A recent study in Genome Medicine provides a possible genetic explanation for this. The focus is on the PAM gene, which encodes peptidyl-glycine alpha-amidating monooxygenase.

This enzyme is involved in the amidation of numerous bioactive peptides—including GLP‑1. Two hypomorphic PAM variants studied, p.S539W and p.D563G, are associated with an increased risk of type 2 diabetes; combined, they are carried by about one in ten people.

More GLP‑1 does not mean increased effectiveness

In the study, PAM activity was significantly reduced in carriers of these variants: by about 52% for p.S539W and by about 20% for p.D563G.

Interestingly, carriers also had elevated circulating GLP‑1 levels. While this may initially sound like an advantage, it does not translate into a stronger effect. Reduced endogenous GLP‑1 sensitivity was particularly evident with p.S539W—consistent with the concept of GLP‑1 resistance.

The mouse data also fit this picture: Pam knockout mice exhibited accelerated gastric emptying, responded less well to exendin‑4, and showed attenuated signal transduction via the GLP‑1 receptor in the pylorus.

So what does this mean for treatment?

Clinically, the effect was measurable: In a meta-analysis of three cohorts with 1,119 participants, the reduction in HbA1c under GLP-1RA therapy was lower in p.S539W carriers than in non-carriers. This difference was not observed for metformin, sulfonylureas, and DPP‑4 inhibitors.

This does not yet change any guidelines. But PAM could help identify GLP-1RA non-responders earlier —and make treatment decisions less based on the principle of “let’s see if it works.”

Umapathysivam MM et al. Type 2 diabetes risk alleles in peptidyl-glycine alpha-amidating monooxygenase influence GLP‑1 levels and response to GLP‑1 receptor agonists. Genome Medicine (2026).

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Asymptomatic for years

Infection usually goes unnoticed. The parasite’s tiny eggs can be ingested via contaminated soil, unwashed berries, or contact with infected animals. In the human intestine, small larvae hatch from the eggs, migrate through the intestinal wall, and enter the bloodstream. The larvae then preferentially settle in the liver and grow there in an infiltrative manner—almost like a malignant tumor.

The symptoms are nonspecific: years later, complaints such as fatigue, upper abdominal pain, weight loss, or jaundice may appear. It is precisely these nonspecific symptoms that make diagnosing the disease so difficult. It is not uncommon for the condition to be discovered by chance—for example, during an ultrasound or CT scan.

Difficult Differential Diagnosis

Radiologically, the disease can indeed quickly resemble a tumor. This is precisely why the fox tapeworm is gaining importance in clinical practice. Especially in southern Germany, doctors should also consider the fox tapeworm when faced with unclear liver findings.

The good news: When detected early, the disease can be treated much more effectively today than in the past. Curative resection is performed, supplemented by benzimidazoles such as albendazole—sometimes for life.

Prevention remains crucial

The fact that the fox tapeworm is spreading increasingly is also changing perceptions of the disease. What was long considered a rare zoonosis is becoming more relevant to human and veterinary medicine.

While widespread panic is unwarranted, vigilance is certainly called for. Simple measures—thorough handwashing, cleaning food grown close to the ground, or regular deworming of pets—can already significantly reduce the risk.

The fox tapeworm remains rare. Nevertheless, it should not be underestimated. Therefore:

· Wash hands after gardening or contact with animals

· Clean berries, mushrooms, and windfall fruit before consumption

· Have dogs and cats dewormed regularly

Casulli, Adriano et al. Unveiling the incidences and trends of alveolar echinococcosis in Europe: a systematic review from the KNOW-PATH project. The Lancet. Infectious Diseases vol. 26,1 (2026): e49-e61.

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What has long been underestimated: The consequences don’t just manifest as obesity or metabolic disorders. The negative effects of a high-fat diet seem to begin much earlier—right in the gut. There, it affects gut immunity, meaning the interaction between the gut barrier, immune cells, and the gut microbiota.

Fat acts faster than you think

And unfortunately, damage can occur after just a short time. A recent preclinical study suggests that just a few days of “fatty meals” are enough to impair key immune functions in the gut—at least in mice.

The focus is on so-called ILC3 cells. They are crucial for a stable intestinal barrier and control how closely the contact between intestinal contents and the immune system is regulated. It is precisely these cells that are sensitive to fat: their numbers decline rapidly. At the same time, the intestinal barrier becomes more permeable, and inflammatory processes increase.

