mardi 30 septembre 2014

Lipoproteins and prediction of CVD, CHD and stroke

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ApoB reduction and risk of CVD, CHD and stroke

Current Opinion in Endocrinology, Diabetes & Obesity:
doi: 10.1097/MED.0b013e32835ed9cb
LIPIDS: Edited by Annabelle Rodriguez

Update on the detection and treatment of atherogenic low-density lipoproteins

Sniderman, Allana; Kwiterovich, Peter O.b

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Purpose of review: To explain why epidemiological studies have reached such diverse views as to whether apolipoprotein B (apoB) and/or low-density lipoprotein particle number (LDL-P) are more accurate markers of the risk of cardiovascular disease than LDL-C or non-high-density lipoprotein cholesterol (HDL-C) and to review the treatment options to lower LDL.
Recent findings: The Emerging Risk Factor Collaboration, a large prospective participant level analysis, a meta-analysis of statin clinical trials, and the Heart Protection Study have each reported that apoB does not add significantly to the cholesterol markers as indices of cardiovascular risk. By contrast, a meta-analysis of published prospective studies demonstrated that non-HDL-C was superior to LDL-C, and apoB was superior to non-HDL-C. As well, three studies using discordance analysis each demonstrated that apoB and LDL-P were superior to the cholesterol markers. Two approaches to resolve these differences are brought to bear in this article: first, which results are credible and second, how does taking the known differences in LDL composition into account, help resolve them. The best identification of individuals at risk of coronary artery disease or with coronary artery disease allows the most efficacious treatment of elevated LDL-P and will permit a more extensive use of some of the more novel LDL-lowering agents.
Summary: Much of the controversy vanishes once the physiologically driven differences in the composition of the apoB lipoprotein particles are taken into account, illustrating that epidemiology, not directed by physiology, is like shooting without aiming.

Saturated fats and lipid profile

And the combined effect of med diet and weight loss

Current Opinion in Lipidology:
doi: 10.1097/MOL.0b013e3283613ba2
LIPID METABOLISM: Edited by Ernst J. Schaefer

Dietary fatty acids and lipoprotein metabolism: new insights and updates

Ooi, Esther M.M.a; Ng, Theodore W.K.a; Watts, Gerald F.a; Barrett, P. Hugh R.a,b

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Purpose of review: Dyslipidemia is a powerful risk factor for cardiovascular disease (CVD). Dietary fatty acid composition regulates lipids and lipoprotein metabolism and may confer CVD benefit. This review updates understanding of the effect of dietary fatty acids on lipoprotein metabolism in humans.
Recent findings: High dietary fish-derived n-3 polyunsaturated fatty acid (PUFA) consumption diminished hepatic triglyceride-rich lipoprotein (TRL) secretion and enhanced TRL to LDL conversion. n-3 PUFA also decreased TRL-apoB-48 concentration by decreasing TRL-apoB-48 secretion. High n-6 PUFA intake decreased liver fat, and plasma proprotein convertase subtilisin/kexin type 9, triglycerides, total-cholesterol and LDL-cholesterol concentrations. Intake of saturated fatty acids with increased palmitic acid at the sn-2 position was associated with decreased postprandial lipemia, which might be due to decreased triglyceride absorption. Replacing carbohydrate with monounsaturated fatty acids increased TRL catabolism. Ruminant trans-fatty acid decreased HDL cholesterol, but the mechanisms are unknown. A new role for APOE genotype in regulating lipid responses was also described.
Summary: The major advances in understanding the effect of dietary fatty acids on lipoprotein metabolism have focused on n-3 PUFA. This knowledge provides insights into the importance of regulating lipoprotein metabolism as a mode to improve plasma lipids and potential CVD risk. Further studies are required to better understand the cardiometabolic effects of other dietary fatty acids.

Fermented raw milk improves your lipid profile

Lipid profile and lifestyle in healthy men

The shift toward an atherogenic profile is correlated with increased BMI and moderately with age. But one must keep in mind that lipid profile is neither the only risk factor of CVD and nor the most predictive...

Quel est votre avis sur les sodas à volonté?

samedi 27 septembre 2014

More mothers than fathers in humanity

Great review on ancestral diets

Hypertension is not a consequence of Aging

K+ and Paleodiet

Saturated fats and cardiovascular diseases, replacement by omega 6 PUFA

Look at the reference number eight!

