by Dr Rob Verkerk 

Obesity and its related diseases are the biggest threats to human health in the modern age and it’s facile to say those afflicted simply haven’t heard the message to eat less and exercise more. Getting on top of the over-fat epidemic isn’t about helping people feel good or bad about their bodies – positive or negative. It’s about health and longevity and ensuring that the fabric of society continues in a self-sufficient manner to support future generations. Humans are not built to carry excess fat beyond a certain level designed for energy storage and survival, and when they do, there are severe health consequences.

There is wide consensus that the causes of obesity are myriad and complex. However the good news from published and clinical evidence is that for those afflicted, type 2 diabetes can often be reversed.

Once upon a time, type 2 diabetes was a rare occurrence. Now it threatens to overwhelm health systems globally. In 2017 it is estimated that 425 million adults globally, aged 20-79 years, were living with diabetes (type 1 and type 2). More shocking are estimates that by 2045 this is set to rise to 625 million. Of these, 90% of all cases of diabetes are type 2 – which again, are almost entirely preventable.

Speak to most conventional authorities and they’ll tell you the cause is too much sugar in the bloodstream causing insulin resistance. In reality, it’s far from being that simple.

Hormones: Drivers of Change

Behind visible and internal symptoms created by metabolic disruption lie multiple, upstream, causative factors. Ranging from early and childhood trauma, too much stress, poor sleep, social (and nature) disconnection and exposure to too many environmental toxins, to the ultra-processed, sugar and refined vegetable fat-laden foods that are now ever-present. Designed to hit the ‘bliss point’, these calorie-dense, sugary, fatty foods speak to our primordial survival hormones, keeping us wanting more and pretending to comfort our unmet needs.

The reasons so many of us are getting fat, sick and tired are not the same for everyone. There may be a genetic and epigenetic element, but our gene expression is in turn greatly affected by our behaviour which includes what, when and how we eat; when and how we move; when and how we respond to and recover from stress, and our environmental toxin burden. And each of these actions drives – and is driven by – our gene expression, our biochemistry and our hormones.

Key Hormonal Drivers for Appetite Management

We still have a lot to learn about the hormones that regulate appetite and food intake. Insulin is the key hormone released from the pancreas that determines how much blood sugar will be allowed into cells where it can be used by mitochondria to produce energy. If the sugar is not burned, it’s converted to fat. We know the consequences of becoming insulin resistant – our blood sugar starts going up and then it’s all downhill towards type 2 diabetes. But insulin also has other effects, with insulin receptors being widely distributed throughout the central nervous system and insulin playing an important role, in particular in concert with glucagon, to regulate blood sugar, as well as energy storage or use.

Our appetite hormones are responsible for telling the brain when to eat and when to stop. These hormones are so intimately involved with our evolutionary development that they can be regarded as primordial drivers. When correct signalling stops working as intended, the dysregulation can predispose you to gaining weight, becoming insulin resistant and heightening your risk of developing type 2 diabetes amongst many other chronic diseases.

•  Leptin is a peptide, but it functions like a hormone. It’s often called the ‘satiety hormone’ and regulates the size of the adipose (fat) deposits in the body. Leptin is part of our survival response as it regulates energy intake and fat stores within a narrow margin. When fat mass decreases, the level of leptin decreases and the appetite is stimulated until fat is regained. There is also a decrease in body temperature and energy expenditure is reduced. When fat deposits increase, so do leptin levels, suppressing appetite until weight loss occurs. Interestingly, leptin also plays a role in puberty as a woman has to have sufficient fat stores if she’s to nourish a foetus and ensure the survival of the human race. When leptin levels are persistently high due to over eating, the leptin receptor becomes ‘deaf’ causing reduced sensitivity to the hormone. The absence of leptin, or the leptin receptor, leads to uncontrolled eating, therefore increasing the risk of obesity.

•   Ghrelin is produced mainly by the stomach and is commonly known as the ‘hunger hormone’. Whilst it stimulates appetite, increases food intake and promotes fat storage, it also does so much more, and is even involved in cancer development and metastasis.

•   Peptide YY (PYY) is secreted from cells in the GI tract. Released after eating, it helps to induce satiety and reduce appetite. Low levels lead to feelings of hunger and enhanced cravings.

•  Glucagon works alongside insulin to control levels of glucose in the blood (blood sugar). Glucagon is released to stop blood sugar levels dropping too low (hypoglycaemia), while insulin works to regulate blood sugar from becoming too high.

•  Adiponectin, like leptin, is also secreted by fat cells. It plays a role in the regulation of blood glucose and helps burn fat for energy. Low levels of adiponectin have been implicated in the development of obesity and insulin resistance.

  Leptin – resistance is futile

You would think the more fat cells a person has, the more leptin is produced and the less the desire to eat. But in the same way that insulin signalling becomes ‘muted’, the same is true of leptin – and the body becomes leptin resistant. Even with a hefty load of fuel on-board (as food or stored fat) , the brain doesn’t get a clear signal and thinks the body is starving. The body ignores this ‘ample food on-board’ message and the brain sends out messages to eat more to top up our reserves so we don’t starve, and conserve energy by becoming more sedentary. Hence the leptin-resistant individual is unable to eat less and exercise more. For the record, eating more and exercising less is not the only root cause of weight gain, but it is a direct consequence of leptin resistance and disrupted hormones which are implicated in obesity and the development of type 2 diabetes.

The drug-free fix

The fix is not merely down to diet alone.

The fix is about recognising that there are multiple upstream causes that have created a situation in which metabolic dysregulation has occurred.

Whilst a diet closer to our evolutionary origins will certainly help, it won’t address the emotional/psychological wounds that may have contributed to this status. Hence, any strategy for truly addressing the metabolic (obesity, type 2 diabetes, chronic disease) crisis must address the upstream causes that have caused the downstream effects.

*This is an edited article. To read the full article please go to the website shown below and/or conduct your own further research.