So, which diet offers more weight loss, the Keto or the Mediterranean diet?
We would not be surprised if, these days, this were the most frequently asked question when it comes to dieting, and we now may have an answer from a study by Spanish investigators, published very recently in BMC Medicine.¹
In a three-month, parallel-arm, randomized clinical trial including 160 adults with obesity, they randomized participants to several groups against a Mediterranean diet control, MedDiet. They were: a ketogenic diet (KD), a very low carbohydrate diet, early time restricted eating (eTRE), late time restricted eating (lTRE), and modified alternate day fasting (mADF). The primary outcome was the difference in weight loss after 3 months between caloric restricted MedDiet and the other 5 diets. Secondary outcomes were changes in BMI, body composition, and cardio-metabolic risks.
The mean age of patients was 45.7 years, and 70.6% were women; 140 participants completed the study.
Significant differences in weight loss were found between KD and the control group [− 3.78 kg], between mADF and the control group [− 3.14 kg], and between lTRE and the control group [− 2.27 kg], but there were no outcome differences between eTRE and the control group [− 1.22 kg].
The authors concluded that in obesity (the definition was quite broad with a BMI range of 30-45 kg/m2), calorie-restricted KD, mADF, or lTRE may be more effective for weight loss than a calorie-restricted MedDiet.
Once again, caution is probably indicated before jumping to conclusions. The BMI range of study subjects was huge, going from mildly obese to morbidly obese. One wonders whether all of these weight classes can be thrown into the same patient pool. We really don’t think so!
Reference
Martinez-Monoro et al., BMC Medicine 2025;23:368
The increasing importance of the gut-brain axis
Once more, Eric Topol, MD’s Ground Truths on Substack offered an important posting, this time describing in much detail the increasing knowledge that is accumulating regarding the very important gut-brain axis (see Figure 1 below).¹
Topol describes the axis as made up of 4 interactions through which the gut influence the brain and vice versa: 2 neural pathways (also called the “second brain”) reflecting, first, the gut’s nervous system made up of the cells that line the gut and communicate through the vagus nerve with the brains (and vice versa) and, second, the autonomous nervous system (sympathetic and parasympathetic) branches and spinal cord innervations to the gut, primarily communicated through the autonomous nervous system.
The gut’s endocrine cells also produce a family of hormones, some of which have entered medical practice in a grand way as medications for diabetics and, more recently, for weight loss (glucagon-like peptides, GLP-1 agonists), but also others, like gastric inhibitory peptide (GIP), peptide YY, secretin, gherlin, gastrin, etc. And the hormonal interaction through these hormones with the brain also affects the hypothalamic-pituitary -adrenal axis (and, therefore, also must affect the ovaries).
In addition, trillions of cells of over 3,000 species of bacteria and their metabolites influence, to a significant degree, the production and stimulation of different neurotransmitters like 5-HR and GABA, and of metabolites that then communicate with the brain and the immune system. The communication with the immune system is of special importance because it is supposed to maintain the integrity of the gut lining, which can lead to the “leaky gut syndrome” when it is not properly maintained. And the same applies regarding the integrity of the blood-brain barrier. In this context, he also noted a recent paper in Nature which demonstrated that CD4+ T cells from the inflamed gut can infiltrate the brain.²
He then goes on to describe “a plethora of new gut hormones” now under investigation for their potential clinical use and, as always, a tour-de-force and absolutely worthwhile reading.
Reference
Topol E. Ground Truths. Substack. June 22, 2025. https://erictopol.substack.com/p/the-gut-brain-axis-takes-center-stage
White et al., Nature. 2025;643(8071):509‑518.