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jeudi 28 février 2013

Even if you need statins don't forget this

Manage your residual risk... And don't believe that statins will reduce CV deaths, they mainly reduce CV events in trials where strict compliance is obtained about diet.

Pregnant women should think to wild fatty fish...


1. 
 2013 Jan;97(1):58-65. doi: 10.3945/ajcn.112.044198. Epub 2012 Nov 14.

Fetal growth, omega-3 (n-3) fatty acids, and progression of subclinical atherosclerosis: preventing fetal origins of disease? The Cardiovascular Risk in Young Finns Study.

Source

Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders, University of Sydney, Sydney, Australia. michael.skilton@sydney.edu.au

Abstract

BACKGROUND:

Impaired fetal growth is independently associated with an increased risk of cardiovascular events in adulthood. Prevention strategies that can be implemented during adulthood have not been identified.

OBJECTIVE:

The objective was to determine whether habitual omega-3 (n-3) fatty acid intake is associated with the rate of increase of carotid intima-media thickness during adulthood in individuals with impaired fetal growth.

DESIGN:

This was a population-based, prospective cohort study of 1573 adults in Finland. Carotid intima-media thickness was assessed in 2001 (at ages 24-39 y) and in 2007. Participants were categorized as having had impaired fetal growth (term birth with birth weight )

RESULTS:

In multivariable models, the 6-y progression of carotid intima-media thickness was inversely associated with dietary omega-3 fatty acids in those with impaired fetal growth (P = 0.04). Similarly, serum omega-3 fatty acid concentrations were inversely associated with the 6-y progression of carotid intima-media thickness in those with impaired fetal growth (P = 0.04) but were not noted in those with normal fetal growth (P = 0.94 and P = 0.26, respectively).

CONCLUSION:

Dietary intake of omega-3 fatty acids is associated with a slower rate of increase in carotid intima-media thickness in those with impaired fetal growth.
2.

 2013;8(1):e53972. doi: 10.1371/journal.pone.0053972. Epub 2013 Jan 16.

Increased Carotid Intima-Media Thickness and Reduced Distensibility in Human Class III Obesity: Independent and Differential Influences of Adiposity and Blood Pressure on the Vasculature.

Source

Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.

Abstract

Carotid intima-media-thickness (cIMT) and carotid distensibility (distensibility), structural and functional properties of carotid arteries respectively, are early markers, as well as strong predictors of cardiovascular disease (CVD). The characteristic of these two parameters in individuals with BMI>40.0 kg/m(2) (Class III obesity), however, are largely unknown. The present study was designed to document cIMT and distensibility in this population and to relate these to other factors with established association with CVD in obesity. The study included 96 subjects (65 with BMI>40.0 kg/m(2) and 31, age- and gender-matched, with BMI of 18.5 to 30.0 kg/m(2)). cIMT and distensibility were measured by non-invasive high resolution ultrasonography, circulatory CD133(+)/KDR(+) angiogenic cells and endothelial microparticles (EMP) by flow cytometry, and plasma levels of adipokines, growth factors and cytokines by Luminex immunoassay kits. The study results demonstrated increased cIMT (0.62±0.11 mm vs. 0.54±0.08 mm, P = 0.0002) and reduced distensibility (22.52±10.79 10(-3)kpa(-1)vs. 29.91±12.37 10(-3)kpa(-1), P<0 .05="" bmi="" in="" individuals="" with="">40.0 kg/m(2). Both cIMT and distensibility were significantly associated with traditional CVD risk factors, adiposity/adipokines and inflammatory markers but had no association with circulating angiogenic cells. We also demonstrated, for the first time, elevated plasma EMP levels in individuals with BMI>40.0 kg/m(2). In conclusion, cIMT is increased and distensibility reduced in Class III obesity with the changes predominantly related to conventional CVD risk factors present in this condition, demonstrating that both cIMT and distensibility remain as CVD markers in Class III obesity.

mercredi 27 février 2013

Low concentrations of added sugars in industrial foods

Sugars are named so differently that people don't care of that. so they eat a continuous low concentration of sugars from entrée through dessert.
Processed meats, even smoked fish or Roll Mops, soups etc do contain added sugars like sucrose, saccharose, HFCS, dextrose, inverted glucose, glucose, starch, lactose, agave syrup, maple syrup, maltose...
These added sugars are counterbalanced in salted dishes by a supplementary sodium chloride.
Even if it is argued by food giants that it is a very tiny glycemic load for the consumer, the consequences on taste and brain addiction to sugars are far from neutral.
So instead of checking all the stickers on your packed food products buy raw whole food...

mardi 26 février 2013

Le bio sucré comme la plupart des produits industriels

Sirop de glucose, lactose et sucre bien sur de canne!
Vous en voulez des sucres pour manger encore plus de saucisse?
Et bien vous l'avez et on vous le dit!
Pendant ce temps l'état s'occupe des étiquettes de la viande française, oui c'est du porc français d'après l'étiquette, so what!
En revanche non ce n'est pas une recette artisanale.



The paradox of PAHs


The primary soup and the major role of PAHs

Life needs organic molecules. Those organic molecules were initially synthesized endogenously and delivered exogenously.













