It has been called the ‘Banting for Babies Trial’ and ‘Nutrition Trial of the Century’. The Health Professions Council of SA (HPCSA) hearing against UCT emeritus professor Tim Noakes is becoming the ’Inquisition of a Modern-day Gallileo’. Those comparisons may not just be the febrile output of sensationalist journalistic poetic licence. With all the high drama attendant on this hearing, and ongoing attempts by the HPCSA to stop Noakes giving crucial evidence in his own defence, uncomfortable grains of truth are emerging. (Banting pun unintended. It doesn’t favour grains). One grain is that this ‘trial’ may very well have been a set up from the start. The hearing, chaired by Pretoria advocate Joan Adams, has heard evidence of irregular conduct by top academics and doctors, including the head of bioethics at the University of the Witwatersrand, Prof Ames Dhai, aimed not just at ensuring that Noakes was charged but that the hearing goes against him. If the HPCSA and the Association of Dietetics for SA (ADSA) – whose former president Claire Julsing Strydom lodged the complaint that led to the charge – hoped the hearing would effectively muzzle Noakes, the very opposite appears to be happening, thanks in part to the law of unintended consequences on social networks.
In his evidence in chief, Noakes is presenting the science behind low-carb, high-fat (LCHF) lifestyles and is helping to spread it fast across the planet – ironically, thanks to Twitter, the social network that got him into trouble in the first place, and Facebook. Last week Noakes called for medicine to move in a radically new direction. The ‘power of the annointed’ is becoming the ‘wisdom of the crowd’. He told the hearing: ’We can continue to teach a failed model that has caused the diabetes/obesity epidemic. We can continue to train more doctors, build more hospitals and tell people they must eat lots of carbs. Or like Winston Churchill said, maybe it’s time to look at the results and outcomes and say: Maybe we got it wrong.’ Medical students need to learn that there are two models of chronic disease, Noakes said: one that has always been taught and one that needs to be taught. ‘If we don’t teach our medical students, they will get it on Twitter,’ he said. Students will soon ‘know more about the disease than their lecturers’, and that’s a ‘problem for the future of medicine’. Here, in the fifth part of a series, science and business writer Rob Worthington-Smith looks at those models. In the final part of this series, Worthington-Smith will look at another nub of this hearing: should infants be weaned onto an LCHF diet, or is this dangerous advice to be broadcasting to our nation’s young mothers? – Marika Sboros
By Rob Worthington-Smith
In Part Four, we saw from population studies, both ancient and modern, that as soon as a society ‘modernised’ its diet towards carbohydrate as the primary source of energy in place of traditional animal-based fats, this was generally accompanied by obesity and the onset of metabolic diseases.
For Noakes to be successful in making the case for a diet high in healthy fat and low in carbohydrate (less than 75g per day), he will have to present a compelling model for how we metabolise carbohydrate and fat – a model that both explains and predicts the outcomes of these polar opposite dietary regimes.
The conventional view is the so-called “energy imbalance model of obesity”. In this model, overweight people get fat because they eat more calories than they can burn. So far, the model makes sense. What this model doesn’t explain is why obesity is so closely correlated to carbohydrate intake and not fat intake (note: carbohydrate cannot be present in significant quantities in the high fat diet for this statement to hold true). Nor does this model explain why it is that people who are obese don’t experience satiety when their energy needs are already satisfied.
On the contrary, overweight patients seem to be constantly hungry. Why is it that as we put on more weight, our brains demand more food, in particular, starchy and sugary carbs? This model provides no explanation for this erroneous brain messaging other than the “sins of decadence”: gluttony and sloth. Yet in the previous article we saw that many of the poorest populations studied suffer the worst.
No, this model neither fits nor explains the phenomenon.
The model that Noakes presented at the HPCSA hearing regards the metabolism of fat for energy as being normal and the metabolism of carbohydrate as an equally vital pathway, but in terms of its evolved use, a seasonal alternative. The logic being that when our ancestors had reached the apex of the food chain and were mostly eating prey, the only significant carbohydrate in their diet would have been seasonal fruit, berries, or in times of desperate food shortage, plant energy storage organs, such as tubers.
The model for this pathway evolved to store this food in the body and make sure that the early human continued eating during this food’s abundant, but short season to lay down the necessary fat reserves.
Considering the ease with which carbohydrate can be broken down by the body into glucose, and the over-abundance of fruit when in season (often just before a period of food stress, encouraging our ancient ancestors to eat as much as they could), the body needed a metabolic process that would ensure that the flood of glucose entering the bloodstream is quickly dealt with before causing damage. And not just dealt with, but stored against expected, periodic conditions of famine.
