Take home message
- One calorie is not the other. Physiologically, milk has a low impact on our physiology unlike Coca-Cola and that despite, both products provide the same amount of energy (calories) per glass.
- Fructose plays a key role in this, especially because of our permanent state of abundance in Western societies.
Six months diet of milk or Coca-Cola?
A Danish study (Maersk et al., 2012) looked, how two types of Coke (regular Coca-Cola and Diet Coke) had effects on weight development and physiological and body parameters around Metabolic Syndrome and Diabetes. As a counterpart to the Coca-Cola, milk with 1.8% fat was taken. The milk had the same amount of calories as Coca-Cola, while Diet Coke had the same amount as the control group, which drank water.
The group was followed up for 6 months, and nothing was changed about their subsequent eating habits, except that each drank 1L of liquid either water, or milk 1.8%, or Coca-Cola, or Diet coke. The men and women were 39 years old, and quite heavy (about 95 kg) with a high BMI (about 32). Thus, obesity was present. The researchers took regular blood samples, and the metabolism was assessed. Below is the difference in the outcome as an increase or decrease compared to the ‘water’ group (Table 1).
Table 1. The increase or decrease (%) after 6 months’ consumption of semi-skimmed milk (1.8%) or Coca-Cola or Diet coke compared to the water group as control.
| Change relative to water (in %) | Milk (1.8%) | Coca-Cola | Diet coke |
| Physical changes: | |||
| Body weight | 0.8 | 0.7 | -0.5 |
| Total fat mass | 0.9 | 2.7 | -1.0 |
| Subcutaneous fat | 7.4 | 9.3 | 1.5 |
| Ratio Organ/ subcutaneous fat | -16.4 | 14.2 | 0.7 |
| Lean mass | 1.6 | 0.6 | 1.1 |
| Bone mass | 1.5 | -0.5 | -0.0 |
| Fat in fat store (tissue): | |||
| Organ fat (visceral) | -9 | 23 | 1 |
| Liver fat | -11 | 129 | -6 |
| Muscle fat | -100 | 120 | 0 |
| Blood values: | |||
| Leptin | 5.4 | 21.5 | -5.9 |
| Total cholesterol | 0.8 | 11.6 | -5.7 |
| HDL cholesterol | 1.6 | -0.1 | -5.4 |
| Triglycerides | 13.9 | 46.9 | 0.1 |
| Insulin resistance (HOMA) | -11.8 | 4.8 | -5.9 |
| Blood pressure: | |||
| Systolic blood pressure | -6 | 3 | -7 |
| Diastolic blood pressure | -5 | 6 | -8 |
Diet coke gives hardly any differences to water. In particular, the differences arise between the Coca-Cola and milk groups; however, in two different directions. Most intriguing are those results in which the Coca-Cola moves up, while the value in the milk group actually decreases. Differences are seen around fat storage in the different adipose tissues, in blood pressure, insulin resistance and bone formation.
The extra calories in milk and Cola give a (slight) weight gain in both groups. The already overweight Danes gain slightly more (0.7-0.8%) in both groups. That translates to almost 3/4 kg of extra weight in 6 months. However, milk has more impact on both bone (and muscle) mass, while Coca-Cola leads to additional fat storage. There is bone weight loss in the Coca-Cola group. Not insignificant is the shift where fat is stored: Coca-Cola gives more storage in fat around the vital organs. The amount of suspended fat in the blood (triglycerides) is increased after Coca-Cola, while the increase is smaller after milk consumption. The value to express insulin resistance (HOMA) gives a decrease after milk, however an increase after Coca-Cola.
Chronic metabolic syndrome and insulin resistance
Blood sugar levels rise more sharply after Coca-Cola than after milk. This causes a strong spike in the hormone insulin, which causes conversion of glucose and fructose into glycogen, among other things. Cola-sugars ultimately lead to more fat storage in liver and vital organs. Prompted by insulin, this leads to the so-called ‘non-alcoholic fatty liver syndrome’ (NAFL). Fats (triglycerides) are deposited everywhere in the body, including in places you would rather not have them, namely around the vital organs and in the muscles instead of the normal fat pads (padding fat) on the outside of the body.
