Overweight and obesity
Excess weight is not a willpower issue — it is a hormonal, metabolic and neurobiological condition. For most people the root cause is not "too many calories, too little movement", but chronically high insulin, leptin resistance and a disrupted satiety loop.
- 70%+ of Estonian adults are overweight or obese
- "Calories in — calories out" ignores hormonal context
- Reversible with the right protocol and patience
What is overweight, metabolically?
Medically, overweight is classified by BMI: 25–29.9 overweight, ≥30 obesity. But BMI is a blunt metric — it doesn't distinguish muscle from fat, nor where the fat sits. Waist circumference and visceral fat are clinically more meaningful.
Adipose tissue is not passive storage — it is an active hormonal organ. It secretes leptin (satiety), adiponectin (insulin sensitivity) and inflammatory cytokines. Chronic excess fat — especially visceral — shifts the hormonal balance and locks in the weight-gain pattern.
In most cases overweight is a consequence of insulin and leptin resistance, not a cause. High insulin blocks fat burning; high leptin fails to reach the brain as an "I'm full" signal. Hence the hunger, fatigue and weight gain — regardless of willpower.
Signs the problem runs deeper than "eating too much"
- Waist ≥94 cm men, ≥80 cm women
- Weight won't budge despite calorie restriction
- Evening sugar cravings, hard to stop at dinner
- Hunger within 2–3 h of a meal
- Post-lunch fatigue, drooping eyelids
- Night eating or waking hungry
- Puffiness (face in the morning, tight rings in the evening)
- Weight rebounds immediately after every "diet"
Why calorie deficits fail long-term
Sharp calorie restriction lowers thyroid activity (T3), leptin and muscle mass. The body enters "conservation mode" — resting metabolism can drop 20–25% (Rosenbaum, Am J Clin Nutr 2008). Once the diet ends, you eat as before but burn less — weight rebounds, often above baseline.
A 6-year follow-up of Biggest Loser contestants found their resting metabolism stayed suppressed even after regaining weight (Fothergill, Obesity 2016). The issue isn't willpower — it's metabolic adaptation.
Main root causes
- Insulin resistance and chronically high insulin — blocks lipolysis
- Leptin resistance — the brain doesn't "hear" satiety
- Liquid and refined carbs — insulin swings and hunger 2 h later
- Snacking and long feeding windows (>14 h) — insulin never falls to fat-burning range
- Sleep loss — one bad night raises ghrelin and lowers leptin (Spiegel, Ann Intern Med 2004)
- Chronic stress and cortisol — retain abdominal fat and drive sugar cravings
- Thyroid hypofunction (Hashimoto, subclinical hypothyroidism)
- Endocrine disruptors (BPA, phthalates) — "obesogens" that alter adipocyte differentiation
- Low muscle mass — lower resting metabolism, smaller glucose buffer
- Medications — corticosteroids, some antidepressants and antipsychotics, insulin
- Peri- and menopause — falling oestrogen raises visceral fat
Why fat location matters more than weight
Visceral fat (intra-abdominal, around organs) is metabolically active and dangerous. It secretes inflammatory cytokines and is directly linked to fatty liver, insulin resistance, cardiovascular disease and several cancers.
Subcutaneous fat is relatively inert — on hips and thighs it may even protect metabolism. A "pear-shaped" person can be metabolically healthier than an "apple-shaped" one at the same BMI.
Holistic approach
Weight loss without restoring metabolic health is temporary. Four pillars for durable change:
Nutrition
Prioritise protein (1.4–1.8 g / kg body weight) — protects muscle, raises satiety and thermogenesis. Cut refined carbs and liquid calories. Eat 2–3 times a day, no snacking. Feeding window 8–10 h. Vegetables at every meal.
Strength training first
Weight loss without strength = 25–30% of the loss comes from muscle. That lowers resting metabolism and programmes rebound. Strength 2–3×/week preserves muscle, improves insulin sensitivity and burns fat at rest. Cardio is a supplement, not the base.
Sleep and stress
Under 7 h sleep = 55% less fat loss at the same calorie deficit (Nedeltcheva, Ann Intern Med 2010). Chronic stress keeps cortisol high and locks in abdominal fat. Sleep and stress management aren't bonuses — they are preconditions.
Patience and measurement
Realistic fat loss is 0.3–0.7 kg per week. Faster = muscle loss. Track waist, body composition and photos — not just the scale. Weight can stall for weeks while composition improves.
Supplements that support fat and weight metabolism
No supplement replaces nutrition, strength training and sleep. But some support fat metabolism and satiety. Consult your doctor if you take medications or have chronic conditions.
- Protein powder (whey or pea) — a practical protein source to help support satiety and muscle retention
- Berberine — improves insulin sensitivity, supports fat burning; caution with drug interactions
- Omega-3 (EPA/DHA) — lowers metabolic inflammation, supports muscle protein synthesis
- Magnesium glycinate — supports sleep and glucose metabolism
- Vitamin D — deficiency links with higher body fat; test before supplementing
- Creatine monohydrate (3–5 g/day) — boosts performance, preserves muscle
- Fibre (psyllium, acacia) — prolongs satiety, supports the gut
- L-carnitine — supports fatty-acid transport into mitochondria during endurance work
Time-restricted eating and fasting
Shortening the eating window to 8–10 h lowers average insulin, extends the fat-burning window and eases calorie control without leaning on willpower. For most people it is more sustainable than classic calorie restriction.
