jeudi 29 janvier 2015
mercredi 28 janvier 2015
mardi 27 janvier 2015
Is fat good for your health?
Lhttp://www.cbc.ca/thecurrent/episode/2015/01/26/fat-doesnt-make-you-fat-nina-teisholz-has-a-big-fat-surprise/
I am not a fan of cooked fats, nor of grain fed fatty animals. But mainly she is right. Whole foods with high fat content are good, either from animal or vegetal origin and the war against fats is counter productive. Unrefined fats are either necessary like W3PUFA in fishes or ALA in veggies, or LA from meats and whole grains, or non necessary like unfiltered olive oil, tropical oils and sat fat from meats but with a major advantage which is to induce a low insulin state.
I am not a fan of cooked fats, nor of grain fed fatty animals. But mainly she is right. Whole foods with high fat content are good, either from animal or vegetal origin and the war against fats is counter productive. Unrefined fats are either necessary like W3PUFA in fishes or ALA in veggies, or LA from meats and whole grains, or non necessary like unfiltered olive oil, tropical oils and sat fat from meats but with a major advantage which is to induce a low insulin state.
lundi 26 janvier 2015
samedi 24 janvier 2015
mercredi 21 janvier 2015
Leptin vs Insulin
Garron T. Dodd, Stephanie Decherf, Kim Loh, Stephanie E. Simonds, Florian Wiede, Eglantine Balland, Troy L. Merry, Heike Münzberg, Zhong-Yin Zhang, Barbara B. Kahn, Benjamin G. Neel, Kendra K. Bence, Zane B. Andrews, Michael A. Cowley, Tony Tiganis. Leptin and Insulin Act on POMC Neurons to Promote the Browning of White Fat. Cell, 2015; 160 (1-2): 88
mardi 20 janvier 2015
Huile de Palme - Palm Oil
1. Is consuming palm oil good or bad for us?
There is no such thing as good and bad in term of diet... Safety of food and food products has never been so high in developed countries. You probably want to mean is consuming palm oil threatening our health? The answer is No. But when I took this line of reasoning even further your next and linked question could be: is fat threatening our health? And the answer is another time No. No food alone could threaten our health. Conversely smoking, obesity, sitting, junk food products could ruin our health very fast.2. What do you say to those who want to ban palm oil as a food ingredient?
On a human health perspective they have no point. Saturated fats are not the culprit for CVD. And even if you back this assertion meats, cheese and dairy are the main sources of sat fats not palm oil.
- About the saturated fats debate.
Why do you think saturated fats and, in particular palm oil, have a reputation that they are bad for you? And, indeed, why do so many scientists advise us to limit our intake of saturated fats? Also, what does cause CVD?
Sat fats controversy
My first comment is to avoid to comment other opinions. I would focus on facts and it is rather to the sat fat enemies to justify their position.
Some facts.
Why the recent meta analysis on sat fats did not find any increasing risk of CVD in people who consumed more sat fats than others?
Read Siri Tarino paper about it.
Why France where the sat fat consumption is the highest in the EU does have since a long time the lowest rate of CVD? No it couldn't be explained by wine.
Palm oil controversy
For Palm oil the main reason of the bad reputation is the green bashing. It is perhaps based on facts but it is not in my field of expertise.
Limiting our sat fats intake
Let me be clear about experimental models.
All very rich diets in fat lead to disease in mice. But it is the same for very rich diets in sugar or protein...
Some animals are more prone to develop atheroma and atheroma is a very complex disease. So clinical data are the only data we can rely on. Experimental data are only tracks to further developments.
Clinical data
Sat fats consumption is not associated with increased risk of CVD. Sat fats modify the blood lipid profile. But these changes are more neutral than previously thought.
Total cholesterol is increased but by equally increasing HDL and non HDL cholesterol. LDL particles are not smaller or denser. So this claimed assertion about the deterioration of blood lipid profile is an old story which is not backed by a more detailed evaluation of risk.
3. What is your advice on eating palm oil?
We need fats. We need unadulterated fats (http://www.foodnavigator-usa.com/Suppliers2/Foods-with-artificial-trans-fats-should-be-considered-adulterated). I mean lard, fat of meats, butter, cheeses, unfiltered olive oil, tropical oils like coconut and palm for cooking. So if I choose to eat palm oil I would choose red palm oil and I would not overheat it. Refined palm oil is acceptable but partially hydrogenated palm oil is adulterated.
Availability of red Palm oil
Is red palm oil readily available and how would you use it? What effect does overheating it have? Why is partially hydrogenated palm oil not advisable and in what food products would we find it?
