From The Desk Of Clarence Bass

“Compared with metabolically healthy normal-weight individuals, obese persons are at increased risk for adverse long-term outcomes even in the absence of metabolic abnormalities,
 suggesting that there is no healthy pattern of increased weight.”                                               Kramer et al, Annals of Internal Medicine, December 3, 2013

“Body fat is just an inert layer of blubber, right? If Only. New research shows that it’s a toxic parasite that doesn’t want to let go. The good news: if you exercise and eat right, you can force it to.”
                                                                                  Bill Gifford, Outside Magazine, March 2013

Healthy Obesity a Pipe Dream

Fat Cells Tell the Tale

Fat Fights Muscle

In 2005, I wrote an article titled “Fit But Fat Risky.” The bottom line was that being physically fit doesn’t cancel out the risk of being overweight. If you want to reduce the risk of dying before your time, it’s best to be lean and fit. No amount of exercise can overcome the hazards of being overweight or obese. While that’s still true, researchers have uncovered many more important details. As usual it’s complex—fascinating and empowering.

A new meta-analysis of eight well-designed studies by Caroline K. Kramer, MD, PhD, and colleagues followed 61,386 persons for ten or more years to tease out the links between body fat, health, and mortality/cardiovascular events.

The primary aim of the analysis was to compare the effect of metabolic status—blood pressure, cholesterol, blood sugar—on normal weight, overweight, and obese persons. Metabolically healthy-normal-weight individuals were the reference group; the risk in each of the other groups was compared to the risk in this group. That group, as expected, had the lowest risk.

The most thought-provoking finding was that the metabolically healthy obese group was at increased risk—but only after 10 years. The researchers had to follow this group for at least 10 years to find increased risk. Like a slow boat to China, obesity takes a long time to deliver its toxic load.

 Metabolically healthy overweight persons had a risk similar to the reference group, but were still not out of the woods. Their risk appeared to be gaining more weight and becoming obese.

The trend may be the most significant finding. The researchers found that metabolic problems went up in sync with body fat. Be that as it may, normal body weight isn’t necessarily an all-clear sign. The researchers found that metabolically unhealthy normal weight people are just as likely to have a stroke or heart attack as those who are obese and metabolically unhealthy. That’s a surprise because obesity and metabolic dysfunction have long been considered the most dangerous combination.

It’s important to consider both body weight and metabolic status. “Metabolically healthy obese individuals are at increased risk for death and cardiovascular events over the long term compared with metabolically healthy normal-weight persons, suggesting that increased body mass is not a benign condition even in the absence of metabolic abnormalities,” Kramer and colleagues concluded. “In addition, all metabolically unhealthy individuals (normal weight, overweight, obese) had increased risk for events compared with metabolically healthy normal-weight individuals.”

“[It appears that] there is no healthy pattern of increased weight,” Kramer et al wrote in summary.

Fat Cells Tell the Tale

A chiropractic student told us a few days ago that he was determined not to be fat. He’d seen the harm fat can do. While dissecting cadavers, he’d observed that the fat bodies are very different than lean ones. Reinforcing his concern, a New York Times piece by Anahad O’Connor (October 9, 2013) took an in-depth look at the difference between healthy and unhealthy fat cells. O'Connor's account helps to explain how obesity eventually took its toll on the metabolically healthy obese subjects in the Kramer study. Unhealthy fat cells look and act differently than healthy fat cells. The difference is clearly visible under a microscope.

A study in the journal Diabetologia found that metabolically unhealthy obese persons have impaired mitochondria (cellular components that convert food into energy), along with a reduced ability to generate new fat cells. Instead of making new cells to store more fat, the original fat cells in unhealthy obese people swell to their breaking point, straining the cellular machinery, generating inflammation, and causing fat to accumulate where it doesn’t belong, such as the liver, heart, and skeletal muscle. Heart disease and high blood pressure often result. A fatty liver frequently leads to insulin resistance and Type 2 diabetes.  

The fat cells in healthy obese people, on the other hand, are smaller and make new fat cells when needed. The new fat cells usually reside in the padding under the skin, where the harm is mostly cosmetic.

“The metabolically healthy obese individuals are in the minority,” Dr. Jussi Naukkarinen, a research specialist at the University of Helsinki who took part in the new study, told the New York Times. “Most people tend to go along the not so healthy lines.”

Dr. Naukkarinen and his colleagues have studied pairs of identical twins in which one twin is obese and the other is not. In one study, Naukkarinen et al divided 16 pairs into two groups. In both, the average weight difference between twins was about 40 pounds. But in one group, the obese sibling had high blood pressure, undesirable cholesterol levels, and unhealthy measures of blood sugar and insulin production, as well as seven times the amount of fat in their liver. In the other group, the obese twins’ blood work and liver fat was similar to that of the lean twin. So we have healthy obese twins matched against unhealthy obese twins. It seems that genetics is not the controlling factor.

