vendredi 30 octobre 2015

Relative risk of cancer, refined nutrients and specific foods

Sugar increases pancreatic cancer risk.

"During a mean follow-up of 7.2 y, we identified 131 incident cases of pancreatic cancer. The consumption of added sugar, soft drinks, and sweetened fruit soups or stewed fruit was positively associated with the risk of pancreatic cancer. The multivariate hazard ratios for the highest compared with the lowest consumption categories were 1.69 (95% CI: 0.99, 2.89; P for trend = 0.06) for sugar, 1.93 (1.18, 3.14; P for trend = 0.02) for soft drinks, and 1.51 (0.97, 2.36; Pfor trend = 0.05) for sweetened fruit soups or stewed fruit."

Fructose sucrose and GL increase the risk of colorectal cancer in men

Meat and colorectal cancer
Viande rouge neutre pour le risque de cancer colorectal

Essentiellement les saucisses
Red Meat:
The summary RRs for the highest versus lowest red meat intake comparison were 1.10 (95% CI  = 1.00−1.21), 1.18 (95% CI  = 1.04−1.35), and 1.14 (95% CI  = 0.83−1.56) for colorectal, colon, and rectal cancer respectively (Table 1). The mean of the highest category of red meat intake ranged from 26 to 197 grams per day in the studies. In dose-response meta-analyses, red meat was statistically significantly associated with increased risk of colorectal (RR for 100 g/day increase  = 1.17, 95% CI  = 1.05−1.31) (8 studies, 4314 cases) and colon cancer (RR for 100 g/day increase  = 1.17, 95% CI  = 1.02−1.33) (10 studies, 3561 cases) (Table 1) (Figure 4). No significant association was observed with rectal cancer (RR for 100 g/day increase  = 1.18, 95% CI  = 0.98−1.42) (7 studies, 1477 cases). Influence analyses did not suggest strong influence from any of the individual studies on the summary estimates.
Processed meat:
Eighteen studies were included in the highest versus lowest meta-analyses [18][20][22],[26][28][33][34][49][50][52][54][56][57][60][62][64][65]. Processed meat intake was significantly related to the risk of colorectal (RR highest vs lowest  = 1.17, 95% CI  = 1.09−1.25), colon (RR highest vs lowest  = 1.19, 95% CI  = 1.11−1.29), and rectal cancer (RR highest vs lowest  = 1.19, 95% CI  = 1.02−1.39) (Table 1). The mean of the highest category of processed meat intake ranged from 16 to 122 grams per day in the studies. Four studies could not be used to derive dose-response estimates [20][28][62][66]. The summary RR for every 50 g/day increase in processed meat was 1.18 (95% CI  = 1.10−1.28) (9 studies, 10863 cases) for colorectal cancer and 1.24 (95% CI  = 1.13−1.35) (10 studies, 6727 cases) for colon cancer (Table 1) (Figure 5). For rectal cancer, no significant dose-response association was observed (RR for 50 g/day increase  = 1.12, 95% CI  = 0.99−1.28) (8 studies, 2565 cases). Influence analyses did not suggest strong influence from any of the individual studies on the summary estimates.


Absolute Risk of breast cancer

According to the current report, the risk that a woman will be diagnosed with breast cancer during the next 10 years, starting at the following ages, is as follows:

  • Age 30 . . . . . . 0.44 percent (or 1 in 227)
  • Age 40 . . . . . . 1.47 percent (or 1 in 68)
  • Age 50 . . . . . . 2.38 percent (or 1 in 42)
  • Age 60 . . . . . . 3.56 percent (or 1 in 28)
  • Age 70 . . . . . . 3.82 percent (or 1 in 26)
  1. Howlader N, Noone AM, Krapcho M, et. al. (eds). SEER Cancer Statistics Review, 1975–2009 (Vintage 2009 Populations), National Cancer Institute. Bethesda, MD, 2012. Retrieved September 7, 2012.