A protective system is thrown off balance

As a possible explanation, the researchers describe an interplay between inflammatory signals from the gut microbiota and metabolic stress in the immune cells. The exact processes are complex—but what is crucial is that the very cells that are supposed to stabilize the barrier are the ones being compromised.

At least: The data suggest that these changes can, at least partially, be reversed. The immune system in the gut thus appears to be not only sensitive but also adaptable. One more reason to start thinking about a healthy diet as soon as possible.

Torrico E et al. High-fat diet causes rapid loss of intestinal group 3 innate lymphoid cells through microbiota-driven inflammation and mitochondrial stress. Immunity, 2026;0

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Prevention rather than treatment

Studies show that the effect is particularly evident in women with recurrent urinary tract infections. The number of new infections can decrease with regular consumption. According to a Cochrane review, the risk of recurrent infections is reduced by about 25–30% in women; the effect appears to be slightly stronger in children. Some groups, such as pregnant women and nursing home residents, did not benefit.
In cases of acute bladder infections, there is hardly any positive effect. Once the infection has taken hold, the mechanism simply comes too late—the bacteria have already attached themselves to the mucous membrane and are multiplying.

What’s Behind the Effect

According to studies, simply drinking more water alone can significantly reduce the number of recurrent urinary tract infections. However, the effect of cranberries is not about “flushing,” but rather the active compounds contained in the plant: proanthocyanidins (PACs), which make it difficult for bacteria to attach to the bladder lining. E. coli, the most common cause of urinary tract infections, relies on this adhesion. Without it, it becomes significantly harder for the bacteria to establish themselves in the urinary tract.

Juice, capsules, or extract—and how much, exactly?

And how and in what quantity is it best to take cranberry? There is no standard dosage recommendation. Studies often use about 36 mg of proanthocyanidins per day. It is not possible to give a general figure for how much juice is needed, as the proanthocyanidin content varies significantly depending on the product. When taking dietary supplements, you should pay attention to the information regarding PAC content.

Williams G et al. Cranberries for preventing urinary tract infections. Cochrane Database Syst Rev. 2023;4(4):CD001321.

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• Against toothache and cavities: “Rinse your mouth with fresh morning urine for at least three minutes and keep it in the oral cavity as long as possible.”
• For middle ear infections: “Let urine run into the ear canal and leave it there for 15 minutes.”
• For skin impurities or minor burns: “In the morning, after your normal facial cleansing, wash your face with concentrated morning urine and do not rinse it off for as long as possible.”

Behind such recommendations lies a surprisingly persistent myth: urine is a natural disinfectant. In fact, it was already used for this purpose in ancient and medieval medicine.

Overcoming the disgust — is it worth it?

The idea that urine is sterile is now considered outdated. Modern microbiological studies show that the human urinary tract does indeed have a bacterial colonization. The supposed antiseptic thus turns out to be simply a bodily fluid which—like many others—can contain microorganisms and therefore has little place near wounds.

In addition, urine consists mostly of water, along with a small percentage of electrolytes and metabolic waste products that the body is actively trying to eliminate. There is no convincing mechanism for an antiseptic effect.

If it burns, it must work against bacteria?

The fact that urine can sting on injured skin is sometimes interpreted as evidence of a “disinfecting effect.” In reality, this is more likely due to its salt concentration and slightly acidic pH.

In short: urine can sting—but not for the same reasons as an antiseptic, rather for roughly the same reasons as saltwater on an abrasion.

No — urine is not a disinfectant

Today, we have clean water, simple wound care, and sterile dressings. Urine-based applications therefore seem about as advisable as some other classics of historical medicine: bloodletting for fever, mercury treatments for syphilis, or leeches for nearly everything.

Nevertheless, this old myth has still not been completely eradicated.

Have you ever come across advice like this?

Morand A et al. Human Bacterial Repertoire of the Urinary Tract: a Potential Paradigm Shift. J Clin Microbiol. 2019 Feb 27;57(3):e00675-18.

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Same diet.

Same training volume.

Different results:

He loses four kilos. She loses her patience. But what are the reasons for this “gender weight gap”?

Muscle mass: The starting point is not identical

On average, men have around 10–15% more fat-free mass than women of the same age. The share of skeletal muscle is about 40–45% of body weight in men, and more like 30–35% in women. More muscle mass, however, also means a higher basal metabolic rate: One kilogram of fat-free mass burns about 13–15 kcal per day at rest.

