Your Genes Can Control Your Cholesterol Levels

Genetic mutations can effect the production or function of lipoproteins, which transport and store cholesterol. This mutation is called FH, which occurs when there is a mutation in one of your chromosomes for the LDL receptor , which plays an important role in balancing cholesterol levels. Homozygous FH occurs when both parents pass down the gene to the offspring and it leads to very high levels of LDL (low density lipoprotein), which leads to increased cholesterol levels in the blood, blocked arteries, and cholesterol skin deposits. This also occurs early in life, even during childhood, and it is difficult to treat. Treatment can include filtering to blood to remove the LDL particles, known as LDL apheresis. Heterozygous FH is when only one parent passes down the mutated gene and it still leads to elevated LDL levels, high cholesterol, and cholesterol deposits under their skin or on their Achille's tendon, but it does not occur early in life like Homozygous FH. Heterozygous FH is usually detected after the patient's first coronary event such as a heart attack, but it is easier to treat than Homozygous FH and treatment usually consists of oral medication. If one parent is heterozygous and the other parent does not have the mutation at all, all of their children will have a 50% chance of getting the mutation. Meanwhile if One parent is homozygous and the other does not have the mutation, all of their children will have a 100% chance of getting the mutation. Therefore, this mutation is a dominant trait because you only need one allele to express it. 

https://www.healthline.com/health/high-cholesterol/genetics-of-inherited-high-cholesterol#key-tips-to-manage-risk 

Gene Found to be Associated with Common Cause of Blindness

CFH is red, FHL-1 protein is green

        About 50 million people are affected by Age-related Macular Degeneration (AMD). The victims of this condition are thought to be genetically predisposed. Complement factor H (CFH) is found to be one of the most important genes involved in the risk for AMD. CFH encodes for a protein called factor H (FH); factor H protects our eyes from attack by our complement system, which is apart of our immune system. FH prevents the complement system from causing damage by sticking to tissues in sufficient quantities.
        Scientists from the Faculty of Medical and Human Sciences, at The University of Manchester, have excluded protein factor H from being the main regulator of immunity in the back of the eye. They have discovered that factor H-like protein 1 (FHL-1), which is made from the same CFH gene is the main regulator of immunity. Dr Simon Clark, a Medical Research Council Career Development Fellow, led the research and had a lot to say about the results.
        "FHL-1 is a smaller version of FH, in fact it is about a third of the size. However, it has all the necessary components to regulate the immune system and is still subject to the genetic alterations that affect AMD risk. Our research has shown that the FHL-1, because it is smaller than FH, can get into structures of the back of the eye which cannot be reached by the larger FH. Therefore, this research suggests that it is FHL-1 rather than FH which protects the back of the eye from immune attack and that insufficient FHL-1 in the back of the eye may result in inflammation that eventually results in vision loss from AMD. FHL-1, although similar to FH in many ways, does not have a totally unique 'tail' structure at its end. This tail seems to mediate how FHL-1 binds tissue. As such, this work has identified a new target for therapeutics aimed at readdressing immune imbalance in the eye, thereby preventing or slowing down AMD," says Dr. Clark.
        I believe just as Dr. Clark said, this can open new doors for treatments involving imbalances in the eye. New information, targets, and ideas are always a step forward in the medical field. I know nothing about Age-related Macular Degeneration, but since it is the major cause of blindness in the western world, preventing or slowing down AMD will help out many people. 

Main Article: http://www.sciencedaily.com/releases/2014/11/141114085839.htm
Related Article: https://www.nei.nih.gov/news/statements/genes_amd