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Preventive investigative biology in the service of Nutritional & Functional Medicine
In nutritional and functional medicine, the contents of the plate no longer reflect the patient's real biological status, and staying within a laboratory's statistical ranges does not mean having an optimal status. This training teaches you to master preventive investigative biology as a genuine tool for…
21 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
In nutritional and functional medicine, the contents of the plate no longer reflect the patient's real biological status, and staying within a laboratory's statistical ranges does not mean having an optimal status. This training teaches you to master preventive investigative biology as a genuine tool for personalisation, to validate your clinical hypotheses and build precise micronutritional protocols.
What you will learn
- Distinguish statistical reference values from optimal health values, and reason in terms of intermediate health states rather than the sole deficiency-or-disease logic
- Define the minimal effective assessment for each patient, selecting the biomarkers that are truly useful and prioritising according to the clinical context and budget
- Interpret the main functional assessments, from the erythrocyte fatty acid profile to microbiota analysis, spotting pre-analytical conditions and pitfalls such as false negatives
- Link each result to a concrete strategy, combining nutritional recommendations and supplementation targeted on the right forms and doses
- Reason systemically, linking the functions to one another rather than cutting the patient into isolated organs
On the programme
- Generalities about functional biology, known as preventive investigative biology, and its place in the micronutrition consultation
- The erythrocyte fatty acid profile, membrane fluidity, omega-3, omega-6, omega-7, omega-9, saturated fats, trans fatty acids and ratios of interest such as the omega-3 index and the AA-to-EPA ratio
- Assessing the functionality of the gut ecosystem, microbiota and dysbiosis, metagenomics, mucus quality and FUT2 polymorphism, intestinal hyperpermeability with zonulin and LBP
- Inflammation and the immune system, low-grade inflammation, high-sensitivity CRP, calprotectin, and modulating micronutrients such as vitamin D, zinc and selenium
- Cardiometabolic function, early screening for metabolic syndrome, hyperinsulinism and insulin resistance with HOMA and QUICKI, as well as independent cardiovascular markers such as Lp(a), homocysteine and TMAO
- Assessment of mitochondrial function and oxidative stress, oxidation markers and enzymatic and micronutritional antioxidant defences
- Hepatic detoxification function, its successive phases, and the question of toxic trace metals
- Micronutrient status, iron panel, magnesium, fat-soluble and water-soluble vitamins, as well as genetic polymorphisms of interest
- Functional hormonal assessment, thyroid, adrenals and gonads, and exploration of central nervous system function
Who it is for
This training is for healthcare professionals already engaged in micronutrition and functional medicine, doctors, pharmacists, naturopaths and other practitioners, who wish to integrate preventive investigative biology into their clinical practice.
At the end of the training
You will be able to select and prescribe the relevant assessments according to your patient's clinical picture, then interpret the results against optimal health values. You will be able to translate these results into concrete management strategies, linking terrain and symptom, and combining dietary recommendations and appropriate supplementation. You will thus gain accuracy and confidence in offering personalised micronutritional support.
Programme
Total video duration: 8 h 36 min
CCM ELEARNING BIP
- Quiz de début de formation
- INTRO9 min
- GENERALITES32 min
- PAGE1 h 07 min
- ECO DIG1 h 01 min
- IMMUNOINF32 min
- CARDIOMET34 min
- MITO8 min
- STRESS OX18 min
- DETOX17 min
- MICRONUTRIMENTS1 h 03 min
- POLYMORPHISME46 min
- HORMONO INTRO4 min
- HORMONO SURRENALES23 min
- HORMONO GONADES27 min
- HORMONO THYROIDE22 min
- SNC19 min
- CONCLUSIONS10 min
- QUIZ POST FORMATION2 min
- CORRECTION QUIZ23 min
- Formulaire de satisfaction
Video Audio PDF handout
Frequently asked questions
What are the essential pre-analytical conditions for a DMI (intestinal dysbiosis and mycosis) test?
The DMI is a dynamic test that requires a substrate load the evening before: carbohydrates (rice, pasta, potato, a sweet dessert) for the fungal module, fermentable vegetables for the fermentation bacteria, and animal protein for the putrefaction bacteria. The sample is collected on the first morning urine (from 5am). Fluid restriction the evening before is advised in patients with nocturia to avoid false negatives.
What is the "minimum effective workup" and why does Dr Anne Lucas, PharmD, emphasize it?