• In practice, this often results in a daily energy expenditure that is about 100–300 kcal higher for men.

Energy regulation: Earlier counter-regulation

In women, hormonal regulation reacts more sensitively to energy deficits. The level of the satiety hormone leptin can drop by 30–50% even with moderate restriction, while the hunger hormone ghrelin increases. At the same time, adaptive thermogenesis reduces energy expenditure by 5–15%.

• A woman’s body therefore dampens expenditure earlier and more consistently.

Cycle: Weight is not a fixed reference value

Weight fluctuations of 1–2 kg within a cycle are physiological. In the luteal phase, basal metabolic rate increases by 2–10%, while at the same time, in many women spontaneous energy intake increases by 90–500 kcal per day. Progesterone additionally promotes fluid retention.

• Short-term scale values therefore often show the hormonal dynamics — not actual fat change.

Menopause: When distribution changes

With menopause, visceral fat volume increases by around 40–60%, while muscle mass decreases significantly — even if total body weight increases only moderately.

• On the one hand, visceral fat is metabolically active and promotes insulin resistance, inflammatory processes and cardiovascular risk. On the other hand, with less muscle mass, resting energy expenditure can be around 100–200 kcal per day lower.

So what is especially important for women

• Strength training + sufficient protein: 2–3×/week progressive training; 1.6–2.0 g protein/kg BW, to secure muscle mass and basal metabolic rate
• Moderate calorie deficit: about 300–500 kcal instead of crash diet
• Plan for cycle & life stage: 1–2 kg cyclical fluctuations are physiological; postmenopausal, focus more on waist circumference, strength values and metabolic markers)

What do you think: Do weight-loss strategies sufficiently take sex differences into account?

Szeliga A et al. The Impact of the Menopausal Transition on Body Composition and Abdominal Fat Redistribution. J Clin Med. 2026 Jan 16;15(2):740.

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What makes the difference in practice

For this to actually work, the way you do it matters. If your nose is blocked, it makes sense to use a decongestant nasal spray or drops before doing the rinse. For the irrigation, use about 150–250 ml of isotonic saline solution per nostril. The simplest option is pre-portioned nasal rinse salts from a pharmacy or drugstore; you can also get suitable nasal douches or squeeze bottles there. Alternatively, you can mix the solution yourself (about 9 g of salt per 1 liter of water). The water is important: ideally sterile or boiled and then cooled to lukewarm. Lean your head slightly forward over the sink, keep your mouth open, and continue breathing calmly so the nasal secretions can drain properly. Forceful nose blowing is counterproductive because it stresses the mucosa and can push fluid into the sinuses or the middle ear. So it’s better to blow your nose gently, one nostril at a time.

Unspectacular, but effective

The whole procedure isn’t particularly elegant, but it works. Nasal irrigation can be used as often as needed. Symptoms usually improve noticeably after just a few days. Sea salt nasal sprays do not replace irrigation because they simply lack the necessary volume.

Hygiene also determines how useful it is: prepare the solution fresh, clean the irrigation device regularly, and let it dry thoroughly. When used correctly, nasal irrigation is a simple, inexpensive addition to symptomatic therapy – and a good example of how a seemingly unspectacular home remedy can turn out to be surprisingly evidence-based on closer inspection.

Pecoraro L, Di Muri E, Lezzi G, Picciolo S, De Musso M, Piazza M, Bosoni M, Indrio F. Nasal Irrigations: A 360-Degree View in Clinical Practice. Medicina (Kaunas). 2025 Aug 1;61(8):1402.

By the way: This text is part of our series “Naturally effective?”. In it, we take a close look at home remedies and similar approaches – focusing on what makes physiological sense and has at least a bit of scientific backing.

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The focus is shifting away from individual workouts…

… toward overall daily activity.

A 40-minute jog in the morning, then proudly off to the office – followed by eight hours of sitting. Many people consider this a success, even though their step counter may still show less total movement than on a day filled with small errands, stairs, and “just” a walk.

Everyday exercise, short walks, or simply spending less time sitting often contribute more to the overall balance than isolated intense sessions. But exercise not only changes daily activity—it also changes how the body responds to training.

Strength training changes the body – even without weight loss.

Fat mass can decrease, muscle mass can increase.

Dwayne Johnson weighed around 120 kilograms in his action roles – your office-working neighbor at the same weight would likely present a very different physique and fitness level.

The number on the scale may stay stable while function, posture, and metabolic markers improve. Progress, therefore, isn’t defined by weight alone.

