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.
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.
Dysnutrition: une vision globale et évolutionniste de la nutrition humaine
A global and evolutionary approach of human diet
D'un point de vue évolutionniste l'alimentation des humains a connu depuis 100 ans des transformations inconnues pendant les millions d'années qui ont précédé notre ère. Ces transformations résultent de l'industrialisation et de l'utilisation de végétaux et d'animaux non sauvages profondément transformés pour en faire des produits alimentaires. Un grand nombre de ces produits ne sont adaptés ni à notre physiologie ni à notre génomique et produisent des pathologies chroniques même s'ils permettent un apport calorique stable voire excessif pour les pays industrialisés et émergents. Toute la problématique est là. Analyser comment ces transformations bouleversent nos régulations cérébrales et générales et entraînent l'obésité, le diabète, la majorité des cancers, l'athérome et les démences chez certains d'entre nous.