Low fat versus low sugar

jeudi 29 octobre 2015

Lipids in Acute Myocardial Infarction

Critical Care Medicine:
doi: 10.1097/CCM.0000000000000946
Clinical Investigations

Lipid Paradox in Acute Myocardial Infarction—The Association With 30-Day In-Hospital Mortality

Cheng, Kai-Hung MD1,2,3; Chu, Chih-Sheng MD, PhD1,2,3; Lin, Tsung-Hsien MD, PhD1,2,3; Lee, Kun-Tai MD1,2; Sheu, Sheng-Hsiung MD1,2; Lai, Wen-Ter MD1,2

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Objectives: Elevated low-density lipoprotein cholesterol and triglycerides are major risk factors for coronary artery disease. However, fatty acids from triglycerides are a major energy source, low-density lipoprotein cholesterol is critical for cell membrane synthesis, and both are critical for cell survival. This study was designed to clarify the relationship between lipid profile, morbidity as assessed by Killip classification, and 30-day mortality in patients with acute myocardial infarction.
Design: A noninterventional observational study.
Setting: Coronary care unit in a university hospital.
Patients: Seven hundred twenty-four patients with acute myocardial infarction in the coronary care program of the Bureau of Health Promotion were analyzed.
Interventions: None.
Measurements and Main Results: Low-density lipoprotein cholesterol and triglyceride levels were significantly lower in high-Killip (III + IV) patients compared with low-Killip (I + II) patients and in those who died compared with those who survived beyond 30 days (both p < 0.001). After adjustment for risk factors, low-density lipoprotein cholesterol less than 62.5 mg/dL and triglycerides less than 110 mg/dL were identified as optimal threshold values for predicting 30-day mortality and were associated with hazard ratios of 1.65 (95% CI, 1.18–2.30) and 5.05 (95% CI, 1.75–14.54), and the actual mortality rates were 23% in low low-density lipoprotein, 6% in high low-density lipoprotein, 14% in low triglycerides, and 3% in high triglycerides groups, respectively. To test the synergistic effect, high-Killip patients with triglycerides less than 62.5 mg/dL and low-density lipoprotein cholesterol less than 110 mg/dL had a 10.9-fold higher adjusted risk of mortality than low-Killip patients with triglycerides greater than or equal to 62.5 mg/dL and low-density lipoprotein cholesterol greater than or equal to 110 mg/dL (p < 0.001). The lipid paradox also improved acute myocardial infarction short-term outcomes prediction on original Killip and thrombolytic in myocardial infarction scores.
Conclusions: Low low-density lipoprotein cholesterol, low triglycerides, and high Killip severity were associated with significantly higher 30-day in-hospital mortality in patients presenting with acute myocardial infarction. The initial lipid profile of patients with acute myocardial infarction may therefore hold prognostic value.

Antioxidants supplements deadly?

  1. Mejia, Paula. “Antioxidants May Lead to Cancer Spread, Study Says.” Newsweek. 17 October 2015. Available
  2. Piskounova E, Agathocleous M, Murphy MM, et al. Oxidative stress inhibits distant metastasis by human melanoma cells. Nature. 2015.
  3. Chen AC, Martin AJ, Choy B, et al. A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention. The New England journal of medicine. 2015;373(17):1618-1626.

