Browsing by Subject "cholesterol"

In general the amount of fat in cow’s milk, what consists mostly of fatty acids, is about 4%, and more than half of the milk fatty acids are saturated. Dairy fat, due to its saturated fat and cholesterol content, is related to the risk of cardiovascular disease. Moreover, energy from fat can also be related to obesity. These relations also concern cow’s milk, however, its fat content remains around 4% and besides fat, there are a lot of positive effects on health, as milk is a good source of some vitamins and minerals. Milk consumption in Finland per capita has been the largest in the world for many years. There is also a market for milk substitutes, i.e. non-dairy drinks, produced mostly from oat, soy, and almond. This master’s thesis focuses on cow’s milk fat content and its relations to human health, especially the cardiovascular health and obesity. According to the hypothesis, consumer attitude towards cow’s milk is strongly affected by assumptions associated with the impact of dairy fat on health as well as the impact of dairy industry on climate change. The aim of this research was to study how detrimental or beneficial the dairy fat in milk is for human health on the basis of cow’s milk chemical composition, health related reports by authorities, research findings, historical perspectives, and consumer preferences. According to the literature, the chemical composition and nutrients properties of whole milk show that more nutrients of health benefit are present in comparison than of detrimental compounds. Most of present evidence suggest that milk and dairy products have neutral or beneficial effect on human cardiovascular health alhtough it is generally recognized in dietary recommendations that saturated fat is a risk factor for cardiovascular disease. The experimental part investigated Finnish consumers attitudes and preferences regarding milk consumption and overall preferences and issues affecting attitude toward food choice. It appears that the study hypothesis partly refuted, as the majority of participants were not much affected by assumptions associated with the impact of dairy fat on health. However, the impact of dairy industry on climate change was a very important issue related to attitude and preference regarding milk consumption. The majority of the study participants made their choice of drinking milk on the basis of taste, and the impact on health was considered mainly as beneficial rather than detrimental.

Familial combined hyperlipidemia (FCH) is a complex and common familial dyslipidemia characterized by elevated total cholesterol and/or triglyceride levels with over five-fold risk of coronary heart disease. The genetic architecture and contribution of rare Mendelian and common variants to FCH susceptibility is unknown. In 53 Finnish FCH families, we genotyped and imputed nine million variants in 715 family members with DNA available. We studied the enrichment of variants previously implicated with monogenic dyslipidemias and/or lipid levels in the general population by comparing allele frequencies between the FCH families and population samples. We also constructed weighted polygenic scores using 212 lipid-associated SNPs and estimated the relative contributions of Mendelian variants and polygenic scores to the risk of FCH in the families. We identified, across the whole allele frequency spectrum, an enrichment of variants known to elevate, and a deficiency of variants known to lower LDL-C and/or TG levels among both probands and FCH affecteds. The score based on TG associated SNPs was particularly high among affected individuals compared to non-affected family members. Out of 234 FCH affecteds across the families, seven (3 %) carried Mendelian variants and 83 (35 %) showed high accumulation of either known LDL-C or TG elevating variants by having either polygenic score over the 90th percentile in the population. There was large between-family variation in how much the polygenic scores contributed to the FCH phenotype. FCH is highly polygenic, supporting the hypothesis that variants across the whole allele frequency spectrum contribute to this complex familial trait. This reinforces the clinical tenet that FCH is a cluster of overlapping genetic defects instead of an etiologically homogenous disease entity.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide and the major cause for them is atherosclerosis. Atherosclerosis is a state of chronic inflammation of the arterial wall, which slowly progresses to form plaques that can eventually obstruct blood flow. The resulting hypoxia in the tissues affected by the ischemia manifests as clinical symptoms such as chest pain. All this begins with chronically high LDL-C concentrations in the blood. LDL-C is transported into the intima of the arterial wall where it is modified with for example oxidizing enzymes. Intimal macrophages remove oxidized LDL via phagocytosis, which leads to lipid accumulation that turns macrophages into foam cells. At first, foam cells die via apoptosis as they are removed by other macrophages. At some point, macrophages cannot remove all the apoptotic material, which leads to a necrotic release of the cell contents. This creates a necrotic core in the center of the atherosclerotic plaque. The inflammatory environment makes vascular smooth muscle cells proliferate and form a fibrous cap to protect the prothrombotic necrotic core. Eventually the plaque can rupture, which leads to the formation of a thrombus and possibly even thrombosis. To prevent this, drugs including statins, ezetimibe and PCSK9 inhibitors are widely used along with certain dietary modifications. More options for diagnosing, preventing, and treating atherosclerosis are still needed to decrease the burden of atherosclerosis and CVDs on both the individual and healthcare systems. A potential example of such methods is presented in this review. This method utilizes synthetic LDL receptors to isolate LDL from the blood, which is needed for determining the quality of LDL particles. The knowledge of LDL quality helps predict the individual risk for developing atherosclerosis.