First we grow longer. Then we grow wider. People assume that weight gain is just another unavoidable insult in the aging process. They’re wrong.

Such thinking characterizes many of our notions about “normal” aging. Other casualties in this category include your bone, balance, muscle and marbles. This may hold true in a statistical sense but is not a biological necessity.

The first order of business in any discussion about weight is to correct a fundamental misconception. No one really wants to lose weight. People want to look better, fit into clothing, move more easily, feel more energetic or improve health. These things are not achieved by losing weight.

Body composition, the ratio of muscle to fat, defines all of them. This is not a trifling distinction. In fact, this confusion dooms most attempts at changing both our appearance and our health.

Aging is characterized by changes in body composition. CT studies demonstrate that as we age, subcutaneous fat (below the skin, SF) decreases and visceral fat (in abdominal cavity, VF) increases. VF is the enemy. Because it causes systemic inflammation, it is an independent risk factor for coronary artery disease, stroke and death. If that’s not enough, VF also provides the Buddha-belly mid-life midriff.

The other most common age-related change in body composition is muscle loss. Because muscle has a high metabolic rate, its loss is associated with a reduction in energy expenditure. This decrease in caloric burn lends itself to weight (fat) gain.

Both increased VF and decreased muscle mass are linked to a loss of insulin sensitivity. The lower the insulin sensitivity, the more insulin the body secretes. The compromise of this master metabolic hormone causes a cascade of problems. Insulin is a storage hormone. It therefore activates glucose uptake and fat production while inhibiting the burning of fat and stored glucose (glycogen).

In other words, if you don’t address the loss of muscle and increase in fat that can occur with aging, you’re stuck in a vicious cycle. The good news is that we know how to counteract this downward spiral. In doing so, these techniques not only curb weight gain but prevent much of the pathology people mistakenly associate with normal aging.

Body composition problems, like most contemporary health issues, are almost always caused by lifestyle. By lifestyle we mean the quantity and quality of our eating, sleeping and moving. Recently a third variable has been added to lifestyle analysis. When we eat, sleep and move has been shown to be as important as quantity and quality. Neglect of the timing issue can destroy an otherwise perfect program.

Body Time:

We evolved on a rotating planet that created days divided into light and dark periods. The human day (until recently in our history) consisted of an active (daylight) phase and a resting night (dark) phase.

This resulted in the evolution of a metabolic day shift, so to speak, bearing little resemblance to the night shift. Daytime metabolism excelled at being alert, eating, energy harvesting and storage while nighttime metabolism was designed for sleep, fasting and accessing stored energy for regeneration and repair.

These contrasting functions are synchronized with the 24 hour day by an internal clock. In fact, every cell has a clock. These biological timepieces direct metabolism and physiology by turning on and off thousands of genes, depending on the time of day.

This means that our bodies have a preferred schedule in order to function properly. To assure daily synchrony of biology and behavior our internal clocks must keep good time.

So how are the body clocks set?

The two most powerful regulators of our internal clocks are light and food. Light sets the central body clock in the brain and energy (food) sets the peripheral clocks.

As the sun sets, Melatonin, the body’s expression of darkness, is secreted. Traditionally, melatonin was considered primarily as a sleep cue. It is now recognized as a powerful messenger to switch from active to resting metabolic function, a chemical signal of day’s end. A robust release of this ancient hormone requires unadulterated darkness. Light, whether natural or artificial, blocks melatonin secretion.

Melatonin exerts its effect on weight by modulating the action of several key metabolic hormones such as insulin, ghrelin and leptin. These hormones orchestrate appetite, satiety, calorie uptake and fat storage.

Animals who have had the pineal gland (location of melatonin production) removed become overweight. Timed administration of melatonin reverses the weight gain. In addition, middle-aged fat animals given melatonin and studied to old age showed decreased weight and visceral fat. These changes were eliminated if melatonin was withheld.

Like light, food intake sets the clock to active phase. The nighttime fast, like darkness, sets our clock to resting metabolic mode. Here contemporary culture and biology clash. And so the trouble begins.

Dining after dark is antithetical to our biology. It provides strong signals (both light and food) that the body is in active phase. This signal is not easily extinguished when you go to bed a few hours later.

Disconnection from nature’s clock is now considered an important cause of our struggle with weight gain. By limiting eating to a 10 hour period that coincides as much as possible with daylight, one can lose fat without cutting calories or changing what one eats.

Such Time Restricted Feeding, nature’s darkness diet, synchronizes metabolism and circadian rhythms. This tuning has been shown to decrease inflammation, obesity, diabetes, cardiovascular disease, sleep disorders and depression.

Eating

In addition to when, what you eat is critical. My focus here is the reframing of weight problems as body composition problems. This shifts the goal from weight loss to increasing muscle and decreasing fat. Adequate protein intake is key here.

Mechanistically, muscle atrophy is the result of an imbalance between muscle protein synthesis and muscle protein breakdown. Muscle work and protein consumption both act as powerful stimuli for muscle protein synthesis or anabolism.

Whether 9 or 90, the body maintains its ability to build new muscle throughout life. However, older muscle has a blunted response to anabolic stimuli. You therefore need more protein to stimulate muscle maintenance and growth. In a 75 kilogram (165 pound) individual, about 60grams of protein daily. (.8g/kg)

As you age there is a greater need to distribute the protein equally across 3 daily meals. Therefore, 20 grams of protein 3 times per day would be ideal. Exercise should be in close proximity to one or more of these feedings.

Nitty Gritty: For more details on eating for muscle maintenance see http://www.huffingtonpost.com/entry/muscle-and-aging-how-to-prevent-muscle-loss-and-why_us_589b7f96e4b0985224db5d13

Muscle work for body composition

Moving more is essential for general health. Exercise of any kind is beneficial. But when it comes to counteracting the body composition changes associated with aging, both target and technique are specific.

Research has demonstrated that low load high intensity lifting at 30% of the one repetition max (1RM) to failure can elicit similar rates of muscle protein synthesis as traditional, high load low intensity lifting at 90% of 1RM. Data suggest that low and high load lifting performed to failure yield equivalent hypertrophy over time. So exercise volume (repetitions x sets x load) can achieve maximal muscle fiber activation, including the important larger type II fibers. This is also much less likely to cause injury, an important consideration at any age.

Nitty Gritty: For more details on exercise for muscle maintenance see http://www.huffingtonpost.com/entry/muscle-and-aging-how-to-prevent-muscle-loss-and-why_us_589b7f96e4b0985224db5d13

How we envision aging has a potent effect on how we actually age. Negative stereotypes about aging are a public health problem. Follow the emerging story on the new aging and join those who will not “go gentle into that good night.”


Originally published at www.huffingtonpost.com on February 26, 2017.