Anti-oxidants and Skin Cancer
Major news outlets hyped the dangers of antioxidant consumption from sources such as “blueberries,” citing they may promote tumor metastasis.[1]
The original study’s aim was to better understand metabolic changes in metastatic tumors. The authors first characterized the potential of human melanoma lines to form new tumors when explanted into immunodeficient mice.  Successfully metastasizing melanomas were found to have higher levels of NADPH, a critical enzyme within the folate pathway that recycles glutathione, which is known to help with oxidative stress. To test whether increased glutathione promotes tumor metastasis, three highly metastatic melanoma cell lines were injected into mice and received either subcutaneous N-acetyl cysteine (NAC) or control. The authors found a 10-fold increase in tumor formation with NAC (p<0 .0001="" p="">
A separate phase 3 double-blind randomized control trial published this week showed that antioxidant compounds might also have protective effects in cancer. Investigators tested vitamin B3 in the prevention of skin cancer in patients with a history of previous non-melanoma skin cancers. The rationale for using Vitamin B3 is that Vitamin B3 is a precursor of nicotinamide adenine dinucleotide (NAD+), an essential co-factor for ATP production, which is otherwise depleted with UV-radiation induced DNA damage. The study included 386 patients who underwent dermatological evaluations every 3-month for 18-months to evaluate for new skin lesions. The results showed that at 12-months, there were 23% fewer new non-melanoma skin cancers with a number needed to treat (NNT) of 2.2 for basal cell carcinoma and 5.0 for squamous cell carcinoma. Vitamin B3 also led to a 13% greater decline in the number of actinic keratoses from baseline in the nicotinamide group vs. the placebo group, which equates to 3 – 5 fewer per patient on average. However how the number of actinic keratoses corresponds to risk of recurrent malignancy is unclear. There was no comparative benefit during the 6-month post-intervention surveillance period after nicotinamide was discontinued nor were there any adverse effects throughout the study.[3] Overall this study provides support for the role of vitamin B3 as a chemoprevention agent in patients at high risk for recurrent non-melanoma skin cancer as it is safe, well tolerated and cheap. However it remains unclear whether this will lead to true clinical benefit as non-melanoma tumors are frequently slow growing and easy to excise. Larger and longer studies are necessary to assess effects on morbidity and mortality.
These two recent studies present opposing conclusions regarding the harm or benefit of antioxidants in cancer. One possibility is that antioxidants provide a protective effect during tumor initiation but a deleterious effect during tumor progression. This could explain why Vitamin B3/nicotinamide decreases the risk of new tumors while NAC promotes melanoma metastasis. Alternatively, the biology of non-melanoma and melanoma tumors may be different. Either way, the role of antioxidants in cancer is likely to be more complex than represented in the popular press. Additional pre-clinical and clinical trials will be essential to further understand the effects of antioxidants on cancer.

Meat and meat products consumption in France

My advices:
Eat fresh or frozen grassfed meat from beef, bison, lamb or free range pork. Don't forget snails.
Eat offal especially liver
Eat fresh or frozen fish, seafoods 
Eat rabbit and game meat.
Don't transform them at high temperature. 
No meat without a salad.

Egg and D2 in women

mercredi 28 octobre 2015

It is mainly a problem of the irrational mind

All the problems we are discussing now in human nutrition and health are biased by irrational minds and thoughts in the media or by incompetent commentators. it is the case for meat, vaccines, sugar, fat, cholesterol, statins, and this is a short list.
One of the major irrationality is about complexity of issues. All irrational minds hate complexity, they want to sum a scientific paper of 10 pages in two sentences...
The other bias is a complete misunderstanding of uncertainty and probability.
This later marker is linked to irrationality for most of the people but it is perhaps not an accident. In avoiding uncertainty they pave the way to oversimplify the issues and to push people to think in black and white.
Aside irrationality media and lobbying commentators are pushing their agendas through the controversy about scientific papers.
Agendas of these big interests mix those of the agricultural industry, drug manufacturers, energy and transport industries, public structures and politicians.

Meat or not meat

Food: a stuff full of data and signals

Sugar calories are not fat calories, actually?

Balsamic vinegar: trendy but full of sugars

Balsamic vinegar is a shot of fast sugars
17g/100g of sugars
A table spoon is 14,5g of sugar.
A cube is 2,3 g of sugar so 100 g of balsamic vinegar is 7,5 sugar cubes and 100ml id est 1 liter is 75  sugar cubes....

Instead Cider vinegar is only 0,93g sugars /100g, less than half a sugar cube in 100 ml and 4 sugar cubes for a liter...

For red wine vinegar the content of carbs is still less 0,27g/100 ml and 2,7 g/liter. A liitle bit more than a sugar cube...

For your information a regular Cola is 9,94 g of sugar/100ml or 99,4 g of sugar a liter.

But, as a matter of facts there are more sugared Balsamic vinegar: 34 g/ 100g quite a marmelade...

mardi 27 octobre 2015

IARC, meat and the economy

This paper is a sum of stupidities...

Useful classification of IARC: completely arbitrary however

lundi 26 octobre 2015

FTO sitting and obesity

 2015 Sep 22. doi: 10.1038/ijo.2015.190. [Epub ahead of print]

FTO association and interaction with time spent sitting.

Author information

  • 1Department of Epidemiology and Biostatistics, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA.
  • 2School of Anthropology, University of Arizona, Tucson, AZ, USA.



