Skipping Meals Regularly May Be Good for Your Health

Skipping Meals Regularly May
Be Good for Your Health

How often you eat may be more important than how much you eat
By Dr. Edward R. Rosick

ow the landscape of human health has changed in just a hundred years. In our grandparents’ day, epidemics of smallpox and typhoid ravaged the country and sent countless thousands of people, from infants to the elderly, to their graves every year. Today, smallpox is talked about only as a bioterror weapon, and typhoid is a disease confined to a few third-world countries.

Yet even today, with our miracles of modern technology and Western medicine, we face epidemics that debilitate and kill hundreds of thousands of people a year. Unlike the epidemics of a century ago, however, the killer epidemics of today, including diabetes and Alzheimer’s disease, are due not to germs but, in large measure, to our own self-indulgent and unwittingly self-destructive behavior.

Overweight and Obesity Are Epidemic

We must eat to live. The problem is that many people live to eat. Our seemingly insatiable appetite has spawned an explosion of obesity, particularly in the United States, where the rate increased by 61% between 1991 and 2000.1 It’s now thought that 25–30% of all adults in the USA are obese. If we include overweight individuals (those with a body mass index greater than 25), then 56% of American adults are overweight or obese. Since many studies have shown that these conditions contribute significantly to such devastating diseases as cancer, cardiovascular disease, type 2 (adult-onset) diabetes, and Alzheimer’s disease, our excessive food consumption, particularly of high-calorie foods, is a deadly addiction.

Obesity Links Diabetes and Alzheimer’s

At first glance, the notion that diabetes and Alzheimer’s disease could have a common cause might seem preposterous. After all, isn’t diabetes a disease in which high glucose levels and decreased insulin sensitivity contribute to a myriad of severe health problems, whereas in Alzheimer’s there is a degeneration of brain neurons resulting eventually in total mental incapacity? Well, yes—but scientists are coming up with some intriguing hypotheses that tie these two modern epidemics together.

Obesity is by far the greatest risk factor for type 2 diabetes, and the link is very strong: for every kilogram of increase in self-reported weight, the risk of diabetes increases approximately 9%, and as we grow ever fatter in the United States, the number of diabetics is rising rapidly, with a 33% increase seen between 1990 and 1998.2

AGEs and Free Radicals Will Do You Harm

One of the many harmful conditions associated with type 2 diabetes is the excessive accumulation of advanced glycation end products, or AGEs. These sugar/protein complexes accumulate in the blood and tissues of all of us as we age, and some researchers believe that they’re implicated in the pathogenesis of such modern epidemics as heart disease and Alzheimer’s disease.3 Their link with diabetes stems from the fact that elevated blood glucose levels, which are a characteristic of that disease, promote the rapid formation and accumulation of AGEs.

Another way in which the effects of obesity may link diabetes and Alzheimer’s is through the increased production of free radicals, destructive molecules that are produced inside brain neurons and all the other cells in the body when the cells generate energy from their primary source of fuel, glucose. In high concentrations, free radicals can cause serious problems, including DNA damage and the oxidation of proteins and lipids. Studies have shown that cellular signs of excessive free radical damage are significantly higher in people who are obese.4

Caloric Restriction Extends Lifespan

A simple (but far from easy) way to decrease your weight and avoid the major health problems of obesity is to eat less, thereby taking in fewer calories. In fact, a significant body of evidence shows that long-term dietary caloric restriction of 30% or more (i.e., taking in at least 30% fewer calories than normal) can slow the aging process and maintain health and vitality in a great variety of species, from simple invertebrates to primates.5 Such extreme caloric restriction (CR), in fact, is the only environmental variable that has been shown to markedly slow the rate of aging over a wide range of species.

Most significantly, CR can extend lifespan, by up to 50% in some cases. Exactly how this is accomplished is not known, but tantalizing clues are found in several biomarkers of aging. In primates, CR has been shown to decrease plasma glucose and insulin levels, increase insulin sensitivity, decrease cholesterol and triglyceride levels, lower blood pressure, and increase DHEA levels. Another notable effect of a CR diet is, not surprisingly, major weight loss, resulting in an extremely lean physique—no excess body fat.

Has Evolution Destined Us to Fast?

Let’s assume that intermittent fasting is as healthful for humans at it is for mice—which does not seem unreasonable. The question is, why?