When not only the how much but also the how is decisive, the focus automatically shifts to training intensity.

More intensity is not automatically better.

Current discussions emphasize sustainability over extreme programs.

A workout can feel great—until the next day when muscle soreness sets in and suddenly every staircase is avoided. If you end up asking your partner to take out the trash instead, that session may have been harder than what makes sense long term.

Routines that can be permanently integrated into everyday life are more effective in the long term than short bursts of extreme effort.

The old question used to be: How hard was the workout?

Today, it’s more like: How active was the day overall?

Dog owners, by the way, meet physical activity recommendations significantly more often than people without dogs. On gray, rainy days they still go outside — not because they’re more motivated, but because daily life demands it.

So — what ideas do you have?

Zablan K, Melvin G, Hayley A. Dog ownership, physical activity, loneliness and mental health: a comparison of older adult and younger adult companion animal owners. BMC Psychol. 2024 Nov 1;12(1):618.

Dorling JL, Apolzan JW, Johannsen NM, Thomas DM, Höchsmann C, Hsia DS, Martin CK. Exercise-induced Changes in Central Adiposity During an RCT: Effect of Exercise Dose and Associations With Compensation. J Clin Endocrinol Metab. 2024 Feb 20;109(3):e997-e10

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Misconception 1: Weight is a valid marker for therapeutic success.

Body weight is easy to measure, but it says little about fat distribution, insulin sensitivity, inflammatory status, or cardiometabolic risk. Numerous interventions improve precisely these parameters without causing any significant change on the scales. If success is measured solely in terms of weight, relevant health effects remain invisible – and effective measures are mistakenly considered to have failed.

Misconception 2: More effort leads to more weight loss.

This assumption sounds plausible, but often does not stand up in practice. An energy deficit triggers a physiological counter-regulation: resting energy expenditure decreases. At the same time, behavior and well-being change – those affected unconsciously move less outside of planned activities, for example by sitting more or moving less spontaneously. This compensates for part of the deficit. More effort therefore does not automatically lead to more weight loss.

Misconception 3: Losing weight is primarily a behavioral problem.

This view overestimates willpower and underestimates biology – and thus also the psychological strain. Studies show that the body actively regulates weight and fat mass. Hunger, energy consumption, and storage adapt to the nutritional situation, regardless of motivation, insight, or good intentions. For many affected individuals, a lack of success therefore feels like personal failure, even though it is a biological reaction.

Does this sound familiar from your own experience?

Three errors in thinking, many disappointed expectations. In the following articles, we classify these findings based on evidence.

Müller MJ, Bosy-Westphal A. Adaptive thermogenesis with weight loss in humans. Obesity (Silver Spring). 2013;21(2):218–228.

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The metBMI is not based on body measurements, but on an AI-supported model of blood metabolites. It was developed by researchers at the Universities of Leipzig and Gothenburg. The starting point is a known weakness of the BMI: up to 30% of people of normal weight already have metabolic disorders, whereas some overweight people remain metabolically normal. The BMI does not capture the functional quality of adipose tissue.

The new index is the result of a study published in Nature Medicine involving almost 2,000 participants, in which extensive multi-omics data was analysed. From over 1,000 metabolites, the authors identified a clinically manageable panel of 66 markers that accurately reflect obesity-related dysfunctions. An elevated metBMI was associated with a two- to five-fold higher risk of metabolic fatty liver, type 2 diabetes, visceral fat accumulation, insulin resistance and systemic inflammation – regardless of actual BMI. In addition, individuals with high metBMI lost around 30% less weight after bariatric surgery, suggesting metabolic ‘therapy resistance’.

Particularly exciting is the link with the gut microbiome: as metBMI increased, the diversity of gut bacteria decreased, as did their ability to produce protective short-chain fatty acids such as butyrate – a possible mechanistic link between obesity, chronic inflammation and insulin resistance.

What does this mean in practice? While the Body Roundness Index (BRI), Waist-to-Hip Ratio (WHR) and Waist-to-Height Ratio (WtHR) primarily quantify fat distribution, metBMI addresses the biological quality of adipose tissue. It could help to identify high-risk patients earlier, personalise treatment decisions and break the ‘weight equals risk’ paradigm. The scales remain important – but they now have metabolic competition.

Chakaroun RM et al. Multi-omic definition of metabolic obesity through adipose tissue-microbiome interactions. Nat Med. Published online 2 January 2026.

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