|
This entire chapter boils down to
one simple statement: You’re stuck with the genetics you’ve got, so suck it up.
Got screwed genetically? Boo fucking hoo. Take it up with mom and dad, God, or Charles Darwin for all I care. I could go
into excessive details about how I got buggered in the genetic lottery, but that would result in me being cut out of my parents’
will so I’m going to elect to keep that information private.
I’ll admit that this is one area
of obesity research where there is a helluva lot more that we don’t know than do. There are potentially thousands
of genetic markers for obesity and researchers have identified only a handful. Some people get more, some get less. Maybe
you got a lot of them, but acting like a victim won’t make the situation any better.
Don’t Be a Victim of Your Genetics
You want to bitch and whine about how you’re genetically
programmed to be fat? Then go do it somewhere else. People who adopt the victim mentality royally piss me off, so if you’re
one those, then fuck off. This is not a book that preaches fat acceptance. I won’t cater to your “poor me”
attitude. I won’t tell you what you want to hear. I will tell you the truth, and even if evolution played a joke on
you, I will still offer hope. Obesity is a major problem and a leading cause of death, so you shouldn’t just accept
it. You should do something about it.
Many fat acceptance authors preach what amounts to
“You can’t win, so don’t try.” Don’t pay attention to such crap, because you can win. You may
never have a hope at getting six-pack abs. You may never look like a fitness model. However, you CAN achieve your maximum
genetic potential. Like the old U.S. Army slogan said: “Be all that you can be.” Don’t be a victim and don’t
make excuses. Just do what you can with what you have. Your body is the only one you’ve got. Even if you own a mint-condition
1966 Corvette Stingray, your body is still your most prized possession, so stop treating it so poorly.
If you found the above statements offensive, then you’re welcome.
Yes, there is an Obesity Epidemic, and No, it Wasn’t Caused by Genetics The fact is that a lot of people blame genetics when in reality the obesity epidemic is caused by two simple
things: a decrease in physical activity and an increase in caloric intake. For example, during the 24-year period between
1976 and 2000 the prevalence of obese people (BMI >29.9) in the U.S. more than doubled, rising from 15% of the population
to 30.9%.1 The increase has nothing to do with genetics; genes don’t change that much in a single generation.2
Maybe it’s your genetics and maybe it’s not.
Maybe it’s pie. Maybe it’s pizza. Maybe it’s beer. Maybe it’s the fact that you scarf all three while
your ass is glued to the couch. You’ll never find out what you’re capable of if you’re not willing to work
hard and be adaptable. Maybe you suck at fat loss but build muscle easily, so you would want to increase your aerobic activity
and focus more on creating consistent caloric deficits (much more on that later). That’s just one example.
Pay attention to what works for you and what doesn’t. Like I wrote earlier, be an active participant in the creation
of your program.
If you are interested in broadening your mind a little, then lets
get down to the nasty business of explaining the genetics of obesity and response to physical activity from a non-geneticist.
This could be painful.
Nature vs. Nurture
Researchers are well aware that both genetics and familial environment play important roles in who we are and who
we become which is why there have been numerous studies that control for the nurture factor by utilizing twin and adoption
studies to single out genetic causes for specific outcomes. We all know of families where every member is obese, and other families where all are fit and trim. The question becomes,
what portion is genetic and what part is influenced by familial habits? Are the fat family members all that way because none
of them exercise and they all eat large portions of junk food, or are there also genetic elements at play? In many cases the
answer is “both.” Genetics can actually influence whether or not people are physically active and even impact
taste preferences. This isn’t about making excuses; it is about increasing your understanding so you know how to play
your best hand with the cards you’ve been dealt. The following pages provide a brief summary of how genetics influence
a variety of traits relevant to getting in shape.
Differences in Trainability
There is debate on this subject because some studies have
shown that a portion of the population is essentially untrainable. Before you say, “Well, then screw it!” and
throw this book on the fire, allow me to explain further about this research and what it means.
Dr. Claude Bouchard is one the most respected and well-known researchers in the field of the genetics of obesity and physical
fitness. