Our ancestors and alcohol

http://www.bbc.co.uk/earth/story/20170222-our-ancestors-were-drinking-alcohol-before-they-were-human

Danger et risque de cancer, une différence fondamentale

Un agent capable de causer un cancer dans certaines circonstances, représente un danger, alors qu'un risque de cancer ou d'une autre affection est une estimation des effets cancérogènes attendus de l'exposition à cet agent. Les études expérimentales ont pour but de rechercher si un cancer peut survenir dans l'exposition des animaux ou des humains à cet agent, les études cliniques ont pour but si un danger de cancer existe d'authetifier la relation causale et de quantifier le risque. La distinction entre danger et risque est importante et une étude expérimentale peut identifier un danger de cancer même lorsque les risques sont très bas aux niveaux d'exposition actuels des populations, car de nouvelles utilisations ou des expositions imprévues pourraient engendrer des risques nettement plus élevés.

Just have a look at pesticides residues in food: last data from the EU

http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2017.4791/epdf

Remember this issue with lemons:
http://dysnutrition.blogspot.fr/2010/01/pourquoi-payer-moins-cher-avec-imazalil.html

Retinal damage of LED

http://www.sciencedirect.com/science/article/pii/S0306452216305243

Primary prevention could be summed by a poem

http://www.bmj.com/rapid-response/2011/10/30/polypill-life%E2%80%A6in

Polypill a life…in

Instead of delicious butter margarin
For bad cholesterol statin
For thick blood aspirin
For diabetes metformin
For high blood pressure nicardipin
As I stopped smoking a full patch of nicotin
And tomorrow a nightmare, imagine !

Don’t be foolish !
Take fresh spinach and fatty fish
Roquette, nuts, kiwis and have a large meal
Pour your glass with wine and make a deal
After a snap I will go running
Work a bit and get light dining
Smoke a big havana once a year
And forget doctors for ever

Grosse manipulation journalistique au sujet du thon en boîte

Un tissu de mensonges. Un exemple: la moitié de la valeur réglementaire c'est parfaitement réglementaire. Des manipulateurs.

http://www.ladepeche.fr/article/2016/04/22/2330496-thon-boite-enquete-choc-60-milllions-consommateurs.html

Chronobiology of food intake: the truth and the myths

Figure 1. The day-night cycles set the regular oscillations of eating (purple line) and locomotor activity (blue line), which are coupled during a healthy state. Intake of hypercaloric diets, leading in obesity, disrupts the eating daily patterns, producing small but frequent bouts of ingestion even during the normal resting period. The locomotor activity and eating pattern rhythms are uncoupled in an obese state. The effects of a hypercaloric diet over the rhythmicity of the reward system are unknown but as the evidence suggest that the rhythmicity in the hypothalamus is mainly unaffected (blue dotted line), the reward system might be influencing the disturbances of the daily eating patterns (purple dotted line). In the diet-induced obese state, the rhythmicity of the peripheral organs are altered (green line), causing an internal desynchrony of central and peripheral oscillators (green dotted line).

http://journal.frontiersin.org/article/10.3389/fnins.2017.00023/full

This clearly proven. Other relationships between more specific food intakes and chronobiology are not backed by solid experimental or clinical studies.

This study (http://ajpregu.physiology.org/content/308/5/R337.long) is considering those issues:

"This review has focused on the effects of fatty acids and sugar on the circadian clock. Studies have shown that high-fat and high-sugar intake can lead to alterations in clock gene expression in peripheral tissues, in non-SCN brain nuclei, as well as in the SCN. Putative mechanisms through which this can occur were discussed with an important role for signaling components that link nutrient status to the molecular clock mechanism. Indeed, it was shown that alterations in circulating levels of fatty acids and glucose can affect various nutrient sensing mechanisms, which can affect the molecular clock, thereby linking fat and/or sugar intake to the circadian clock. Furthermore, many studies have focused on how altered energetic status can affect the clock. Current evidence supports the idea that the amount of nutrients may be more important for resetting the molecular clock than the source of nutrients, but it remains elusive whether the specific metabolites of fatty acids and sugar can contribute to alterations in the circadian clock and whether there are differential mechanisms through which fatty acids and sugar regulate the clock."