What does hyaluronic acid do in the skin?

Hyaluronic acid (HA) occurs naturally in the skin – and decreases dramatically with age. At 25, the skin still produces enough, but by 40 the level has fallen by over 50%. When applied as a serum, it penetrates into the upper layers of the skin and provides:

• Intensive hydration: Immediate moisture boost, visible after the first application
• Volume effect: fine lines are plumped up by moisture
• Barrier strengthening: the skin barrier is stabilized, less transepidermal moisture loss
• Soothing: Hyaluronic acid is suitable for all skin types, including rosacea skin

Low molecular weight vs. high molecular weight: Which is better?

This is the most common question when buying hyaluronic serums. In the K-Beauty world, many brands already rely on multi-weight formulas:

• High molecular weight HA (over 1,000 kDa): Stays on the skin surface, acts as a moisture-binding film – quick visible shine effect
• Low molecular weight HA (less than 500 kDa): Penetrates deeper into the skin, more effective in the long term
• Multi-weight HA: combination of both molecule sizes – the smartest option. Most high-quality serums today rely on

The best hyaluronic serums in comparison

Budget (under 20 Euro)

• The Ordinary Hyaluronic Acid 2% + B5 (~8 euros): Reliable, well formulated, ideal for beginners
• Garnier Hyaluron Filler Serum (~15 euros): Widely available, for dry and normal skin
• COSRX Hyaluronic Acid Intensive Cream (~18 euros): More of a cream than a serum, but hugely hydrating

Mid-range (20-60 euros)

• Vichy Liftactiv Supreme H.A. Epidermic Filler (~35 euros): Dermatologically tested, 1.5% HA concentration
• La Roche-Posay Hyalu B5 Serum (~42 euros): Gold standard for sensitive skin – Bakuchiol plus HA
• Paula’s Choice Hyaluronic Acid Booster (~52 euros): Multi-weight formula, excellent tolerance

Premium (over 60 euros)

• SkinCeuticals H.A. Intensifier (~115 euros): Clinically tested, 1.3% HA with Proxylane and Licorice Root
• Drunk Elephant B-Hydra Intensive Hydration Serum (~75 euros): Light, layerable, ideal for combination skin

Application: When and how to apply?

Hyaluronic serum works best on slightly moist skin – this increases penetration. A common mistake is to apply it to completely dry skin – HA then draws moisture from the skin instead of from the outside. Further tips for optimal integration into the Glass Skin morning routine:

1. Cleanse face
2. Apply toner or essence – leave slightly damp
3. Press on hyaluronic serum (do not rub in – gently tap in)
4. Moisturizing cream over it – seals the HA
5. SPF in the morning

Combination with other active ingredients

Hyaluronic acid is compatible with almost everything. Good combinations:

• HA + niacinamide: hydration plus pore refinement – classic K-Beauty combination
• HA + vitamin C: layer serum in the morning, vitamin C underneath or on top
• HA + retinol: apply HA before retinol – buffers irritation and keeps skin moisturized

What is retinol and how does it work?

Retinol is a form of vitamin A – the upper category of retinoids. In the skin, it is converted into retinoic acid, which acts directly on the cell nuclei. The result:

• Cell renewal is accelerated: Old cells are shed faster, new ones form more quickly
• Collagen production increases: The main cause of the anti-aging effect
• Pigment spots fade: Melanin synthesis is inhibited
• Pores refine: less sebum, tighter pore structure

Retinol strengths: What to start with?

This is the most common mistake: too much concentration when getting started. The result: redness, flaking, over-irritation. Combining retinol with a good hyaluronic serum significantly reduces irritation. Start right:

• Beginners: 0.025% – 0.1%: start once a week, then increase slowly
• Advanced: 0.3% – 0.5%: 2-3x per week when the skin is accustomed
• Experienced: 0.5% – 1%: Daily, but always with moisturizer underneath (sandwich method)

The sandwich method: retinol without irritation

The sandwich method is the best beginner’s technique: moisturizer – retinol – moisturizer. The cream “dilutes” the retinol contact with the skin and drastically reduces irritation without completely eliminating the effect. Ideal for the first 4-8 weeks.

