la caseine, le gluten
Sébastien a écrit:Franck a écrit:L'excès ("excès" est variable selon les individus...) de viandes et de certaines légumineuses (riches en purines) peut provoquer des crises de gouttes et des calculs rénaux.
Tu peux avancer quelques études allant dans ce sens?
Ca m'intéresserait de les lire car je n'ai encore jamais vu qu'une sur-alimentation de prots conduisait à des calculs rénaux.Franck a écrit:Les protéines d'origine animales sont acidifiantes car contiennent beaucoup d'acides aminés riches en soufre (méthionine...) qui seront métabolisés en acide sulphurique, si bien que le corps pour éviter de s'acidifier (faire tampon) va taper dans dans les réserves calciques du corps, avec à la longue risque d'ostéoporose.
Seignalet tenait le même discours mais ce n'est que des suppositions.
As-tu des études allant dans ce sens?Franck a écrit:Par contre comme je l'ai dit plus haut pour faire tampon le corps va taper dans nos réserves de calcium, ce dernier sera excréter, par la suite pouvant contribuer à la formation de calculs rénaux et à l'ostéoporose.
La fuite de calcium occasionne un dépouillement de l'os mais je ne vois pas trop ce que vient faire les calculs rénaux là -dedans?
Tu peux m'expliquer ?Franck a écrit:Les épinards sont riches en acides oxaliques pouvant chez les sujet susceptibles provoquer des crises de gouttes, calculs rénaux...mais en général les apports nutritionnels sont suffisamment bas pour que cela soit sans incidence sur la santé.
L'acide oxalique est particulièrement déconseillé pour les gens qui ont la goutte et le foie fragile mais que vient faire, à nouveau, les calculs rénaux là -dedans ?!
A high ratio of dietary animal to vegetable protein increases the rate of bone loss and the risk of fracture in postmenopausal women. Study of Osteoporotic Fractures Research Group.
Sellmeyer DE, Stone KL, Sebastian A, Cummings SR.
Division of Endocrinology, the General Clinical Research Center, and the Department of Epidemiology and Biostatistics, University of California, San Francisco, USA. dsellmeyer@psg.ucsf.edu
BACKGROUND: Different sources of dietary protein may have different effects on bone metabolism. Animal foods provide predominantly acid precursors, whereas protein in vegetable foods is accompanied by base precursors not found in animal foods. Imbalance between dietary acid and base precursors leads to a chronic net dietary acid load that may have adverse consequences on bone. OBJECTIVE: We wanted to test the hypothesis that a high dietary ratio of animal to vegetable foods, quantified by protein content, increases bone loss and the risk of fracture. DESIGN: This was a prospective cohort study with a mean (+/-SD) of 7.0+/-1.5 y of follow-up of 1035 community-dwelling white women aged >65 y. Protein intake was measured by using a food-frequency questionnaire and bone mineral density was measured by dual-energy X-ray absorptiometry. RESULTS: Bone mineral density was not significantly associated with the ratio of animal to vegetable protein intake. Women with a high ratio had a higher rate of bone loss at the femoral neck than did those with a low ratio (P = 0.02) and a greater risk of hip fracture (relative risk = 3.7, P = 0.04). These associations were unaffected by adjustment for age, weight, estrogen use, tobacco use, exercise, total calcium intake, and total protein intake. CONCLUSIONS: Elderly women with a high dietary ratio of animal to vegetable protein intake have more rapid femoral neck bone loss and a greater risk of hip fracture than do those with a low ratio. This suggests that an increase in vegetable protein intake and a decrease in animal protein intake may decrease bone loss and the risk of hip fracture. This possibility should be confirmed in other prospective studies and tested in a randomized trial.
Kidney stone disease.
Coe FL, Evan A, Worcester E.
Renal Section, University of Chicago, Chicago, Illinois 60637, USA. f-coe@uchicago.edu
About 5% of American women and 12% of men will develop a kidney stone at some time in their life, and prevalence has been rising in both sexes. Approximately 80% of stones are composed of calcium oxalate (CaOx) and calcium phosphate (CaP); 10% of struvite (magnesium ammonium phosphate produced during infection with bacteria that possess the enzyme urease), 9% of uric acid (UA); and the remaining 1% are composed of cystine or ammonium acid urate or are diagnosed as drug-related stones. Stones ultimately arise because of an unwanted phase change of these substances from liquid to solid state. Here we focus on the mechanisms of pathogenesis involved in CaOx, CaP, UA, and cystine stone formation, including recent developments in our understanding of related changes in human kidney tissue and of underlying genetic causes, in addition to current therapeutics.