The minimum effective workup refers to the precise selection of biomarkers to propose to a given patient, based on their functional signs and etiopathogenic hypotheses. Dr Anne Lucas, PharmD, contrasts this with the practice of prescribing a standardized battery of tests to all patients, which can cost several hundred euros or more than a thousand euros without clinical justification. The goal is to prioritize the workup according to the patient's budget and clinical picture.
Which biological biomarkers should be measured to assess phase 1 of hepatic detoxification?
Phase 1 (functionalization) depends on the cytochrome P450 enzymes, whose optimal function requires a good iron status. Iron testing (ferritin, transferrin saturation) therefore serves as an indirect marker of this first phase. An iron deficiency can slow cytochrome P450 activity and compromise the neutralization of xenobiotics.
In which clinical contexts should mitochondrial function be assessed?
Dr Anne Lucas, PharmD, recommends assessing mitochondrial function in all patients presenting with chronic fatigue, in athletes, and in the context of long COVID, fibromyalgia, metabolic disorders and neurodegenerative diseases. She emphasizes that this assessment should be almost systematic in functional medicine and micronutrition.
Why should fasting glucose alone not be relied on to detect a metabolic disorder early?
Blood glucose is a highly regulated variable: it takes several years, even decades, for it to exceed 1.26 g/L. Dr Anne Lucas, PharmD, stresses the need to combine glucose testing with other biomarkers, particularly fasting insulin, HOMA-IR and triglycerides, which reflect the onset of insulin resistance much earlier.
What are Dr Anne Lucas, PharmD's qualifications in functional biology?
Dr Anne Lucas, PharmD, holds a doctorate in pharmacy (thesis 2009, Toulouse). She holds 9 university diplomas covering micronutrition, functional nutrition, physionutrition and psychonutrition. She also completed the BSN university diploma (Health Nutrition Biomarker) at the Faculty of Medicine and Pharmacy of Dijon in 2015, to date the only university diploma specialized in nutritional and functional biology, reserved for doctorate holders.
Why should the iron panel always be paired with a high-sensitivity CRP test?
Ferritin is a positive acute-phase protein: it rises with inflammation independently of iron status. Without knowing the patient's inflammatory level, an elevated or low ferritin cannot be correctly interpreted. Measuring high-sensitivity CRP at the same time helps put the result in context and avoid a poor treatment decision.
What is the difference between PAGE and SAGE, and how often should this workup be prescribed?
PAGE (erythrocyte fatty acid profile) and SAGE (erythrocyte fatty acid status) refer to exactly the same test. Since the half-life of red blood cells is about 120 days, there is no point retesting before 4 months. In practice, Dr Anne Lucas, PharmD, recommends two workups per year at the start to optimize the profile, then an annual workup once the values have stabilized.
What is the difference between 8-OHdG and anti-oxidized LDL antibodies for assessing oxidative stress?
8-OHdG, measured in urine, reflects oxidative damage at the DNA level (guanine base). Anti-oxidized LDL antibodies, measured in blood, provide information on oxidative stress at the protein and lipid level. Dr Anne Lucas, PharmD, recommends combining both to avoid false negatives with 8-OHdG, particularly when the DNA repair system is impaired.
What is the difference between standard CRP and high-sensitivity CRP, and when should each be prescribed?
Standard CRP detects high-grade inflammation (infections, acute flares) with a usual threshold around 5 to 10 mg/L. High-sensitivity CRP (hs-CRP), a more precise immunoturbidimetric assay, reveals low-grade inflammation. An optimal health value is below 0.75 mg/L, or even 0.1 to 0.3 mg/L. hs-CRP is indicated as part of a systematic workup whenever the goal is to assess cardiovascular risk or chronic low-grade inflammation.
What is the connection between Dr Anne Lucas, PharmD, and the LIMS-MBnext laboratory?
Prof. Castronovo invited Dr Anne Lucas, PharmD, to join his team when the LIMS MBnext laboratory opened. She contributed to the development of the BIP Academy / BIP School webinars, and hosts daily peer workshops bringing together 5 to 6 healthcare professionals (physicians, pharmacists, naturopaths) around functional biology case studies.
Why should a functional workup not be prescribed if the associated therapeutic strategy is not mastered?
A functional biology workup only has value if the practitioner is able to interpret the results and propose an appropriate management plan (dietary recommendations, supplementation, treatment). Prescribing without mastering the interpretation makes the patient spend money for no benefit. Dr Anne Lucas, PharmD, points out that the tool does not replace clinical competence.
