Juvenon Health Journal Vol. 5 No. 1, January 2006
By Benjamin V. Treadwell, Ph.D.
As the graphic (right) indicates, carbohydrates can be converted to fat, but not vice versa. A net synthesis of carbohydrates from fat cannot occur in our body. This is important. It implies that certain carbohydrates can be more dangerous to our health than fat! However, too much of either food type is detrimental to our health, and too much of both types can result in an even more serious assault on our health. We explain below.
Why is obesity associated with type 2 diabetes?
Diabetes is characterized by a high level of glucose (sugar) in our blood. Normally, the insulin-producing cells of the pancreas (beta cells) recognize high blood-glucose and respond by secreting insulin. A glucose-sensing protein (glucose transporter 2) attaches to the beta cell surface and signals to the cell’s interior that glucose is in the blood. This signal flips a chemical switch in the cell that activates machinery involved in insulin production. The newly manufactured insulin is subsequently secreted from the beta cell into the blood stream and delivered to our muscle, fat, and liver cells, where it binds to the membranes of these cells and opens a door, allowing glucose to enter.
A recent study demonstrates, in mice, that a high-fat diet impairs the cell’s ability to attach the glucose transporter to the beta cell’s outer surface. The fat, through some mechanism, inhibits an enzyme involved in attaching specific recognition molecules to the glucose-sensing protein. Thus, the protein fails to be secured to the beta cell, which relies on this sensor protein to monitor blood glucose. In this way, the cell loses its ability to recognize glucose in the blood. Blood-glucose levels rise and remain high, causing a pre-diabetic condition, known as Syndrome X. Sustained or chronic high blood-glucose eventually results in full-blown type 2 diabetes.
Why does the pyramid now recommend fewer simple carbohydrates if fat is so bad for our health?
Simple carbohydrates, especially those with a high glycemic index (candy, soda, junk food), are rapidly converted to simple sugars such as glucose, and transported in the bloodstream. If the pancreas is functioning normally, it produces and secretes insulin into the bloodstream, which in turn activates muscle, fat and liver cells to take in glucose from the blood. This is a positive effect as it lowers blood-glucose, and prevents it from reaching toxic levels.
If the cells of the body are in an energy deficit, they will quickly utilize this fuel and convert it to energy. However, if our energy storage tank is already full (the obese state), as a result of over consumption of fuel, the excess glucose spills over into the fat-producing pathway, converts to fat, and is stored in fat cells. So guess what? Now we have two bad things happening to our body. First, we have an excess of blood-glucose, and second, now our cells are converting this excess fuel, in the form of glucose, to fat. If this condition is chronic, it eventually results in numerous bloated fat cells, the hallmark of obesity. (As described above, high body fat impairs the production of insulin, thus interfering with the removal of the blood-borne glucose we put into our bodies with a high-carbohydrate diet.) The eventual consequence is full-blown type 2 diabetes. There are two toxic effects, one from high glucose, or glycotoxicity, and the other from high fat (lipid), or lipotoxicity. These toxic effects result in the characteristic symptoms of diabetes, which include hypertension, insulin insensitivity, increased thirst, and atherosclerosis (coronary heart disease or hardening and/or thickening of the arteries).
The healthy life-style: Keep your fat reserves low by utilizing them for energy on a regular basis.
Use of fat for energy is healthy if the fat used is stored fat. Our bodies, even lean bodies, have fat reserves, and these should be regularly tapped for energy. The evidence supporting this statement is obvious: the lean are healthier. Now research is unraveling the complex story behind fat-promoted disease. For example, it has been demonstrated that people on restricted caloric diets (1,500 to 1,700 kcal/day) have lower blood pressure, lower cholesterol, lower insulin levels, and lower blood glucose. Animal studies have shown those on restricted diets live longer and have fewer age-associated diseases, including cancer. The metabolic property shared by these animals is increased production of energy from fat stores relative to non-diet restricted animals (controls). In effect, they are keeping their fat stores at a minimal level; they have fewer bloated fat cells.
In addition to improving the health of the beta cell, low fat stores also help keep inflammation at a low level. Since it is now known that high fat content increases fat-associated inflammatory cells, and inflammation is associated with numerous disease states, it is not surprising that low body-fat produces a wide range of health benefits.
The biochemical equation for maximum health is: Energy taken in (food) should equal energy utilized for work. A diet low in saturated fat and low in the bad type of carbohydrates will help keep the left side of the equation in check. You can address the right side, and help prevent the accumulation of bloated fat cells, by increasing energy expenditure. Diet and exercise together can keep blood glucose levels in check, and help ward off Syndrome X and type 2 diabetes.
To increase understanding of how a high-fat diet leads to type 2 diabetes, a 2005 study induced diabetes in laboratory mice through chronic ingestion of a high-fat diet. Researchers then isolated the mechanism that impedes production of the insulin needed to ward off type 2 diabetes. To read the peer-reviewed article on this study and see its color photographs, click here.
“Dietary and Genetic Control of Glucose Transporter 2 Glycosylation Promotes Insulin Secretion in Suppressing Diabetes”
Cell, Vol 123, 1307-1321, 29 December 2005.
This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.
I’ve read that nitric oxide (NO) is hard on cells. You wrote in last month’s issue that Juvenon increases NO. How can that be helpful?
J.A.F., via email
NO can sometimes be harmful, especially if produced by an enzyme known as iNOS (inducible nitric oxide synthase). This enzyme is activated during inflammation and in fact promotes inflammation by activating another enzyme, COX 2, which is involved in synthesis of an inflammatory substance known as prostaglandin E2.
Exercise and high levels of HDL promote the synthesis of the good enzyme involved in NO synthesis, namely eNOS (endothelial nitric oxide synthase). This enzyme helps promote vascular relaxation and is associated with the cells that line the walls of vessels. In contrast, iNOS is associated with inflammatory cells and is stimulated by much different environmental factors, such as smoking, infection and inflammatory carcinogens.
So whether NO is good or bad depends on its source of production (endothelial cells or inflammatory cells) and on environmental factors.
Benjamin V. Treadwell, Ph.D. is former associate professor at Harvard Medical School.