Publication Types:
* Review
PMID: 16200192 [PubMed - indexed for MEDLINE]
L'étude complèteUrine oxalate concentration affects CaOx SS exactly as does urine calcium concentration (68); therefore, any conditions that increase oxalate absorption from food or lead to increased oxalate production can cause CaOx stone formation.
Dietary hyperoxaluria in idiopathic CaOx SFs. Whereas the 95th percentiles for urinary oxalate excretion for females and males are 45 mg/d and 55 mg/d, respectively, and the corresponding 70th percentiles are 31 mg/d and 41 mg/d (12), values up to approximately 80 mg/d are common among idiopathic CaOx SFs and are often unexplained by a systemic cause (69). A low-calcium diet that reduces CaOx crystallization in the gut lumen, thereby facilitating oxalate ion absorption, is easily identified and corrected (70). High protein or oxalate intake are other causes of this condition (71, 72). Oxalate absorption from food may depend upon gastrointestinal transporters (73, 74), and genetic variations in oxalate transporting proteins in red blood cells have been linked to CaOx stone formation (73).
Enteric hyperoxaluria. If colon is present and receiving small bowel effluent, fat malabsorption of any cause (e.g., small bowel disease, resection or bypass, or exocrine pancreatic insufficiency) results in increased colon oxalate absorption and urine oxalate excretion in the range of 80–140 mg/d (69). Undigested fatty acids promote colon oxalate absorption (75). Diarrheal fluid losses and low urine pH and citrate levels resulting from stool bicarbonate losses increase urine CaOx SS and UA SS; stones usually contain 1 or both of these phases (69).
Among patients with enteric hyperoxaluria resulting from small bowel bypass for the treatment of obesity (19), some terminal CDs are plugged with apatite crystals (Figure 3) and show epithelial cell death and surrounding interstitial inflammation. How the apatite plugs form remains unknown; possibly high oxalate concentrations in tubule fluid injure epithelial cells and disturb pH regulation so that lumen pH increases. Plugging and consequent nephron damage may account for renal function loss in such patients and may benefit from urine dilution.
Treatment involves high fluid intake and reducing dietary oxalate and fat intake to the extent that nutritional requirement guidelines permit. Calcium supplements (500–1,000 mg) taken with each meal can bind food oxalate and hinder absorption. Cholestyramine (2–4 g with each meal) binds oxalate and fatty acids and reduces urine oxalate excretion. If stones contain UA, potassium alkali is needed to increase urine pH (76). No formal trials have validated these treatment approaches.
Primary hyperoxaluria. Mutations in 1 of 2 genes — AGXT or GRHPR (77) — leads to oxalate overproduction and urine oxalate excretion rates above 100 mg/d or even 200 mg/d, resulting in PH (Table 2). When gene alterations divert active enzyme into mitochondria, where it cannot function effectively, pyridoxine may reduce urine oxalate concentration by increasing enzyme activity (78). When loss-of-function mutations inactivate enzymes, actively increasing urine volume and perhaps treatment with orthophosphate supplements may be advised (79). In type I PH, renal failure is frequent and presently treated by combined segmental liver and renal transplantation (80). Type II PH, being milder, seldom causes renal failure.
. Extrait tiré de...Stones may develop just because the urine is very concentrated. Not surprisingly, stones are therefore more likely to occur in hot climates. On the other hand, stones can occur because the output of a given chemical waste product is increased. Calcium stones occur when there is too much calcium in the urine. This may happen if there is too much calcium in the diet from milk, cheese or bread. Some people seem to absorb more calcium from the gut and there is nowhere for it to go other than into the urine. Other people may have an overactive parathyroid gland (hyperparathyroidism). This results in calcium being leached out of the bones and again it has nowhere else to go but the urine. More often, no obvious cause can be found. Oxalate stones can occur if there is too much oxalate in the diet (spinach, rhubarb, chocolates and certain nuts). They are more likely to occur in people who have a bowel problem in which fat is not being absorbed properly. Uric acid stones form when there is too much uric acid in the urine. This comes as a direct result of too much uric acid in the blood. This is particularly likely in people who are prone to the condition of gout. Cystine stones are an uncommon problem where the kidneys leak high quantities of a chemical called cystine...
