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Micronutritional management of overweight and obesity: Part 1, theory and clinical cases
Your overweight patients go from diet to diet, lose a few kilos then regain everything, sometimes more, and end up feeling guilty. This training invites you to change paradigm by revisiting the real metabolic causes of weight gain, to understand, step by step, why "eat less, move more" fails and how to build coherent,…
7 lessons · Lifetime access · Online
These trainings are delivered in French. This page is translated for your convenience; the course videos and materials remain in French.
Overview
Your overweight patients go from diet to diet, lose a few kilos then regain everything, sometimes more, and end up feeling guilty. This training invites you to change paradigm by revisiting the real metabolic causes of weight gain, to understand, step by step, why "eat less, move more" fails and how to build coherent, personalised and genuinely physiological management.
What you will learn
- Why hyperinsulinism and insulin resistance are the central cause of overweight and obesity, and how to reason from this root rather than from symptoms alone.
- How to screen for metabolic syndrome in the practice from waist circumference, fasting glucose, triglycerides, HDL and blood pressure, and how to assess insulin sensitivity (HOMA, QUICKI).
- How to build nutritional interventions tailored to the degree of insulin resistance, working on carbohydrate quality (glycaemic index and load), the rehabilitation of good lipids and dietary restriction windows.
- Which micronutrients support insulin signalling, glucose metabolism and the mitochondria, and in which situations to consider assessment then targeted supplementation.
- How to spot the other metabolic locks that block weight loss, in particular the neurotransmitter, digestive and cardiometabolic profiles, as well as the thyroid, chronic stress and sleep debt.
On the programme
- The clinical observation and the revision of the obesity paradigm, beyond BMI and the simple energy balance.
- The main pathophysiological mechanisms of the terrain, low-grade inflammation, oxidative stress, glycation and carbonyl stress, acid-base balance.
- Glucose metabolism, lipogenesis and lipolysis, the role of insulin as the storage hormone, glycogen, gluconeogenesis and ketogenesis.
- The metabolic syndrome, its definition, criteria and link with cardiometabolic risk and type 2 diabetes.
- Low-carbohydrate and high-fat dietary models, intermittent fasting and eating windows, as well as the place of prebiotic fibres, fructose and sweeteners.
- The micronutrients of interest, chromium, zinc, selenium, magnesium, omega-3, vitamin D, cinnamon, vitamins B1, B3, B6, alpha-lipoic acid, glutathione, L-carnosine, berberine.
- The weight-loss resistance profiles inspired by the functional approach, neurotransmitter (dopamine, noradrenaline, serotonin), digestive (candidiasis, metabolic endotoxaemia, Akkermansia, dysbiosis), cardiometabolic and micronutritional deficiencies.
- The often overlooked aggravating factors, thyroid and reverse T3, functional hypercortisolism and chronic stress, sleep debt, hepatic detoxification and physical activity.
- Clinical cases to link theory to consultation reasoning and train you to formulate hypotheses and strategies.
Who it is for
This training is for healthcare professionals who support patients with overweight, obesity or weight-loss resistance, in particular doctors, pharmacists, as well as practitioners trained or training in micronutrition and functional medicine.
At the end of the training
You will be able to reframe overweight and obesity as a multifactorial problem whose central axis is insulin, and identify the metabolic blocks that coexist in the same patient. You will be able to screen for metabolic syndrome, assess insulin resistance and choose the relevant assessments to personalise your approach. You will have a clear reasoning framework to offer nutritional interventions and supplementation tailored to each patient's profile, in a logic of progressive support and therapeutic alliance.
Programme
Total video duration: 14 h 09 min
CCM SURPOB MICRONUT THEORIE
- Leçon 13 h 27 min
- Leçon 22 h 29 min
- Leçon 31 h 08 min
- Leçon 44 h 55 min
MODULE MISE À JOUR (NOVEMBRE 2025)
- Chapitre 1 : Activité physique56 min
- Chapitre 2 : Tolérance aux glucides56 min
- Conclusion : Individualisation des apports glucidiques17 min
Video Audio PDF handout
Frequently asked questions
Why does the classic low-calorie diet not work in the long term?