Best retinol products

Beginner

• The Ordinary Retinol 0.2% in Squalane (~7 Euro): Inexpensive, effective, well tolerated due to squalane base
• CeraVe Retinol Serum (~18 euros): With niacinamide and ceramides – soothes at the same time
• Eucerin Anti-Pigment Dual Serum (~35 euros): 0.1% retinol, specially formulated for pigmentation spots

Advanced

• RoC Retinol Correxion Line Smoothing Serum (~35 euros): Classic with proven effect
• Paula’s Choice Clinical 1% Retinol (~60 euros): High concentration, well buffered with hyaluronic acid and vitamin C
• Medik8 Crystal Retinal 3 (~57 euros): Retinaldehyde instead of retinol – more effective and better tolerated

Retinol and sun: the most important rule

Retinol belongs exclusively in the evening routine. It makes the skin more sensitive to light. In the morning: always use SPF 50+. This is not an option – it’s mandatory. More on optimal sun protection in the K-Beauty product guide (Korean sunscreens are among the best on the market).

What should retinol not be combined with?

• AHA/BHA: Never use at the same time – too irritating. Alternate: Retinol Mon/Wed/Fri, peeling Tue/Thu
• Vitamin C: Different pH ranges – vitamin C in the morning, retinol in the evening, no problem
• Benzoyl peroxide: Deactivates retinol – never use together

When will we see the first results?

The first improvements can be seen after 4-6 weeks: smoother texture, more even complexion. Significant results for pigmentation spots and fine lines after 3-6 months. Retinol is not a sprint – those who are consistent will be rewarded in the long term.

What is cannabis microdosing?

Microdosing means taking cannabis in such low doses that the therapeutic or mood-enhancing effects are noticeable, but there is no perceptible high. For THC, this is typically 1-5 mg per dose. The concept is particularly relevant for:
– Medical users who want to maintain everyday functionality
– People with low THC tolerance
– Anxiety patients for whom high THC doses trigger panic
– Creative work (slight opening of perception without functional impairment)

Biphasic THC effect: less is more

THC shows a classic biphasic dose-response curve – a basic principle of cannabinoid pharmacology:

Low dose (1-5 mg): Anxiolytic, mood enhancing, mildly focusing, analgesic without sedation

Medium dose (10-20 mg): Euphoria, relaxation, hunger, slight time distortion – classic recreational high

High dose (25-50 mg+): paranoia, anxiety, disorientation – especially in beginners or without tolerance

The paradox: if you want to take cannabis for anxiety, you have to dose low. Higher doses worsen anxiety in many cases.

Microdosing protocol according to experience level

CBD microdosing: why even too little is too little

CBD also shows a biphasic dose effect:
– Too low (<10 mg): Often no noticeable effect
– Moderate (30-100 mg): Anxiolytic, anti-inflammatory, sleep-inducing
– High (150-300 mg): Sleep-inducing, antiepileptic (clinically relevant)

For anxiety: at least 25-50 mg CBD daily for consistent effects. Many users take too little (10 mg softgel) and report no effect – this is a dosing issue.

Practical microdosing methods

Vaporizer: Most precise method for THC. Small puff = ~1-2 mg THC, depending on strain. Effect noticeable in seconds, quick adjustment possible.

Sublingual oil: pipette with 1/4 drop of THC oil or precise CBD oil dosage. Good control.

Microdosing capsules: 2.5 mg THC capsules are medically available; simplest form for precise daily dosing.

Tincture: dropwise control; alcohol-based = fastest oral absorption.

FAQ: Cannabis microdosing

Summary

Microdosing utilizes the biphasic THC dose-response: 1-5 mg THC produces therapeutic effects without intoxication. CBD microdosing starts at 25-50 mg daily for measurable anxiolytic effects. Methods: vaporizer (most precise), sublingual oil, capsules. For daily use: cycling (5 days on, 2 days off) for tolerance avoidance. Tolerance break guide; CBD dosage guide for all indications.