The fat cells of the unhealthy obese twins were larger—and fewer—than those of the other group. They were swollen and riddled with inflammation. Their mitochondria were also malfunctioning.

Properly functioning mitochondria stimulate the creation of new fat cells, which explains why the unhealthy obese twins had fewer fat cells.

So we have a clear difference between healthy and unhealthy fat cells. What can be done about it remains an open question. Dr. Naukkarinen suspects that alcohol consumption and exposure to high glycemic foods that create spikes in blood glucose and insulin levels, like sugar and white flour, may play a role. So healthy eating is clearly a viable avenue of attack.

Poorly functioning mitochondria in the metabolically unhealthy twins suggests that exercise may also be an important factor. Both strength and endurance exercise create healthy mitochondria; see my book Take Charge.

For a look at the role of exercise we’ll turn to a comprehensive and enlightening article by Bill Gifford in the March 2013 Outside Magazine: “Your Fat Has a Brain.”

Gifford calls fat a “toxic parasite that doesn’t want to let go” and exercise and eating right the way “you can force it to.” His main focus is on exercise. Authoritative support is provided throughout the piece. A feature story, it’s long. We’ll summarize the main points and let you refer to the magazine online for more detail and references.  

Fat Fights Muscle

Gifford built his article around Phil Bruno, a 47-year-old, six-three man who stopped working out in his mid-twenties. Bruno gorged his way to 470 pounds and had the metabolic profile to prove it. His blood pressure was 230 over 150 and his A1C—an important marker for diabetes—was 16, when the upper limit of normal is 6. After prescribing numerous medications, including Lipitor for sky-high cholesterol, his doctor held out little hope: “Bruno, you should drop dead any second.”

Fat has traditionally been thought of as evolution’s unsightly way of storing energy for leaner times that almost never come in today's world. That has changed. “Starting in the 1990s,” Gifford observed, “scientists began to realize that fat is best understood as a single huge endocrine gland, one that wields powerful influence over the rest of the body.” For the majority of Americans, he added, fat tissue has become their biggest organ.  (The endocrine system is a large group of glands and other structures that exert powerful effects throughout the body.)

As indicated above, healthy fat is mostly under the skin, while unhealthy fat builds up in the midsection, infiltrating vital organs, bathing them in a “nasty chemical stew” that causes heart disease, diabetes and other major problems. Visceral fat also appears to accelerate the aging process. Removing abdominal fat from obese rats has been found to extend their life span.

Exercise was the only feasible option for Phil Bruno, Gifford concluded. Liposuction was not an option, because it only removes the protective subcutaneous fat. (It works best for people who really don’t need it.)  And visceral fat can’t be safely removed because it is so deeply intertwined with blood vessels and vital organs. “So Bruno called on the only thing in his body that was powerful enough to fight [fat] off: muscle.”

In June of 2004, about a month after his dooms-day diagnosis, “Bruno did the one thing his doctor hadn’t prescribed.” He joined his local Gold’s Gym. His doctor suggested he lose weight, but stopped short of recommending exercise.

After looking around the gym, Phil decided the only piece of equipment suitable for a 470-pound man was an exercise bike. He lasted only five minutes on the first go, but was soon able to manage 30 minutes. A few weeks later, with encouragement from a helpful female instructor, he joined a class. He soon became a regular, spinning six times a week. He was finally making a serious effort to change the course of his life.

Without knowing it, Phil had kicked off a war for control of his body, with fat on one side and muscle on the other. Like fat, muscle was once considered a passive organ; it simply moved the body around. “But muscle is now known to be one of the most dynamic systems in the body,” Gifford related. “When it contracts, it undergoes huge changes at the cellular level. And its mortal enemy is fat.” (See my article Muscle Talk: http://www.cbass.com/MuscleTalk.htm )

In sedentary people, including those who aren’t heavy, fat invades all parts of the body. “Pools of fat, which occur in both the liver and the muscles, block a key step in the conversion of glucose,” a prominent diabetes researcher told Gifford, “leading to the insulin resistance that’s a prerequisite for diabetes.”

More fat means less muscle, which means fewer mitochondria, which are most plentiful in muscle tissue. The majority of fat contains almost no mitochondria. “This explains one of the nagging problems with obesity,” Gifford wrote; “the more fat you accumulate, the harder it becomes for your body to burn off that stored energy.”