Multiple studies have revealed an interaction between a variant in the FTO gene and self-reported physical activity on body mass index (BMI). Physical inactivity, such as time spent sitting (TSS) has recently gained attention as an important risk factor for obesity and related diseases. It is possible that FTO interacts with TSS to affect BMI, and/or that FTO's putative effect on BMI is mediated through TSS.


We tested these hypotheses in two cohorts of the Framingham Heart Study (FHS) (Offspring: n=3430 and Third Generation: n=3888), and attempted to replicate our results in the Women's Health Initiative (WHI; n=4756). Specifically, we examined whether an association exists between FTO and self-reported TSS, and whether an interaction exists between FTO and TSS on BMI, while adjusting for several important covariates such as physical activity.


In FHS, we find a significant positive association between the BMI-increasing FTO allele and TSS. We find a similar trend in WHI. Mediation analyses suggest that the effect of FTO on BMI is mediated through TSS. In FHS, we find a significant interaction of FTO and TSS on BMI, whereby the association of TSS with BMI is greatest among those with more FTO risk alleles. In WHI, we also find a significant interaction, although the direction is opposite to that in FHS. In a meta-analysis of the two data sets, there is no net interaction of FTO with TSS on BMI.


Our study suggests that FTO exerts its effect on BMI, at least partly, through energy expenditure mechanisms such as TSS. Further research into the intersection of genetics, sedentary behavior and obesity-related outcomes is warranted.International Journal of Obesity advance online publication, 13 October 2015; doi:10.1038/ijo.2015.190.

If you eat mainly or a lot of processed meat it is time to shift

First and above all we have to rephrase the media:
Processed meat consumption is associated with an increase risk of cancer. Not completely the same meaning.
But the most important is coming: what is the magnitude of the risk? It is small, rather very small. 11-12 % increase of all cancers risk.
Cutted meat (id est red meat) is associated with a smaller risk so the group of IACR qualified it as uncertain.

1/ Cutted meat is less carcinogenic especially if eaten raw or cooked very gently. Yes the main source of carcinogens in red meat is the result of cooking especially high temperature cooking. That is not news.
Charcoal on meat is carcinogenic as soot for the skin of chimney-sweeps.
2/ What processed meat is less carcinogenic? Obviously processed meat freshly prepared or dried meat like jerky or raw ham.
3/ Cheeses are probably better with less or no TMAO production in your gut
Abstract Image

Processed meat is carcinogenic according to IARC group and red meat is probably carcinogenic. Mechanisms are less clear:
"Substantial supporting mechanistic evidence was available for multiple meat components (NOC, haem iron, and HAA). Consumption of red meat and processed meat by man induces NOC formation in the colon. High red meat consumption (300 or 420 g/day) increased levels of DNA adducts putatively derived from NOC in exfoliated colonocytes or rectal biopsies in two intervention studies.19,20 Few human data, especially from intervention studies, were available for processed meat. Haem iron mediates formation of NOC, and of lipid oxidation products in the digestive tract of human beings and rodents. Haem iron effects can be experimentally suppressed by calcium, supporting its contribution to carcinogenic mechanisms. Meat heated at a high temperature contains HAA. HAA are genotoxic, and the extent of conversion of HAA to genotoxic metabolites is greater in man than in rodents. Meat smoked or cooked over a heated surface or open flame contains PAH. These chemicals cause DNA damage, but little direct evidence exists that this occurs following meat consumption." 
So if you have to choose eat preferably cut meat, raw (tartare) or gently cooked... Avoid products with processed meat. Indeed fresh saucisse or saucisson or jerky or raw dried ham are OK but other products are highly processed... 
Evil in the details as usual.


Acrylamide is a compound that is formed through the Maillard reaction from the reaction between free asparagine and carbonyl compounds (mainly reducing sugars) during heating at temperatures > 120 °C of plant-derived, carbohydrate-rich foods such as French fries, potato chips, bakery products, and coffee. Acrylamide is neurotoxic in humans and carcinogen in rodents and the associated margin of exposure is quite high for a widespread food contaminant, which would indicate a high concern from a public health point of view. Only few epidemiological studies have indicated an increased cancer risk related to acrylamide dietary intake; however, a principle of precaution should be applied reducing as much as possible its concentration in foods.

