E = MC2
Einstein’s iconic formula defines the theory
of relativity. We think of this formula mainly in quantum physics and space
exploration, but it also applies to our body. The theory specifies that a body
that weighs say 68kg (150 lbs.) will have 6,111,535,215,410,359,952 Joules of
energy. This is 6,111 Petajoules (PJ) which translates to 1,697,500 giga watt
hour. In comparison, 31.5 PJ is the electrical annual output of a large power
plant, while 210 PJ is equivalent to about 50 megatons of TNT. This is the
amount of energy released by thirty Tsar Bomba, the largest man-made nuclear
explosion ever.
One person is a walking universe of
restrained energy. We can only access a small percentage of this energy so most
of this energy remains inaccessible. But our biology knows how to utilize part
of this energy. And one way that it uses energy is by storing it in fat. It is
a reserve that our biology does very well. This balance is based on the first
law of thermodynamics applied to an open system. It is an open system because
energy can be added to the system by ingesting food. Energy that is not used by
the body is stored in the form of glycogen, lipids (mainly in the form of fatty
acids), and protein. Unlike glucose, fat can be stored in large quantities for
extended lengths of time. As a result, fat mass is the main long-term energy
storage mechanism of the human body.
Surprisingly, we are built with two systems of energy: glucose and ketones. In ketosis, once we run-out of glucose, we switch to our fat for energy. We break down fat into fatty acids, and those fatty acids which the liver transforms into ketones, which are then used as the energy source by the brain, muscles, and other tissues. Ketosis occurs through high fat intake, fasting, or reduction of carbohydrates.
The average adult has as much energy stored in fat as a one-ton battery. Fat is a very good system when there is energy shortage, but becomes problematic when there is an abundance of food since the body is excellent at storing fat. Especially since the body protects any loss of fat. Weigle et al (1988) reported that the body is aware of how much energy is stored. So for someone who lost a lot of stored energy (say after dieting) the body uses 18% less daily energy than those of the same relative body weight conducting the same activity, as those who had never dieted. This is a clever energy conservation system that we see in action better in older age.
The average adult has as much energy stored in fat as a one-ton battery. Fat is a very good system when there is energy shortage, but becomes problematic when there is an abundance of food since the body is excellent at storing fat. Especially since the body protects any loss of fat. Weigle et al (1988) reported that the body is aware of how much energy is stored. So for someone who lost a lot of stored energy (say after dieting) the body uses 18% less daily energy than those of the same relative body weight conducting the same activity, as those who had never dieted. This is a clever energy conservation system that we see in action better in older age.
The average human, at rest, produces around
100 watts of power. This equates to around 2000 kcal (kilocalorie =4184 joules)
of food energy, which is why your recommended daily intake of calories is
around 2000 kcal. Over periods of a few minutes (or a few hours in the case of
trained athletes), we can comfortably burn 300-400 watts of energy—and in the
case of very short bursts of energy, such as sprinting, some humans can output
up to 2,000 watts.
As we get older this equation changes
dramatically. We become less efficient. The idea that aging is simply an
attrition of energy is one of the oldest theories in gerontology starting with Aristotle (384-322 BC) and was later
adopted by the Romans, Muslims and Western European medical
establishments. It became the basis for our early understanding of
how the human body works. Essentially, Aristotle held that the human
body was filled with four humors: black bile, yellow bile, phlegm, and blood. Any
imbalance in these four humors resulted in diseases and disabilities. Aging is
caused by the drying out and cooling of these humors. This idea had a wide
following, and involved numerous hot baths and saunas in order to maintain our
wetness and heat.
Surprisingly, older adults do have
slightly lower temperatures. The 98.6° F benchmark for body temperature comes
from Carl Wunderlich—a 19th-century German physician—is not accurate for older
adults. In 2005, Irving Gomolin from Winthrop University Hospital in New
York, found that older people have lower temperatures than younger adults. In a
study of 150 older people with an average age of 80-plus, they found an average
temperature of 97.7°. What is fascinating is longer you survive the lower your
body temperature…or is it the other way round?
Although most have seen lower temperature as correlated with mortality,
lower temperature might be a protective function, knowing that the body likes
to conserve energy. And that is exactly what a 2006 research study found. An Italian
researcher Bruno Conti at the Scripps Research Institute showed that a decline
in body temperature is beneficial. The study found that mice that had lower
core body temperatures lived 12% (male) to 20% (female) longer than mice with higher
core body temperatures. The difference in temperatures between "cold"
and "normal" mice was 0.5-0.9 F (0.3-0.5 C), which is the same
difference between the average young person and the average older adult.
Perhaps the body is conserving energy by reducing its operating temperature and
therefore reducing metabolic rate, free radicals and stress on the system.
The science behind this anomaly is just now
becoming clear. One of the known ways to increase longevity is to restrict calorie
intake—eating fewer calories. Caloric restriction increases lifespan in all
sorts of animals. Several studies have reported that animals on
reduced calorie diets also had a lowering of core body temperature. By
conserving energy and reducing temperature, our body is also slowing the aging
process. One interpretation from this is that the reason older adults may have
lower body temperature is not because they are dying, but because it is our
body’s way of preserving energy, resulting in living longer. In the Baltimore
Longitudinal Study of Aging, men with a core body temperature below the average
(median) lived significantly longer than men with body temperature above the
average. But how does Caloric Restriction (CR) result in lower temperature and
conserving of energy?
