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"I was told to try the Snack-All-Day diet plan, but it has been a disaster. I was eating 7 or 8 small snacks per day but instead of losing weight, I have gained weight. Why?"
It is quite clear that obesity is a major public health problem and contributes to a substantial burden of disease at a population level. Why do we get obese? This is complex, but a lot of it can be explained by the food environment we live in and the change in our eating habits over the last 3 or 4 generations.
The study below shows that the extent of the postprandial dip in glucose, which occurs 2-3 hours after a meal predicts hunger, a shorter time until the next meal and greater additional energy intake at 3-4 hours.
The reason why we get low blood glucose 2-3 hours after a meal is that there is too much insulin released relative to the amount of sugar or glucose in the baseline meal. In other words, our bodies produce too much insulin in anticipation of the continued absorption of glucose. When there is too little glucose being absorbed relative to insulin this results in relative hypoglycaemia, which triggers counter-regulatory mechanisms to raise glucose levels in the blood one of which is hunger and food-seeking behaviour. This leads to a vicious cycle of snacking, a rise in blood glucose, a rise in insulin, a fall in blood glucose, which is then followed by further food-seeking behaviour and the cycle repeats itself. Over time being trapped in this cycle leads to excessive calorie intake in the presence of high insulin levels, which leads to obesity. Insulin is the master hormone that drives adipose tissue to convert excess glucose into adipose tissue.
The driver of the vicious cycle above are foods with a low glycaemic index, i.e. foods that release their sugars very rapidly. These foods are typically processed and ultra-processed carbohydrates, but can happen with unprocessed foods, for example, some fruits.
To break this cycle you need to change your diet to carbohydrates with a low glycemic index or to eat a low carbohydrate diet. The latter includes high-fat or high-protein diets that if eaten for prolonged periods of time result in ketosis, which is why they are often referred to as ketogenic diets.
A positive effect of ketogenic diets is that the ketones themselves affect the brain in other positive ways and are anorexigenic (reduce appetite). Ketosis triggers complex hormonal changes in the body that reduce appetite. Contrary to what people expect caloric intake on high-fat high-protein diets actually drop spontaneously and people don’t overeat. This rule however only holds true if you are ketotic. As soon as you eat carbohydrates, and switch off ketosis, your appetite comes back with a vengeance and you tend to overeat to compensate for the adipose tissue you may have just lost.
From an evolutionary perspective, people with lots of adipose tissue were protected in times of famine. This is why when carbohydrates became available to our ancestors, e.g. seasonal fruits, nuts and honey, they were endowed with the metabolic programme to store the excess calories as fat and to not switch off their appetites when eating carbohydrates; the so-called gorging response. The fact that most modern societies don’t live a seasonal life, i.e. we now have access to a high carbohydrate diet all year round, explains why obesity has reached such epidemic proportions.
What we really need is a public education programme around how the body responds to specific food and how we can hack our physiology by changing our diets to lose weight and control our appetites. I am aware that this is easier said than done. However, we have to start somewhere otherwise many people in our society will remain primed for earlier death and a more unhealthy old age.
If you are interested in reading more about this topic I have written a piece on Medium on why low-fat diets are bad for you and another article on diet as a philosophy.
Wyatt et al. Postprandial glycaemic dips predict appetite and energy intake in healthy individuals. Nature Metabolism volume 3, Pages 523–529(2021). Published: 12 April 2021.
Understanding how to modulate appetite in humans is key to developing successful weight loss interventions. Here, we showed that postprandial glucose dips 2–3 h after a meal are a better predictor of postprandial self-reported hunger and subsequent energy intake than peak glucose at 0–2 h and glucose incremental area under the blood glucose curve at 0–2 h. We explore the links among postprandial glucose, appetite and subsequent energy intake in 1,070 participants from a UK exploratory and US validation cohort, who consumed 8,624 standardized meals followed by 71,715 ad libitum meals, using continuous glucose monitors to record postprandial glycaemia. For participants eating each of the standardized meals, the average postprandial glucose dip at 2–3 h relative to baseline level predicted an increase in hunger at 2–3 h (r = 0.16, P < 0.001), shorter time until next meal (r = −0.14, P < 0.001), greater energy intake at 3–4 h (r = 0.19, P < 0.001) and greater energy intake at 24 h (r = 0.27, P < 0.001). Results were directionally consistent in the US validation cohort. These data provide a quantitative assessment of postprandial glycaemia in appetite and energy intake modulation.
Conflicts of Interest
MS Research
Twitter
LinkedIn
Medium
Disclaimer: Please note that the opinions expressed here are those of Professor Giovannoni and do not reflect the position of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust.
To break this cycle you need to change your diet to carbohydrates with a low glycemic index or to eat a low carbohydrate diet. The latter includes high-fat or high-protein diets that if eaten for prolonged periods of time result in ketosis, which is why they are often referred to as ketogenic diets.
A positive effect of ketogenic diets is that the ketones themselves affect the brain in other positive ways and are anorexigenic (reduce appetite). Ketosis triggers complex hormonal changes in the body that reduce appetite. Contrary to what people expect caloric intake on high-fat high-protein diets actually drop spontaneously and people don’t overeat. This rule however only holds true if you are ketotic. As soon as you eat carbohydrates, and switch off ketosis, your appetite comes back with a vengeance and you tend to overeat to compensate for the adipose tissue you may have just lost.
From an evolutionary perspective, people with lots of adipose tissue were protected in times of famine. This is why when carbohydrates became available to our ancestors, e.g. seasonal fruits, nuts and honey, they were endowed with the metabolic programme to store the excess calories as fat and to not switch off their appetites when eating carbohydrates; the so-called gorging response. The fact that most modern societies don’t live a seasonal life, i.e. we now have access to a high carbohydrate diet all year round, explains why obesity has reached such epidemic proportions.
What we really need is a public education programme around how the body responds to specific food and how we can hack our physiology by changing our diets to lose weight and control our appetites. I am aware that this is easier said than done. However, we have to start somewhere otherwise many people in our society will remain primed for earlier death and a more unhealthy old age.
If you are interested in reading more about this topic I have written a piece on Medium on why low-fat diets are bad for you and another article on diet as a philosophy.
Wyatt et al. Postprandial glycaemic dips predict appetite and energy intake in healthy individuals. Nature Metabolism volume 3, Pages 523–529(2021). Published: 12 April 2021.
Understanding how to modulate appetite in humans is key to developing successful weight loss interventions. Here, we showed that postprandial glucose dips 2–3 h after a meal are a better predictor of postprandial self-reported hunger and subsequent energy intake than peak glucose at 0–2 h and glucose incremental area under the blood glucose curve at 0–2 h. We explore the links among postprandial glucose, appetite and subsequent energy intake in 1,070 participants from a UK exploratory and US validation cohort, who consumed 8,624 standardized meals followed by 71,715 ad libitum meals, using continuous glucose monitors to record postprandial glycaemia. For participants eating each of the standardized meals, the average postprandial glucose dip at 2–3 h relative to baseline level predicted an increase in hunger at 2–3 h (r = 0.16, P < 0.001), shorter time until next meal (r = −0.14, P < 0.001), greater energy intake at 3–4 h (r = 0.19, P < 0.001) and greater energy intake at 24 h (r = 0.27, P < 0.001). Results were directionally consistent in the US validation cohort. These data provide a quantitative assessment of postprandial glycaemia in appetite and energy intake modulation.
Conflicts of Interest
MS Research
Medium
Disclaimer: Please note that the opinions expressed here are those of Professor Giovannoni and do not reflect the position of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust.
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