The muscle Bruno built cycling created more mitochondria and enabled him to burn off more fat. The new muscle also changed his body chemistry, making it a better and healthier fat fighter. A prominent example is Interleukin-6 (IL-6). When produced by visceral fat, IL-6 causes chronic inflammation. But when released during exercise it promotes fat burning and controls inflammation. (Again, see my article Muscle Talk: http://www.cbass.com/MuscleTalk.htm)

Overeating is a notoriously difficult habit to break, especially if you’re already fat. The reason, Gifford explained, is a hormone produced by fat tissue called leptin. “Ordinarily, leptin tells the brain, ‘Dude, we’re fat. It’s time to stop eating.’ But the brain of obese people often become deaf to leptin, so they don’t get the message.”

Exercise helps restore sensitivity to leptin. While it wasn’t easy, exercise helped Phil Bruno cut out fried food, fast food, and soda. He and his wife started eating more sensibly. As he kept exercising, Bruno found that he not only lost weight but also felt less hungry.

A year after Bruno was diagnosed with Type 2 diabetes, he surprised his doctor. His insulin resistance was gone; his A1C was down to 5.5. “[His] doctor had never seen anyone do that,” Gifford wrote. “Bruno no longer needed his medications.”

He kept spinning, got certified, and “became one of the most popular instructors at that branch of Gold’s Gym,” Gifford reported.

In four years, he had lost more than 200 pounds, getting down to 260. “He kept moving, kept riding, knowing he could never stop,” Gifford wrote.

And then tragedy struck. “His legs suddenly gave out. He couldn’t stand; they were pretty much paralyzed.”

An MRI revealed pinched nerves from inflammation at the base of his spinal cord. A short time later, he had another setback—atrial fibrillation, probably related to the enlarged heart he’d acquired from all those years when he was heavy. “Ironically, a-fib is also known to be a side effect of long-term, intense exercise, particularly in middle-aged (or older) men,” Gifford added. (A-fib or atrial fibrillation is heart beat irregularity characterized by disorganized electrical activity.)

Gifford closed by telling readers that Phil was on medication to regularize his heart beat and back to spinning at a lower level.

Bruno parting words: “The bright spot in all this craziness is that my working out over the years has saved my life.”

***

With a more balanced and varied exercise regimen—and more rest—Phil Bruno’s story may have had a happier ending.

Phil's laser-beam focus on spinning left half of his body unused and untrained. A more varied approach would have put all of his muscles to work and allowed more opportunity for recovery. For example, the push-pull arm action of the Schwinn Airdyne would have spread the stress to his upper body.  Rowing would’ve strengthened his back. And the Concept 2 Ski Erg would have stressed his body from yet another angle. There are many other options which would have rotated the stress around his body, encouraging recovery and putting all of his muscles to work against the huge fat burden engulfing his body.

A once-a-week strength training program—four or five multi-joint movements—would have put more focus on his fast-twitch muscle fibers, insuring that his entire body was growing stronger and better able to fight the war on fat.

More rest days—minimum three—walking or just moving around—would have allowed his body to recover fully and grow stronger, making the entire routine more effective.

It would, of course, take time to add all of these elements. Spinning was a good place to start—walking is probably uncomfortable for someone Phil’s size—but it became counter-productive over time.

Bill Gifford nailed a major problem with his aside that a-fib is known to be a side effect of long-term exercise. That’s especially true of long term endurance exercise. The streakers who never miss a day of training are especially at risk.

Hans R. Larsen, Editor of THE AFIB REPORT, has written that long-term endurance training profoundly affects the body’s physiology. Among other things it significantly reduces heart rate and testosterone. Vigorous, long-term endurance exercise has also been associated with increased inflammation.

Phil Bruno’s relentless spinning, including the added pressure of becoming an instructor, was a likely cause of his a-fib—and his leg paralysis. (Recall that Phil’s leg paralysis was attributed to an inflamed lower back.)

Decades of being grossly overweight was undoubtedly a contributing factor--heart and back. Excess weight compressed his low spine.

The Wall Street Journal recently ran an article titled "One Running Shoe in the Grave." The focus of the article was an editorial in the British journal Heart. The editorial discusses two new studies. One involving 52,600 people followed for three decades found that the runners in the group had a 19% lower death rate than non-runners, but those who ran a lot--more than 20 to 25 miles a week--lost that mortality advantage. Another large study found no mortality advantage for those who ran faster than 8 miles an hour, while those who ran slower reaped significant mortality benefits. "Running too fast, too far and for too many years may speed one's progress toward the finish line of life," the editorial concluded.

Too much of good thing for too long can become a harmful, even deadly, pursuit.

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