summarize: Fasting, or time-restricted (TR) eating (regulating when you eat), presents us
with a tactical conundrum. On the one hand, it is a powerful tool for
accomplishing some of our goals, large and small. On the other, fasting has
some potentially serious downsides that limit its usefulness. While
intermittent fasting and eating “windows” have become popular and even
trendy in recent years, I’ve grown skeptical of their effectiveness. And
frequent longer-term fasting has enough negatives attached to it that I am
reluctant to use it in all but the most metabolically sick patients. The jury is
still out on the utility of infrequent (e.g., yearly) prolonged fasts. Overall, I’ve
come to believe that fasting-based interventions must be utilized carefully and
with precision.
There is no denying that some good things happen when we are not
eating. Insulin drops dramatically because there are no incoming calories to
trigger an insulin response. The liver is emptied of fat in fairly short order.
Over time, within three days or so, the body enters a state called “starvation
ketosis,” where fat stores are mobilized to fulfill the need for energy—yet at
the same time, as I often noticed when I was undergoing regular lengthy fasts,
hunger virtually disappears. This paradoxical phenomenon is likely due to the
ultrahigh levels of ketones that this state produces, which tamp down feelings
of hunger.
Fasting over long periods also turns down mTOR, the pro-growth and
pro-aging pathway we discussed in chapter 5. This would also be desirable,
one might think, at least for some tissues. At the same time, lack of nutrients
accelerates autophagy, the cellular “recycling” process that helps our cells
become more resilient, and it activates FOXO, the cellular repair genes that
may help centenarians live so long. In short, fasting triggers many of the
physiological and cellular mechanisms that we want to see. So why don’t I
recommend it to all my patients?
It’s a tricky question, because the scientific literature on fasting is still
relatively weak, notwithstanding the many popular books that have been
written about fasting in its various forms. I have recommended (and
practiced) different forms of fasting myself, from time-restricted feeding
(eating in a defined time period each day) to water-only fasting for up to ten
days. Because my thinking about fasting has evolved considerably, I feel that I
need to address the topic here. I still think it can be useful sometimes, in
some patients—typically the ones with the most severe metabolic dysfunction
—but I am less persuaded that it is the panacea that some believe it to be.
There are really three distinct categories of time-restricted feeding, and
we’ll look at each of them in order. First, we have the short-term eating
windows that we’ve mentioned previously, where someone will limit their
consumption of food to a specific time frame, such as six or eight hours out
of the day. In practice, that could mean skipping breakfast, eating a first meal
at 11 a.m. and finishing dinner by 7 p.m. every evening; or someone could eat
breakfast at 8 a.m., another meal at 2 p.m., and nothing thereafter.
There are an almost infinite number of variations on this, but the trick is
that it works only provided you make the feeding window small enough. The
standard 16/8 (sixteen hours of fasting, eight hours to eat) is barely enough
for most people, but it can work. Usually a narrower window, such as 18/6 or
20/4, is needed to eke out enough of a caloric deficit. For a time, I was
experimenting with a two-hour eating window, which basically meant that I
would eat one huge meal per day. I always enjoyed the look on a waiter’s face
when I would order multiple entrees.
In my experience, most people find this to be the easiest way to reduce
their caloric intake, by focusing on when they are eating rather than how
much and/or what they are eating. But I am not convinced that short-term
time-restricted feeding has much of a benefit beyond this.
The original 16/8 model came from a study conducted in mice. This study
found that mice fed in only eight hours out of the day, and fasted for the other
sixteen, were healthier than mice fed continuously. The time-restricted mice
gained less weight than the mice that ate whenever they wanted, even though
the two groups consumed the same number of calories. This study gave birth
to the eight-hour diet fad, but somehow people lost sight of the fact that this
is a big extrapolation from research in mice. Because a mouse lives for only
about two to three years—and will die after just forty-eight hours without
food—a sixteen-hour fast for a mouse is akin to a multiday fast for a human.