To bath not to bath?

jeudi 25 septembre 2014

FODMAP or gluten?

Neurobiological approach of obesity

Sugar consumption and oral inflammmation

Added sugars and periodontal disease in young adults: an analysis of NHANES III data1,2,3

  1. Antônio AM Silva
-Author Affiliations
  1. 1From the Departments of Public Health (ECOL and AAMS) and Dentistry (CCCR and CMCA), Federal University of Maranhão, São Luís, Brazil, and the Department of Preventive and Social Dentistry, Federal University of Rio Grande do Sul, Porto Alegre, Brazil (FNH).
-Author Notes
  • 2 Supported by the Fundação de Amparo à Pesquisa e ao Desenvolvimento Científico e Tecnológico do Maranhão (grant PAEDT 01342/12).
  • 3 Address reprint requests and correspondence to CCC Ribeiro, Universidade Federal do Maranhão, Centro de Ciências da Saúde, Departamento de Odontologia II, Campus do Bacanga, São Luís, MA 65085-580, Brazil. E-mail:


Background: Added sugar consumption seems to trigger a hyperinflammatory state and may result in visceral adiposity, dyslipidemia, and insulin resistance. These conditions are risk factors for periodontal disease. However, the role of sugar intake in the cause of periodontal disease has not been adequately studied.
Objective: We evaluated the association between the frequency of added sugar consumption and periodontal disease in young adults by using NHANES III data.
Design: Data from 2437 young adults (aged 18–25 y) who participated in NHANES III (1988–1994) were analyzed. We estimated the frequency of added sugar consumption by using food-frequency questionnaire responses. We considered periodontal disease to be present in teeth with bleeding on probing and a probing depth ≥3 mm at one or more sites. We evaluated this outcome as a discrete variable in Poisson regression models and as a categorical variable in multinomial logistic regression models adjusted for sex, age, race-ethnicity, education, poverty-income ratio, tobacco exposure, previous diagnosis of diabetes, and body mass index.
Results: A high consumption of added sugars was associated with a greater prevalence of periodontal disease in middle [prevalence ratio (PR): 1.39; 95% CI: 1.02, 1.89] and upper (PR: 1.42; 95% CI: 1.08, 1.85) tertiles of consumption in the adjusted Poisson regression model. The upper tertile of added sugar intake was associated with periodontal disease in ≥2 teeth (PR: 1.73; 95% CI: 1.19, 2.52) but not with periodontal disease in only one tooth (PR: 0.85; 95% CI: 0.54, 1.34) in the adjusted multinomial logistic regression model.
Conclusion: A high frequency of consumption of added sugars is associated with periodontal disease, independent of traditional risk factors, suggesting that this consumption pattern may contribute to the systemic inflammation observed in periodontal disease and associated noncommunicable diseases.

Caffeine consumption by teen agers

One word: stable.

mercredi 24 septembre 2014

Statins impairs glucose uptake by cells

Junk food


The most frequent causes of cancer which are not clearly recognised by people

Unsustainable costs of type two diabetes for healthcare systems

This study presents the arguments for preventative medicine in type two diabetes. However we know that prevention do have extreme difficulties to lower the cost of chronic illnesses. So we need a very extraordinary innovative approach of preventative medicine for chronic illnesses like type two diabetes.

Don't waste your money in sentiments to prevent chronic illnesses


lundi 22 septembre 2014

Curcumin and mesothelioma

Low PIAS3 Expression in Malignant Mesothelioma Is Associated with Increased STAT3 Activation and Poor Patient Survival

  1. Afshin Dowlati1,*
+Author Affiliations
  1. 1Division of Hematology and Oncology, Case Comprehensive Cancer Center and University Hospitals Case Medical Center, Cleveland, Ohio.
  2. 2Division of Pathology, Case Comprehensive Cancer Center and University Hospitals Case Medical Center, Cleveland, Ohio.
  3. 3Division of Biostatistics, Case Comprehensive Cancer Center and University Hospitals Case Medical Center, Cleveland, Ohio.
  4. 4Institute for Biomedical Research, Georg-Speyer-Haus, Frankfurt, Germany.
  1. *Corresponding Author:
    Afshin Dowlati, Department of Medicine, Division of Hematology and Oncology, University Hospitals Case Medical Center, 11100 Euclid Avenue, Mail Stop LKS 5079, Cleveland, OH 44106. Phone: 216-286-6741; Fax: 216-844-5234;