What is the reference biomarker for diagnosing digestive candidiasis, and how should it be interpreted?
D-arabinitol is the gold standard marker for excessive proliferation of Candida albicans. The D/L arabinitol ratio provides additional information: an elevated ratio indicates not only the presence of candidiasis but also poor-quality fermentation flora (L-arabinitol being produced by the eubiotic flora). An isolated elevated arabinose level, without a positive D-arabinitol, is not sufficient on its own to make the diagnosis of candidiasis.
Why is membrane fluidity a central pillar in micronutrition?
Cell membranes are phospholipid bilayers whose fluidity governs signal transduction and the function of all transmembrane receptors. The nature of the fatty acids incorporated into these membranes directly determines this fluidity: polyunsaturated fatty acids increase it, while excess saturated fatty acids or trans fatty acids stiffen it. Cholesterol plays a buffering role and is essential, particularly for the central nervous system.
Which form of iron should be chosen for supplementation and at what dosage?
Dr Anne Lucas, PharmD, recommends iron bisglycinate for its good bioavailability and digestive tolerance, to the exclusion of ferrous sulfate. The recommended dosage is 14 to 28 mg per day, possibly every other day, so as not to trigger the homeostatic mechanisms that reduce absorption. She advises against combining vitamin C with iron supplementation (risk of a pro-oxidant effect via the Fenton reaction), contrary to what is often read.
Why measure homocysteine as part of the detoxification workup?
Homocysteine is an indirect marker of phase 2 of hepatic detoxification, which mobilizes the methylation and transsulfuration pathways. Hyperhomocysteinemia can signal a deficiency in B6, B9 or B12 (and B2), which compromises the ability to conjugate toxins. If suspected, it is worth adding testing for the MTHFR polymorphism.
In which cases should fecal calprotectin be prescribed, and what target value should be aimed for?
Calprotectin is reserved for patients with chronic diarrhea or a suspected inflammatory bowel disease (IBD). It is not indicated in everyone. The target value is below 50 micrograms per gram of stool. Dr Anne Lucas, PharmD, recommends retesting it every four months to assess the effectiveness of the gut protocol put in place.
Why can a low 8-OHdG level be a false negative?
A low urinary 8-OHdG level means either that there is no DNA oxidation, or that the patient is unable to repair and eliminate the oxidized guanine base. In this second case, the absence of urinary elimination masks major oxidative stress. Dr Anne Lucas, PharmD, therefore advises always cross-checking this result with another marker, such as anti-oxidized LDL antibodies.
What are the diagnostic criteria for metabolic syndrome that must absolutely be known?
Dr Anne Lucas, PharmD, retains five criteria: increased waist circumference (strict thresholds: 80 cm in women, 94 cm in men), fasting glucose above 1 g/L, triglycerides above 1.5 g/L, low HDL cholesterol (below 0.5 in women, 0.4 in men), and treated high blood pressure or blood pressure above 130/85 mmHg. She emphasizes that one should not be too rigid about the thresholds: a patient can be building toward metabolic syndrome without yet crossing all of them.
Which testable micronutrients are directly involved in mitochondrial function?
Dr Anne Lucas, PharmD, cites vitamin B1 (cofactor of pyruvate dehydrogenase), iron (complexes 1 and 2), copper (complex 4, cytochrome c oxidase), coenzyme Q10 (electron transport), vitamin A (antioxidant), vitamin E (protection of the phospholipid bilayers) and vitamin B2 (precursor of FAD). These micronutrients are testable, unlike PQQ, alpha-lipoic acid or resveratrol, which remain of interest for empirical supplementation.
How often are patients seen in a micronutrition-functional medicine follow-up?
The usual pace is three consultations per year: an initial workup consultation, a workup interpretation consultation (a few weeks later), then a biological follow-up at three to four months to assess the effectiveness of the protocol. Once the imbalances are corrected, follow-up moves to twice a year, then an annual check-up.
What is the role of coenzyme Q10, and what values should be targeted?
Coenzyme Q10 (ubiquinone) collects electrons from complexes 1 and 2 and transports them to complex 3 of the mitochondrial respiratory chain. Reference values lie between 0.85 and 2.8 micromoles per liter, but Dr Anne Lucas, PharmD, recommends targeting high values, even slightly above the upper limit, since there is no risk of overdose.
What are the main topics covered by this training?
