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Since 53.5% of the population in Germany (as of 2020) are overweight, many will be familiar with this scenario.

We will now explain how this comes about and what you can do about it.

The master metabolic hormone

Leptin is a satiety hormone and is produced in fatty tissue. The more body fat, the more leptin is produced. Leptin thus serves the brain as a kind of body fat sensor.

In addition to this “long-term component”, there is also an acute one: Leptin formation in fatty tissue is also stimulated by high energy availability and a strong insulin effect!

Leptin works, among other things, by binding to specific receptors in the hypothalamus, the brain’s top control center. There, energy consumption and energy intake are controlled.

So if the body has enough stored fat or the body’s energy status is in the green, a lot of leptin is produced, which in turn ensures that the excess energy is consumed through various processes. At the same time, further energy intake is reduced.

Leptin gives us

• less hunger and a feeling of satiety
• more glucose utilization
• more fat burning and less fat storage
• more thyroid hormones (conversion of T4 to T3)
• new blood vessels and bone substance
• new mitochondria
• sexual hormones (stimulates the reproductive axis)

That sounds wonderful!

What’s the catch? Let’s take a look at what happens when the leptin system goes off the rails in one direction or another.

Scenario 1: Leptin resistance

Anyone who is overweight (= a lot of fatty tissue) has high leptin levels. Theoretically, this person should experience the above-mentioned effects of leptin, i.e. not be hungry and burn their excess, stored energy.

To a certain extent, this is even true, which is why the body “defends” itself against further fat gain when fat mass increases. However, you can overstretch this arc…

Then the opposite happens: Overweight people suffer from severe cravings. This is due to so-called leptin resistance.

This means: leptin is high, but can no longer work. We know this from insulin resistance (insulin high, but poor effect).

Several causes are discussed for this, such as reduced transport of leptin through the blood-brain barrier due to high leptin levels or too many triglycerides.

But also low-grade inflammation, i.e. low-level inflammation, which is triggered by being overweight, among other things, can reduce the sensitivity of the leptin receptors and thus cause resistance. And: There is evidence that the wheat protein gliadin also inhibits the binding of leptin to the receptor.

This creates a vicious circle: The overweight person no longer has a sufficient feeling of satiety and therefore tends to gain more and more weight.

Scenario 2: Leptin deficiency

Ironically, a well-trained bodybuilder in the definition phase with his 5% body fat can suffer from cravings, lack of energy and low libido for the exact same reason as the obese couch potato.

Even in very athletic, slim people, it can happen that leptin does not work, this time due to too little leptin.

Excessive exercise and radical diets lower leptin levels, and faster than you lose body fat. This is probably a protective mechanism of the body to protect valuable fat reserves in the event of a famine.

So if you run too large a calorie deficit for too long, you reduce your leptin levels and thus also your metabolism. If you increase your calorie intake again after the diet, the dreaded yo-yo effect occurs.

The body is then still in “energy saving mode” and cheerfully stores all the fat it can get. It doesn’t check that you’re not in a life-threatening famine, but just want a cool six-pack 😉

By the way, lack of sleep has a similar effect: A short sleep duration is associated with reduced leptin and increased ghrelin (hunger hormone) and thus with increased appetite. The authors of the relevant study come to the following conclusion:

“A habitual sleep duration of less than 7.7 hours was associated with an increased BMI.”

Let leptin work

It should now be quite clear what needs to be done to enjoy the effects of leptin.

A healthy body fat percentage, neither too high nor too low, is desirable. This is not so easy with obesity due to the vicious circle of leptin resistance mentioned above.

A first step here would be to switch the diet to unprocessed, protein-rich foods (how about the edubily-KD?) and to reduce inflammation, for example with omega-3 fatty acids.

Then you should choose a moderate calorie deficit during diets (300-500 kcal) and also integrate regular refeeds, i.e. individual meals or entire days on which more is eaten again, especially more carbohydrates.