The question is about availability of fats and I would like to emphasize that in order to consume Palm oil voluntarily you need to make choices as for every raw or crude fat.
Let me clear about buying food: if you buy products you will not find red Palm oil nor coconut oil nor butter nor olive oil. You will buy a mix of real foods rearranged and highly transformed to make a packaged product. If you look at the label you can know what it contains but nothing can be discarded.
If you buy real foods in order to prepare your meal you will find the fats mentioned above.
But obviously in our countries you will more easily find
1/ olive oil
2/ butter
And it will be more difficult to find tropical oils than seed oils like sunflower, rapeseed or peanut or a mix of them. Only because the trees which produce these fruits grow on hotter climates!
But in all of these fats the trend for years is to sell refined oils.
You will easily find filtered olive oil and for Palm fully refined one that means without carotenes, vitamins and polyphenols.
Unfiltered olive oil or red Palm oil are rarer. But their micronutrient content is higher which is of paramount importance to preserve our resistance to oxidative stress, inflammation, aging and cancer. And I have to add that the present process of making food products tend to be more successful with highly refined crude foods like glucose or fructose syrups refined cereal flours refined Palm oil or sunflower oil, milk protein powder and so on...
The agrofood industry is able to change its processes in order to keep more micronutrients in foods but it will take research and development and a demand from the public. It is probable that final cost, preservation and storage will be impacted.
Other points
1/ I will use Palm oil to spread or to cook.
2/ overheating PO could lead to some trans fat production as grossly 30% of PO fatty acids are unsaturated. Overheating red palm oil will destroy carotenes thermolabile vitamins and poly phenols.
3/ partially hydrogenated PO is an industrialized product which does contain trans fat mainly from the transformation of oleic acid in elaidic acid. Industrialized trans fats are atherogenic according to compelling evidences.
4/ read the labels in countries where labelling trans fats is mandatory without threshold! If not you cannot know.
- about the irrelevance of experimental studies of high fat diets in mice
- about trans fats of industrial origin
dimanche 18 janvier 2015
samedi 17 janvier 2015
vendredi 16 janvier 2015
jeudi 15 janvier 2015
dimanche 11 janvier 2015
Vitamins K: the Rotterdam study
Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study
TABLE 2
Association of coronary events and all-cause mortality with intake of phylloquinone in 4807 Dutch men and women aged 55 y and over1
Energy-adjusted phylloquinone intake (μg/d) P for trend <200 th=""> 200–278 >278 n 1588 1608 1611 Median intake, μg/d 154.6 236.5 336.9 Nonfatal MI Person-years 11323 11556 11766 Events, n 48 56 40 RR, model 12 1 1.19 (0.81, 1.75) 0.86 (0.56, 1.30) 0.44 RR, model 23 1 1.14 (0.77, 1.70) 0.84 (0.54, 1.31) 0.42 Incident CHD4 Person-years 11323 11556 11766 Events, n 82 81 70 RR, model 1 1 1.01 (0.74, 1.38) 0.89 (0.64, 1.22) 0.45 RR, model 2 1 1.00 (0.73, 1.37) 0.89 (0.63, 1.25) 0.48 CHD mortality5 Person-years 11502 11764 11880 Events, n 36 30 33 RR, model 1 1 0.86 (0.53, 1.40) 0.98 (0.67, 1.57) 0.94 RR, model 2 1 0.90 (0.55, 1.48) 1.02 (0.61, 1.69) 0.93 All-cause mortality Person-years 11502 11764 11880 Events, n 246 240 215 RR, model 1 1 0.98 (0.82, 1.17) 0.91 (0.75, 1.09) 0.28 RR, model 2 1 1.02 (0.85, 1.23) 0.94 (0.77, 1.14) 0.53
-
1 RR obtained by Cox proportional hazard analysis, with 95% CI in parentheses and P for linear trend across the tertiles.
-
2 Model includes age, gender, and total energy intake.
-
3 Model includes age, gender, total energy intake, BMI, smoking status, pack-years of cigarette smoking, diabetes, education (3 categories), and intake of alcohol, SFA, PUFA, flavonols (quercetin, myricetin, and kaempferol), and calcium.
-
4 CHD comprises fatal and nonfatal MI, sudden cardiac death, and other forms of acute and chronic ischemic heart disease (ICD-10 codes I20–I25 and I46).