The training is structured into 13 parts: general principles of functional biology, erythrocyte fatty acid profile, gut ecosystem function, inflammation and immunity, metabolic function, mitochondrial assessment, oxidative stress, detoxification and heavy metals, micronutrient status, genetic polymorphisms, hormonal assessment (thyroid, adrenal, gonadal) and assessment of brain function.
Why must the balance between SOD and GPx be monitored?
SOD acts first and produces hydrogen peroxide, a radical intermediate subsequently handled by GPx. If SOD is very active and GPx insufficient, hydrogen peroxide accumulates and, in the presence of excess iron or copper, triggers the Fenton reaction with production of the hydroxyl radical, the most oxidizing radical species. Synchronized activity between these two enzymes is therefore essential.
How should a high AA/EPA ratio be interpreted in a patient with a chronic inflammatory disease?
The AA/EPA ratio reflects the balance between series 2 eicosanoids (pro-inflammatory, derived from arachidonic acid) and series 3 eicosanoids (anti-inflammatory, derived from EPA). An optimal ratio is around 1; a ratio between 1 and 4 is acceptable. The French population shows an average ratio of about 25, a sign of an exaggerated inflammatory response. Correction involves reducing AA (quality of animal products, omega-3-enriched supply chains) and increasing EPA (small oily fish 3 times a week, supplementation of 1 to 3 g/day).
What is the practical difference between the DMI and 16S rRNA metagenomics, and how should one choose between the two?
The DMI (urinary organic metabolites) is a functional and metabolomic test that detects what the microbiota produces. 16S rRNA metagenomics is a genotypic test that precisely identifies which bacteria are present and in what quantity. Dr Anne Lucas, PharmD, recommends combining the MI (fungal module alone, about 50 euros) with 16S rRNA metagenomics rather than running the full DMI, in order to obtain both a qualitative and a quantitative view of the microbiota.
Which biological test should be chosen to assess magnesium status, and why not the serum assay?
Magnesium is 99% intracellular, which makes serum or plasma levels unreliable. Dr Anne Lucas, PharmD, recommends erythrocyte magnesium testing as the best reflection of true status, targeting high-normal values. The decision to supplement, however, remains primarily clinical: a picture of stress, chronic fatigue, adrenal exhaustion, anxiety-depressive disorders.
How do heavy metals disrupt metabolism without being directly measured?
Heavy metals exert their toxicity by substituting for physiological metals (selenium, copper, zinc, iron) without performing their functions. For example, a heavy metal can take the place of selenium in thyroid deiodinases, explaining functional hypothyroidism or chronic fatigue of mitochondrial origin. This concept of antagonism should guide the clinical history-taking before any testing.
What is the value of the tryptophan/kynurenine ratio in anxio-depressive disorders?
In cases of inflammation, tryptophan is diverted into the kynurenine pathway (the indoleamine-2,3-dioxygenase pathway) at the expense of serotonin synthesis. A decreased tryptophan/kynurenine ratio signals this diversion and a neuroinflammatory component. This test is relevant in patients with anxio-depressive disorders to objectively demonstrate the link between inflammation and serotonin deficiency.
How should the triglycerides/HDL ratio and the AIP index be interpreted in clinical practice?
The triglycerides/HDL ratio should ideally be below 1.5 (a target of at least below 3): the higher it is, the greater the cardiometabolic risk. The AIP (the logarithm of the TG/HDL ratio) distinguishes phenotype A (large LDL particles, protective) from phenotype B (small, dense LDL particles, strongly atherogenic). An online calculator can derive the AIP from just these two basic lipid values.