Metabolic syndrome is a preliminary stage of Diabetes-2, when the liver is overworked. Blood pressure rises and insulin resistance develops over time. Even 40% of normal-weight people suffer from insulin resistance, which stems from the Western diet with a constant excess of sugars in every meal. As a result of the decades-long rejection of animal fat and its replacement by sugars and fructose, insulin resistance and metabolic syndrome has made us susceptible to further increases in obesity, cardiovascular disease, chronic, inflammatory reactions from the adipose tissue with all the consequences for immunity, as well as depression and alzheimer’s disease.
One calorie is not the other
The main representation, how we digest our food is based on thermodynamics or the ‘Energy Balance Model’ (EBM). In short: food has a certain energy value or caloric value, we count calories. By living, moving, exercising, we consume energy. You get fat because you take in too many calories in relation to consumption: every pound goes through the mouth. So in the eyes of calorie-counters, too much food and too little exercise are the cause of the obesity epidemic. And of course there is a grain of truth in this, but it does not answer why we have started consuming more and more and portions of food have become larger and larger over the years: we have become hungrier, we want to eat more. EBM’s outdated representation is not entirely accurate and sometimes not at all. For example, the system does not take into account ‘satiety’ or ‘reward/addiction’ of a food. Based on the EBM, we started changing and ‘improving’ foods. Replacing high-energy fat with sugar; replacing full-fat products with low-fat or other light varieties. Stevia instead of sugar, as in Diet coke.
Just as one milk is not the other (raw milk or heated milk), neither is one calorie (from sugar or from fat) exchangeable for another. The above study shows this very clearly. Milk with 1.8% fat and 3.4% protein has a neutral effect on your metabolism, while Coca-Cola with the same caloric value greatly boosts sugar metabolism.
A different model is therefore needed from the over-simplified EBM of calorie-in and calorie-out. This is the so-called sugar-insulin model (Eng.: Carbohydrate-Insulin-Model = CIM). Sugars trigger an insulin response, accelerating the removal of sugars from the bloodstream and storing them in fat droplets via glycogen. A side effect and disadvantage, however, is that this is precisely what triggers hunger; the CIM model indicates that the many sugars that have to be processed in one go give rise to even more food. So the insulin response to excess sugars stores fat on the one hand, but also triggers a lasting feeling of hunger. The hormone leptin plays a role in this and mice without leptin (leptin resistance) continue to eat and become fat. We also speak of empty calories, food that does not satiate. Finally, fructose inhibits the conversion of fat into energy in the form of ATP.
Fatty liver syndrome
The pictures below are from a rat study, which were either fed a diet with a low or high glycaemic index (Pawlak et al., 2004; Ludwig et al., 2020; Ludwig, 2023). High represents lots of easily digestible carbohydrates. As in the goose liver, where animals are stuffed daily with an excess of corn-starch, the picture of the classic ‘non-alcoholic-fatty liver’ emerges (high GI). The fat ends up around the vital organs and in the abdominal cavity. The liver ‘swells’ enormously.
Figure 1. Rats fed a diet with low GI (left) and high GI (right); (From: Ludwig et al., 2020)
Glycaemic index and glycaemic load
To compare foods in terms of insulin load, two outcomes are relevant. The glycaemic index describes the impact on our blood sugar levels. In 1-2 hours after ingestion, the first sugar is released into the blood and blood sugar levels rise. The index thus reflects the claim food makes on the immediate insulin requirement. The glycaemic load additionally discounts the amount of carbohydrates in the product. Because it includes the absolute amount of carbohydrates, the charge is a measure of the amount of carbohydrates per serving.