Purpose: Deregulation of STAT3 activation is a hallmark of many cancer cells, and the underlying mechanisms are subject to intense investigation. We examined the extent of PIAS3 expression in mesothelioma cells and human tumor samples and determined the functional effects of PIAS3 expression on STAT3 signaling.
Experimental design: We evaluated the expression of PIAS3 in mesothelioma tumors from patients and correlated the expression levels with the course of the disease. We also measured the effects of enhanced PIAS3 activity on STAT3 signaling, cellular growth, and viability in cultured mesothelioma cells.
Results: Gene expression databases revealed that mesotheliomas have the lowest levels of PIAS3 transcripts among solid tumors. PIAS3 expression in human mesothelioma tumors is significantly correlated with overall survival intervals (P = 0.058). The high expression of PIAS3 is predictive of a favorable prognosis and decreases the probability of death within one year after diagnosis by 44%. PIAS3 expression is functionally linked to STAT3 activation in mesothelioma cell lines. STAT3 downregulation with siRNA or enhanced expression of PIAS3 both inhibited mesothelioma cell growth and induced apoptosis. Mesothelioma cells are sensitive to curcumin and respond by the induction of PIAS3. Corroborative evidence has been obtained from STAT3 inhibition experiments. Exposure of the cells to a peptide derived from the PIAS3 protein that interferes with STAT3 function resulted in apoptosis induction and the inhibition of cell growth.
Conclusion: These results suggest that PIAS3 protein expression impacts survival in patients with mesothelioma and that PIAS3 activation could become a therapeutic strategy. Clin Cancer Res; 20(19); 1–9. ©2014 AACR.

Curcumin: A Double Hit on Malignant Mesothelioma

  1. Arti Shukla
+Author Affiliations
  1. Authors' Affiliation: Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont
  1. Corresponding Author:
    Arti Shukla, Department of Pathology, University of Vermont College of Medicine, 89 Beaumont Avenue, HSRF 216, Burlington, VT 05405-0068. Phone: 802-656-8253; Fax: 802-656-8892; E-mail:


Inflammation is a key mediator in the development of malignant mesothelioma, which has a dismal prognosis and poor therapeutic strategies. Curcumin, a naturally occurring polyphenol in turmeric, has been shown to possess anticarcinogenic properties through its anti-inflammatory effects. Inflammasomes, a component of inflammation, control the activation of caspase-1 leading to pyroptosis and processing of proinflammatory cytokines, interleukin (IL)-1β and IL-18. In the present study, we investigate the role of curcumin in pyroptotic cell death of malignant mesothelioma cells. Using in vitro models with mouse and human malignant mesothelioma cells, curcumin is shown to induce pyroptosis through activation of caspase-1 and increased release of high-mobility group box 1 (HMGB1) without processing of IL-1β and IL-18. Absence of IL-1β processing in response to curcumin-mediated caspase-1 activation is attributed to blockade of pro-IL-1β priming through inhibition of the NF-κB pathway. Furthermore, curcumin's cytotoxicity in malignant mesothelioma cells is demonstrated to be dependent on pyroptosis as inhibition of caspase-1 resulted in protection against curcumin-induced cell death. We also demonstrate that curcumin-mediated caspase-1 activation is oxidant dependent by using N-acetyl-L-cysteine (NAC) to inhibit pyroptosis. PCR array analysis using the human inflammasome template revealed that curcumin significantly downregulated levels of inflammasome-related gene expression involved in inflammation, e.g., NF-κB, toll-like receptors (TLR), and IL-1β. Our data indicate that curcumin has a double effect on malignant mesothelioma cells through induction of pyroptosis while subsequently protecting against inflammation. Cancer Prev Res; 7(3); 330–40. ©2014 AACR.