Thus is the scene set for the insulin model of obesity. In this model, rising blood glucose concentration stimulates increased production of the hormone insulin by the pancreas, resulting in a chain of complex metabolic reactions, simplified here.
The metabolic pathway governed by insulin both prevents an overload of glucose in the bloodstream, and crams the fat (converted from this energy) into the liver and nearby tissue. It then uses a ratchet mechanism to prevent this fat from escaping again. In other words, once it’s there, it can’t easily be used to provide for daily energy requirements until there is again a food shortage indicating impending starvation.
Finally, to make sure early man continues to gorge on the bounty while still available, the carbohydrates present in the food send messages to the brain telling it to continue feeling hungry. Thus, the body is eager for the next snack as soon as it’s available. Not surprisingly, the first noticeable effect of this addictive eating pattern is an expanding waistline.
As the liver takes up more fat, it begins to establish a resistance against the effectiveness of secreted insulin. When the next carbohydrate meal arrives, the insulin released by the pancreas has to work harder in order to convert the excess glucose into stored glycogen and fat. It is at this point that the body enters a pre-diabetic state as the pancreas begins to lose its ability to manufacture sufficient insulin. The result is elevated levels of glucose in the bloodstream and the onset of diabetes (type II).
Taking these two side-effects together, the feeling of constant hunger, as well as increased resistance to insulin, one is faced with the classic symptoms of addiction. The metabolic processes for the addiction to nicotine, cocaine and indeed some modern medicines, results in the same outcome for the patient: decreasing effectiveness of the drug in the face of increasing desire for more.
(Interestingly, this perspective may also explain why some populations appear to thrive on a carbohydrate diet. Canadian nephrologist Dr Jason Fung makes a compelling case that rural Chinese, by eating a small bowl of rice just once a day, give their bodies 23 hours in which the body’s metabolism can recover and rebuild its sensitivity to the hormone before the next daily meal.)
But for the high-carbohydrate eater there is worse to come: Immune cells mistake the fat being stored in the liver and the adipose tissue for alien intruders. This declaration of war by the body’s auto-immune system breaks open the fat cells and releases harmful by-products, such as cytokines.
Further contributors to such metabolic mayhem derive from other cultivated or manufactured foods, such as fructose – fruit, confectionary and anything containing high fructose corn starch (HFCS) – as well as alcohol and vegetable seed oils. These, though metabolised for energy primarily in the liver, escape the regulation of insulin and can’t be put into glycogen storage. Their energy products are thus sent unregulated to the body’s cells, more specifically to the mitochondria (essentially our cell’s energy batteries). Overloaded mitochondria then cause the formation of free radicals (carriers of reactive oxygen).
Free radicals in the organic chemical world attack anything they can get their hands on. Amongst their actions, they attack the body’s anti-oxidant defences and interfere with the accurate production of protein from the cell’s DNA, thus damaging both the DNA and the cell. Is it any coincidence that back in the 1800s cancer was practically unheard of, whereas these days about one in three of us will develop cancer before the age of 60?
These metabolic disorders, taken together, were originally termed Syndrome X by their discoverer, Dr Gerald Reaven, but are now commonly called the metabolic syndrome. Other researchers have also coined the term systemic inflammation, which more accurately describes the consequences of the civil war going on in the body.
Illnesses now recognised by many medical research papers as being caused by the metabolic syndrome include: Type 2 diabetes, cardiovascular disease, diet-induced obesity, osteoarthritis, certain cancers, Alzheimer’s disease and other dementias, as well as gout, tinnitus, schizophrenia and even autism.
Noakes, recognising the role of insulin and advanced insulin resistance as the main mechanism responsible for the metabolic syndrome, refers to the underlying condition, Hyperinsulinaemia, and supports the growing view that it may be a unifying theory that describes the real cause of chronic disease. And following the trail of evidence just one step back, we arrive at the constant and convenient availability of carbohydrate in our diet as the primary driver of this ultimately lethal condition.
In the last article in this series, we will get to the nub of the issue being debated at the HPCSA hearing: should infants be weaned onto an LCHF diet, or is this dangerous advice to be broadcasting to our nation’s young mothers?
- Rob Worthington-Smith is a science and business writer. While his day job is to analyse companies’ non-financial capitals for the responsible investor, he also pursues a wide range of interests including evolutionary biology and behavioural economics. Rob enjoys the challenge of bringing perspective to contentious issues, such as the moral landscape, how to address inequality in a developing economy, progressive approaches to education, parenting (as a widowed, single parent of four), and the science and pseudo-science behind health and nutrition. Rob holds a BSc Honours degree in Agricultural Economics from Stellenbosch University. Disclosure: Whilst as yet undecided on every aspect of the issue, Rob is currently working with Professor Noakes to bring perspective and balance to the current debate on dietary guidelines.