The answer can probably be found in evolutionary biology. Long before the very recent advent (on an evolutionary timescale) of agriculture, it was probably common for prehumans and early humans to have to endure intermittent fasting, owing to the unreliability of their hunting or gathering forays. Those who thrived under such tough conditions—perhaps going hungry for several days before gorging—were the most likely to reproduce and transmit their genes to future generations, including, eventually, us.

Thus we are probably “hard-wired” by evolution to be intermittent fasters, even though the reproductive advantage in that has disappeared and has been replaced, apparently, by health and longevity advantages.

Intermittent Fasting—A Shortcut to Major Health Benefits

Although caloric restriction seems to be the way to live a longer, healthier life, a reality check suggests that few, if any, people would ever do it—there are just too many tempting foods out there, and a lifetime of voluntary food deprivation doesn’t sound too appealing. But wait—some exciting research has just been published indicating that it might be possible to obtain the health benefits of a CR diet without actually having to go on one.


Obesity is by far the greatest risk
factor for type 2 diabetes, and
the link is very strong.


Researchers at the National Institute on Aging in Baltimore have found that, in laboratory mice, a long-term (20-week) program of intermittent fasting—a total fast every other day, interspersed with unlimited food every other day—conferred virtually all the health benefits of a CR diet, and it did so with little or no attendant weight loss (which could be a plus or a minus in humans, depending on what level they were starting from).6*


*In previous studies of a similar kind with mice and rats, the IF animals usually lost weight, but the strain of mice used in this particular study did not.


The researchers did not record the effects of intermittent fasting on longevity, because the nature of the study required that the mice be killed so their brains could be microscopically examined. In two previous studies well over a decade ago, however, it was found that the same kind of intermittent fasting regimen in the same strain of mice did result in significant extensions of lifespan.7,8

IF Mice Were Not Calorically Restricted

For the new study, the NIA researchers compared the effects of eating patterns in three test groups of mice, starting when the mice were 15 weeks old: (1) mice that were given unlimited food, called an ad libitum (AL) diet; (2) mice on a “limited daily feeding” (LDF) diet, entailing a 40% caloric restriction regimen, i.e., one that provided only 60% of the amount of food that AL-fed mice normally eat; and (3) mice subjected to intermittent fasting (IF), as described above.

Because the IF mice were given all the food they wanted to eat every other day (when they would predictably gorge themselves), they were in no way calorically restricted in the long run. As a control against possible hidden physiological factors associated with intermittent fasting, a fourth group of mice was given a daily food allotment equal to the average daily intake of the IF mice, so that the total food intakes of these two groups in the long run were identical.

Could 5-HTP Help You Skip a Meal?

If intermittent fasting is not your cup of tea—and who could blame you?—take heart from the fact that there are other ways to obtain at least some of its remarkable health benefits. Ironically, one of the best ways is through weight loss (the other, of course, is exercise), which was not observed in the intermittently fasting mice described in the accompanying article (but then, they weren’t overweight to begin with). You can, and should, eat sensibly and exercise regularly, and you can take nutritional supplement formulations designed to help you shed unwanted pounds.

Among the best supplements for that purpose is 5-HTP (5-hydroxytryptophan), an amino acid precursor to the neurotransmitter serotonin, which helps to regulate appetite, among other things. With low serotonin levels, there is a tendency to feel sluggish and depressed and to overeat. Raising serotonin levels with 5-HTP can raise your spirits while curbing your appetite, thereby reducing your energy intake.

Another supplement that’s helpful for weight loss, but by an entirely different mechanism, is the green tea catechin EGCG (epigallocatechin gallate), which is an effective stimulator of thermogenesis, the generation of heat by physiological processes, e.g., fat “burning.” Although EGCG is effective by itself in this regard, adding caffeine, that well-known stimulant in coffee and tea, can boost the thermogenic potential of EGCG, thereby increasing energy output—and caffeine also helps to suppress appetite, a bonus.

Thus, a combination of 5-HTP, EGCG, and caffeine could be just what you need to win the battle of the bulge and slim down to where you want to be. (For more on this subject, see “Lose Weight with 5-HTP and EGCG” in Life Enhancement, April 2003.)

