samedi 23 juin 2018

Where can you buy a good Maragogype?

https://www.cafenegril.fr/

https://www.mokamalo.fr/produit/mexiquemaragogype-bio/ 34,5

A blend
http://www.cafes-savina.fr/brulerie-du-goyen/36-maragogype-choi.html

https://www.comptoirsrichard.fr/cafe-colombie-maragogype-excelso.html

http://www.lagrangedirect.com/produit_detail.php?p=279&decli=346

http://www.paul-et-arthur.com/mon_panier.php 37,6

http://www.toobeautyfood.com/fr/commande 37

http://www.vert-tiges.com/cafes-d-exception/357-cafe-nicaragua-maragogype-finca-buenos-aires.html 27,84

Oysters

https://www.theatlantic.com/technology/archive/2014/09/todays-oysters-are-mutants/380858/

vendredi 22 juin 2018

Read it ASAP, it is worth the time spent...

https://thepaleodiet.com/ketogenic-diets-long-term-nutritional-and-metabolic-deficiencies/?inf_contact_key=955ca3d259651034252673cd773f15316badb169c0963923d24f110899dde5e6

jeudi 21 juin 2018

Magnesium

Table 1. Negative effects of Magnesium
deficiency on the body and organs.

General: anxiety, agitation, irritability, headache, loss of appetite,
nausea.

Musculature: muscle spasm and tetany.

CNS/Nerves: nervousness, migraine, depression, poor memory,
low-stress tolerance, paraesthesia, tremor, and seizures.

Cardiovascular system: HTN, a risk of arrhythmias, coronary spasm,
atherosclerosis, endothelial dysfunction, low-grade
vascular inflammation, arterial stiffness, vascular ECM remodelling,
arterial calcification, vascular ageing, increased
platelet aggregation potentiates Ca2+-mediated vasoconstriction,
potentiates the vasoconstrictor effects of ATII,
ET-1, NA, Adr, and TxA2.

Electrolytes: sodium retention, hypokalemia, and hypocalcemia.

Metabolism: dyslipoproteinemia, insulin resistance,
pancreatic β-cell dysfunction, decreased glucose tolerance,
increased risk of MetS and T2D, disorders of vitamin D metabolism,
resistance to PTH, and osteoporosis.

Pregnancy: pregnancy complications (e.g., eclampsia).

Gastrointestinal tract: constipation.

http://www.mdpi.com/1422-0067/19/6/1724

mardi 19 juin 2018

Breaking news: Vitamin D level and breast cancer

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0199265

It is an association in an epidemiological study. But,

The chart above shows the proportion of participants who were not diagnosed with breast cancer according to vitamin D level over the course of the study.
The proportion of participants with breast cancer was 78% lower for women with vitamin D levels at 60 ng/ml or above compared to women with levels less than 20 ng/ml.

Poitrine fraîche aux girolles: un plat paléo très gouteux

Girolles des Pyrénées, récompense d'un printemps pluvieux

Elles sont dans la grande casserole avec une huile d'olive non filtrée, du sel de Guérande, du basilic frais et du piment d'Espelette. On couvre.

La poitrine est cuite après que les Girolles aient sué dans une grande casserole. Bien sur on mange la couenne!

Accord très satisfaisant de vin très fin et subtil

L'intérêt de cette viande c'est la race du porc et son élevage en extensif

lundi 18 juin 2018

Red Tuna with wild lemons: fast paleo recipe

Omega3 PUFAs are here... I love the tuna belly!

mercredi 13 juin 2018

A new approach to the prevention of heart attacks during sport

mardi 12 juin 2018

Alcohol tolerance and human genetic diversity

Two key enzymes.

The chemical name for alcohol is ethanol (CH3CH2OH). The body processes and eliminates ethanol in separate steps. Chemicals called enzymes help to break apart the ethanol molecule into other compounds (or metabolites), which can be processed more easily by the body. Some of these intermediate metabolites can have harmful effects on the body.

Most of the ethanol in the body is broken down in the liver by an enzyme called alcohol dehydrogenase (ADH), which transforms ethanol into a toxic compound called acetaldehyde (CH3CHO), a known carcinogen. However, acetaldehyde is generally short-lived; it is quickly broken down to a less toxic compound called acetate (CH3COO-) by another enzyme called aldehyde dehydrogenase (ALDH). Acetate then is broken down to carbon dioxide and water, mainly in tissues other than the liver.

Alcohol metabolism and cancer

Alcohol consumption can contribute to the risk for developing different cancers, including cancers of the upper respiratory tract, liver, colon or rectum, and breast (19). This occurs in several ways, including through the toxic effects of acetaldehyde (20).