Le titre du pire article sur le gras en français vient d'être décerné!

Faire de la pub pour les acides gras trans en 2012 est une faute.
Tout le reste est à l'avenant du relativisme scientifique.

Low carb diets are doing better on weight loss and CVD risk factors.
Still a great difference between races:
Fig 3.  Bayesian probabilities for mean differences in (a) weight loss and (b) estimated 10-year ASCVD risk scores.
This is not negligible and side effects are few.

Stone after stone the destruction of the low fat myth which fueled so many mistakes and so much benefit for agro-industry.
The results of this study on conventional biomarkers of CVD are amazing.
Another time looking at those results marker by marker is totally irrational. The risk is far better appreciated by the combination of factors.
Example: LDL
Low fat works better on LDL BUT we don't know if the LDL particles are the same on low fat diets and low carb diets... And several studies showed that LDL particles profile is more atherogenic on high carb diet and very atherogenic if the carbs do have a high GI.
In the same comparison low fat diets DO NOT improve substantially HDL contrary to low carb diets and we know that the ratio between HDL/LDL particles is a potent risk factor. In the same perspective of global lipid evaluation low carb drastically decrease TG. TG is an independent risk factor of atheroma through chylomicron remnants and VLDL especially in the postprandial period. 
My point is that low carb diets moderately decrease all cholesterol containing particles and improve the number and/or size of the HDL particles so the non HDL cholesterol particles decrease. These non HDL cholesterol particles are the major biomarker of atheroma in the lipid heart hypothesis. In summary low carb diets impact all the biomarkers of atheroma instead of low fat diets which are only decreasing LDL cholesterol. Another time total cholesterol is in only some studies poorly correlated with CVD and should not have been mentioned in this comparison.
But lipids are not by far the only biomarkers of atheroma.
Low carb diets which are very efficient on weight (-12 vs -6,5 %) decrease systolic blood pressure which is the major factor of extracranial atheroma in the supra-aortic trunks where originate 25% of TIA and Stroke.
What about acceptance of those diets?
"The magnitude of carbohydrate and fat restrictions were calculated from the time of lowest daily intake (Table 2), at which time the average carbohydrate intake was 145 g/day lower in the LoCHO vs. LoFAT group. The LoFAT group averaged lower protein intake (by 36 g/day) and lower fat intake (by 53 g/day) with an average minimum fat intake of 24% of daily energy (95% CI: 21, 27). At the time of the strictest carbohydrate restriction for the LoCHO group, the total caloric intake was not significantly different between groups (1504 vs. 1449 kcal/day for LoCHO and LoFAT, respectively)."
Eventually the data showed that in low carb diets the minimum CHO intake was 29,5 g/d which is easily doable in an everyday life. 
In conclusion this study is in keeping with strong observational nutritional data: Switzerland and France which have the most important consumption of sat fat in Europe (around 15% of TEI) have the lowest rate of CVD. And their sat fats come primarily from animal fat with a high % of cheeses.

Should you advice a closely related to follow a ketogenic diet if he or she suffers cancer?

This question is difficult, it is an emerging field. We have to keep very near from our basic principles:
"primum non nocere" but we have to avoid any delay in front of new chances to cure!

1/ During chemo it is well backed that fasting and enhanced nutrition improve the efficacy and tolerance (stem cells recovery) of chemo. The last study is a RCT!  free full text

Hematologic parameters compared between both groups. Values are measured on day 0 of cycle 1 immediately before the chemotherapy infusion, on day 7 of cycle 1–5 combined and day 21 of cycle 1–5 combined. * P value <0 nbsp="" p="">

2/ Ketogenic diet is on the rise. It is a lie to assert that it can cure cancer. It is very difficult without advice to implement a keto diet when you are the kind of people who eats the standard western diet. Counselling is very difficult to find in Europe.
There are good indications of keto diet in cancer like brain tumors. But another time don't embark alone in keto diet especially if you have cancer.
- caloric restriction is key
- low carb diet is mandatory only one raw juicy fruit at each meal
- you need high fat diet to survive so eat it! Pork, lamb, bone marrow broth, butter, cream, cheeses with long fermentation and affinage in order to avoid any residual lactose, nuts macadamia Brazil nuts and groundnuts.
- eat your protein too, you cannot do it without meat or fish and obviously with eggs.
- no carbs but a lot of veggies, kale, sauerkraut, tomatoes, salads, celery, broccoli no tubers.
You can improve your metabolism and starve your cancer cells.