Which tests are reliable for investigating heavy metal poisoning, and which should be avoided?Full answer inside the training →
Which cofactors should be measured to assess the activity of antioxidant enzymes?Full answer inside the training →
Why is a dietary survey alone not enough to assess a patient's micronutrient status?Full answer inside the training →
What is the target value for fasting insulin, and how should HOMA-IR be used?Full answer inside the training →
Why should magnesium not be given in "cures", and how should doses be spread out?Full answer inside the training →
How often should a DMI or 16S rRNA metagenomics test be repeated during follow-up?Full answer inside the training →
Why combine LBP with hs-CRP, and what optimal value should be retained for LBP?Full answer inside the training →
What is the purpose of the pre-training quiz and how should it be approached?Full answer inside the training →
When should EPA and DHA be supplemented directly rather than providing precursors such as ALA?Full answer inside the training →
Can coenzyme Q10 be supplemented without prior testing, and what dosages should be applied?Full answer inside the training →
Which forms of zinc are recommended, and how should the zinc/copper balance be monitored?Full answer inside the training →
Why measure vitamin A alongside vitamin D?Full answer inside the training →
Why does Dr Anne Lucas, PharmD, emphasize "small oily fish" in her dietary recommendations?Full answer inside the training →
Which form of vitamin E should be prescribed and at what dosage?Full answer inside the training →
What link exists between mitochondrial function and fatty acid status?Full answer inside the training →
What is the difference between a deficiency and a deficit in micronutrients in clinical practice?Full answer inside the training →
What is the value of C-peptide in assessing insulin-pancreatic function?Full answer inside the training →
What is the clinical role of N-butyrate, and in which situations should it be tested or supplemented?Full answer inside the training →
What is the pedagogical goal of this training in relation to clinical practice?Full answer inside the training →
What is the risk of supplementing with GLA without accounting for FADS1/FADS2 polymorphisms?Full answer inside the training →
How should a carotenoid panel showing elevated beta-carotene and low vitamin A be interpreted?Full answer inside the training →
Why is chromium the priority micronutrient in insulin resistance?Full answer inside the training →
What role does intestinal hyperpermeability play in micronutrient bioavailability?Full answer inside the training →
How can natural trans fatty acids be distinguished from industrial trans fatty acids in the PAGE, and why does this matter?Full answer inside the training →
Should dental amalgams systematically be removed to reduce mercury exposure?Full answer inside the training →
What is the role of vitamin D in immune modulation, and what values should be targeted?Full answer inside the training →
How should the alpha-tocopherol level be interpreted relative to total cholesterol?Full answer inside the training →
Why assess the FUT2 genetic polymorphism, and what is its clinical relevance?Full answer inside the training →
What are the differences between zonulin and LBP for assessing intestinal hyperpermeability?Full answer inside the training →
Which form of vitamin B9 should be favored for supplementation, and why avoid synthetic folic acid?Full answer inside the training →
When should Lp(a) be tested, and what course of action should be taken in case of an elevated result?Full answer inside the training →
How does selenium contribute to the immune response, and which form should be supplemented?Full answer inside the training →
When should directly supplemented glutathione be favored over NAC?Full answer inside the training →
What are the main clinical indications for prescribing a PAGE?Full answer inside the training →
In which clinical cases should hepatic detoxification systematically be supported?Full answer inside the training →
What are optimal health values and how do they differ from laboratory reference values?Full answer inside the training →
What does the LIMS laboratory oxidative stress status panel (BIP) include?Full answer inside the training →
What natural chelators can be used in routine micronutrition practice?Full answer inside the training →
What are the natural modulators of the NF-kB pathway usable in clinical practice?Full answer inside the training →
Why is LDL cholesterol alone insufficient to assess cardiovascular risk?Full answer inside the training →
Why is chewing factored into thinking about micronutrient bioavailability?Full answer inside the training →
Which dietary supplements are indicated as first-line in cases of intestinal hyperpermeability?Full answer inside the training →
How can the LA/DGLA ratio (RLAD) be used to assess delta-6 desaturase activity?Full answer inside the training →
Why measure active vitamin B12 (holotranscobalamin) rather than total serum B12?Full answer inside the training →
What is the overall recommended approach when facing chronic low-grade inflammation?Full answer inside the training →
In which clinical situations is it appropriate to order an oxidative stress panel?Full answer inside the training →
Why is rapeseed oil preferred over walnut oil to optimize the omega-6/omega-3 balance?Full answer inside the training →
How does the concept of epigenetics and the metagenome justify a personalized approach?Full answer inside the training →
How should an elevated level of Fusobacterium in the gut metagenome be interpreted?Full answer inside the training →
What is the optimal value for homocysteine, and how should it be corrected in practice?Full answer inside the training →
In which types of patients should vitamin B12 be measured as a priority?Full answer inside the training →
Which forms of vitamin B12 should be favored for supplementation, and which route of administration should be chosen?Full answer inside the training →
What is the role of Akkermansia muciniphila in the gut ecosystem, and how can it be supported?Full answer inside the training →
How should elevated TMAO be interpreted, and what management should be proposed?Full answer inside the training →
Why should management not be limited to boosting antioxidant defenses in the face of oxidative stress?Full answer inside the training →