Intermittent Fasting Reduced Glucose and Insulin Levels

By the end of the study, the IF mice were consuming essentially the same amount of food as the AL mice, simply by eating twice as much food on their “on” days as the AL mice ate every day. Meanwhile, the LDF mice ate 40% less food than the AL mice, and they lost 49% of their weight (they were very skinny and hungry—but healthy—mice).

Blood tests done after 14 weeks (and following a 14-hour fast for all the mice) showed that the concentrations of glucose and insulin were significantly decreased in both the IF mice and the LDF mice—which is good! Remarkably, in fact, they were lower in the IF mice—this despite the fact that the IF mice ate the same amount of food as the AL mice, which did not show a significant decrease in their glucose and insulin levels and thus continued to be good candidates for diabetes in the long run.

It could be expected that binge eating, such as that indulged in by the IF mice every other day, would have some negative health effects, notably the excessive generation of free radicals or of AGEs (advanced glycation end products, remember?). Remarkably, however, it seems that these potentially harmful effects were more than offset by the evident benefits of alternate-day fasting. As the authors put it:

Apparently, confining bouts of high caloric intake to a limited time window with long intervening periods of fasting results in adaptive responses that do not occur when meals are more frequent. . . . It may be that alternating periods of anabolism [the metabolic buildup of complex biomolecules] and catabolism [the metabolic breakdown of complex biomolecules] play a mechanistic role in triggering increases in cellular stress resistance and the repair of damaged biomolecules or cells.
Intermittent Fasting Protected Brain Neurons

After 24 weeks, the researchers injected the brains of the mice with a substance, kainic acid, that causes neurological damage similar to that seen in the brains of Alzheimer’s victims. The damage was induced in the hippocampus, a part of the brain that is associated with memory and learning and that is characteristically impaired in Alzheimer’s disease. Then, 24 hours later, the mice were killed and their brains examined.

The AL brains showed major pathological changes, as expected. In the LDF brains, by comparison, there was a significant increase in the survival of hippocampal neurons, and remarkably, the neuronal survival rate was even higher in the IF brains than in the LDF brains. This seems to show that intermittent fasting is neuroprotective, independently of overall caloric intake—and that too is remarkable.

Lose Weight and Live Better and Longer

Since it is known that caloric restriction extends lifespan in a wide variety of animals and that intermittent fasting, which confers essentially the same health benefits as CR, can extend lifespan in mice, one is tempted to think that IF might also extend lifespan in humans—provided, of course, that they made a lifetime practice of it. It’s also intriguing to speculate whether a less rigorous regimen, such as skipping one meal (or even two) every other day, or eating only two meals a day instead of three, might have some health benefits. It’s hard to say, but the chances seem good, and it’s almost certain to do no harm.

In any case, one thing is for sure: combating overweight and obesity so as to maintain a healthy weight and keep your blood glucose and insulin levels (not to mention cholesterol levels) well under control is one of the best things you can possibly do for your health and your prospects for a long and happy life.

References

  1. Bianchini F, Kaaks R, Vainio H. Overweight, obesity, and cancer risk. Lancet Oncol 2002;3(9):565-74.
  2. Hamdy O, Goodyear LJ, Horton ES. Diet and exercise in type 2 diabetes mellitus. Endocrin Metab 2001;30(4):883-907.
  3. Raj DSC et al. Advanced glycation end products: a nephrologist’s perspective. Am J Kidney Dis 2000;35(3):365-80.
  4. Dandona P et al. The suppressive effects of dietary restriction and weight loss on the generation of reactive oxygen species by leukocytes, lipid peroxidation, and protein carbonylation. J Clin Endo Metab 2001;86(1):355-62.
  5. Roth GS, Ingram DK, Lane MA. Caloric restriction in primates and relevance to humans. Ann NY Acad Sci 2001;928:305-15.
  6. Anson RM et al. Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proc Natl Acad Sci 2003 May 13;100(10):6216-20.
  7. Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider N. Effects of intermittent feeding upon body weight and lifespan in inbred mice: interaction of genotype and age. Mech Ageing Dev 1990 Jul;55(1):69-87.
  8. Ingram DK, Reynolds MA. In Woodhead AD, Thompson KH, eds. Evolution of Longevity in Animals, Plenum Press, New York, 1987.


Dr. Rosick is an attending physician and clinical assistant professor of medicine at Pennsylvania State University, where he specializes in preventive and alternative medicine. He also holds a master’s degree in healthcare administration.

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