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Preventing diseases of civilisation: focus on cardiovascular disease
Faced with a patient with a chronic disease, the reason for the consultation almost always hides the same major pathophysiological mechanisms, which medicine compartmentalised by specialty too often leaves aside. This training invites you to understand them one by one, then apply them concretely to cardiovascular…
6 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
Faced with a patient with a chronic disease, the reason for the consultation almost always hides the same major pathophysiological mechanisms, which medicine compartmentalised by specialty too often leaves aside. This training invites you to understand them one by one, then apply them concretely to cardiovascular prevention, to move from a reading centred on cholesterol alone to a global, micronutritional and genuinely personalised approach.
What you will learn
- Identify and investigate the major mechanisms that pave the way for chronic diseases, systematically starting with the gut ecosystem and its four players (microbiota, mucus, mucosa and hyperpermeability, immune system).
- Understand and modulate chronic low-grade inflammation and oxidative stress, from NF-kB to kinase activity modulators, including fatty acid balance and the AA-to-EPA ratio.
- Link together carbonyl stress and insulin resistance, acid-base balance, hepatic detoxification, mitochondrial function and cellular senescence, to reason as a map rather than organ by organ.
- Revisit the cholesterol paradigm by looking at LDL oxidation, and work on the real cardiovascular levers of the omega-3 index, membrane rigidity and platelet aggregation.
- Spot the often overlooked independent risk factors, such as lipoprotein(a), TMAO and homocysteine, and know what to offer for each.
- Build dietary recommendations and supplementation tailored to each patient's budget, drawing on detailed clinical cases and the interpretation of real assessments.
On the programme
- The gut ecosystem at the heart of management: exploring the microbiota, the mucus and FUT2 polymorphism, intestinal hyperpermeability (LBP, IgG, zonulin), prebiotics, probiotics and rebalancing strategies.
- Chronic low-grade inflammation: signalling pathways, turmeric and green tea, fatty acid balance, long-chain omega-3 EPA and DHA, GLA and DGLA, caution on palmitic acid and trans fatty acids.
- Oxidative stress: antioxidant enzymes and their cofactors, glutathione, alpha-lipoic acid, coenzyme Q10, and the logic of antioxidant recycling.
- Carbonyl stress and insulin resistance: glycated haemoglobin, glycation, advanced products, L-carnosine and micronutritional levers.
- Acid-base balance, hepatic detoxification, mitochondria and cellular senescence: sodium-potassium balance and PRAL, detoxification phases and homocysteine, mitochondrial support, senolytics.
- The cardiovascular FOCUS: atherosclerosis and LDL oxidation, erythrocyte fatty acid profile and omega-3 index, metabolic syndrome and metabolic endotoxaemia, lipoprotein(a), TMAO, homocysteine, support of the patient on statins, vitamins D, K2, A and E, glutathione, nattokinase and resveratrol.
- The dietary model and lifestyle: Cretan-inspired Mediterranean diet, choice of oils, intermittent fasting and a low-carb approach according to the profile, sleep, stress management, getting moving again and smoking cessation.
- Putting it into practice: several commented clinical cases, with reading of assessments, choice of biomarkers and construction of the protocol.
Who it is for
This training is for healthcare professionals who wish to integrate micronutrition and functional medicine into their practice: pharmacists, doctors, as well as practitioners supporting patients in health prevention. It suits beginners discovering these mechanisms as well as more experienced practitioners wishing to review and refine their protocols.
At the end of the training
You will be able to link your patient's clinical picture to the major pathophysiological mechanisms at play, choose the relevant biological assessments and interpret their results. You will be able to build a coherent strategy combining dietary recommendations, lifestyle and targeted supplementation, adapting it to each person's profile and budget. You will approach cardiovascular prevention globally, in addition to conventional medical follow-up, rather than through the cholesterol level alone.
Programme
Total video duration: 6 h 56 min
MCV
- Quiz de début de formation
- Leçon 11 h 46 min
- Leçon 21 h 39 min
- Leçon 31 h 45 min
- Leçon 41 h 46 min
- Quiz de fin de formation
Video Audio PDF handout
Frequently asked questions
How should the erythrocyte fatty acid profile be interpreted for cardiovascular prevention?