Try to adjust the leptin balance so well for you that you don’t need a leptin boost at McDonald’s, but also produce enough leptin through sufficient energy and carbohydrate availability to be well satiated.

And last but not least: Get enough sleep (at least 7 hours) to prevent a drop in leptin.

Let’s be clear: Work with your biology and not against it. We need to understand that our body only wants to protect us with such mechanisms. If you regularly give it the signal that it is safe (enough calories, enough sleep), fat loss will also work.

After you got to know the ketogenic diet last week, today we want to talk a little about its possibilities and limitations.

Admittedly, some study results make a ketogenic diet (KD) appear very attractive. In the past, we have often talked about the use of the ketogenic diet in certain diseases such as epilepsy1, chronic kidney disease2 and metabolic derailments such as type 2 diabetes3 and severe obesity4.

A ketogenic diet has always proven to be a potent remedy without any major side effects.

In a freshly printed pilot study by Stanford University, KD has even proven to be helpful for psychiatric disorders.5 Recent findings suggest that schizophrenia and bipolar disorder may be due to metabolic disorders that can negatively affect synapses and the excitability of nerve cells.

Keto forever?

We have long been aware that the healing effect of ketone bodies can be a real game changer for some people with specific diseases. And it’s no secret that most people in our affluent society would benefit from a slight ketosis from time to time.

That’s why we also advise you to do less “carbohydrate fattening” and instead of snacking on bread and pasta every day, rather increase the protein and vegetable content.

But does it have to be a permanent (massive) restriction of carbohydrates? In most cases, the answer is “No”. The fact that a keto diet even carries certain risks is often – intentionally or unintentionally – ignored. More on that in a moment.

To lose weight and thus automatically become more metabolically healthy, there are simpler ways and means than going directly full keto…

As a much-cited study from 2019 showed, overweight subjects automatically consumed ∼500 calories less per day through an unprocessed diet than the subjects who were given highly processed foods.6 And the people in each group were allowed to eat as much as they wanted.

There’s no magic behind it: a potato simply keeps you full longer than toast.

White flour products are automatically eliminated by the unprocessed diet – and thus also a lot of carbohydrates. And here we are again with the edubily keto diet (see our Instagram post from Monday).

Everything cyclical, nothing chronic

But now let’s take a look at what can go wrong with the KD.

For one thing, keto is often misunderstood. Some think that eating ketogenic is a free pass for unlimited butter coffee, salami, bacon, cheese and cream-nut cake.

At the end of the day, they then wonder why the promised weight loss fails to materialize, but the blood lipid levels get worse and worse.

Anyone who already has many free fatty acids in their blood due to being overweight does not need to refuel with dietary fats. Ultimately, you can lose weight just as well with carbohydrates. The crucial thing is to get into an energy deficit at all and live off your own reserves – how is irrelevant at first.

On the other hand, there are some pitfalls even with a well-thought-out keto diet. We have often mentioned it: Biology wants to oscillate. Chronic processes, no matter in which direction, almost never lead to the goal in the long run.

Hormonal effects of a chronic KD

With the growing popularity of the ketogenic diet, the number of scientific publications has also been increasing exponentially since the 2000s. While there were just under 300 publications on KD in total from the first publication in 1931 to the year 2000, there were more than twice as many in the last year alone, with over 600!

There’s the thing with the hormone balance. Under a strictly low-carbohydrate diet (here we are talking about less than 100 g of carbs a day), for example, the thyroid hormones decrease, more precisely the T3.7 Even an iodine administration cannot prevent this.8

Closely related to this is the satiety hormone leptin. This drops quite a bit under a diet that is too low in carbohydrates.9 Little leptin means cravings, slowed metabolism, non-existent libido and a compromised immune system, to name just a few of the consequences. You don’t want that.

In addition, the testosterone level in men can drop due to a KD, while the cortisol level increases.10 Nobody wants a permanently elevated cortisol level, because the stress hormone can lead to insulin resistance, sleep disorders and the storage of (abdominal) fat in the long term, among other things.