Ironically, the very genes that protect some people from alcoholism may magnify their vulnerability to alcohol-related cancers. The International Agency for Research on Cancer (21) asserts that acetaldehyde should be classified as a carcinogen. Acetaldehyde promotes cancer in several ways—for example, by interfering with the copying (i.e., replication) of DNA and by inhibiting a process by which the body repairs damaged DNA (5). Studies have shown that people who are exposed to large amounts of acetaldehyde are at greater risk for developing certain cancers, such as cancers of the mouth and throat (5). Although these individuals often are less likely to consume large amounts of alcohol, Seitz and colleagues (5) suggest that when they do drink their risk for developing certain cancers is higher than drinkers who are exposed to less acetaldehyde during alcohol metabolism. Many heavy drinkers do not develop cancer, and some people who drink only moderately do develop alcohol-related cancers. Research suggests that just as some genes may protect individuals against alcoholism, genetics also may determine how vulnerable an individual is to alcohol’s carcinogenic effects (5).
Acetaldehyde is not the only carcinogenic byproduct of alcohol metabolism. When alcohol is metabolized by CYP2E1, highly reactive, oxygen-containing molecules—or reactive oxygen species (ROS)—are produced. ROS can damage proteins and DNA or interact with other substances to create carcinogenic compounds (22).

Our tools of epidemiology and meta-analysis do work when there is an increased RR of cancer;

THE GENETICS BEHIND METABOLISM

Regardless of how much a person consumes, the body can only metabolize a certain amount of alcohol every hour (2). That amount varies widely among individuals and depends on a range of factors, including liver size (1) and body mass.

In addition, research shows that different people carry different variations of the ADH and ALDH enzymes. These different versions can be traced to variations in the same gene. Some of these enzyme variants work more or less efficiently than others; this means that some people can break down alcohol to acetaldehyde, or acetaldehyde to acetate, more quickly than others. A fast ADH enzyme or a slow ALDH enzyme can cause toxic acetaldehyde to build up in the body, creating dangerous and unpleasant effects that also may affect an individual’s risk for various alcohol-related problems—such as developing alcoholism.

The type of ADH and ALDH an individual carries has been shown to influence how much he or she drinks, which in turn influences his or her risk for developing alcoholism (11). For example, high levels of acetaldehyde make drinking unpleasant, resulting in facial flushing, nausea, and a rapid heart beat. This “flushing” response can occur even when only moderate amounts of alcohol are consumed. Consequently, people who carry gene varieties for fast ADH or slow ALDH, which delay the processing of acetaldehyde in the body, may tend to drink less and are thus somewhat “protected” from alcoholism (although, as discussed later, they may be at greater risk for other health consequences when they do drink).

Genetic differences in these enzymes may help to explain why some ethnic groups have higher or lower rates of alcohol-related problems. For example, one version of the ADH enzyme, called ADH1B*2, is common in people of Chinese, Japanese, and Korean descent but rare in people of European and African descent (12). Another version of the ADH enzyme, called ADH1B*3, occurs in 15 to 25 percent of African Americans (13). These enzymes protect against alcoholism (14) by metabolizing alcohol to acetaldehyde very efficiently, leading to elevated acetaldehyde levels that make drinking unpleasant (15). On the other hand, a recent study by Spence and colleagues (16) found that two variations of the ALDH enzyme, ALDH1A1*2 and ALDH1A1*3, may be associated with alcoholism in African-American people.

Although these genetic factors influence drinking patterns, environmental factors also are important in the development of alcoholism and other alcohol-related health consequences. For example, Higuchi and colleagues (17) found that as alcohol consumption in Japan increased between 1979 and 1992, the percentage of Japanese alcoholics who carried the protective ADH1B*2 gene version increased from 2.5 to 13 percent. Additionally, despite the fact that more Native American people die of alcohol-related causes than do any other ethnic group in the United States, research shows that there is no difference in the rates of alcohol metabolism and enzyme patterns between Native Americans and Whites (18). This suggests that rates of alcoholism and alcohol-related problems are influenced by other environmental and/or genetic factors.

https://pubs.niaaa.nih.gov/publications/aa72/aa72.htm

C2H5OH metabolism

Where? Alcohol is metabolized in the body mainly by the liver. The brain, pancreas, and stomach also metabolize alcohol.

lundi 4 juin 2018

GMO and Round up without any carcinogenic nor toxic effects in rats according to the verification experiments of the EFSA

https://www.g-twyst.eu/files/Conclusions-Recommendations/G-TwYSTConclusionsandrecommendations-final.pdf

OGM et Round up sans effets cancérigènes ni toxiques chez les rats selon les expériences de vérification de l'UE.

