the period of slow adoption of more sedentary living, more groupings, adoption of resident shelter with gardening, animal herding and use of natural local grains, already adapted.The nature and number of food items contracted slowly as hunter and gathering practice fell. There is bone biochemical evidence that protein consunption fell and the possibility that enteropathies from grains contributed also, like Celiac disease and syndromes.Group proximity living aided viral and bacterial spread which with time would have been helped with a variable malnutrition that was responsible for the height reduction and skeletal changes. Immunity in this context suffers and would have contributed to infection. From a biological perspective the nature and extent of these changes show how sensitive we as a species are to nutrition changes.This was a state of relative malnutrition as Neolithic practices spread over the globe. Encephalisation in our species reached its zenith near a century ago and plateaued, then shrunk a degree post Neolithic practice. What adaptions did all the organ systems make in this context?
Metabolism changed to deal with the limited variety of foods and the quantities of them. The Carbohydrate load increased and animal protein fell, so insulin demands inched up and more so as grain was dehusked and flour contents free for food and gruels and later beer brews. With time the CHO load in an individual reached a level that glucose the CHO source in blood was excessive and certain tissues adapted mechanisms to prevent overload of glucose in each cell and its known today as Insulin resistance. The extra CHO as glucose is returned to the liver and converted to triglycerides that make their way to adipose tissue, where it is stored as fat. Insulin facilitates that. My Endocrine colleagues will be un-impressed with my simple version of fat accumulation.
So overtime and it has and does vary, consumption of CHO as grain flour, cane and root sugar with fructose in an exploded processed food industry has provided excess CHO that accumulates as fat. That fat is available for future use as energy if required.This process was very useful as hunter-gatherers when food times were lean, Protein, CHO as muscle glycogen, fat can be mobilised at times of need such as deprivation, malnutrition and starvation.
As CHO has become increasingly available in its extensive range of processed food as flour sugar and fructose more glucose is converted to Triglycerides and deposited as fat. In this context we will have excess glucose and triglycerides circulating in our blood.Accumulation of fat tissue is a means of adaptation but becomes excessive. This fat tissue now can function like an endocrine organ producing cytokines and other biological factors that are playing a part in metabolic behaviour.
The simple sequence of metabolic changes that arise when consuming excess CHO is the template for the origin of chronic degenerative diseases that we know as Atheromatous Vascular disease(AVD) which manifests as Cerobrovascular Disease(CVD), Coronary Heart Disease(CHD) PeripheralVascular Disease( PVD), Overweight, Obesity(OWOB) Diabetes (T2DM), Hypertension, Alzheimers Disease and the cancers of the Breast, Bowel and Prostate.Arguably this cohort of diseases is resposible for the majority of non-infective disease on the planet, so its ‘cost’ in human death misery and financial cost is immense and I am making a case for its origins at the Neolithic period and seems mostly the result of human judgement.
The role of CHO in OWOB has been described. Interestingly the site of fat plays some part in its endocrine activity. Omental abdominal fat appears to be most active in this respect compared with subcutaneous fat.This ‘organ’ can increase insulin resistance and effect chronic inflammation. As such chronic hyperisulinemia persists and is responsible for arguably many of the complications of diabetes. AVD now appears to be a consequence of Triglycerides producing small dense LDL, the lipoprotein that enters the the artery endothelium and arguably initiates the early atheroma lesion. Its possible an infective agent like CMV may be the very early injury agent, often in childhood. The most common Hypertension, essential hypertension is aggravated by alcohol and definitely improves or is eliminated with weight reduction, fat tissue depletion. Currently it appears the risk factors for AVD are those for Alzheimers disease. The three common cancers have the same risk factors also and one large European Study suggests most cancers have the same risk factors. That has not been proven but fits the trend and also my hypothesis.prior to this.
Where does Tabacco and alcohol fit in this hypothesis. Alcohol provides quanta of CHO as alcohol and from its production. Some early gruels with grains fermented and alcohol was introduced to humans. Berries and grapes could have self fermented and been used seasonally. Tabacco was considered benign until recently. Its link with the commonest lung cancer was a triumph but is effect on artery function, sytemic inflammation, hypertension, IR, and atheroma are more recent. The treatment of hypertension and smoking rfeduction appear to be thr major factors resposible for the marked reduction in CVD mortality, but prevalence persists at the same level and in some areas is increasing.