Table 2. Direct insulin entitlement after consumption as Glycaemic Index (from 0-100 = min – max), and total sugar load per serving of product as Glycaemic load (grams/portion).
| Glycaemic Index | Glycaemic load | |
| milk, cream | 30 | 1,4 |
| kefir, yogurt | 32 | 1,2 |
| cheese, etc | 39 | 5,3 |
| sweetened milk product | 52 | 4,6 |
| ice cream | 51 | 13,1 |
| plant-based drinks, etc | 38 | 4,1 |
| soft-drinks | 60 | 6,0 |
Traditional milk and milk products (milk, cream, yoghurt and cheese) contribute little or nothing to sugar levels. It is mainly protein and fat, while milk sugar is digested differently from sucrose. The increase is caused by added sugars (fruit yogurt, chocolate milk and ice cream). Ice cream has the highest glycaemic load among dairy products and is dangerous in the context of weight gain: high glycaemic index combined with high energy and fat content. Plant-based alternatives are diverse, with much higher index values among cereal-derived drinks (rice or oats), lower among the higher-fat ones (soy, almond). By comparison, the group of soft drinks, which consist of water and sugar, their GI is 2x as high as milk (Table 2).
Milk sugar is a different sugar from sucrose or the breakdown products from sucrose: glucose and fructose. Milk sugar is broken down differently and, moreover, some of the calories from milk are available not as sugar but as fat. Rather, this milk fat has a satiating effect and does not drive your need to eat more. Traditional dairy products like milk, farmer’s cheese, fermented dairy like yogurt and kefir, as well as butter, all provide satiety precisely because of dairy’s fat and low glycaemic index. Indeed, the simple idea, that fat made you fat, was also not true, and that you had to avoid fat to prevent some kind of fat secretion in your arteries was also not true. That, what Westernised people do with excess sugar intake is most like the annual preparation for hibernation (of bears, etc), (Johnson et al., 2023). There is a problem with humans, firstly, we do not go into hibernation (fasting) and secondly, the period of excess does not come to an end; constantly we live in a kind of idle land. Fructose plays an important role in the way fat is stored, but it depends on the conditions (intermittent fasting, permanent excess).
Conclusion
- Understanding the metabolism of sugar and in particular fructose versus fats (CIM model) makes it clear that the current threat to Western health is based on insulin, associated type-2 diabetes and metabolic syndrome. The overload of sugar is converted into fat, which permanently ends up in the wrong places in our body, around the vital organs, and triggers a constant low-grade inflammation.
- Because we eat empty calories due to excess sugars, we are constantly hungry. As a result, we eat more than we use energetically, but we keep feeling hungry. We are full, but not satiated.
- Because milk contains a different sugar than beet sugar (there is no fructose), and because milk also contains fat and protein, we do get satiated from the high-fat milk products. Milk products do not put any strain on the liver.
Literature
- Johnson, R. J., Lanaspa, M. A., Sanchez-Lozada, L. G., Tolan, D., Nakagawa, T., Ishimoto, T., … & Stenvinkel, P. (2023). The fructose survival hypothesis for obesity. Philosophical Transactions of the Royal Society B, 378(1885), 20220230.
- Ludwig, D. S., Ebbeling, C. B., Bikman, B. T., & Johnson, J. D. (2020). Testing the carbohydrate-insulin model in mice: the importance of distinguishing primary hyperinsulinemia from insulin resistance and metabolic dysfunction. Molecular metabolism, 35.
- Ludwig, D. S. (2023). Carbohydrate-insulin model: does the conventional view of obesity reverse cause and effect? Philosophical Transactions of the Royal Society B, 378(1888), 20220211.
- Maersk, M., Belza, A., Stødkilde-Jørgensen, H., Ringgaard, S., Chabanova, E., Thomsen, H., … & Richelsen, B. (2012). Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. The American journal of clinical nutrition, 95(2), 283-289.
- Pawlak, D. B., Kushner, J. A., & Ludwig, D. S. (2004). Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and plasma lipids in animals. The Lancet, 364(9436), 778-785.