Home made carcinogens

This is the type of cooking to avoid

Fracture risk, osteoporosis and chronic low-grade inflammation

You definitely need an anti-inflammatory diet, and among the different diets appears that Palio diet is one of the most potent anti-inflammatory diet.

samedi 20 septembre 2014

Taxe sur les boissons énergisantes: l'état est mal conseillé et gaspille

Agriculture and food industry: they don't need subsidies

The future of agriculture: Shift to solar produced food

Epigenetics across generations

Wine and your Health

And a recent interview about the last European society of cardiology in Barcelona 

The last paper is in french

Paleo how to do it

vendredi 19 septembre 2014

Sugar is killing your cells or worse sugar is accelerating cancer

Low carb calories in/out


Coke: the bottle and the liquid

Statins seem to kill the benefit of exercise

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Figure 1. 
Cardiorespiratory Fitness
(A) Peak oxygen consumption (Vo2peak) before (Pre) and after (Post) 12 weeks of supervised aerobic exercise training (Ex) or combination exercise-plus-statin therapy (St+Ex). (B) Vo2peak presented as within-group change (Δ) from baseline. Data are expressed as mean ± SE. p < 0.005 for within-group change from baseline. §p < 0.005 for between-group difference in change from baseline.

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Figure 2. 
Citrate Synthase Activity, a Marker of Skeletal Muscle Mitochondrial Content
(A) Citrate synthase activity before and after 12 weeks of supervised aerobic exercise training or combination exercise-plus-statin therapy. (B) Citrate synthase activity presented as within-group change from baseline. Data are expressed as mean ± SE. p < 0.05 for within-group change from baseline. §p < 0.05 for between-group difference in change from baseline. Abbreviations as in Figure 1.

lundi 15 septembre 2014

Des décennies de conseils alimentaires qui s'effondrent

Butter: It has long been thought that consuming too much saturated fat, such as that found in butter, increases the risk of heart disease but a recent study found no significant link. 

Cheese: Once seen as a risk for heart disease, some experts now consider it is rich in fats that may be good for the body. One study found eating cheese might reduce the risk of diabetes. 

Low-fat yoghurts: The public health campaign against fat led to a huge range of lower fat products but many contained added sugar and are often not the healthiest option. 

Red wine: It contains the chemical resveratrol which has been considered to have long-term health benefits. However, a report published earlier this year found no evidence that it stops heart disease or prolongs life. 

Coffee: Once considered detrimental to heart health, it is now thought to have health benefits, including protection against type 2 diabetes and liver disease. 

Chocolate: Dark chocolate is believed to improve cardiovascular health by acting like a natural anti-inflammatory to reduce blood pressure.

 French version (largely modified)

Beurre: vous pouvez manger du beurre car les graisses saturées en quantité raisonnable n'augmentent pas le risque de maladie cardiovasculaire (MCV)
En particulier les fromages d'alpage contiennent des graisses qui peuvent diminuer le risque de MCV
Les yaourts et autres produits allégés: 
outre le fait que les graisses saturées (qui ont été enlevées) des produits laitiers peuvent améliorer le profil de risque, l'addition systématique de sucre favorise la prise de poids et le diabète type 2
Vin rouge: consommé isolément il n'améliore pas le profil de risque biologique, ce n'est que combiné à l'exercice physique qu'une telle amélioration se produit
Café: loin d'être défavorable à la santé la consommation de café peut abaisser le risque de syndrome métabolique, de diabète type 2 et de surcharge graisseuse du foie
Chocolat: le chocolat noir diminue la pression artérielle, est antioxydant et améliore l'artérite des membres inférieurs. Lui attribuer une pastille couleur défavorable parait inapproprié.

Vegan ?

Protein in your breakfast!

Increased glycolysis: carcinogenic per se?

vendredi 12 septembre 2014

Brain and PUFA

i apps in medicine and food advice

Is carbohydrate in the mouth sufficient to enhance motor performance?

The answer is yes! When you put CH in your mouth a direct circuitry enhances motor activity via your brain.

Added sugar should be limited

You told me sugar?

"Today the average person consumes 17 times more added sugar than we used to in the early 19th century. My kids' friends think that limiting soda intake means only being allowed one can per day. When is enough going to be enough? And when will we realise it’s already too much?"

Stupidity of correlations