The randomised trial by Moro et al. (2016, J Transl Med) showed 16:8 time-restricted eating in trained men reduced fat mass and preserved muscle and performance versus a normal eating pattern — at matched protein and calories.
Start with a 12-hour window (dinner to breakfast), extend gradually. Don't fast through training when starting out. Not appropriate in pregnancy, lactation, eating-disorder history or with certain medications.
Labs that give the real picture
- Body composition (bioimpedance or DEXA) — muscle vs fat vs water
- Waist circumference (<94 cm men, <80 cm women)
- Fasting insulin and HOMA-IR
- Fasting glucose and HbA1c
- Triglycerides / HDL ratio (>1.5 = red flag)
- Thyroid panel: TSH, free T4, free T3, TPO antibodies
- Vitamin D (25-OH), ferritin
- hs-CRP (low-grade inflammation)
- Cortisol (morning salivary or 4-point curve)
- Sex hormones: testosterone, oestradiol, SHBG
Go deeper: metabolic-health webinars
Recorded webinars on insulin resistance, blood sugar and the root causes of weight loss — with Dr Saadi.
BMI, vööümbermõõt ja kehakoostise normid
Riskihindamine täiskasvanule
| Marker | Optimaalne | Ülekaal | Kõrge risk |
|---|---|---|---|
| BMI (kg/m²) | 18,5–24,9 | 25,0–29,9 | ≥ 30,0 |
| Vööümbermõõt (M) | < 94 cm | 94–102 cm | > 102 cm |
| Vööümbermõõt (N) | < 80 cm | 80–88 cm | > 88 cm |
| Vöö / puusa suhe (M / N) | < 0,90 / 0,85 | 0,90–1,0 / 0,85–0,90 | > 1,0 / > 0,90 |
| Kehatasand rasva % (M) | 10–20 % | 20–25 % | > 25 % |
| Kehatasand rasva % (N) | 18–28 % | 28–33 % | > 33 % |
| Vistseraalne rasv (skoor) | 1–9 | 10–14 | ≥ 15 |
BMI on ligikaudne — lihaselisel inimesel võib olla „ülekaal" ilma rasvahaiguseta. Vööümbermõõt ja kehakoostise analüüs on täpsemad.
Frequently asked questions
Go deeper: related materials
Related topics
Metabolic health is interconnected — explore the other deep-dives:
Insulin resistance
The root of metabolic disease — 5–10 years before diabetes appears.
ReadVagus nerve
The rest-and-repair system — digestion, heart, inflammation, stress.
ReadCholesterol & ApoB
Expanded lipid panel — ApoB, Lp(a), homocysteine, A vs B phenotype.
ReadSleep
The foundation of metabolic health — hormones, cortisol, insulin, brain recovery.
ReadChronic inflammation
The 'silent fire' behind cardiovascular disease, diabetes and autoimmunity.
ReadLow-carb and keto
Carbohydrate restriction — IR, T2D, fatty liver, metabolic syndrome.
ReadTeaduslikud allikad
- Fothergill E et al. Persistent metabolic adaptation 6 years after "The Biggest Loser" competition. Obesity, 2016. doi.org/10.1002/oby.21538
- Hall KD, Kahan S. Maintenance of Lost Weight and Long-Term Management of Obesity. Medical Clinics of North America, 2018. doi.org/10.1016/j.mcna.2017.08.012
- Frayling TM et al. A common variant in the FTO gene is associated with body mass index and predisposes to obesity. Science, 2007. doi.org/10.1126/science.1141634
- Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). NEJM, 2021. doi.org/10.1056/NEJMoa2032183
- Leidy HJ et al. The role of protein in weight loss and maintenance. American Journal of Clinical Nutrition, 2015. doi.org/10.3945/ajcn.114.084038
- Jakubowicz D et al. High caloric intake at breakfast vs. dinner differentially influences weight loss. Obesity, 2013. doi.org/10.1002/oby.20460
- Westerterp-Plantenga MS. Sleep, circadian rhythm and body weight. Proceedings of the Nutrition Society, 2016. doi.org/10.1017/S0029665116000227
- Villareal DT et al. Aerobic or Resistance Exercise, or Both, in Dieting Obese Older Adults. NEJM, 2017. doi.org/10.1056/NEJMoa1616338
Dr Sergey Saadi — expert in metabolic health and the root causes of weight gain
Dr Sergey Saadi is a physician with over 15 years of clinical practice.
- Thousands of consultations for metabolic-health and weight concerns
- Author of "Dangerous secrets of blood sugar" (Varrak)
- Clinical approach: body composition + hormonal panel + lifestyle audit
- No one-size-fits-all diets — individual root-cause analysis
Want to know why the weight won't move?
In the consultation we review your labs, body composition, HOMA-IR and hormonal context and build an individual plan you can discuss with your GP and/or other treating clinicians.
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