The fatty acid profile makes it possible to assess omega-3 status (ALA, EPA, DPA, DHA), omega-6 status (GLA, DGLA, AA), and saturated or trans fatty acid status. The omega-3 index is the most reliable marker of cardiovascular risk: it should be between 8 and 12% for prevention. Dr Anne Lucas, PharmD, stresses the need to read the numerical value rather than the graph, since the latter can be misleading. Elevated palmitic acid and low DGLA are two particularly important abnormalities to correct.
Which lab tests does Dr Anne Lucas, PharmD, recommend first to explore intestinal permeability?
Dr Anne Lucas, PharmD, primarily recommends testing LBP (LPS Binding Protein) and a few food IgGs (5 maximum). Zonulin can be added in the context of significant digestive disorders, gluten intolerance, or celiac disease, but its sensitivity remains limited. These panels are not reimbursed.
What is the optimal target for homocysteine in cardiovascular prevention, and why should it be systematically tested?
Dr Anne Lucas, PharmD, recommends a homocysteine level below 7-7.5 micromoles, since above that threshold this molecule is endothelium-toxic: it promotes oxidative stress, platelet aggregation, and arterial wall thickening. The test costs about 15 euros at functional biology laboratories and should be performed whenever there is a family or personal history of cardiovascular disease.
Why test for anti-oxidized-LDL antibodies rather than oxidized LDL directly?
Dr Anne Lucas, PharmD, recommends testing for anti-oxidized-LDL antibodies because they are more stable than oxidized LDL itself and constitute a genuine marker of autoimmunity. This test reflects the immune system's reaction to an LDL modified by oxidative stress and no longer recognized as 'self.' It should systematically be combined with a lipid panel (EAL) to obtain a complete functional view of cardiovascular risk.
How to assess and correct an intestinal mucus defect related to the FUT2 polymorphism?
A salivary or blood genetic test (59 euros, performed only once in a lifetime) makes it possible to determine whether the patient is a non-secretor. In the case of a polymorphism on the FUT2 gene, Dr Anne Lucas, PharmD, advises gradual supplementation with fucosyllactose up to 2 grams per day, starting at 500 mg to avoid digestive intolerance. This supplement can be given even to those who are lactose intolerant.
What supplement is essential for any patient on statins, and why?
Coenzyme Q10 is an absolute priority: statins inhibit HMG-CoA reductase and thereby block not only cholesterol synthesis but also that of coenzyme Q10. This deficiency explains the muscular adverse effects, which can go as far as rhabdomyolysis. Dr Anne Lucas, PharmD, recommends systematically combining coenzyme Q10 and omega-3 with any statin prescription, without questioning the allopathic treatment.
Which cofactors should be tested and corrected in cases of hyperhomocysteinemia?
A deficiency in vitamins B12, active B9 (methyltetrahydrofolate), B2 (MTHFR cofactor), and B6 (which is also involved in methylation) should be sought. The MTHFR polymorphism, present in more than 45% of the population, can explain an inability to convert folic acid into its methylated form; in that case, direct supplementation with methylated vitamin B9 is indicated.
What are the practical recommendations to correct a DGLA deficiency, and what is its impact on cardiovascular prevention?
DGLA is the precursor of series 1 eicosanoids, which are anti-inflammatory and anti-platelet-aggregating, making it a key marker in cardiovascular prevention. Correcting it relies exclusively on supplementation with borage oil or evening primrose oil, since there is no sufficient dietary equivalent. Dr Anne Lucas, PharmD, notes that while some practitioners advise separating the intake of omega-3s and omega-6s, she now gives both at the same time without observing any problem, although a competition for absorption is theoretically possible.
What is the practical difference between recommending rapeseed oil and giving EPA or DHA directly to an elderly patient?
Delta-6-desaturase, the key enzyme converting alpha-linolenic acid into EPA and DHA, functions poorly at the extreme ages of life and in cases of hyperinsulinism. In a patient over 60, rapeseed oil will therefore not be sufficient to optimize long-chain omega-3 status. EPA/DHA must then be provided directly through small oily fish (sardines, mackerel, anchovies) or a fish oil-based supplement.
What is the value of the DMI (intestinal metabolite panel) in cardiometabolic management?