The Seralinigate is obviously lasting!

"1.2. No potential risk for humans and animals was identified in the original assessment of the GM maize NK603. In particular, no triggers for animal feeding studies were identified from the molecular characterization and the compositional, phenotypic and/or agronomic analyses of NK603. Therefore, the G-TwYST 90-day and long-term animal studies were conducted in the absence of a specific hypothesis. The G-TwYST data from 90-day and long-term rodent feeding studies did not identify potential risks as well, and therefore support the results from the initial analyses.

1.3. No potential risk has been identified in the course of the 90-day rat feeding study with NK603. The G-TwYST data from the long-term feeding rat study with NK603 did not identify potential risks as well, and therefore support the results from the initial analyses and 90-day rat feeding studies.

1.4. Three immune function assays (proliferative activity of lymphocytes upon mitogen and protein stimulation, production of cytokines, and phagocytic activity and respiratory burst of leukocytes) not included in the OECD Test Guideline 408 for single substances were performed in the course of the two 90-day rat feeding trials with the GM maize NK603. The GM maize NK603 did not affect the immune functions tested in both studies. Many of the measured variables had a low precision and, therefore, only very large differences can be detected with 80% power. Taken together, the above-mentioned analyses did not increase the scientific value of the 90- day rat feeding trials."

There are other reassuring data:
https://link.springer.com/content/pdf/10.1007%2Fs00204-016-1798-4.pdf

GMO Mon810 is totally safe in rats.

You can also read a commentary:
https://pubs.acs.org/doi/pdf/10.1021/acs.jafc.7b03686
or
http://www.grace-fp7.eu/en/content/final-results-and-recommendations-eu-research-project-grace

dimanche 3 juin 2018

Are you afraid of red meat?

The fallacy of a Relative Risk of cancer with red meat consumption is very well shown by this meta-analysis. 10% only after 90g/day. 10% for a very complex food which is not the same all over the planet and whose cooking is also very different is not an actual risk. More there is no increased risk with the amount of meat consumed except for the threshold of 90g/d.

Tiny increased risk after 90g/day

No clear effect of the amount of red meat consumed

Do you cook your bone broth?

https://ketodietapp.com/Blog/lchf/Keto-Bone-Broth

samedi 2 juin 2018

A frequent question of CKD patients about the best diet

October 01, 2013

RENAL NUTRITION UPDATE

High Fat, Low Carb Diet Beneficial for CKD Patients

Share this content:

In a study, higher intake of processed meats led to a nearly 70% increase in CVD mortality.

For years, dietary recommendations have focused on reducing saturated fat and its potential sources. This advice includes a focus to reduce red meat and other high-fat meat products because of their higher saturated fat content.

Recent analyses have begun to find no significant associations between fresh meat intake and cardiovascular events.

Instead, confounding factors appear to be more indicative of cardiovascular risk. The European Prospective Investigation into Cancer (EPIC) found no significant increased risk associated with unprocessed meat or poultry intake, whereas increased intake of processed meat led to a nearly 70% increase in cardiovascular disease (CVD) mortality (BMC Med 2013; published online ahead of print).

A large meta-analysis in 2010 also demonstrated that risk of coronary heart disease (CHD) was not associated with unprocessed meats, but instead processed meats increased risk by 42% (Circulation 2010;121:2271-2283). Another meta-analysis found that saturated fat sources did not always consistently increase mortality risk; processed and unprocessed meats analyzed together increased risk while high-fat dairy products were not associated (Am J Public Health2013;103:e31-e42).

Together, these analyses beg the question of whether processed meat has been a confounding variable in the analysis of meat and saturated fat intake on CVD.

Analyzing LDLs

Chronic kidney disease (CKD) populations are at increased risk for CVD mortality. Typical recommendations for reduced saturated fat intake often are derived from cholesterol-lowering strategies and the fact that saturated fat is associated with increases in total cholesterol, LDL, and HDL. LDL particle size, however, is becoming a more appreciated risk factor for CHD and mortality, more notably in CKD populations.

In a prospective cohort of hemodialysis (HD) patients, researchers found that conventional lipid profiles did not predict mortality, whereas smaller, high-density LDL particles were associated with a 55% increase in mortality risk (Clin J Am Soc Nephrol 2011;6:2861-2870).

Carbohydrate intake and LDL particle size

LDL particle size is influenced by carbohydrate intake. Higher carbohydrate intake increases the release of triglyceride-rich, very low density lipoproteins (VLDL) and increased serum triglycerides (Curr Opin Clin Nutr Metab Care 2012;15:381-385). Small, dense LDL particles are released in response to sequester triglycerides.

