One of the important aspects of fat is that it is not water-soluble. In order to begin the digestion process, the liver makes bile, which in collected in the gallbladder and is secreted into the small intestine. The bile acts as a detergent. The bile salts in it have a lipophilic side, which binds to the fat droplets, and a hydrophilic side, which suspends the droplets in the watery mixture of the food we have just eaten.

The triglycerides or fats in the suspended droplets cannot be absorbed by the intestine. To accomplish absorption. the pancreas secretes an enzyme called pancreatic lipase into the small intestine, Pancreatic lipase breaks down each triglyceride molecule into two free fatty acids plus a monoglyceride. “Mono” means one, and in this case it means that one of the fatty acids remains attached to the original glycerol backbone. When the triglyceride is broken down into subunits, it is able to pass into the absorptive cells of the intestinal mucosa. After the three subunits have transited the wall of the intestine, the fatty acids are added back to the glycerol backbone and they form a triglyceride once more.

Inside the cells of the intestine, triglycerides are packaged into chylomicrons. Chylomicrons are large diameter (75-1200 nanometer) particles that contain a bit of protein, a bit of cholesterol and lots of triglycerides. The chylomicrons are not secreted directly into the blood but into the lymphatic system. They eventually arrive at the thoracic duct and then are deposited into the blood at the left subclavian vein. Once they enter the blood, they are transported into capillaries and are able to reach the entire body.

One of the proteins in a chylomicron is called apo C-II. This protein has the ability to activate an enzyme called lipoprotein lipase or LPL. Lipoprotein lipase resides on the capillary walls of tissues that have a high requirement for triglycerides, such as cardiac muscle cells, skeletal muscle cells and fat (adipose) cells. The activated lipoprotein lipase acts on the triglyceride molecules (called triacylglycerols in the illustration above) stored inside the chylomicron. It hydrolyzes or breaks down the triglycerides into two fatty acids plus a monoglyceride. Just as we saw in the intestine, intact triglycerides cannot pass through the cell walls, but when they are hydrolyzed into subunits, they can be absorbed into the cells. Once inside, they can be used for energy in the muscle cells or reassembled into triglycerides and stored in the adipose cells.

When we eat a piece of bacon, we start with fat and end with fat (or for the low-carber–energy from the fat). But, as you can see, there are may steps involved in getting from the beginning of the process to the end.

A biracial group of 475 girls was studied first at ages 9-10 years and then at ages 18-19 years. In the first stage of the study, the invesigators determined the body mass index (BMI) of each girl. They also determined a score called the HOMA-IR, or homeostatis model assessment of insulin resistance. Insulin resistance can be measured using an oral glucose tolerance test (OGTT), but this requires several hours and numerous blood draws. In the HOMA-IR, the fasting levels of insulin and glucose are determined, multiplied, and converted into a score that correlates well with the insulin resistance determined by more technically-demanding methods. The girls were divided in two ways: (1) according to whether their BMI put them in the bottom, middle or top third of the group with regard to to relative obesity (2) according to whether their HOMA-IR score put them in the bottom, middle or top third with regard to relative insulin resistance.

Nine years later the girls were assessed for five metabolic syndrome risk factors. These included:
Triglycerides
High-density lipoprotein cholesterol
Systolic/diastolic blood pressure
Waist circumference
Blood glucose
Each risk factor measurement was converted to a z score, which is a way of expressing the relationship of a specific measurement to the population average and the standard deviation of that particular variable. The five z scores were added for each individual. If the total z score was negative, that meant that the individual had a lower risk of metabolic syndrome. (The more negative the total, the better in this instance.) If the total z score was positive, that meant that the individual had a higher risk of metabolic syndrome.

The results were not surprising. The girls who had the lowest BMI and the lowest insulin resistance at ages 9-10 were found to have the lowest risk of metabolic syndrome at ages 18-19. As initial BMI and insulin resistance scores rose, the subsequent scores for risk of metabolic syndrome also rose. The girls who had the highest BMI and the highest insulin resistance at ages 9-10 had the highest risk of metabolic syndrome at ages 18-19. It appears that childhood obesity and insulin resistance interact to produce a higher risk of metabolic syndrome in early adulthood.

Taking it one step farther, the significance of metabolic syndrome in childhood was underlined by a study recently published in the journal Pediatrics, Metabolic Syndrome in Childhood Predicts Adult Cardiovascular Disease 25 Years Later. In this study, the investigators found that the incidence of cardiovascular disease for their 31 patients with pediatric metabolic syndrome was 19.4%, while the incidence was 1.5% for the subjects without metabolic syndrome as children. If these findings are correct, children with metabolic syndrome are significantly more likely than their peers to experience cardiovascular disease twenty five years later as adults.

The obvious question becomes, what happens to these children if intervention takes place between their pre-teen years and their forties? And what would that intervention be? Would it be pharmacological? Would it involve a change in dietary habits? There is a bias at this blog for at least trying a low-carb eating strategy to lower BMI, reduce insulin resistance, avert childhood metabolic syndrome and prevent the progression to adult cardiovascular disease. Whether or not that approach will be tested in the scientific community remains to be seen.

In spite of the increasing incidence of heart disease, the death rate from heart disease is decreasing. According to the figure below, from the New York Times, the one-year heart attack survival rate in Medicare patients went from about 58% in 1986 to just under 70% in 2000. The second graph suggests the reason for this: Medicaid hospital spending doubled during that time period.

Patient survival is good. Increasing Medicare costs is bad. Some people have proposed limits on medical spending as a way to cope with the increased costs. One of these is Tom Daschle, who was recently nominated to be head of the Health and Human Services Department. Mr. Daschle’s sudden withdrawal from that nomination was unexpected, and he had already provided much advice about acting quickly to ensure that health care legislation could be enacted without the debate and delay that had caused the 1994 health care overhaul to be abandoned.

In 2008 Mr. Daschle wrote a book called Critical: What We Can Do About the Health-Care Crisis. In it he advocated many of the provisions that have found their way into the 2009 economic stimulus package. These include moving medical record keeping to an electronic format that will be available to a new federal bureaucracy, the National Coordinator of Health Information Technology. This organization has a mandate to reduce costs and “help guide medical decisions at the time and place of care.”

Mr. Daschle also recommended the creation of another bureaucracy to be modeled the after United Kingdom’s National Institute for Clinical Excellence (NICE). This entity is found in the stimulus package as the Federal Coordinating Council for Comparative Effectiveness Research. It is described in the draft report for the bill as being expected to apply a cost-effectiveness standard to approve or reject treatments using a formula that divides the approximate cost for a treatment by the years the patient is expected to benefit from that treatment. The Council will enforce the standard by evaluating doctors and hospitals based on whether or not they are “meaningful users” of the new system. Translation: as Americans get older, they should expect to receive less medical care.

It is hard to contemplate health care reform built on the principle of denial of care to the elderly. However, Mr. Daschle has said that health care reform will not be pain free. He believes that Americans should be more like Europeans in their ability to accept hopeless diagnoses, to do without experimental treatments and to refrain from expecting too much from the health care system. It may be necessary in such a system to provide health care benefits for younger citizens and then ask citizens to be willing to sacrifice those benefits in their later years.

One hopes that all of this has very little to do with low-carbing. It is still permissible to buy eggs, cheese, meat and fresh vegetables. It is still permissible to avoid refined carbohydrates. As far as the health care system, following a low-carb lifestyle will prevent or lessen the impact of many medical conditions including diabetes, heart disease, gallstones, and dental cavities. And being able to achieve excellent health without resorting to medication and hospitalization is a good thing.