After Caloric Restriction (CR) was initially
discovered in 1935 in mice, it has been tested with varied organisms and it has
been shown to increase the lifespan in yeast, insect, and in non-human
primates. In humans CR is still undergoing testing, although initial
results suggest prolongation of life as well as prevention of age-related diseases
are likely outcomes. The mechanism seems to emulate the genetic work of life
prolongation, in that the CR elicits a hormesis event—a low level stressor that
stimulates a positive response. The system is believed to involve genes that
become active when stress occurs. These genes are referred to as epigenetic.
Epigenetics are genes once thought to be “junk” genes, but now we are finding
that they can be switched on or off. In most cases they are triggered by
environmental factors. The best way to study the effect of genetics on
longevity is to look at twins. Monozygotic twins, those that split from a
single egg, have nearly similar genetic makeup at birth. In contrast, twins
that have a different egg (dizygotic) only share the same level of genotype as
with any other siblings.
More than three decades ago, Cook and his
associates published a study looking at the onset of dementia among monozygotic
twins who were both affected by Alzheimer's dementia. In one case study,
dementia began in her late 60s, while in the other twin the onset of dementia
was at age 83. Subsequent studies confirm that although monozygotic twins might
both have the disease, how they express them and when they express the disease
might differ. The difference was used attributed to the environment. In support
of this interpretation recent studies are blurring the difference between
genetics and the environment. In 2000 biologists Randy Jirtle and Robert
Waterlanda from Duke University modified the expression of a gene—called agouti
gene--which made mice fat, yellow and prone to cancer and diabetes. These mice did not live very long. After an
intervention however, these researchers produced young mice that were slender
and healthy, evading their parents' susceptibility to cancer and diabetes living
to an active old age. The researchers virtually erased the effect of the agouti
gene. Remarkably, the researchers
modified the expression of this gene not by altering the mice genes, but by
changing the moms' diet. Feeding the
mother a diet rich in onions, garlic, beets, and in food supplements often
given to pregnant women the researchers provided a chemical switch that reduced
the agouti gene's harmful effects.
These foods—known as methyl donors, folic
rich foods—enhance or diminish gene activation and gave birth to a whole new
science of epigenetics.
The same changes in our genetic expression
are seen throughout our life. With older adults expressing more variance in
their genetic expression. In 2012, Jordana Bell of King's College London and
colleagues looked at the genes of 86 sets of twin sisters aged 32 to 80, and
repeated with another 44 sets of younger twins aged 22 to 61, and discovered
that 490 genes linked with ageing showed signs of epigenetic change. In
particular, among this epigenetic expression were four genes that relate to
cholesterol, lung function and maternal longevity. What is phenomenally
interesting is that these changes are not just brought about by diet and methyl
rich donors, but also by such lifestyle factors such as smoking, environmental
pollution, stresses, and attitude.
There are many studies in this area of how
genetic manipulation changes longevity through the conservation of energy. The
three seminal research studies all have
one thing in common and it is to do with how the body reserves energy through
growth hormones. The first type is a classic experiment by Michael Rose who
began manipulating the life spans of fruit flies by allowing them to reproduce
only at late ages. The subsequent progeny of flies evolved longer life spans
and greater reproduction over the next dozen generations. If our parents delayed producing us, then our body seems to know
to conserve energy in order to make the body live longer to enable it to pass
on its genes at this delayed period.
The second type of experiment uses examples
from nature, which were then emulated in the laboratory at U.C San Francisco by
Cynthia Kenyon. Here they chemically knocked out certain genes in flatworms,
the gene daf-2 which partially disables receptors that are sensitive to two
hormones—insulin and a growth hormone called IGF-1. This had the effect of
nearly doubling the flatworms’ lifespan. These long-lived worms looked and
acted younger than their control group, implying that extending the lifespan
also extends healthy life. By conserving energy by weakening insulin and a growth
hormone, the flatworms lived longer.
Then there is the third type of genetic
observation with mice, in particular the work done by Richard Miller, and his
infamous mouse called Yoda (who is now deceased.) Like other dwarf mice, Yoda
had a natural genetic mutation that obstructs the production of growth and
thyroid hormones. Dwarf mice tend to grow to only about a third the size of
normal mice, which helps them live about 40 percent longer. The common
denominator in all these experiments and observations is that stunted growth and
a conservation of energy correlates with increased lifespan. Surprisingly there
are two inclusive and complimentary theories that can explain these findings.
The theory of Antagonistic Pleiotropy argues
that some genes have contradictory effects at different age. Genes which might
enhance your reproductive success at a younger period in our life—genes that
increase testosterone in men, resulting in more muscle mass and masculine
secondary sexual characteristics—may at an older age have detrimental effects
on survival later in life—in the testosterone example it is the elevated risk
of cancer. Natural selection tends to favor these kinds of genes because they
maximize fitness and the passing of genes while the higher mortality occurs in
post-reproduction stage will have little impact on increasing the number of
offspring. The second theory is that of Disposable Soma which states that given
that there are finite resources to maintain and repair cells and organs, the
body conserves energy and protects itself just long enough so that we are able
to pass on our genes.
As with all genetic work there are many
confounders. There is no direct translation from the genotype to the phenotype.
The environment can intervene as is being shown with epigenetics. Even if we
accept that stunted growth might preserve energy and improve lifespan, other
factors might negate such gains. And
that is the case with a southern Ecuador group where more than 250 individuals
are thought to have Laron syndrome—IGF-1 deficiency in primary growth hormone—caused
by a mutation in the growth hormone receptor gene with affected individuals
growing to less than 4 feet tall. Although Laron patients appear to be protected
against developing cancer, this apparent protection does not translate to a
longer lifespan due to trauma and alcoholism. There is a schism between
lifespan and theoretical lifespan…human behavior. The ability of the body to
preserve energy might be negated by our negative behavior.
© USA Copyrighted 2015 Mario D. Garrett
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