the-psoriasis-treatment

What are the specific reasons for hypoglycemia seen in hereditary fructose intolerance? Hereditary fructose intolerance (HFI) an autosomal recessive disorder in which there is subnormal activity of the enzyme fructose 1-phosphate aldolase B (1;2). Largely found in the liver, the enzyme is needed for normal fructose metabolism for splitting fructose 1-phosphate to form dihydroacetone and glyceraldehyde (1). Hypoglycemia after consumption of fructose (also sucrose or sorbitol) results because of the lack of maintenance of proper blood glucose levels by the liver (2). The fructose ingestion and the lack of aldolase B results in the accummulation of fructose 1-phosphate in cells, particularly in the liver (1). The accumulation leads to depletion of Pi, which in turn keeps mitochondria in hepatocytes from producing ATP causing cell damage, and inhibition of glycogenolysis and, thus, guconeogenesis (1;2). HFI often goes unrecognized and is life-threatening due to hypoglycemia along with poss

NIACIN FOR HIGH CHOLESTEROL The recommended daily intake for niacin, or vitamin B3, is only 14 mg for women and 16 mg for men with a tolerable upper intake level of 35mg (1). Nutrition professionals should also be aware that niacin, as nicotinic acid (not nicotinamide), has also been used in much larger doses—up to 6 g per day—for decades as a treatment for hyperlipidemia (1). Note that nicotinic acid is available as a dietary supplement. Use as a Drug High-dose niacin, in fact, was the first-ever lipid-modifying drug treatment. It helps increase HDL cholesterol while lowering total serum cholesterol, triglycerides and LDL cholesterol (2). After initial discovery in the 1950s and research in the ‘70s, it was found that niacin helped prevent myocardial infarction and reduced risk of death from myocardial infarction when used in doses of 3 g daily (2;3). The mechanism of high-dose nicotinic acid is broad and unique. It inhibits lipolysis in adipose tissue decreasing free fatty plasma le

B-complex supplement products are popular commodities, often marketed for "stress" or "energy." Is there scientific justification for these claims? Why should anyone choose a B-complex supplement as opposed to either broader multivitamin-mineral supplements or narrower single B-vitamin supplements? You might remember in the early ‘90s when a neuropathy epidemic broke out in Cuba among unsuspecting tobacco growers. They complained of burning sensations in their feet, pain in their arms and legs, frequent urination, blurred vision, weight loss, sensitivity to sunlight, and, well, lots of stress and fatigue (1). After assessing their diets it was discovered they were deficient in B complex vitamins and the amount of alcohol they drank daily contributed to loss of the little Bs they had (1). The tobacco growers may have not known that B vitamins play essential roles in the health of their bodies relating to energy metabolism and stress, but let’s be sure we do. Energy

Vitamin E refers to eight compounds (vitamers: tocopherols and tocotrienols) and is found in both plants and animal foods (1). The most studied natural source of vitamin E is alpha-tocopherol because of its prevention of lipoprotein oxidation and inhibition of platelet aggregation, which suggests prevention of cardiovascular disease (1). Alpha-tocopherol is the only one with biological activity and offers the most protection against oxidative stress through its oxygen-quenching capacity (2). The natural and most active form is designated by its steroisomer RRR alpha-tocopherol and continues to be found on supplement labels as d-alpha tocopherol (2). Beta-tocopherol also exhibits oxygen-quenching capacity albeit not as much as alpha-tocopherol and its abilities are followed by gamma- and delta-tocopherol (2). The tocotrienols may not exhibit significant antioxidant role, but have another role in which they reduce plasma cholesterol concentration (2). A recently discovered natural form o

Could it be that when Bugs Bunny chose his special diet of carrots because he knew that the discovery of vitamin A in 1915 found it was an essential growth factor in animals (1)? Maybe he knew that vitamin A kept his skin healthy under all that fur (1). Or, more likely, that vitamin A kept his eyes healthy for seeing underground (1). Bugs can also celebrate that his enjoyment of carrots might keep him from later having to say, “What’s up doc?” This is because clinical evidence has led the U.S. Food and Drug Administration to approve a cancer health claim for a low-fat diet rich in fruits and vegetables when it includes vitamin A (1). Vitamin A’s benefits are all appealing to humans too. But while vitamin A deficiency is not common in developed countries, a few are deficient not being regular eaters of foods high in vitamin A like carrots, sardines or liver (1). How much should you get? What kind of vitamin A should you be getting? And, how do you know when you should supplement? Clinic

Which will keep the doctor way? The orange contains about 10 times more vitamin C, which is an essential antioxidant for many complex roles in the human body (1). On the other hand, the apple contains quercetin, which has been shown to have a higher antioxidant capacity than vitamin C, thus, potentially offering better protect against free radicals (2;3). Clearly these antioxidants are not equal. Free radicals are atoms or molecules that have one or more unpaired electrons. These are mainly result of the mitochondria leaking electrons that bind to oxygen; however, there are a variety of other free radicals from exposure to smog, ozone, drugs, and drugs (1). Because “oxidative stress” is thought to be associated with many diseases including cancer, antioxidant nutrients are frequently evaluated for ability to neutralize free radicals, particularly the oxygen-centered radicals: superoxide, hydroxyl and peroxyl radicals (1). While antioxidants help decrease neutralize free radicals, they