vendredi 23 octobre 2015

The début of biotech

¨Ancient bread baking
¨Wine brewing
¨Cheese making
¨Yogurt fermentation

¨Animal and plant breeding

Symptomatic atheroma

Save your cash for whole foods

The Blue Zones of centenarians

High fat diet in mice and glucose tolerance: not a reliable model for humans
This title recalled me how reporting science is difficult...
1/ figures 3,4 and 5 of the paper are not available...
2/ reference:
3/ The HFD in mice is a model to study GLUCOSE intolerance!

4/it is not a matter of specific fatty acids except for W3 PUFA which are not associated with glucose intolerance:
"Also, in our own study, we were not able to detect significant correlations between the saturation level of free fatty acids and insulin action as estimated from whole-body glucose disposal after an insulin challenge (Figure 2)."

As usual those exp studies on rodents should be reported with extreme caution about any translational knowledge applicable to humans. issues about carbs and fats are complex and extremely controversial so a more balanced approach should be to report also other studies by instance this one:

"Results: Higher TC, higher HDL-C, and lower triglycerides were associated with higher age 70 cognitive scores in most cognitive domains. These relationships were no longer significant after covarying for childhood IQ, with the exception a markedly attenuated association between TC and processing speed, and triglycerides and age 70 IQ. In the fully adjusted model, all conventionally significant (p < 0.05) effects were removed. Childhood IQ predicted statin use in old age. Statin users had lower g, processing speed, and verbal ability scores at age 70 years after covarying for childhood IQ, but significance was lost after adjusting for TC levels.
Conclusions: These results suggest that serum cholesterol and cognitive function are associated in older age via the lifelong stable trait of intelligence. Potential mechanisms, including lifestyle factors, are discussed."

The surge of nut oils in EU

The message that consumers send to manufacturers is simple: in EU taste is key!

Do you bet on this prediction?

jeudi 22 octobre 2015

Toujours le sucre mais vous le savez c'est écrit sur presque tous les produits...

Il arrive que l'on soit un peu étonné de la naiveté de certains journalistes... 
Sur le sucre ajouté cette naiveté est partagée par nos concitoyens qui ne lisent pas les ingrédients contenus dans les produits qu'ils achètent car ils sauraient que l'inondation à petit débit est un fait. Pas plus qu'ils ne lisent les recommandations pour les médicaments ou bien qu'ils ne lisent le programme des hommes politiques pour lesquels ils votent...

Après il y a le mythe naturaliste:
"Ce sucre artificiel (qui n’a rien à voir avec le fructose des fruits)" 

Si, si le fructose du maïs des fruits ou de la synthèse chimique sont les mêmes molécules...

"Les Etats-Unis ont inventé le "fructose de maïs" pour exploiter au maximum leur stock de maïs. C’était économiquement intelligent."

Non, non pas intelligent but heavily subsidised. Like in Europe and singulièrement en France ou le maïs demande une grande quantité d'eau et de pesticides.

"La chimiste américaine voit dans le sucre «  l’héroïne légale de l’alimentation familiale »."
En réalité il faut comparer cliniquement, il est beaucoup plus facile de se passer de sucre que d'héroïne. Fin de l'histoire, on ne gagne pas à surdimensionner une vérité car cela en fait une propagande. Oui certains sont plus dépendant du sucre pur que d'autres comme pour la caféine ou l'alcool ou me^me l'héroïne mais le niveau de dépendance n'est pas le même et l'héroïne impacte beaucoup plus le fonctionnement du cerveau car c'est un neurotransmetteur alors que le sucre est un nutriment.