CBN: The cannabinoid of aged cannabis

Cannabinol (CBN) is produced when THC oxidizes – heat, light and oxygen gradually break down THC into CBN. Old, poorly stored cannabis therefore contains more CBN than fresh material. CBN is weakly psychoactive (around 10% of the potency of THC) and is primarily associated with sedative, sleep-inducing properties.

CBN pharmacology

CBN and sleep: what the evidence really shows

CBN is popularly regarded as the “sleep cannabinoid” – but the evidence is weaker than often claimed:

Older Study (Musty et al. 1976): 5 subjects received CBN alone vs. THC alone vs. CBN+THC. CBN alone: hardly any sedation. CBN+THC: stronger sedation than THC alone. Conclusion: CBN potentiates THC sedation in combination, but does not have a strong sedative effect on its own.

Mechoulam & Ben-Shabat 1998: CBN mentioned as part of the entourage effect – sedative effect mainly in combination with other cannabinoids.

Current reviews (2022-2024): Human clinical studies on CBN and sleep are largely lacking. The “CBN is the sleep cannabinoid” claim is marketing-driven and not as scientifically proven as often claimed.

Real effect: CBN has a sedative effect mainly through its weak CB1 activation and in combination with THC. Monoproducts with CBN have limited clinical evidence.

CBN for pain and inflammation

Wong & Cairns 2019 (Arch Oral Biol): CBN desensitizes TRPA1 nociceptors more strongly than CBD. Relevant for neuropathic pain and joint pain.

Antibacterial: Like CBG, CBN shows antibiotic activity against MRSA in vitro (Appendino et al. 2008, J Nat Prod).

Neuroprotective: Weydt et al. 2005 (Neuroreport): CBN significantly delayed disease progression in ALS mouse model – one of the first cannabis animal model neuroprotection results.

Storing cannabis correctly: THC preservation vs. CBN formation

Who wants to get THC:
– Cool (15-20°C), dark, airtight (vacuum seal)
– UV light is the main enemy: THC → CBN through photooxidation
– No refrigerator (humidity → mold)

Who wants CBN-rich (for sleep products):
– Store old cannabis intentionally: 1-2 years in a slightly open container at room temperature

FAQ: CBN Cannabinol

Summary

CBN is the degradation product of THC through oxidation – old cannabis contains more of it. Slightly psychoactive (10% THC potency), sedative mainly in combination with THC (not alone). Well documented for TRPA1 pain modulation, antibacterial (MRSA), neuroprotective (ALS model). Clinical sleep studies are lacking – CBN is better proven than often claimed for pain, worse for sleep. CBG guide for another non-THC cannabinoid; entourage effect for CBN in a full-spectrum context.

CBG: The mother cell of all cannabinoids

Cannabigerol (CBG) is often referred to as the “mother cell of all cannabinoids” because CBGA (the acid form) is the precursor from which THC, CBD and CBC are biosynthesized. In mature cannabis plants, CBG is therefore only present in small amounts (usually <1%) – most CBGA has already been converted into THCA and CBDA.

Young cannabis (before flowering) contains more CBG. Specially bred CBG strains today reach 10-15 % CBG content.

CBG pharmacology: How it works

CBG in glaucoma: a historical finding

Glaucoma is caused by increased intraocular pressure (IOP). CBG shows a strong IOP-lowering effect in animal models – stronger than THC:

Colasanti et al. 1984 (J Ocul Pharmacol): CBG lowered IOP in cats more than THC. Mechanism: α2-adrenoceptor agonism (same mechanism as timolol eye drops in glaucoma therapy).

Clinical human studies are still lacking for CBG specifically, but the mechanism is pharmacologically sound.

CBG for inflammatory bowel disease

Borrelli et al. 2013 (Biochem Pharmacol): CBG in mouse colitis model. CBG reduced significantly:
– Inflammation parameters (TNF-α, IL-1β)
– Intestinal damage histologically
– iNOS expression (inflammatory nitric oxide)

Mechanism: CB2 activation on intestinal immune cells + PPAR-γ agonism. Conclusion: CBG is an interesting experimental target for Crohn’s disease and ulcerative colitis.

