Juvenon Health Journal – March 2013, No. 3
In last month’s Juvenon Health Journal, we discussed a recent study conducted by the Harvard School of Public Health that identified the top preventable risk factors for premature mortality. Smoking tops Harvard’s list of preventable risk factors with high blood pressure and obesity closely following.
The Harvard study revealed that obesity accounts for about 216,000 premature deaths in America each year. Additionally, the Centers for Disease Control and Prevention (CDC) report just over a third of U.S. adults are obese and forecasts that by 2030, this may grow to 42 percent. What’s more, Duke University researchers concluded that the already obese are getting fatter. If the trend continues, severe obesity will double by 2030, when 11 percent of adults will be nearly 100 pounds overweight, or more.
Equally troubling is the fact that being overweight increases one’s risk of diabetes, heart disease and many other ailments. According to CDC studies, obesity-related problems account for at least 9 percent of the nation’s yearly health spending, or $150 billion a year. Indeed these are sobering statistics and a multimillion industry has been based upon obesity and its causes and cures.
Mitochondria – Turning on the Cellular Powerhouse
However, researchers are now exploring the notion that some clues to obesity may be found at the cellular level, in the mitochondria. But before we get into the nitty gritty of the research, let’s review the role of the mitochondria, the powerhouse of the cell. The mitochondria are located throughout the body. Like a furnace uses fuel and oxygen to generate heat, nutrients and oxygen enter the mitochondria where energy is generated. Approximately 95% of the energy needed by muscles and organs is generated locally by the mitochondria. However, when the mitochondria are not functioning properly, the food and oxygen can’t be used properly and virtually all of your bodily systems are compromised.
Is Obesity Caused by Impaired Mitochondrial Function?
A growing body of research is demonstrating that altered mitochondrial energy production, particularly in skeletal muscles, is a major anomaly capable of setting off a chain of metabolic events leading to obesity.
The fact that mitochondrial defects can be accumulated over time and as a normal part of aging explains why a person can eat all sorts of foods and remain a normal weight while he or she is young. However, when middle-age approaches, as often as not, so will the middle-age spread.
When a meal of fats and carbohydrates is eaten, both substances are broken down and absorbed by the cells. Although both macronutrients are available to be converted into energy, when carbohydrate is present, the mitochondria will favor the carbohydrate. When free fatty acids are present, but carbohydrates are in short supply, the mitochondria will normally switch over to using fatty acids for fuel. This is called metabolic flexibility.
Evidence supports that obese individuals have a depressed ability to oxidize free fatty acids for use as energy in skeletal muscle. It further appears that defects in the mitochondria of skeletal muscle are responsible for this impaired lipid oxidation, which causes the person to store body fat for fuel instead of burning it.
The Battle of Fatty Acid Oxidation
There are several possible reasons why obese people may have a harder time oxidizing fatty acids than they should:
- They have fewer mitochondria.
- They have smaller mitochondria.
- Their mitochondria have structural problems that are visible by electron microscopy, and some of their mitochondria may even have degenerated completely.
- Their mitochondria have reduced oxidative activity.
Mitochondrial dysfunction may be a plausible explanation for some forms of obesity. If mitochondria fail to oxidize fatty acids, both ingested and de-novo synthesized fatty acids will be preferentially routed to and will tend to remain in storage. Studies show that weight loss by itself does not improve fatty acid oxidation in mitochondria and this explains why it is so easy to regain weight on a diet that is fairly high in carbohydrate.
How Mitochondrial Biogenesis Can Help Fight The Battle of the Bulge
Improving mitochondria through regeneration (mitochondrial biogenesis) might be a way to permanently avoid or reverse obesity. Recent technological advances like genetic microarray chips and sophisticated microscopes have allowed researchers to identify the molecules in the body that support growth/regeneration of healthy mitochondria. The primary molecule in the body that stimulates growth of mitochondria and is activated by exercise is now believed to be PGC-1alpha, also called “The Exercise Molecule.”
Transient scarcity of cellular energy is a “triggering stressor” that induces the growth of new healthy mitochondria through the PGC-1alpha pathway. Exercise creates a short-term energy shortage that triggers mitochondrial renewal. Temporary fasting or caloric restriction also triggers mitochondrial renewal. A low carbohydrate diet, which removes the “easy calories” from the diet, is also a “stressor” that triggers mitochondria renewal.
In contrast, easy living with limited exercise and excess calories, especially carbohydrates, discourages mitochondrial renewal. The Exercise Molecule PGC-1alpha activates the growth of new mitochondria so that even older people can have youthfulness – strong muscles, endurance, brain power, memory – and obese people can have the fat metabolism they had when they were younger.
How to Grow New Mitochondria
- Regular exercise stimulates PGC-1alpha and the growth of new healthy mitochondria over time.
- Transient caloric restriction may also stimulate PGC-1alpha and the generation of new healthy mitochondria over time.
- Low carbohydrate diets have been shown to stimulate PGC-1alpha and thus, mitochondrial growth.
- It is also possible to supplement with nutrients that activate and elevate PGC-1alpha, to promote mitochondrial growth of new mitochondria and to help recharge mitochondria and activity.
Once the mitochondria are somewhat restored, it is important to take advantage of their renewed state to reduce excess fat. Because carbohydrate will always be metabolized first, it makes sense to decrease the availability of this substrate to the mitochondria. Meals should be low in carbohydrate, moderate in protein and relatively high in fat, to keep the mitochondria in fat oxidation mode as much as possible. Snacks should be avoided because each time carbohydrate is consumed, it moves to the front of the line in the mitochondrial queue.
A recent study by Juvenon founder, Dr. Tory Hagen (see abstract link below), showed (in rats) that supplementation with acetyl-L-carnitine (ALCAR) can reverse the age-related decline in fatty acid transport into mitochondria. This was most likely because the ALCAR stimulated PGC-1alpha and mitochondrial renewal. Acetyl-L-carnitine supplementation also reversed the age-related decline in carnitine palmitoyltransferase 1 (CPT1) activity in interfibrillar mitochondria without changing the L-carnitine content in the rat heart. CPT1 is important because it helps regulate the oxidation of fat into energy in the mitochondria.
Mitochondrial regeneration offers some hope in the battle to fend off and possibly reverse obesity, one of the top preventable risk factors for premature mortality. In the coming months, the Juvenon Health Journal will continue to explore other preventable causes of death cited in the Harvard study. By offering effective, all-natural supplements and health news you can use, Juvenon provides an essential toolkit to battle these aging enemies.
Read abstract here