The Real Meal Revolution: The Radical, Sustainable Approach to Healthy Eating

by Tim Noakes

Hunger is regulated by two factors in the foods we eat – the first is their bulk and the second their nutrient density. Bulky foods fill the stomach and produce a rapid satiation whereas nutrient-dense foods turn off hunger for much longer. Importantly, carbohydrates and protein/fat foods act quite differently on both these directors of our hunger.

carbohydrate-rich foods like pasta, potatoes, cereals, bread and many vegetables – the food encouraged by the 1977 USDGA – are bulky and when eaten, they quickly fill the stomach, producing a more immediate satiation. But because these foods are not nutrient dense, their satiating effect passes quite quickly and hunger usually returns within an hour or two. That is why a pasta meal is never quite enough.

In contrast and in ways that we do not yet fully understand, foods with high nutrient density satiate hunger over much longer periods – six to twelve hours.

Moss describes how the manufacturers of processed foods use a special testing method to identify the ‘bliss point’ which is the ‘precise amount of sugar or fat or salt that will send consumers over the moon’ (p. xxv). So, processed foods are engineered specifically to maximize their addictive potential, to ensure that we will always ‘crave’ these fake foods.

To compound the problem, the industry uses other ‘devious moves: lowering one bad boy ingredient like fat while quietly adding more sugar to keep people hooked’ (p. xxvi). So, the ultimate marketing trick – labelling unhealthy high-sugar processed foods as ‘healthy low-fat’ options. And the whole world fell for the scam.

Stephen Sanger then head of General Mills, a company that was then generating $2 billion a year from the sale of sugary breakfast cereals. ‘Don’t talk to me about nutrition. Talk to me about taste, and if this stuff tastes better, don’t run around trying to sell stuff that doesn’t taste good’ (p. xx). And with that the processed food industry in the US turned its back on any possible role it might have in causing the global obesity and diabetes epidemics after 1980.

“We’re just giving people what they want. We’re not putting a gun to their heads,” the refrain goes. Nothing could be further from the truth. Over the years, relentless efforts were made to increase the number of “eating occasions” people indulged in and the amount of food they consumed at each’.

Nor is it plausible that a substance (cholesterol) is produced by our livers with the sole purpose of clogging up our arteries. Human biology simply does not work that way. If cholesterol is produced by the liver and transported in the blood to all the cells of the body, it is because it must serve an important purpose.

The idea that to be healthy we need to block the production of cholesterol in all our cells is perhaps the most ridiculous medical idea since blood-letting became an accepted medical practice more than 2,000 years ago.

But cholesterol is neither ‘good’ nor ‘bad’. It is just cholesterol. And anyone who continues to use this simplistic terminology exposes his or her ignorance of how ‘cholesterol’ is or is not involved in causing heart disease. When anyone uses these terms in your presence, my advice is that you absent yourself since nothing constructive will come from that ignorant discussion. For the truth is that cholesterol does not even exist in the blood as a fat, that is as cholesterol. Instead cholesterol is insoluble in water (and blood) because it is a fat. So it can be transported in the blood only in a water-soluble form. This is achieved by covering the cholesterol with a protein lining. In this way cholesterol in the blood is in fact a protein, not a fat.

Certain lipoproteins are indeed linked to an increased risk of heart disease and so some lipoproteins are indeed ‘bad’. But the simplistic focus on blood ‘cholesterol’ as the key risk factor for heart disease is not just wrong, it is also bad for our health.

In the first place it is biologically impossible for humans to convert saturated fat into ‘bad’ LDL-cholesterol. There is simply no biochemical pathway that allows this to happen.

the ‘bad’ lipoproteins as well as all the other risk factors for heart disease are affected to a far greater extent by the carbohydrate than by the fat content of the diet, regardless of how much saturated fat is ingested.

First, arteries are naturally impervious to the entry of cholesterol. Second, human arterial disease is highly selective; it occurs typically only in short sections of the (damaged) arteries and never affects veins, which constitute a major portion of the vessels in the human circulation. This shows that something other than simply the blood cholesterol concentration determines whether human blood vessels will or will not be damaged by cholesterol. Third, the majority of persons who develop heart disease in countries like the US have blood LDL-cholesterol levels below the cut-off value considered to predict freedom from heart disease risk. Similarly the majority of persons with ‘high’ blood LDL-cholesterol concentrations will never suffer a heart attack.

Sixth is the realization that it is not the ‘clogged artery’ that causes heart attacks and sudden death. Rather, it is the rupture of the arterial plaque, much as an inflamed boil may burst, that causes the sudden development of a blood clot within the coronary arteries that causes a heart attack to occur. This is at its heart an inflammatory process that is not simply due to an elevated blood cholesterol concentration. Rather, it is likely due to many factors, most of which are almost certainly due to an inflamed state within the body caused by high carbohydrate diets in those with IR.