Tiré deI had an oxalate stone. What type of diet should I follow? Do I need to avoid foods high in oxalate?
If you have had a kidney stone that contains oxalate, some evidence (research) suggests that limiting high oxalate foods may help reduce your change of forming another oxalate stone. Foods that are high in oxalate include: peanuts, tea, instant coffee (more than 8 ounces a day), rhubarb, beets, beans, beets, berries (blackberries, raspberries, strawberries, gooseberries, etc.), chocolate, Concord grapes, dark leafy greens, oranges, tofu, sweet potatoes and draft beer. Because the stone contains calcium and oxalate, you may also need to follow the calcium recommendations from the last question. I had an oxalate stone. What type of diet should I follow? Do I need to avoid foods high in oxalate?
Dietary factors and hyperuricaemia.
Schlesinger N.
Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903-0019, USA. schlesna@umdnj.edu
The connection of gout and hyperuricaemia with gluttony, overindulgence in food and alcohol and obesity dates from ancient times. Studies from different parts of the world suggest that the incidence and severity of hyperuricaemia and gout may be increasing. Uric acid (urate) is the end product of purine degradation. Although most uric acid is derived from the metabolism of endogenous purine, eating foods rich in purines contributes to the total pool of uric acid. Sustained hyperuricaemia is a risk factor for acute gouty arthritis, chronic tophaceous gout, renal stones and possibly cardiovascular events and mortality. Before starting lifelong urate-lowering drug therapy, it is important to identify and treat underlying disorders that may be contributing to hyperuricaemia. It is relevant to recognize the strong association of the insulin resistance syndrome (IRS) (abdominal obesity, dyslipidaemia, hypertension, raised serum insulin levels and glucose intolerance) with hyperuricaemia. Consumption of meat, seafood and alcoholic beverages in moderation and attention to food portion size is important. Moderation in the consumption of not only beer but also other forms of alcohol is essential. In the obese, controlled weight management has the potential to lower serum urate in a quantitatively similar way to relatively unpalatable "low purine" diets. Non-fat milk and low-fat yogurt have a variety of health benefits and dairy products may have clinically meaningful antihyperuricaemic effects. In addition, fruits, such as cherries and high intakes of vegetable protein diet may reduce serum urate levels.
Publication Types:
Raphael a écrit:je consomme à la rigueur des prots 3-4 fois par semaines (30 g de prots en plus du mardi au vendredi donc)
j'utilise de l'huile de foie de morue (Carlson, au citron
Raph, se pêter la tête, c'est pas très bon... Non seulement ça déshydrate, ce que les articulations n'aiment pas forcément, mais en plus ça booste les niveau d'oestrogènes
Guen a écrit:J'en ai filé à ma copine en fin de grosesse et début de maternité, c'est pas terrible comme gout qd m^me.
Raphael a écrit:alban sur un autre topic:
"Sur le silicium, ça fait maintenant au moins 1 an, voire plus, que j'utilise un mélange silicium + MSM + glucosamine pour mes pauvres articulations, et l'effet n'est pas placébo. C'est vraiment utile et bénéfique."
tu peux m'en dire plus? perso j'ai bombardé les oméga 3 pas sans grands succès pèour mes genoux, là je prends un autre truc en même temps (reconstituant du cartillage, truc du genre) mais mes vieux genoux craquent toujours autant.
tu as des liens vers les marques de produit que tu utilises? tu as essyé d'âutres trucs qui ont marchés?
Gromit a écrit:Je rajoute à ce que dit alban: a vitamine C qui permet la synthèse du colagène mais aussi les nutriments suivants qui sont souvent négligés et qui interviennent au niveau articulaire et dans la matrice osseuse:
zinc, cuivre, manganèse, bore, magnésium.
Herve Picard a écrit:Enfin quand les articulations sont foutus (cartilage abimé) il n y a plus rien à faire.
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