CBG and neurodegeneration

Valdeolivas et al. 2015 (Neurotherapeutics): CBG in Huntington’s disease mouse model. CBG showed:
– Neuroprotective effect (less striatum neuron loss)
– Reduction of neuroinflammation
– Antioxidant effect

CBG in ALS animal model: similar neuroprotective data (Moreno-Martet 2014).

Antibacterial: CBG against MRSA

Farha et al. 2020 (ACS Infect Dis): CBG showed strong antibiotic activity against methicillin-resistant Staphylococcus aureus (MRSA) in vitro and in a mouse model. CBG effectively disrupted the membrane function of MRSA bacteria.

No human clinical studies on CBG as an antibiotic, but preclinical evidence is remarkable.

FAQ: CBG Cannabigerol

Summary

CBG is the biosynthesis precursor of all cannabinoids. Pharmacological: weak CB1/CB2 agonist, α2-adrenoceptor (glaucoma), 5-HT1A antagonist, antibacterial (MRSA). Study evidence: glaucoma IOP reduction (animal model), colitis improvement (Borrelli 2013), neuroprotection (Huntington’s disease model). No high, legally available in Germany. Entourage effect for CBG in full-spectrum context; CBD vs. THC for main cannabinoid comparison.

Delta-8-THC: What is it?

Delta-8-THC (Δ8-THC) is a naturally occurring cannabinoid that is structurally closely related to the classic delta-9-THC (Δ9-THC). The difference: the double bond is located on the eighth instead of the ninth carbon atom. This small structural difference has pharmacological consequences.

Delta-8-THC is only found in trace amounts (< 0.1%) in the cannabis plant. Commercially available delta-8 products are almost exclusively produced synthetically from CBD by isomerization – which raises toxicological questions.

Delta-8 vs. Delta-9 vs. Delta-10: Pharmacological comparison

Why Delta-8 is marketed as “milder THC”

Delta 8 THC users often report less anxiety and paranoia than with delta 9 THC. This has a neuroscientific basis:

Delta-8 activates CB1 with lower intrinsic activity (lower efficacy) than delta-9 – it is a weaker partial agonist. This could explain the different side effect profile. However, there are hardly any clinical comparative studies.

Manufacturing risks: Synthetic Delta-8

Since natural delta-8 only occurs in traces in cannabis plants, it is produced commercially by chemical isomerization of CBD. This produces potentially problematic by-products:

– Unknown isomers (Δ4, Δ6, Δ7-THC as synthesis by-products)
– Acid catalysts as residues (hydrochloric acid, p-toluenesulfonic acid)
– Heavy metals from uncontrolled synthesis processes

An FDA analysis (2021) found some significant impurities in Delta 8 products. This is a safety risk, especially in an unregulated market.

Legal situation in Germany

Delta-9-THC: narcotic (BtMG Annex III for medical cannabis); regulated recreationally by CanG (max. 25 g in possession).

Delta-8-THC: falls under the BtMG if it is isolated from cannabis or produced synthetically and has a psychoactive effect. Legally no clear “legal gray area” in Germany – the classification follows the psychoactive effect and the production method. Caution: Many online offers are illegal.

Delta-10-THC: Same classification as Delta-8 – psychoactive = BtMG-relevant.

Medical relevance: Is there a benefit?

Delta-8-THC was investigated in an early study (Abrahamov et al. 1995) as an antiemetic agent in children with cancer: 480 mg/m² orally in 8 children with antineoplastic chemotherapy. Result: complete suppression of vomiting in all cases, no reported side effects. This historical study is pharmacologically interesting, but methodologically weak.

FAQ: Delta-8-THC and Delta-10-THC

Summary

Delta-8-THC is a weaker CB1 agonist than Delta-9-THC with a potentially more favorable side effect profile (less anxiety). Commercially produced almost exclusively synthetically from CBD – with risks of contamination. Legally classified as a narcotic in Germany. Delta-10-THC is even weaker and equally regulated. For medical use, certified delta-9-THC and CBD preparations remain the standard. CBD vs. THC for the basics; Legal situation cannabis Germany for current laws.

