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A large portion of the world's population has lactose intolerance. Fundamentally, this condition occurs when the small intestine does not produce enough of the lactase enzyme, which digests the disaccharide lactose in milk. Lactose avoiders might unconsciously decide to limit or exclude milk and dairy products from their diets. This group includes people with lactose intolerance, people with an allergy to milk protein, vegans, and those expressing personal preferences. Lactose avoiders are often self-reported as being milk intolerant. In this review, specific amounts of lactose in different types of milk and milk products are presented. The amounts of micro- and macronutrients in them are compared with the daily requirements established by accepted sources. Foods are suggested that can play vital roles in permanently avoiding lactose-containing dairy products, for example, brussels sprouts, as a good source of vitamin B1; kale, as a source of vitamin K; and cereals at breakfast for vitamin B6. Attention is paid to mature cheeses as they are extremely beneficial for health due to their rich vitamin and elemental compositions, and they are also suitable for people with lactose intolerance due to their low lactose content. This information is rarely provided on packaging. In addition, the current state of labeling for the presence of lactose in food and pharmaceutical products is discussed. The term "hidden lactose" is introduced to include added lactose in unexpected foods, drinks, and even medicines. [ABSTRACT FROM AUTHOR]

The majority (about 70%) of the world's population suffers from lactose intolerance. Lactose intolerance leads to long-term discomfort when consuming milk and dairy products, and hence, to their avoidance. Consequently, the intake of important nutrients is reduced, which potentially has a negative impact on the overall health. Knowing the condition – lactose intolerance – will prevent people from unnecessarily restricting dairy products in their diets. In this study, lactose synthesis and catabolism in the human body are presented, also the types of lactose intolerance, as well as the methods of diagnosing this condition, are discussed. Special attention is paid to the genetic causes of this discomfort and to the tests that can be performed. Solutions for the treatment of lactose intolerance have also been proposed, both up-to-date and easily applicable, as well as future developments. This review highlights the lactose pathway – from the mammary gland production to recipient gut hydrolysis. Lactose intolerance associated SNPs known so far are presented and discussed. Advice for people with lactose intolerance is presented in the form of possible treatments and healthy feeding behaviors. [ABSTRACT FROM AUTHOR]

Introduction: Hepatitis C Virus (HCV) relies on host lipids for its life cycle contributing to lipid abnormalities and hepatic steatosis. Disease progression is influenced by viral factors interacting with host immune and metabolic pathways. The significance of serum lipids for Chronic Hepatitis C (CHC) assessment is not clearly established yet. Aim: Our aim was to investigate serum lipids' association with stage of liver fibrosis, steatosis and genotypes in patients with CHC. Materials and Methods: A total of 112 CHC patients (54 male, 58 female, aged 48.6±13.7 years) were studied - 98 genotype 1 (G1) and 14 genotype 3 (G3). Liver cirrhosis (F4) was diagnosed in 31 cases. Steatosis was present in 75 of all patients on ultrasound. Liver biopsy was done in 65 patients and histology showed steatosis in 28, stages of fibrosis (F1-F3) in 56 and F4 in 9 patients (METAVIR). Laboratory panel included complete blood count, liver tests and serum lipid levels (mmol/l) with Friedewald equation estimations. Indirect noninvasive fibrosis scores FIB-4, Aspartate aminotransferase to Platelet Ratio Index (APRI) and Forns index were calculated. HCV RNA was quantified by RT-PCR. Statistical analysis included Spearman's rho, Mann-Whitney U test, Receiver Operating Characteristic (ROC) curve. Results: Total Cholesterol (TCh) (p=0.002) and Low-Density Lipoprotein (LDL) (p=0.003) in G1 patients were higher when steatosis was present. TCh (p<0.001), High-Density Lipoprotein (HDL) (p=0.018) and LDL (p=0.003) were lower in G1 F4 compared with F1-F3 patients. Triglyceride (TG) levels correlated with FIB-4 (r=0.364, p=0.029), APRI (r=0.333, p=0.047) and Forns index (r=0.423, p=0.010) in G1 patients without steatosis. TG to LDL ratio (TG/LDL) (p=0.001) was higher in F4 than in F1-F3 patients. TG/LDL ratio predicted the presence of F4 in G1 patients without steatosis by an area under the ROC curve 0.900 (p<0.001). TG/LDL ratio > 0.52 was highly specific for F4 without steatosis. Specificity dropped to 76% when steatosis was present. TG/LDL < 0.32 negatively predicted liver cirrhosis. HCV RNA correlated with TG levels (r=0.330, p=0.009) in G1 patients with steatosis and with histological percent of fatty hepatocytes (r=0.585, p=0.028) in G3 patients. Conclusion: Lipid levels in CHC G1 patients depend on the presence of steatosis and cirrhosis. HCV RNA is associated with TG levels in G1 patients with steatosis, but not in G3 patients. In cirrhotic CHC G1 patients cholesterol is low with relatively increased TG. TG/LDL ratio is a potential marker of liver cirrhosis in CHC G1 patients. [ABSTRACT FROM AUTHOR]