These processes typically occur in the presence of insulin resistance. High insulin resistance in the form of diabetes is a known risk factor for renal impairment. Low-carbohydrate, high-protein diets have been shown to reduce triglyceride values as well as decrease LDL, HDL, insulin, free fatty acids, CRP, and glucose in obese women (Am J Clin Nutr 2005;81:1298-1306).

If unprocessed meats are not associated with cardiovascular risks and high-carbohydrate diets alter LDL particles to potentially increase atherogenicity, it would appear that a controlled intervention focusing on a low-carbohydrate diet and unprocessed meats would be necessary in CKD and dialysis populations.

A few studies have indicated that low-carbohydrate, high-protein diets appear to be similarly effective as high-carbohydrate, low-fat diets with regard to improving estimated glomerular filtration rate (eGFR) and microalbumin-to-creatinine ratio (Diabetes Care 2013;36:2225-2232) as well as reductions in serum creatinine and creatinine clearance (Clin J Am Soc Nephrol2012;7:1103-1111).

In the latter study, the low-fat group was required to also undergo caloric restriction, whereas the low-carbohydrate group ate ad libitum fat and protein while slowly increasing carbohydrate intake after a baseline of 20 g/day. Comparing a calorically restricted diet to an ad libitum diet, however, skews the ability to specifically compare the effects of altering macronutrient ratios.

A similar issue confounds the next study. Macronutrient ratios were altered in non-diabetic obese individuals with one risk factor for metabolic syndrome (J Am Diet Assoc 2010;110:633-638). The low-carbohydrate group ate a diet consisting of 4% carbohydrate, 35% protein, and 61% fat, while the high-carbohydrate group consumed 46% carbohydrate, 24% protein, and 30% fat. Both groups also followed a caloric restriction that averaged 1,613 kcal (low-carbohydrate group) and 1,525 (high-carbohydrate group).

Weight loss was similar between groups after one year, and no significant changes were found between groups with regard to creatinine or eGFR. Of note, the average baseline eGFR of each group was 97.4 and 91.8 mL/min/1.73 m2, respectively.

This study helps elucidate whether a higher-protein diet affects eGFR in patients with values greater than 60. The study's high-carbohydrate group was actually lower in carbohydrate percentage than many typical recommendations that promote carbohydrate intakes of 50%-60%. Some larger studies have failed to give useful insights due to minor variations in macronutrient ratios (Diabetologia 2012;55:905-914).

High protein diets and late stage CKD

These studies appear to indicate that high-protein diets do not appear to negatively impact renal function in patients below CKD III-V. Reduced protein intake is known to be beneficial in advanced CKD populations in reducing the effect of uremic toxins (Blood Purif 2013;35:22-25).

Thus, it would beneficial to assess the effect of a low carbohydrate, moderate protein, high fat diet in stages CKD III-V. In healthy individuals without CKD, a 12-week intervention that kept carbohydrate at a static 37% but adjusted protein and fat in the groups found that no significant changes occurred with regard to blood lipids, weight loss, or glucose and insulin responses (Am J Clin Nutr 2005;81:762-772).

In men, there was a reduction in serum creatinine in the higher fat, standard protein group.

From the October 2013 Issue of Renal And Urology News »

vendredi 1 juin 2018

Paleodiet from Loren Cordain

PALEO START UP BREAKFAST

No need to get out of bed early to prepare this hearty Paleo breakfast. From start to finish, this nutrient-packed meal takes less than 10 minutes. Feed your whole family by increasing the ingredient amounts and you are all off to a healthy start to the day!

2 Omega-3 eggs1 tsp avocado oil1 green onion, thinly sliced1 small baby bell pepper, stem and seeds removed and thinly sliced½ cup sliced mushrooms½ tsp salt free Italian herb spice mix1 handful fresh spinach leaves, stems removed½ fresh avocado, thinly sliced

Goose, cane (female duck), hen.

Scramble eggs in small bowl and set aside. In a small fry pan, heat olive oil on low to medium heat. Add onions and bell pepper to the pan and cook for 2-3 minutes, stirring every 30 seconds. Add mushrooms and sprinkle evenly with the spice mix. Continue cooking until mushrooms are softened. Throw in spinach leaves and continue stirring until all ingredients are well mixed and spinach is cooked about 2 minutes. Add scrambled eggs and stir together until eggs are done to your liking. Pair with a side of fresh fruit for a complete Paleo meal. Serves 1.

Thank you, Loren!

https://thepaleodiet.com/a-day-of-paleo-eating/?inf_contact_key=5181cb88b9a07b7b7d7d2283d71600644b491bfba92f04a3ecc143952eb4aa51

Another recipe