Micelles are made up of amphipathic compounds such as bile acids, fatty acids and monoacylglycerols that interact leaving a relatively stable hydrophilic surface and hydrophobic interior (1). They form at certain temperature ranges when a mixture of lipids is present in concentrated amounts (1). Fatty acid and phospholipid micelles are spherical, but pure bile acid micelles are sandwich-shaped rectangles (1p1062). During lipid digestion after hydrolysis of triacylglycerols by lipases, it’s up to the bile acid sandwiches to solubilize the spheres, thereby forming “mixed” micelles that appear not unlike rods (1p1062). These rods become longer as more lipids (including limited cholesterol) are solubilized (1p1062). The bile acid micelles form at concentrations of 2-5 mM and at pH values above pK, meaning in equilibrium with other micelles in solution (1p1061-2). From the lumen, the micelles then transfer the lipids to the mucosal surface for absorption by diffusion (1p1063). Lipid-soluble

When studying the evolution timeline that led to modern biochemistry, one can always turn to studying protein architecture. Proteins have been called “molecular fossils” that serve to mark milestones in the “history of life” (1). There is a wide diversity of proteolytic enzymes in humans and the network of enzymes have a grand complexity that calls for investigation of how they were shaped over time (2). In digestion there is a variety of proteolytic enzymes—pepsins, enteropeptidases, carboxypeptidases, and aminopeptidases (3). Each work to hydrolyse proteins by cleaving off amino acids from differing peptide bonds, in different stages and conditions (gastric, pancreatic and intestinal phases) and at varied pH ranges (3). The system is indeed complex, not exactly perfect (a better system may have used only a one or two enzymes), but it works and that's evolution. Each highly structured enzyme would have evolved accordingly at some time, and some, which may have had major roles in t

Unlike most other mammals, humans and other primates don't synthesize vitamin C because we lack the enzyme glunolactone oxidase (1). The enzyme was lost long ago without affecting our survival due to frequent intake of high-vitamin C fruits and vegetables. Thus, we must continue to get vitamin C from our diet by the same manner (fruits or veggies) or otherwise, lest we succumb to scurvy as British sailors did in the early 1800s before they adopted rationing limes on naval vessels (1). Vitamin C deficiency leading to scurvy is now rare (1) and in the developed world, but studies on North American and European populations have found that many people who do not eat enough fruits and high-vitamin C vegetables continue to have inadequate levels of vitamin C (2;3). Supplementation or dietary change would serve the majority of these patients because—when taken along with other vitamins—vitamin C may lead to reduced risk of chronic diseases such as cancer, cardiovascular disease and catar

Carrageenans are food additives derived from red seaweed such as Chondrus crispus (Irish moss) and other species and are used as a thickening, stabilizing, and texturizing agents in foods and also for reduced-fat meat products (1;2). They nicely replace animal-based gelatin found in many foods such as soymilk, chocolate milk, yogurts, beers and wines. Lamda-carrageenan, for example, is used to provide a creamy texture to dairy products. The polymers are high-molecular-weight polysaccharides made up of repeating disaccharide units have a charged nature and their structure gives them their highly reactive properties (2). Concentration and greater molecular weight increases viscosity further (2). Safety of use of carrageenans in foods has been a matter of controversy and confusion. Leading manufacturers of carrageenan such as FMC corporation have maintained that the use of carrageenan has a centuries-old history of safety in humans that has been confirmed by studies on animals such as dog

GLUT6 is expressed in various tissues in the body, but doesn't encode any functional glucose transport protein (1). Why does it occur at all? It's thought that GLUT6’s nucleotide sequence may have simply occurred from an insertion of GLUT3 reverse transcribed in a region of an untranslated gene (1). Reference List 1. Kayano T, Burant CF, Fukumoto H et al. Human facilitative glucose transporters. Isolation, functional characterization, and gene localization of cDNAs encoding an isoform (GLUT5) expressed in small intestine, kidney, muscle, and adipose tissue and an unusual glucose transporter pseudogene-like sequence (GLUT6). J Biol Chem 1990;265:13276-82.

A currently unpredictable outcome of radiotherapy on lung cancer patients is radiation pneumonitis (lung inflammation). This study was the first performed on humans to determine how antioxidant response may be used to predict this “potentially lethal treatment-related complication”. The oxidative stress link had been established through studies on irradiated mice. Type of study: Observational study on humans; physicians grading for pneumonitis were blinded to antioxidant data Method used to conduct study: Fifteen total lung cancer patients were found eligible for the study after signing informed consents, having stage III disease, receiving concurrent definitive radiotherapy and paclitaxel-based chemotherapy, and having good performance status. Excluded were patients who had received radiotherapy or chemotherapy previously and those with unfavorable Eastern Cooperative Oncology Group performance status or chronic obstructive pulmonary disease. Blood samples were collected at baseline a