When caloric intake is arbitrarily reduced, the body adapts by lowering the basal metabolic rate through a decrease in T3 and an increase in reverse T3. At the same time, ghrelin rises (increased hunger) and satiety mediators collapse, making it physiologically impossible to sustain the diet. This is a homeostatic survival mechanism, not a lack of willpower on the patient's part.
Why is the cardiometabolic profile systematically present in overweight or obese patients?
Insulin resistance is the common metabolic blocking factor in all overweight and obese patients. Dr Anne Lucas, PharmD, explains it as the "backbone" of management: before addressing other blocking factors (digestive, neurotransmitter, deficiencies), this profile is the one that must be treated as a priority. Without resolving hyperinsulinism, other interventions remain of limited effectiveness.
Why is tryptophan as a dietary supplement not recommended in overweight patients with low-grade inflammation?
In overweight patients, chronic low-grade inflammation linked to hyperinsulinism is frequently present. In this inflammatory context, ingested tryptophan is not directed toward serotonin synthesis but is diverted into the kynurenine pathway; this pathway depletes tryptophan and generates neuroactive metabolites (including quinolinic acid) that sustain inflammation. It is therefore preferable to use 5-HTP (griffonia) directly, which crosses the blood-brain barrier without taking this diversion pathway.
Why can sleep debt block weight loss?
A night that is too short is experienced by the body as a major stressor and triggers a significant release of cortisol. Hypercortisolism induces hyperglycemia, then chronic hyperinsulinism leading to insulin resistance. At the same time, sleep deprivation disrupts the chronobiology of leptin and ghrelin, reducing satiety and increasing hunger, which considerably unbalances the day's eating pattern.
How does chronic stress disrupt the synthesis of the neurotransmitters serotonin and dopamine?
In a context of chronic stress, tryptophan (the precursor of serotonin) is diverted into the kynurenine pathway instead of producing serotonin. Similarly, tyrosine (the precursor of dopamine and noradrenaline) is increasingly channeled into its degradation pathway (via tyrosine aminotransferase). These amino acids no longer cross the blood-brain barrier in sufficient quantity to manufacture the neurotransmitters of well-being and motivation.
What is the minimum intermittent fasting window to recommend for an insulin-resistant patient, and should it be positioned in the morning or the evening?
The minimum window recommended as soon as insulin resistance is present is 16:8 (16 hours of fasting, 8 hours of eating). For more severe insulin resistance, one can progress to OMAD (one meal a day) or OMEOD (one meal every other day). From a chronobiological standpoint, it is preferable to position the window in the morning (for example 8am to 4pm) because insulin receptors are more resistant in the evening. That said, the ideal model remains the one the patient can sustain over the long term.
What are the two basic nutritional interventions to resolve insulin resistance?
Dr Anne Lucas, PharmD, distinguishes two complementary approaches: carbohydrate restriction (a low-carbohydrate, therefore higher-fat, diet) with different levels of adjustment depending on the degree of insulin resistance, and restricted eating windows (intermittent fasting, from 16 to 36 hours depending on the case). Neither method is imposed; both are chosen together with the patient according to their preferences and tolerance.
How can an aesthetic overweight be distinguished from a true cardiometabolic risk in consultation?
BMI alone is insufficient: it does not differentiate lean mass from fat mass, nor android fat distribution (abdominal, at risk) from gynoid distribution (hips/buttocks, lower risk). Measuring waist circumference (below 80 cm in women, 94 cm in men) and screening for metabolic syndrome (fasting glucose, HDL, triglycerides, blood pressure) are essential.
How can it be explained that a strategy that does not impose caloric restriction nonetheless results in a negative energy balance?
By working on the regulation of insulin, leptin and ghrelin through intermittent fasting and a low-carbohydrate model, the hormonal signals of satiety are rebalanced. The patient, without being imposed a caloric deficit, naturally eats less because their sensations of hunger and satiety are normalized. This is an indirect and lasting consequence, in contrast to an imposed low-calorie diet, which risks lowering the basal metabolic rate.