The alternate explanation is that arteries are damaged by the entry of only one form of lipoprotein, the small, dense LDL-cholesterol particles, and then only if those small, dense LDL-cholesterol particles have been damaged by becoming oxidized. It is proposed that oxidized small, dense LDL-cholesterol particles have the ability to enter damaged arteries where they become ‘stuck’ within the arterial wall, inducing an inflammatory reaction that leads ultimately to the irreversible arterial damage recognized as the arterial plaque. Thus according to the explanation it is not ‘cholesterol’ which causes arterial damage but rather the entry of small, dense, oxidized LDL-particles into arteries.

It is also known that the increased risk of heart attack in diabetics is not explained by higher blood LDL-cholesterol concentrations since their values are no higher than those without diabetes who also develop heart disease.

A key finding is that the single best predictor of heart attack risk is the blood concentration of glycosylated haemoglobin (HbA1c). The blood HbA1c concentration is a measure of the average blood glucose concentration over the previous twelve weeks. It is an indicator of the extent to which elevated blood glucose concentrations have damaged key body proteins by adding glucose (glycosylation) to any proteins in direct contact with the blood. Glycosylation alters protein function, making them less effective in their various functions. Since haemoglobin is one of the most abundant proteins in blood, the extent to which it is glycosylated gives a good indication of the extent to which other critical body proteins have been damaged by too-high blood glucose concentrations.

This evidence suggests that high blood glucose concentrations are the single most important factor predicting risk that arterial damage causing heart disease will develop. It seems that glucose damages arteries directly through the glycosylation effect on key proteins and also by promoting oxidation of the small dense LDL-cholesterol particles.

High refined carbs foods: 1. Elevate blood sugar, irritating and inflammating the arteries and blood vessels. Excess of blood sugar binds to proteins (glycosilation), hindering their normal functions, as well as becoming toxic for the brain cells and neurons. 2. Spike insulin, increasing the storing of fat, impeding burning fat and likely leading to IR, fatty liver, diabetes, and so forth. 3. Negatively impacts gut bacteria by overgrowing bad bacteria and thus leading to leaky gut, inflammation and digestive issues. 4. Increases production of LDL and tryglicerides in the blood stream, thus raising the chances of heart attack 5. Drives hunger to the roof, leading to overeating and gaining weight 6.

high-carbohydrate diets in those with IR cause elevated blood glucose concentrations and high HbA1c concentrations leading ultimately to type 2 diabetes. But high-carbohydrate diets also cause elevated blood triglyceride concentrations and lower HDL-cholesterol concentrations in those with IR.

In contrast, ingestion of a HCLF Diet increases fat production in the liver (hepatic de novo lipogenesis – itself a risk factor for arterial damage – Table 2), which raises blood triglyceride concentrations and lowers blood HDL-cholesterol concentrations.

Type 2 diabetes mellitus does not increase only one’s risk for developing arterial damage and coronary heart disease. Instead those with type 2 diabetes are also at greatly increased risk of the development of cancer and dementias like Alzheimer’s disease. Is it possible that chronically elevated blood glucose concentrations might also promote those diseases?

High blood sugar levels are toxic for the brain and can lead to dementia It also increases the risk of cancer because most of cancer cells are feed out of glucose and glycosilated proteins

Then there is growing evidence that the key abnormality in cancer is an increased capacity to utilize glucose. In fact, cancer cells do not have the capacity to use any fuel for their growth other than glucose. Unlike the humans in which they occur, cancer cells have an absolute requirement for glucose. Without glucose they starve to death, a point first realized by Dr Otto Warburg, who won the 1931 Nobel Prize for discovering this phenomenon.

What Figure 16 aims to show is that persons with extreme insulin sensitivity – the opposite to IR – can eat as many grams of carbohydrate each day as they wish without ever becoming fat. In this theoretical model someone with extreme insulin sensitivity would be able to eat up to 500 g per day of carbohydrate (left edge of diagram) – about two and a half times what I think is necessary – while retaining a BMI at the bottom of the normal range. Most elite endurance athletes are probably in this group. A person with mild IR would be able to eat perhaps up to 250 g of carbohydrate per day while also maintaining a low BMI. But at higher intakes he or she might show a progressive increase in BMI.

Similarly, individuals with moderate IR would be able to regulate their weight within the safe range at carbohydrate intakes of up to 200 g/day. But above that intake their BMI would increase more steeply so that at intakes greater than about 300 g/day they would no longer be able to control their BMI

Those who are markedly IR might be able to maintain a normal BMI of less than 25 kg/m2 when eating less than about 175 g carbohydrate/day. At higher intakes they would rapidly develop BMIs rated as either overweight or obese. Finally, those with severe and morbid IR are perhaps able to maintain a healthy BMI only on a miniscule amount of daily carbohydrate, perhaps less than about 25–50 g/day.