The PAHs production in human societies and their risks

Both combustion of fossil and biomass fuels and cooking produce PAHs.
They are carcinogenic for animals and human.
But it seems that they are also linked to epigenetic changes which lead to asthma and allergy. So you can cook but try to produce the least of PAHs... As our ancestors probably did because of the scarce avalilability of energy.


lundi 25 février 2013

A quoi servent les questionnaires de l'industrie agro-alimentaire?


Ces questionnaires servent à orienter les neurobiologistes et les publicitaires de leur centre de recherche vers une formulation produit qui vous incitera à manger encore plus...




I'm on a consumer panel for Kraft Foods and today they asked for my opinion on what flavors, textures and other such aspects of Oreo cookies would be appropriate for the various seasons of the year. Here was my simple response: "Oreos should be abolished. These are nothing more than wheat and sugar bombs that perpetuate obesity and metabolic disease." Somehow I don't think that was the answer they were looking for. Can you imagine how the food scientists at Kraft will use the rest of the responses to concoct some scientific lab experiment to make people want to eat more and more and more Oreos? Back in the days before low-carb, I could down a whole package very easily with my 2% low-fat homogenized and pasteurized milk. Ugh, I was such a dope!
Unlike ·  ·  · 54 minutes ago · 
  • You and 21 others like this.
  • J M Leann, you're exactly right. That's why consumer education is so vital. If people learn the truth and still eat this carbage, then that's on them. Richard, true story!
    Like · Reply · 24 minutes ago via mobile
  • W Wow, surprised Kraft lets you on that panel! There is no wheat or sugar that they don't love!!!!!




Caloric restriction: the facts

http://www.nature.com/nature/journal/v489/n7415/pdf/nature11432.pdf

dimanche 24 février 2013

Surprise! A high fat ketogenic diet is not deleterious for lipid levels




Can Children With Hyperlipidemia Receive Ketogenic Diet for Medication-Resistant Epilepsy?

  1. Yeou-Mei Christiana Liu, MSc1
  2. Helen Lowe, MSc1
  3. Maria M. Zak, MN1
  4. Jeff Kobayashi, MD1
  5. Valerie W. Chan, BScN1
  6. Elizabeth J. Donner, MD1
  1. 1Department of Pediatrics, Division of Neurology, The Hospital for Sick Children, Toronto, Ontario, Canada
  1. Yeou-Mei Christiana Liu, MSc, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, M5G 1X8, Canada. Email: christiana.liu@sickkids.ca

Abstract

The very-high-fat ketogenic diet can worsen lipid levels in children with pre-existing hyperlipidemia by increasing serum lipoproteins and reducing antiatherogenic high-density lipoproteins. A retrospective chart review of 160 children treated with the ketogenic diet from September 2000 to May 2011 was performed. Twelve children with pre-existing hyperlipidemia were identified. Lipid levels including total cholesterol, low-density lipoprotein, triglycerides, high-density lipoprotein, and total cholesterol/high-density lipoprotein were measured pre-diet and at 3, 6, and 12 months of treatment. During treatment, there was a significant reduction in mean total cholesterol, low-density lipoprotein, and total cholesterol/high-density lipoprotein. Total cholesterol and low-density lipoprotein were normalized in 8 and 7 children at 6 months; and 9 and 9 children at 12 months respectively. At 6 and 12 months, tot cholesterol/HDL ratio was normalized in 5 and 7 children respectively. Diet modifications were made to achieve healthy lipid levels. By extrapolating the data, it suggests lipid levels can be controlled in children and adults with ketogenic diet treatment.


And a low GL diet with high fat content improves the lipid profile of D2 patients:








http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3510974/

And even Hu acknowledges it:


 2012 Oct 1;176 Suppl 7:S44-54. doi: 10.1093/aje/kws264.

Effects of low-carbohydrate diets versus low-fat diets on metabolic risk factors: a meta-analysis of randomized controlled clinical trials.

Source

Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, Louisiana 70112, USA.

Abstract

The effects of low-carbohydrate diets (≤45% of energy from carbohydrates) versus low-fat diets (≤30% of energy from fat) on metabolic risk factors were compared in a meta-analysis of randomized controlled trials. Twenty-three trials from multiple countries with a total of 2,788 participants met the predetermined eligibility criteria (from January 1, 1966 to June 20, 2011) and were included in the analyses. Data abstraction was conducted in duplicate by independent investigators. Both low-carbohydrate and low-fat diets lowered weight and improved metabolic risk factors. Compared with participants on low-fat diets, persons on low-carbohydrate diets experienced a slightly but statistically significantly lower reduction in total cholesterol(2.7 mg/dL; 95% confidence interval: 0.8, 4.6), and low density lipoprotein cholesterol (3.7 mg/dL; 95% confidence interval: 1.0, 6.4), but a greater increase in high density lipoprotein cholesterol (3.3 mg/dL; 95% confidence interval: 1.9, 4.7) and a greater decrease in triglycerides (-14.0 mg/dL; 95% confidence interval: -19.4, -8.7). Reductions in body weight, waist circumference and other metabolic risk factors were not significantly different between the 2 diets. These findings suggest that low-carbohydrate diets are at least as effective as low-fat diets at reducing weight and improving metabolic risk factors. Low-carbohydrate diets could be recommended to obese persons with abnormal metabolic risk factors for the purpose of weight loss. Studies demonstrating long-term effects of low-carbohydrate diets on cardiovascular events were warranted.