Ustekinumab in Crohn's disease

mercredi 21 octobre 2015

Cholesterol and cognitive function

International Psychogeriatrics (2015), 27: 439-453 
Copyright © International Psychogeriatric Association 2014  
doi: 10.1017/S1041610214001197 Publié en ligne : juil. 2014

Serum cholesterol and cognitive functions: the Lothian Birth Cohort 1936

Janie Corleya1, John M. Starra2a3 and Ian J. Dearya1a2 c1

a1 Department of Psychology, University of Edinburgh, 7 George Square, Edinburgh EH8 9JZ, UK 

a2 Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, 7 George Square, Edinburgh EH8 9JZ, UK 

a3 Royal Victoria Building, Western General Hospital, Porterfield Road, Edinburgh EH4 2XU, UK 


Background: We examined the associations between serum cholesterol measures, statin use, and cognitive function measured in childhood and in old age. The possibility that lifelong (trait) cognitive ability accounts for any cross-sectional associations between cholesterol and cognitive performance in older age, seen in observational studies, has not been tested to date.

Methods: Participants were 1,043 men and women from the Lothian Birth Cohort 1936 Study, most of whom had participated in a nationwide IQ-type test in childhood (Scottish Mental Survey of 1947), and were followed up at about age 70 years. Serum cholesterol measures included total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides, and cholesterol:HDL cholesterol ratio. Cognitive outcome measures were age 70 IQ (using the same test as at age 11 years), general cognitive ability (g), processing speed, memory, and verbal ability.

Results: Higher TC, higher HDL-C, and lower triglycerides were associated with higher age 70 cognitive scores in most cognitive domains. These relationships were no longer significant after covarying for childhood IQ, with the exception a markedly attenuated association between TC and processing speed, and triglycerides and age 70 IQ. In the fully adjusted model, all conventionally significant (p < 0.05) effects were removed. Childhood IQ predicted statin use in old age. Statin users had lower g, processing speed, and verbal ability scores at age 70 years after covarying for childhood IQ, but significance was lost after adjusting for TC levels.

Conclusions: These results suggest that serum cholesterol and cognitive function are associated in older age via the lifelong stable trait of intelligence. Potential mechanisms, including lifestyle factors, are discussed.

(Received March 06 2014)

(Reviewed April 27 2014)

(Revised May 13 2014)

(Accepted May 28 2014)

(Online publication July 15 2014)


c1Correspondence should be addressed to: Ian J. Deary, Department of Psychology, Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, 7 George Square, Edinburgh EH8 9JZ, Scotland, UK. Phone: +44-131-650-3452. Email:

Energy regulation in humans: Extreme complexity

mardi 20 octobre 2015

Palm oil and fires of extension

Have a coach ASAP

Do you believe that there is a link between life expectancy and a healthy diet?

W3/W6 ratio and vegetable saturated fats

There no matter with the w3/w6 ratio if you use saturated fats.
Palm and coconut are neutral .
Peanut oil also is rather neutral.
So you have to make your ratio with foods instead of highly oxydised unsaturated oils!
Fishes, seafoods for long chain W3PUFA and on the other hand seeds for linoleic acid the essential w6 PUFA.
Keep in mind that we presently have an important intake of w6 by the way of grain fed cattle (meat and dairy) and massive use of rich w6 seed oil in industrial products.

lundi 19 octobre 2015

Sugar to fat through the liver

Veganism and sperm quality

"The results showed that the vegetarian diet reduced sperm concentration and motility but did not extend into the infertile range. The findings suggested that estrogenic compounds or chemical residues in the diet had a negative effect on sperm parameters. Hyperactive motility indicative of the CatSper calcium selective channel was compromised in the vegan group. Clinical management would include dietary supplements to offset deficiencies. More studies are needed to corroborate the present findings."

"Lacto-ovo vegetarians had significantly lower sperm concentration (50.7 7.4 M/mL, mean S.E.M.) when compared with nonvegetarians (69.6 3.2 M/mL). Furthermore, total motility was lower in the lacto-ovo group (33.2 3.8% versus non-vegetarian 58.2 1.0%). Similarly, vegans had lower total motility (51.8 13.4%) with a trend towards lower sperm concentration (51.0 13.1 M/mL). Interestingly, hyperactive motility was lowest in the vegan group. The percent strict normal sperm morphology in all groups were within normal range. There were no differences in the remaining parameters: rapid progression, chromatin integrity and SPA capacitation index. "