The DMI makes it possible to detect digestive candidiasis via D-arabinitol, to assess the quality of the fermentative bacterial flora via the D/L-arabinitol ratio, and to identify putrefactive or fermentative dysbiosis. In a cardiometabolic patient, candidiasis not offset by a eubiotic flora often explains fatigue and poor athletic performance, and worsens intestinal hyperpermeability. Elevated citramalate and the presence of methanogenic bacteria confirm the correlation between candidiasis and dysbiosis.
How is metabolic syndrome diagnosed according to the IDF definition?
According to the International Diabetes Federation, the first mandatory criterion is an increased waist circumference (above 94 cm in Caucasian men, 90 cm in men of Asian origin, 80 cm in women). At least two criteria are then required from: treated hypertension or blood pressure above 130/85, triglycerides above 1.50 g/L, glucose above 1.0 g/L, and HDL below 0.40 g/L in men or 0.50 g/L in women. This syndrome markedly increases cardiovascular risk (roughly a doubling) and above all multiplies the risk of type 2 diabetes.
How does vitamin K2 MK7 protect the arteries from calcification?
Vitamin K2 MK7 activates the carboxylation of MGP (Matrix Gla Protein), the most powerful known inhibitor of tissue calcification. Without K2, MGP remains inactive in its decarboxylated form and calcium is deposited in the artery walls, increasing vascular stiffness. Dr Anne Lucas, PharmD, recommends the all-trans K2 MK7 form, between 75 and 180 micrograms per day, systematically combined with vitamin D.
What is TMAO, and why is it an independent cardiovascular risk factor?Full answer inside the training →
How to choose between berberine and rifaximin to treat bacterial dysbiosis with candidiasis?Full answer inside the training →
Why should vitamin D not be supplemented without adding vitamin K2 and vitamin A?Full answer inside the training →
What AA/EPA ratio should be targeted in a cardiovascular-risk patient, and how should it be assessed?Full answer inside the training →
What is the clinical value of the omega-3 index, and what target value should be aimed for?Full answer inside the training →
What protocol should be proposed for a patient with very high Lp(a) and a limited budget for functional lab work?Full answer inside the training →
Why does Dr Anne Lucas, PharmD, advise against combining turmeric with pepper, and what alternative does she propose?Full answer inside the training →
What is the optimal form of vitamin E to recommend, and why is alpha-tocopherol alone insufficient?Full answer inside the training →
Why test LBP (LPS-Binding Protein) in a cardiovascular patient even without overweight?Full answer inside the training →
How to manage significant stress that increases a patient's magnesium needs?Full answer inside the training →
What strategies should be proposed to support glutathione in cardiovascular prevention according to the patient's budget?Full answer inside the training →
How do AGEs (Advanced Glycation End Products) contribute to cardiovascular risk?Full answer inside the training →
What is the role of glutathione in cardiovascular prevention, and how can it be supported?Full answer inside the training →
How to optimize the acid-base balance in clinical practice, and what supplements should be proposed?Full answer inside the training →
What is the minimum lab panel to offer in practice for a patient in cardiovascular prevention?Full answer inside the training →
What lab investigations should be proposed for a presentation of PCOS, PMS, and chronic fatigue in a young woman?Full answer inside the training →
Why recommend L-carnosine in a cardiometabolic profile, and at what dosage?Full answer inside the training →
What warning signs and biological markers should be sought before prescribing a statin to a cardiovascular-risk patient?Full answer inside the training →
What is the nutritional strategy for reducing elevated TMAO?Full answer inside the training →
In which cases should the Mediterranean model be modified by adding a carbohydrate-restriction or fasting protocol?Full answer inside the training →
Which vegetable oils should be recommended for cooking, and why avoid sunflower oil?Full answer inside the training →
What is HIIT, and what is its role in mitochondrial function?Full answer inside the training →
In which cases should adrenal and thyroid support be combined through organotherapy?Full answer inside the training →
At what time of day should omega-3s be taken, and why?Full answer inside the training →
What is SASP, and why do senescent cells represent a cardiovascular risk?Full answer inside the training →
What is the optimal vitamin D status to aim for in a cardiovascular-risk context, and how should supplementation be organized?Full answer inside the training →
What is the link between chronic hyperinsulinism and pathological inflammation?Full answer inside the training →
Which statements about functional cardiovascular markers are true or false, according to the final quiz?Full answer inside the training →