-
5 CHD events followed by death within 28 d after the onset of symptoms.
TABLE 2
Association of coronary events and all-cause mortality with intake of phylloquinone in 4807 Dutch men and women aged 55 y and over1
| Energy-adjusted phylloquinone intake (μg/d) | P for trend | |||
|---|---|---|---|---|
| <200 th=""> | 200–278 | >278 | ||
| n | 1588 | 1608 | 1611 | |
| Median intake, μg/d | 154.6 | 236.5 | 336.9 | |
| Nonfatal MI | ||||
| Person-years | 11323 | 11556 | 11766 | |
| Events, n | 48 | 56 | 40 | |
| RR, model 12 | 1 | 1.19 (0.81, 1.75) | 0.86 (0.56, 1.30) | 0.44 |
| RR, model 23 | 1 | 1.14 (0.77, 1.70) | 0.84 (0.54, 1.31) | 0.42 |
| Incident CHD4 | ||||
| Person-years | 11323 | 11556 | 11766 | |
| Events, n | 82 | 81 | 70 | |
| RR, model 1 | 1 | 1.01 (0.74, 1.38) | 0.89 (0.64, 1.22) | 0.45 |
| RR, model 2 | 1 | 1.00 (0.73, 1.37) | 0.89 (0.63, 1.25) | 0.48 |
| CHD mortality5 | ||||
| Person-years | 11502 | 11764 | 11880 | |
| Events, n | 36 | 30 | 33 | |
| RR, model 1 | 1 | 0.86 (0.53, 1.40) | 0.98 (0.67, 1.57) | 0.94 |
| RR, model 2 | 1 | 0.90 (0.55, 1.48) | 1.02 (0.61, 1.69) | 0.93 |
| All-cause mortality | ||||
| Person-years | 11502 | 11764 | 11880 | |
| Events, n | 246 | 240 | 215 | |
| RR, model 1 | 1 | 0.98 (0.82, 1.17) | 0.91 (0.75, 1.09) | 0.28 |
| RR, model 2 | 1 | 1.02 (0.85, 1.23) | 0.94 (0.77, 1.14) | 0.53 |
- 1 RR obtained by Cox proportional hazard analysis, with 95% CI in parentheses and P for linear trend across the tertiles.
- 2 Model includes age, gender, and total energy intake.
- 3 Model includes age, gender, total energy intake, BMI, smoking status, pack-years of cigarette smoking, diabetes, education (3 categories), and intake of alcohol, SFA, PUFA, flavonols (quercetin, myricetin, and kaempferol), and calcium.
- 4 CHD comprises fatal and nonfatal MI, sudden cardiac death, and other forms of acute and chronic ischemic heart disease (ICD-10 codes I20–I25 and I46).
- 5 CHD events followed by death within 28 d after the onset of symptoms.
Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study
TABLE 3
Association of coronary events and all-cause mortality with intake of menaquinone in 4807 Dutch men and women aged 55 y and over1
Energy-adjusted menaquinone intake (μg/d) P for trend <21 .6="" th=""> 21.6–32.7 >32.7 n 1578 1605 1624 Median intake, μg/d 15.1 26.9 40.9 Nonfatal MI Person-years 11181 11549 11915 Events, n 51 57 36 RR, model 12 1 1.15 (0.79, 1.69) 0.74 (0.48, 1.14) 0.18 RR, model 23 1 1.08 (0.73, 1.62) 0.67 (0.41, 1.09) 0.12 Incident CHD4 Person-years 11323 11556 11766 Events, n 86 89 58 RR, model 1 1 1.05 (0.78, 1.42) 0.71 (0.51, 1.00) 0.048 RR, model 2 1 0.96 (0.70, 1.31) 0.59 (0.40, 0.86) 0.007 CHD mortality5 Person-years 11356 11747 12043 Events, n 41 35 23 RR, model 1 1 0.84 (0.54, 1.33) 0.59 (0.35, 0.99) 0.045 RR, model 2 1 0.73 (0.45, 1.17) 0.43 (0.24, 0.77) 0.005 All-cause mortality Person-years 11356 11747 12043 Events, n 258 248 195 RR, model 1 1 0.97 (0.82, 1.16) 0.81 (0.67, 0.98) 0.030 RR, model 2 1 0.91 (0.75, 1.09) 0.74 (0.59, 0.92) 0.007
-
1 RR obtained by Cox proportional hazard analysis, with 95% CI in parentheses and P for linear trend across the tertiles.
-
2 Model includes age, gender, and total energy intake.
-
3 Model includes age, gender, total energy intake, BMI, smoking status, pack-years of cigarette smoking, diabetes, education (3 categories), and intake of alcohol, SFA, PUFA, flavonols (quercetin, myricetin, and kaempferol), and calcium.
-
4 CHD comprises fatal and nonfatal MI, sudden cardiac death, and other forms of acute and chronic ischemic heart disease (ICD-10 codes I20–I25 and I46).