Edibles: Why oral cannabis use feels so different

Cannabis edibles – cookies, gummy bears, brownies, oils, capsules – have completely different pharmacological kinetics than inhaled cannabis. What many people don’t know: THC taken orally is converted in the liver to a different substance that has a stronger, longer and different effect. This leads to the classic errors associated with edibles consumption.

Liver metabolization: THC becomes 11-OH-THC

When THC is taken orally, it enters the liver via the gastrointestinal tract – subject to the first-pass effect. In the liver, CYP2C9 and CYP3A4 convert THC to 11-hydroxy-THC (11-OH-THC):

– 11-OH-THC is significantly more psychoactive than THC itself
– 11-OH-THC crosses the blood-brain barrier even more efficiently than THC
– Blood plasma concentration of 11-OH-THC after oral ingestion: up to 3× higher than after inhalation
– Half-life of 11-OH-THC: longer than THC → prolonged duration of action

This explains why edibles have a more intense, heavier and longer-lasting effect – not because the dose is higher, but because a stronger metabolite is produced.

Pharmacokinetics: time course

The most common mistake: topping up

The classic scenario: you eat an edible, wait 45 minutes, feel nothing, eat more. An hour later, both doses arrive at the same time – with full 11-OH-THC conversion. Result: overwhelming effect, panic, unpleasant high.

Golden rule: For edibles, wait at least 2 hours before topping up. If you are cannabis-sensitive: 3 hours.

Bioavailability: Why edibles are so unpredictable

The oral bioavailability of THC varies between 4 % and 20 % – depending on:
– Fat content of the meal: THC is lipophilic; up to 3× higher absorption with a meal containing fat
– Individual CYP2C9 activity: Genetic variants determine how quickly THC is metabolized
– Intestinal flora: Intestinal microbiomes modulate cannabis absorption
– Emulsion form: Nanoemulsified THC (water-soluble) has significantly higher and faster absorption

Dosage: recommendations for beginners

What to do if the edible effect is too strong

Overdosing with edibles is unpleasant but not life-threatening. Helpful measures:
– Lying down: safe environment, breathing calmly
– Take CBD: CBD can mitigate the effects of THC (competitive CB1 interaction)
– Sugar: Dextrose can slightly shorten acute THC intoxication (anecdotal)
– Distraction: music, movie, quiet company
– Drink water (not alcohol)
– Effect subsides after 4-6 hours without intervention

FAQ: Cannabis Edibles

Summary

Edibles have a stronger, longer and different effect than inhaled cannabis due to liver metabolization of THC to 11-OH-THC. Onset of effect 30-120 minutes, duration 4-8 hours. Starting dose 2.5-5 mg THC, 3 hours waiting time. Bioavailability is variable (4-20%) and fat-dependent. The most common mistake: topping up early. Variety guide for choosing the right flower; CBD dosage guide for medical use.

CBD dosage: Why there is no standard dose

CBD (cannabidiol) does not have an officially defined standard dosage like conventional medicines. The optimal CBD dose depends on the indication, body weight, metabolism (CYP2C19, CYP3A4), form of administration and individual CB1/CB2 receptor density. Added to this is the high variability in the bioavailability of different products. This guide summarizes scientifically proven dosage recommendations according to indication.

Bioavailability: Why the form of intake is crucial

Practical tip: Always take CBD oil with a fatty meal – increases bioavailability by up to 4× (Millar et al. 2019, Molecules). Coffee, empty stomach = drastically lower absorption.

CBD dosage according to indication

The titration scheme: how to find the right dose

Start low, go slow: the most important principle. CBD has an inverse U-shaped dose-response curve for some indications (e.g. anxiety) – too little and too much can be suboptimal.