It’s just not a valid comparison.
Human trials of this eating pattern have failed to find much of a benefit. A
2020 clinical trial by Ethan Weiss and colleagues found no weight loss or
cardiometabolic benefits in a group of 116 volunteers on a 16/8 eating
pattern. Two similar studies also found minimal benefit. One other study did
find that shifting the eating window to early in the day, from 8 a.m. to 2 p.m.,
actually did result in lower twenty-four-hour glucose levels, reduced glucose
excursions, and lower insulin levels compared to controls. So perhaps an
early-day feeding window could be effective, but in my view sixteen hours
without food simply isn’t long enough to activate autophagy or inhibit chronic
mTOR elevation, or engage any of the other longer-term benefits of fasting
that we would want to obtain.
Another drawback is that you are virtually guaranteed to miss your
protein target with this approach (see “Protein,” above). This means that a
person who needs to gain lean body mass (i.e., undernourished or
undermuscled), should either abandon this approach completely or consume a
pure protein source outside their feeding window (which more or less defeats
the purpose of time-restricted feeding). Also, it’s very easy to fall into the
trap of overindulgence during your feeding window and mindlessly consume,
say, a half gallon of ice cream in one sitting. Taken together, this combo of
too little protein and too many calories can have the exact opposite effect we
want: gaining fat and losing lean body mass. In my clinical experience, this
result is quite common.
As I said, I will sometimes put certain patients on a time-restricted eating
pattern because I’ve found it helps them reduce their overall caloric intake
with minimal hunger. But it’s more of a disciplinary measure than a diet.
Setting time limits around food consumption helps foil a key feature of the
SAD, which is that it’s difficult to stop eating it. Time-restricted feeding is a
way of putting the brakes on snacking and late-night meals—the type of
mindless eating-just-to-eat that the Japanese call kuchisabishii, for “lonely
mouth.” But beyond that, I don’t think it’s particularly useful.
—
Next, we have alternate-day fasting (ADF), which has also become popular.
This is where you eat normally or even a bit more than normal one day, and
then very little (or nothing) the next. There is more extensive research into
this eating pattern in humans—and, of course, there have been books written
about it too—but the results are not particularly appealing. Some studies have
found that subjects can indeed lose weight on alternate-day fasting diets, but
more nuanced research suggests there are some significant downsides. One
small but revealing study found that subjects on an alternate-day fasting diet
did lose weight—but they also lost more lean mass (i.e., muscle) than subjects
who simply ate 25 percent fewer calories every day.
This study was limited because of its small size and short duration, but it
suggests that fasting might cause some people, especially lean people, to lose
too much muscle.
[*14] On top of this, the ADF group had much lower activity
levels during the study, which suggests that they were not feeling very good
on the days they were not eating. With longer-term fasting, these effects only
become more pronounced, particularly the loss of muscle mass. Therefore, I
am inclined to agree with lead investigator James Betts: “If you are following
a fasting diet, it is worth thinking about whether prolonged fasting periods
[are] actually making it harder to maintain muscle mass and physical activity
levels, which are known to be very important factors for long-term health.”
As a result of this and other research, I have become convinced that
frequent, prolonged fasting may be neither necessary nor wise for most
patients. The cost, in terms of lost lean mass (muscle) and reduced activity
levels, simply does not justify whatever benefits it may bring. My rule of
thumb for any eating pattern, in fact, is that you must eat enough to maintain
lean mass (muscle) and long-term activity patterns. That is part of what
makes any diet sustainable. If we are going to use a powerful tool like fasting,
we must do so carefully and deliberately.
But fasting can still prove useful sometimes, in some patients—generally,
patients for whom no other dietary intervention has worked. Case in point:
my friend Tom Dayspring, the lipidologist whom we met in chapter 7. Tom
became a patient of mine a few years ago because I was so concerned about
his metabolic health. Then in his midsixties, he was carrying 240 pounds on
his five-eight frame, giving him a BMI of 36.5, well into the obese range.
