I have argued in my publication, Stone Agers in the Wrong Lane, that we and our fore-bears, pre and post Encephalisation( brain growth) must have made faulty decisions, adaptations, such that extinction occurred 21 times, after seperation ,5-7 million years ago with the Chimpanzee from Concestor three, a large African primate. We now house the most diseases ever to afflict homosapiens at epidemic levels in the affluent and non-affluent world. The Chimp residing still in the Central African rainforest, remains unchanged genotypically, phenotypically, with none of our degenerative diseases, CHD, AVD, DM, OWOB. Do we have better judgement now? I see no evidence of it.
Members of our earliest fore-bears graduated to the forest floor, spent most time there, stood up and moved East. Originally herbivores, then insectivores, scavengers then omnivores. Climate changes, topographical changes lead to nutrition change. The Hominid species that followed the Australopicenes drifted West to the Rift Valley where subsequent species divisions arose, Encephalisation emerged with skeletal growth and a penchant to migrate.
There has been a tendency by commentators to link a homosapiens concept, intelligence with Enchepalisation. Brain mass, size maximised at the birth of the species homosapiens 2-300,000 years ago, plateaued and reversed surprisingly quickly in those who adopted Neolithic nutrition, accompanying other metabolic and skeletal changes. Neolithic nutrition increasingly consumed more seed flour with a major loss of micronutrients, with a range of plant species, animal protein and fats. The skeletal, biochemical, histological and metabolic changes with reduction in brain size, that arose after this nutrition change, where CHO was increasingly consumed, is striking and I believe a major hinge point in our biology, evolution and survival.
Prior to the Neolithic Period, CHO was consumed unmodified in plant, seed, nut, leaf form from 2-500 different species. The CHO was part of an extensive fibrous network, skeleton of a species, as polymers of monosaccharide sugars, starches, proteins, encased in cells,that commenced their ‘digestion’, breakdown in the oral saliva and gastric juices, then the small bowel, where glucose was released and absorbed. This was a slow process and so blood levels were minimal, spikeless, as was the shadow release of pancreatic insulin. Like eating a stalk of celery, or all vegetables, fruit and seeds today, uncooked.
Seed flour released from this fibrous skeleton, incorporated into damper, breads of all kinds, baked biscuits, cakes , confectionary etc. needed little enzymatic digestion and quickly glucose is available for absorption . With sucrose white sugar similarly, glucose enters the blood quickly in large doses, requiring similar response from insulin. Regular ‘overdosing’ with processed CHO, sucrose with time, perhaps 4-5 years, leads to cell receptors for insulin adjusting their sensitivity or becoming resistant and this adds to the levels of blood insulin and glucose. Its a cellular survival mechanism, being presented with excess glucose. This is a pre diabetic or diabetic state and can be reversed by those affected. Persistent raised levels of glucose can effect a process of ‘glycation’ of tissue and inflammation. This is a ‘curable’ state or disease.Except for the seasonal dose of bees honey, we as a species and fore-bears, had experienced nothing like this ever! As a child, I knew DM as ‘sugar diabetes’.
More recently we have high fructose corn syrup, that is converted to fatty acids and parked in fat tissue. In the Period of Decadence after WWII, the consumption of CHO has increased markedly with OWOB and DM as shadows. There is also a large population consuming more CHO than ever previously, often with abdominal, omental fat collections, that have degrees of CHO dyslipidemia, insulin resistance, endocrine fat mediated inflammation, that are at risk for CHD. They can be overweight, but are not pre or diabetic.Most, 80-90% of those with DM and OWOB, die of AVD, or CHD. As Cardiologists our patient cohort is significantly larger in number, than those with OWOB and DM, who are risk factors for AVD, CHD.
As clinicians, if we reduce markedly, or eliminate processed CHO we can reverse or eliminate the dyslipidemia, the insulin resistance and inflammation surprisingly quickly and change the patients morbidity and mortality prognosis, while their mass responds more slowly.
Every cell in our body requires glucose daily as the main energy source for survival. If we choose to consume CHO such there is excess glucose, it is converted to fatty acids in the liver and released to park in fat . Fat tissue assumes endocrine activity with a range of cofactors produced and inflammation also arises. These fatty acids have a propensity to produce small, dense, oxidised LDL that is the primary lipid found in atheroma. This lipid state is known as the CHO Dyslipidemia or Athrogenic Dyslipidemia. Consumed animal, saturated, monosaturated fats and cholesterol play no part in atheroma or CHD. Many in medicine in the 1950-60’s were aware of this but poor science, pressure groups, health agencies, commerce and absence of those trained in medicine, saw evidence and common sense ignored. This was the saturated fat and cholesterol ‘con’.
Tobacco consumption is an important contributor to inflammation, vascular pathology and malfunction. Most hypertension is associated with insulin resistance and inflammation, all risk factors for coronary heart disease.
Not only has this modified CHO consumption spawned our degenerative diseases, I believe it was a major contributor to the population explosion from 1850-2010, where Colonial invasion of the New World, vastly expanded grain production, to effect and grow populations, as Malthaus predicted. It seems grain supplies of energy calories, had more nutrition than today, where degrees of malnutrition and near starvation are reversed, ovulation and conception return, infants and mothers survive better and the population increases. What Malthaus would not know is this calorie provision was poor nutrition, that effected faulty immunity and metabolic states later on . So while populations survived they perished prematurely, by our standards today. In that 150 year period, near 6-7 billion homosapiens came to inhabit the earth. The increase was predominantly in the New World Colonial non-affluent nations.No medicine had very little to do with that. In the latter part of the 20th century some improvement in nersh (nutrition, energy,respiration, reproduction, sanitation,water) with immunisation and improving infant and maternal mortality occured. But energy via the calories provided by CHO provided the universal start. It seems we with other mammals attempt to effect degrees of ovulation during malnutrition, possibly to continue survival and reproduction. Ovulation fails with starvation.
In my series of posts on coronary heart disease, its origin and evolution, its clear that the change of nutrition in the Neolithic period, the introduction of sugars with processed CHO, has accompanied the spawning of CHD, the planet’s leading killer, a food born , self inflicted disease. CHO processed and freed from its plant origins can be argued to be a long term toxin. But as a starch, polysaccharide, fibre or plant sugar in vegetation, it is digested, absorbed and metabolised with insulin as it has been since mammals first consumed plant vegetation.Its another example of HSLC where homosapiens takes another faulty direction, the preperation of food when we evolved, adapted as hunter-gatherers to what was available on the planet.
I will prepare a blog on the large range of vegetable oils and ask why did we produce them and do they contribute to disease?
Dr.Lindsay.A.Green. FRACP. FCSANZ.