The famous longevity researcher Valter Longo also studied the effects of a KD on a mouse model for multiple sclerosis.11 While a cyclical ketosis (“fasting mimicking”) was able to strongly slow down the course of MS and even completely reverse it in some of the animals, a conventional KD only led to a “mild improvement” – without stopping the disease. Again: Cyclical is better than chronic.

Only in May 2024, an animal study was published that shows another downside of the keto diet.12 A continuous KD can trigger the aging of cells, the so-called senescence, in mice. Especially in heart and kidney tissue, which could lead to premature organ damage. Fortunately, the whole thing can be prevented with regular interruptions of ketosis.

By the way, these keto breaks can also be used to increase leptin again. Practical!

Get to know the edubily-KD

Without therapeutic indication, we therefore see no reason to eat strictly ketogenic permanently. On the other hand, it is certainly advisable to reduce the carbohydrate content of the diet more strongly from time to time in order to take advantage of the benefits of ketosis.

This is very easy, for example, by simply having a protein- and fat-rich, i.e. low-carbohydrate, dinner and breakfast. When you wake up in the morning, your ketone bodies are already significantly increased due to the overnight fasting.

You can then take even more advantage of this condition by delaying carbohydrate intake somewhat or continuing to avoid at least refined carbohydrates, such as flour. That’s not rocket science, is it? 😉

Our edubily-KD is a gentle method to temporarily enjoy ketosis without experiencing the disadvantages of an extreme carbohydrate restriction. We have presented you in detail how you can design an edubily-KD day in our Instagram post.

We wish you much success and bon appétit 😉

Sources

1. Lambrechts, D. a. J. E. et al. A randomized controlled trial of the ketogenic diet in refractory childhood epilepsy. Acta Neurol. Scand. 135, 231–239 (2017).
2. Cukoski, S. et al. Feasibility and impact of ketogenic dietary interventions in polycystic kidney disease: KETO-ADPKD—a randomized controlled trial. Cell Rep. Med. 4, 101283 (2023).
3. Correa, L. L. et al. Severe type 2 diabetes (T2D) remission using a very low-calorie ketogenic diet (VLCKD). Endocrinol. Diabetes Metab. Case Rep. 2022, 22–0295 (2022).
4. Moriconi, E., Camajani, E., Fabbri, A., Lenzi, A. & Caprio, M. Very-Low-Calorie Ketogenic Diet as a Safe and Valuable Tool for Long-Term Glycemic Management in Patients with Obesity and Type 2 Diabetes. Nutrients 13, 758 (2021).
5. Sethi, S. et al. Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial. Psychiatry Res. 335, 115866 (2024).
6. Hall, K. D. et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. 30, 67-77.e3 (2019).
7. Iacovides, S., Maloney, S. K., Bhana, S., Angamia, Z. & Meiring, R. M. Could the ketogenic diet induce a shift in thyroid function and support a metabolic advantage in healthy participants? A pilot randomized-controlled-crossover trial. PLoS ONE 17, e0269440 (2022).
8. Reinhardt, W. et al. Effect of small doses of iodine on thyroid function during caloric restriction in normal subjects. Horm. Res. 39, 132–137 (1993).
9. de Luis, D. A. et al. Effects of a low-fat versus a low-carbohydrate diet on adipocytokines in obese adults. Horm. Res. 67, 296–300 (2007).
10. Chen, S. et al. Ketogenic Diet and Multiple Health Outcomes: An Umbrella Review of Meta-Analysis. Nutrients 15, 4161 (2023).
11. Choi, I. Y. et al. Diet mimicking fasting promotes regeneration and reduces autoimmunity and multiple sclerosis symptoms. Cell Rep. 15, 2136–2146 (2016).
12. Wei, S.-J. et al. Ketogenic diet induces p53-dependent cellular senescence in multiple organs. Sci. Adv. 10, eado1463 (2024).