-
5 CHD events followed by death within 28 d after the onset of symptoms.
TABLE 3
Association of coronary events and all-cause mortality with intake of menaquinone in 4807 Dutch men and women aged 55 y and over1
| Energy-adjusted menaquinone intake (μg/d) | P for trend | |||
|---|---|---|---|---|
| <21 .6="" th=""> | 21.6–32.7 | >32.7 | ||
| n | 1578 | 1605 | 1624 | |
| Median intake, μg/d | 15.1 | 26.9 | 40.9 | |
| Nonfatal MI | ||||
| Person-years | 11181 | 11549 | 11915 | |
| Events, n | 51 | 57 | 36 | |
| RR, model 12 | 1 | 1.15 (0.79, 1.69) | 0.74 (0.48, 1.14) | 0.18 |
| RR, model 23 | 1 | 1.08 (0.73, 1.62) | 0.67 (0.41, 1.09) | 0.12 |
| Incident CHD4 | ||||
| Person-years | 11323 | 11556 | 11766 | |
| Events, n | 86 | 89 | 58 | |
| RR, model 1 | 1 | 1.05 (0.78, 1.42) | 0.71 (0.51, 1.00) | 0.048 |
| RR, model 2 | 1 | 0.96 (0.70, 1.31) | 0.59 (0.40, 0.86) | 0.007 |
| CHD mortality5 | ||||
| Person-years | 11356 | 11747 | 12043 | |
| Events, n | 41 | 35 | 23 | |
| RR, model 1 | 1 | 0.84 (0.54, 1.33) | 0.59 (0.35, 0.99) | 0.045 |
| RR, model 2 | 1 | 0.73 (0.45, 1.17) | 0.43 (0.24, 0.77) | 0.005 |
| All-cause mortality | ||||
| Person-years | 11356 | 11747 | 12043 | |
| Events, n | 258 | 248 | 195 | |
| RR, model 1 | 1 | 0.97 (0.82, 1.16) | 0.81 (0.67, 0.98) | 0.030 |
| RR, model 2 | 1 | 0.91 (0.75, 1.09) | 0.74 (0.59, 0.92) | 0.007 |
- 1 RR obtained by Cox proportional hazard analysis, with 95% CI in parentheses and P for linear trend across the tertiles.
- 2 Model includes age, gender, and total energy intake.
- 3 Model includes age, gender, total energy intake, BMI, smoking status, pack-years of cigarette smoking, diabetes, education (3 categories), and intake of alcohol, SFA, PUFA, flavonols (quercetin, myricetin, and kaempferol), and calcium.
- 4 CHD comprises fatal and nonfatal MI, sudden cardiac death, and other forms of acute and chronic ischemic heart disease (ICD-10 codes I20–I25 and I46).
- 5 CHD events followed by death within 28 d after the onset of symptoms.
Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study
TABLE 4
Association of aortic calcification with intake of menaquinone in 4473 Dutch men and women aged 55 y and over,1, 2
| Energy-adjusted menaquinone intake (μg/d) | P for trend | |||
|---|---|---|---|---|
| <21 .6="" th=""> | 21.6–32.7 | >32.7 | ||
| n | 1468 | 1493 | 1512 | |
| Median intake, μg/d | 15.1 | 26.9 | 40.9 | |
| Moderate calcification | ||||
| Controls, n | 916 | 958 | 1000 | |
| Cases, n | 454 | 452 | 453 | |
| OR, model 13 | 1 | 0.93 (0.79, 1.10) | 0.94 (0.80, 1.11) | 0.49 |
| OR, model 24 | 1 | 0.91 (0.77, 1.09) | 0.93 (0.76, 1.12) | 0.45 |
| Severe calcification | ||||
| Controls, n | 916 | 958 | 1000 | |
| Cases, n | 98 | 83 | 59 | |
| OR, model 1 | 1 | 0.75 (0.54, 1.03) | 0.56 (0.39, 0.80) | 0.001 |
| OR, model 2 | 1 | 0.71 (0.50, 1.00) | 0.48 (0.32, 0.71) | <0 .001="" td=""> |
- 1 Aortic calcification was graded according to the length of the calcified area, i.e., no/mild (reference), ≤1 cm; moderate, >1 and <5 cm.="" cm="" p="" severe="">
- 2 OR obtained by multivariate logistic regression, with 95% CI in parentheses and P for linear trend across the tertiles.
- 3 Model includes age, gender, and total energy intake.
- 4 Model includes age, gender, total energy intake, BMI, smoking status, pack-years of cigarette smoking, diabetes, education (3 categories), and intake of alcohol, SFA, PUFA, flavonols (quercetin, myricetin, and kaempferol), and calcium.
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