Hereditary Fuctose Intolerance Research Paper

• Mutations in the ALDOB gene reduce the function of the enzyme, impairing the ability to metabolize fructose.

High-fructose corn syrup is a commonly used artificial sweetener in foods. High-fructose corn syrup is a hydrolyzed version of ordinary corn syrup, which is produced via a steeping process. It is so widely used because it is both economically favorable and it helps to preserve food for extended periods of time. However, the drawbacks of high-fructose corn syrup include issues like potential obesity, diabetes, loss of liver function, malnutrition, and cancer. The fact that the producers of high-fructose corn syrup can deceive people that HFCS is harmless makes matters worse.

However sugar has been linked to some of these problems too but I personally avoid H.F.C.S. at all costs, but not necessarily sugar.

Fructose was considered to be beneficial to diabetics because it is absorbed only forty percent

In correlation with weight gain, HFCS significantly increases the rate of type II diabetes in the United States. Diabetes occurs when there is an insufficient amount of insulin to transport glucose to body cells to be used as fuel. As a result of this, the cells starve, causing the degeneration of tissues and organs. HFCS increases the likelihood of diabetes because the obesity caused by HFCS consumption vastly contributes to the inability of

"The overall prevalence of the lactase non-persistence genotype CC-13910 (170 cases) was 18.1%, with a lower prevalence in the sample from the western region (16.8%) than in the eastern region (18.9%)," (Enattah, 2002). When comparing the overall number from that study for lactose intolerance, which was 18.1%, to the frequency from our pooled data, which was about 25%, it is easy that our data might be skewed. One highly possible reason for this is that because the many people that attend the University of Iowa are of European descent. Another study found "Expression of high levels of lactase in adulthood was considered by people of European descent to be the 'normal' state of affairs," (Ingram et al, 2008). Perhaps if we were in a different part of the United States or even simply at a different university, our results would be either closer to or farther from the results that the Enattah study

We all know that High Fructose Corn Syrup is in our food but we don’t know what it truly is and its hidden health risks it carries. High Fructose Corn Syrup is mad of two main things: fructose and glucose. Fructose is a sugar that is found in many fruits and vegetables, and glucose is a sugar that helps our bodies retain energy. Fructose is a tough energy source for the body to use due to it has to be processed through the liver. “It is also more lipogenic, or fat-producing,

"Crystalline fructose" is an especially deadly form of HFCS. It has a significantly higher percentage of fructose in addition to dangerous chemicals like arsenic and chlorine and metals such as lead. Almost all processed foods contain high fructose corn syrup or some version of it. You will find it in soft drinks and fruit juice. But it is also in breakfast cereals, mayonnaise, peanut butter and jellies, ketchup, yogurt, cookies, candy, mustard, canned soup, potato chips, pancake syrup, beer, and the list goes

Familial Dysautonmia is passed on through genetics. It is very rare because it is a recessive gene. Both parents will have to have a mutilation for a child to get Familial Dysautonmia. Some people may have the mutated gene, but not show symptoms of Familial Dysautonmia. It is from a mutation in the IKBKAP gene. Think of genes

The biochemical basis of this disease is related to the metabolism of fat. It is caused by an abnormality in the ABCD1 gene located on the X chromosome. This prevents the production of ALDP which functions as a

The National Institute of Health (2014) listed the most common form of familial hyperinsulinism to be an autosomal recessive genetic defect that is common among the Ashkenazi Jewish population. This condition affects 1 in 66 carriers who are Ashkenazi Jews since they have reported consanguineous marriages (NIH, 2014). Among Ashkenazi Jews, two single ABCC8 mutations account for 90 percent of cases of familiar hyperinsulinism (Mazor-Aronovitch, et al, 2007). The incidence of FHI in individuals of northern European descendants is approximately 1:30,000 live births. The incidence is increased in genetically isolated populations with a high prevalence of consanguinity (UpToDate.com).

hereditary disorder of Caucasians in the United States and is the most common cause of chronic

Although cells require sugar for energy, it is glucose the cells prefer as a source. However, much of the excess sugar consumed today is fructose. Excess fructose consumption has similar effects on the liver as excessive alcohol intake, as the liver metabolizes alcohol the same way as sugar and converting the carbohydrate into fat (Brandis, Lustig, & Schmidt, 2012). High concentrations of fructose is rare in nature and is typically found along side fiber. However, in the American diet, the fiber is

Primary and congenital lactose intolerance can be explained by the underlying genetic and epigenetics concept. The production of intestinal lactase is coded for by the LCT gene. In primary lactose intolerance, individuals are born with sufficient lactase, which is essential in utilising lactose found in breast milk. Over time, there is a change in dietary patterns, resulting in lower use of the intestinal lactase. As such, transcription of the LCT gene is down-regulated, giving symptoms in of adult-type hypolactasia, or lactose intolerance.

The lipoprotein gene mutation has a penetrance of greater than 90% (Henderson et al., 2016). Heterozygosity takes place when an individual has two dissimilar alleles of a gene. A single dominant gene can manifest itself in a heterozygous person particularly when there is high penetrance property. This is the reason why multiple generation can be affected by the FH disorder as seen in the proband and family members of the followed case discussion. Monogenic FH is largely attributed to mutations in the LDL-receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase, subtilisin/kexin-type 9 [PCSK9] genes (Brautbar et al.,