I have listened to Dr Robert Lustig in his viral YouTube video entitled, “Sugar: The Bitter Truth.” The video is a lecture describing how High Fructose Corn Syrup (and Fructose) are often responsible for the entire metabolic syndrome, namely obesity, fatty liver, insulin resistance, diabetes, leptin resistance, high triglycerides, inflammation, vascular disease, and high blood pressure (hypertension).

The following outline and biochemical analysis only deals with one particular metabolic pathway and process of fructolysis in the liver, which leads to the release of uric acid as a waste product, ultimately resulting in hypertension.  The uric acid causes hypertension by blocking the enzyme in blood vessels known as endothelial nitric oxide synthase, which, if not blocked, would ordinarily create nitric oxide (NO) – a vascular dilator (vasodilator).  The following outline and analysis is derived from Dr. Lustig’s video and a few other technical sources.

HOW DOES FRUCTOSE CAUSE HYPERTENSION?

• Sucrose (table sugar) is ½ Glucose and ½ Fructose. We should instead use Dextrose (Glucose) instead of table sugar because glucose is easier to metabolize, and is basically the staff of life.
• Sugar Soft Drinks and many processed foods contain a lot of high fructose corn syrup (because it’s cheaper to make and it’s sweeter than dextrose).
• Only the liver can metabolize Fructose
• Fructose is foreign to your body – a poison
• Fructose comes in through the transport Glut5 (rather than Glut2). GLUT5 is a fructose transporter expressed on the apical border of enterocytes in the small intestine. GLUT5 allows for fructose to be transported from the intestinal lumen into the enterocyte by facilitated diffusion due to fructose’s high concentration in the intestinal lumen.
• No insulin is stimulated because Fructose does not stimulate insulin
• Fructose gets metabolized (in the liver) by fructokinase to form Fructose-1-P (Fructose 1-phosphate). How? Fructokinase, also known as D-fructokinase, specifically catalyzes the transfer of a phosphate group from ATP (i.e. adenosine triphosphate, the substrate) to fructose as the initial step in its utilization, and in the process ATP gives up one phosphate to become ADP (because the phosphate has to come from somewhere). The reaction equation is as follows: ATP + D-fructokinase = ADP + D-fructose-1-phosphate. Note that ADP is adenosine diphosphate.
• Fructose involves phosphorolating 3-times the calories as compared to glucose (dextrose). It is a volume problem in the liver.
• There is a scavenger enzyme in your liver called AMP deaminase-1 which “rescues” the phosphates (off the rest of the ATP molecule) that takes ADP down to AMP and eventually to IMP and finally to the waste product Uric Acid. In other words, Adenosine monophosphate deaminase is an enzyme that converts adenosine monophosphate (AMP) to inosine monophosphate (IMP), freeing an ammonia molecule in the process.
• Uric Acid causes gout and hypertension.
• Uric Acid causes hypertension by blocking the enzyme in your blood vessels known as endothelial nitric oxide synthase and this enzyme, if not blocked, creates nitric oxide (NO) which is our endogenous blood pressure lowerer (i.e. “NO” keeps your blood pressure low).
• Endothelial NOS is a nitric oxide synthase that generates nitric oxide (NO) in blood vessels and is involved with regulating vascular tone by inhibiting smooth muscle contraction and platelet aggregation.
• Nitric oxide is also known as nitrogen monoxide (chemical formula “NO”). NO is an important cellular signaling molecule involved in many physiological and pathological processes. It is a powerful vasodilator with a short half-life of a few seconds in the blood.
• We have a hypertension epidemic caused by fructose-sweetened beverages increasing uric acid.
• As a proof, in a study, the drug Allopurinol (which is used to treat gout by lowering the uric acid) also lowers blood pressure in obese adolescents having essential hypertension.

Keep looking for the next analysis concerning how Fructose is also converted to and stored as fat in the liver and on our waistlines.  This process is known as de novo lipogenesis.  In other words, sugar (Fructose) is converted to fat (and stored as glycogen).  Fructose is also converted to the small very dense LDL cholesterol known as v-LDL.  LDL is the so-called “bad” cholesterol, and v-LDL is the type of LDL that is actually bad.  This v-LDL is the pattern “B” LDL identifiable in a VAP test (advanced lipid panel).  This dense LDL is supposed to be closely correlated with arteriosclerosis and atherosclerosis (thickening and hardening of the arteries) possibly leading to coronary heart disease (CHD).  The v-LDL together with hypertension (high blood pressure) seems to be a very bad combination for our coronary arteries.