Blood tests revealed that he was also working on a serious case of NAFLD, if
not outright NASH. Over the years, I had nagged him constantly until he
finally agreed to try to do something about it. Given his issues, a ketogenic
diet was the obvious place to start. If we limited his carb intake, I figured,
he’d lose weight and hopefully his NAFLD would have a chance to dissipate,
and his biomarkers and weight would also come under control.
But they didn’t. After Tom struggled for six months to stay on the diet, his
liver enzymes, and his weight, had failed to budge. A year later, same story.
Two years, three years, nothing had changed. In the meantime, his health
continued to deteriorate, to the point where he had difficulty walking a single
city block. He eventually required both a hip replacement and spinal fusion.
The problem was that Tom was simply unable to stay on the strict ketogenic
diet for very long. He would be fine for two weeks or so, but then he would
break down and eat a sandwich or a plate of pasta. It simply wasn’t
sustainable for him.
Tom clearly required some sort of stronger medicine, and I concluded that
he needed to try fasting. Unfortunately, like many SAD-trained North
Americans, Tom hated the very thought of hunger. This was why he had
difficulty adhering to the strict ketogenic diet for very long—he felt hungry,
and he craved his old familiar carb-heavy foods. Thus, he was never able to
switch his metabolism into ketosis and drive down his hunger. Because of his
persistently high insulin, his fat cells were refusing to give up the energy they
had stored. So he felt hungry all the time, and he could not lose any fat.
Clearly, he needed to break out of this vicious cycle.
At first, Tom was horrified by the very notion of fasting. But he is also a
scientist, and after delving into some of the research on nutrient deprivation
and putting that together with what he already knew about lipids and
metabolism and disease risk, he agreed to give it a try. His scientific mind
was persuaded, but I think at some point he also realized that he was staring
down the barrel of what might be the last five years of his life unless he made
some drastic changes. We came up with an aggressive plan, at the limit of
what he thought he could tolerate: one week per month, Monday through
Friday, Tom would subsist on a drastically reduced diet of about seven
hundred calories per day, comprising mostly fat, with a little protein and
almost no carbohydrates.
This kind of fasting is called “hypocaloric” because you are not truly
fasting in the sense of eating no food at all. You are eating just enough to
quell the worst hunger pangs, but not so much that your body thinks you are
fully fed. For twenty-five days out of each month, Tom ate a “normal” diet
(though in his case, very starch- and sugar-restricted), and only between noon
and 8 p.m.; during his fasting week, a typical day’s menu might consist of a
salad with light dressing, an avocado, and some macadamia nuts or olives. He
was surprised at how good he felt. “It wasn’t as horrific as I thought it was
going to be,” he told me later. “After day three, the hunger disappears.”
It did not take long for his blood biomarkers to improve dramatically:
where his complete blood chemistry report used to be largely yellow and red
—meaning, most of his values were borderline to “bad”—it is now almost
entirely green. His lipids are under control, and his liver enzymes have
plummeted back to safe, normal ranges. After several cycles of this, he was
able to do things like climb a flight of steps or walk several city blocks again
without feeling out of breath. His blood pressure is lower, and he has been
able to stop taking many of the countless medications he was on. Last, he
now weighs sixty-seven pounds less than he used to, a sign that his metabolic
health really is back on track, and a powerful incentive for him to keep at it.
“The weight just poured off,” he told me.
Fasting had effectively reset or rebooted his crashed metabolism in a way
that no other dietary intervention was able to achieve. Because it has such
deleterious effects on muscle mass, I only use it in hard-to-fix patients like
Tom. Tom was so overweight to begin with that he could tolerate the loss of
muscle because he was losing so much fat at the same time. But most people
can’t safely lose muscle mass, so fasting is a tool that we can only really use in
extremis, when there are no other viable options.