Which dietary supplements support serotonin resynthesis in a context of chronic stress?
The root cause must be treated with high-dose magnesium and adaptogenic plants. To restore serotonin synthesis, griffonia (5-HTP) is prescribed with its essential cofactors (B6, B9, B12, B2). Vitamin B3 can also be useful: in case of deficiency, the body consumes tryptophan to resynthesize it, thereby reducing its availability for making serotonin. Providing exogenous B3 therefore frees up this tryptophan.
How should a patient's degree of insulin resistance be assessed before defining the protocol?
HOMA-IR is calculated from fasting insulin and fasting glucose. A HOMA-IR above 2.4 signals insulin resistance. The higher the index, the stricter the dietary protocol and the more comprehensive the micronutrient panel need to be. This calculation also guides the choice of carbohydrate model (low carbohydrate, or even ketogenic for severe forms).
How exactly do chronic stress and excess cortisol prevent weight loss?
Functional hypercortisolism leads to persistent hyperglycemia, reactive insulin secretion, and therefore increased insulin resistance. Added to this are an inhibition of T4 to free T3 conversion (in favor of inactive reverse T3), increased leptin resistance, stimulation of preadipocyte-to-adipocyte differentiation via the 11beta-HSD1 enzyme, and a decrease in DHEA. The result: the patient may comply fully with the nutritional protocol without losing weight as long as chronic stress is not treated.
Which micronutrients and tools should be used to manage functional hypercortisolism?Full answer inside the training →
Why should L-carnitine not be supplemented routinely in metabolic patients?Full answer inside the training →
Which micronutrients should be prioritized as first-line options to improve insulin sensitivity?Full answer inside the training →
Why is fructose more problematic than glucose for overweight patients, even though its glycemic index is low?Full answer inside the training →
Which hypotheses should be explored first in the face of resistance to weight loss after multiple pregnancies?Full answer inside the training →
What role does glycation play in the complications of metabolic syndrome?Full answer inside the training →
In what clinical context should griffonia be preferred over a simple tryptophan intake to support serotonin synthesis?Full answer inside the training →
Why is a normal TSH not sufficient to rule out functional hypothyroidism?Full answer inside the training →
How does chronic inflammation worsen insulin resistance?Full answer inside the training →
What are the essential precursors and cofactors for optimizing thyroid function?Full answer inside the training →
How does metabolic endotoxemia induce resistance to leptin and insulin?Full answer inside the training →
What is metabolic endotoxemia and how is it diagnosed in practice?Full answer inside the training →
What is the value of the urinary organic acids (UOA) test in a suspicion of candidiasis?Full answer inside the training →
What role does Akkermansia muciniphila play in overweight issues, and how can its growth be promoted?Full answer inside the training →
What is the difference between glycemic index and glycemic load, and which one should be used in practice?Full answer inside the training →
What role does liver detoxification play in the management of overweight, and how should it be explained to the patient?Full answer inside the training →
Do proteins raise insulin, and which ones should be avoided as a priority in an insulin-resistant patient?Full answer inside the training →
Why do repeated low-calorie diets worsen resistance to weight loss?Full answer inside the training →
How should physical activity be approached in an overweight or obese patient, and what type of exercise should be favored?Full answer inside the training →
How should the dietary model be adapted for a patient presenting both insulin resistance and a neurotransmitter profile with serotonin deficiency?Full answer inside the training →
How can the link between hyperinsulinism and abdominal weight gain be explained to the patient?Full answer inside the training →
How is glycemic load more useful than glycemic index for guiding patients?Full answer inside the training →
When should chronic digestive candidiasis be suspected in a patient consulting for overweight, and what workup should be proposed?Full answer inside the training →
Why should prebiotic fiber not be recommended indiscriminately in all patients with digestive issues?Full answer inside the training →
What is the place of intermittent fasting in the micronutritional management of overweight?Full answer inside the training →
What are the diagnostic criteria for metabolic syndrome, and why does it go beyond the concept of BMI alone?Full answer inside the training →