Recommended titration scheme:
1st week 1-2: 15-25 mg/day (morning or evening depending on the indication)
2nd week 3-4: 50 mg/day (if sufficiently tolerated)
3rd week 5-6: 75-100 mg/day
4. from week 7: increase to 150-300 mg if necessary, depending on the indication

Keep a symptom diary: Record main symptom (0-10), sleep (0-10), side effects daily. Gives a clear picture after 4 weeks whether and how strongly CBD works.

CBD and body weight

Body weight is less important for standard indications (anxiety, sleep) than for epilepsy. As a rough guide:
– Under 60 kg: 15-25 mg entry, max. 100-150 mg
– 60-90 kg: 25-50 mg entry, max. 150-250 mg
– Over 90 kg: 50 mg entry, up to 300 mg possible

Side effects and contraindications

CBD is well tolerated, but not free of side effects:
– Tiredness (especially high doses): Reduce dose or take in the evening
– Diarrhea (especially CBD isolate without carrier oil): Switch to full-spectrum oil
– Elevated liver enzymes (ALT/AST): Possible at >300 mg daily; consult a doctor if liver disease is present
– CYP interactions: CBD inhibits CYP2C19 and CYP3A4 – increased risk of bleeding with warfarin; levels of benzodiazepines, SSRIs, antihypertensives may increase

FAQ: CBD dosage

Summary

CBD dosage depends on the indication: 25-75 mg daily for anxiety and sleep, 50-200 mg for pain, 2.5-20 mg/kg for epilepsy. Bioavailability varies greatly depending on the form of administration – sublingual and inhaled are more efficient than fasting oral intake. Start low, go slow with symptom diary is the only sensible titration strategy. Always clarify CYP interactions with existing medications with your doctor. For specific indications: CBD for sleep disorders, CBD for anxiety and CBD interactions with medication.

What is CBG (cannabigerol)?

CBG (cannabigerol) is referred to as the “stem cell of cannabinoids” – and rightly so: CBGA (cannabigerolic acid) is the biosynthetic precursor of all other cannabinoids in the plant. Enzymes convert CBGA into THCA, CBDA or CBCA; in mature plants, therefore, only little CBG remains (usually <1 % of the total weight). Modern CBG-rich varieties (with up to 20 % CBG) have been specially bred by harvesting before full maturity.

CBG was first isolated in 1964 by Gaoni and Mechoulam, but was long considered an inactive by-product. Since around 2015, interest has grown considerably: CBG has its own pharmacological activity via CB1, CB2, TRPV1, α2-adrenoceptors and 5-HT1A.

Pharmacological mechanisms

CB1 agonism: CBG binds to CB1 – weaker than THC, without a significant intoxicating effect. Via CB1 in the basal ganglia system, CBG shows influence on motor function and pain processing in animal models.

CB2 agonism: CBG acts on CB2 as a full agonist, which explains anti-inflammatory and immunomodulatory effects – similar to CBD, but with a more direct CB2 profile.

TRPV1 antagonism: In contrast to CBD (TRPV1 agonist), CBG blocks TRPV1 – which can counteract an “overstimulation” of pain receptors.

α2-adrenoceptor: CBG is a partial agonist at α2-adrenoceptors. This explains potential blood pressure lowering and anxiolytic effects (analogous mechanism to clonidine).

5-HT1A antagonism: CBG blocks 5-HT1A – in contrast to CBD (agonist). This difference is pharmacologically important and explains why CBG and CBD can have opposite effects in certain indications.

State of research: What the studies show

Possible areas of application

Inflammatory bowel disease (IBD): Crohn’s disease, ulcerative colitis – CB2 in intestinal mucosa and immune cells. CBG showed stronger anticolitis effects than CBD in animal models with the same mechanism. Clinical human studies are still lacking.

Glaucoma: CBG reduces intraocular pressure in animal models – more than THC in some studies. Mechanism: CB1-mediated reduction of aqueous humor production + α2-adrenoceptor activation (similar to timolol eye drops).

Antibiotic of the future: MRSA-resistant germs are a global health problem. CBG acts against gram-positive bacteria through membrane depolarization – a completely different mechanism than classic antibiotics. Particularly interesting: synergism with existing antibiotics.

Neuroprotection in Huntington’s disease/ALS: Valdeolivas 2015 shows CBG neuroprotection in the striatum. Early research on ALS (Loría 2010) shows slowing of motor neuron degeneration by CBG.

Appetite stimulation: In animal models, CBG stimulates food intake more strongly than CBD – without any psychoactive effect (relevant for cachexia in cancer or AIDS).

CBG vs CBD: The most important differences

Buying CBG: What to look out for

CBG oils are available in Germany as food supplements (similar to the former CBD legal situation). Quality criteria:
– COA (Certificate of Analysis) from independent ISO 17025 laboratory
– Full spectrum or broad spectrum (entourage effect with other cannabinoids)
– CBG content and residual THC content (<0.2 %) indicated
– EU-certified hemp cultivation (no pesticides)

Dosage (empirical): 10-50 mg CBG daily. No established clinical dosage guidelines available.

FAQ: CBG – the cannabinoid strain

Summary

CBG is the biosynthetic precursor of all cannabinoids and shows remarkable properties in preclinical studies: strongest antibiotic effect of all cannabinoids against MRSA, CB2-mediated inhibition of inflammation in intestinal diseases, neuroprotection in Huntington’s disease. Compared to CBD, CBG has more direct CB2 binding, but opposite TRPV1/5-HT1A effect. Human studies are largely lacking – CBG remains a high-potential research candidate that is most effective in the entourage effect with other cannabinoids.

5 kilos in one month – but not a sprint

The first month with Mounjaro(weight loss injection) resulted in Nadin losing a total of five kilograms. As she reports, the rapid loss at the beginning was mainly due to water retention. After that, the weight loss leveled off at around one kilogram per week – a realistic and healthy progression.

Through the month without side effects

Particularly positive: even in the second to fourth week of treatment, she did not feel any side effects. There was no nausea, headaches or digestive problems at all. For Nadin, this is a big difference to other weight loss attempts, which often resulted in physical or mental stress.

Hungry? Simply no longer there.

She describes the biggest change as the disappearance of “food noise” – the constant thoughts about food. Nadin says that she no longer plans meals all the time or sees food as a reward. She can now go shopping and cook in a relaxed manner without being overwhelmed by cravings – a completely new attitude to life.

You can find her channel here: Nadin (YouTube)

The complete video of Nadin:

Change of diet with more clarity

Reduced hunger makes it easier for Nadin to make conscious decisions. Instead of eating leftovers from her children’s plates or impulsively grabbing something at the supermarket, she now thinks about what she needs: What does my body need? What gives me energy and nutrients?

Keeping an eye on calories – but not obsessively

With the help of Yazio, she tracks her calories every day. On average, she consumes around 1,000 calories – sometimes less if she is ill. This low intake raises questions: What happens when Mounjaro is discontinued? Can she maintain this discipline without the medication?

“Living on 600 to 1,000 calories a day is not feasible in the long term – at least not without help like Mounjaro.”

The price remains a problem

One topic that remains: The costs. In Austria, the health insurance does not cover anything. The 5 mg dose costs around €330, higher doses such as 7.5 mg or 10 mg cost up to €460 per month. This is a real hurdle for many people. Nevertheless, Nadin sees it as an investment in her health.

Outlook and open questions

• How will her weight develop over the next few weeks?
• How long does the appetite remain so low?
• How do you manage to stop taking medication?

Mounjaro after 30 days: Initial assessment

The first month with Mounjaro was a turning point for Nadin. Five kilos lighter, no side effects, a clear head – and finally less stress around food. But with the new attitude to life also come questions: How long-term is the success? And will she one day be able to maintain her weight without medical help?

More GLP-1 articles

• Ozempic click table: Set dosage 0.25 / 0.5 / 1 mg correctly
• Weight loss syringe comparison: Ozempic vs Wegovy vs Mounjaro
• 14 kg less in 4 months with Mounjaro – long-term experience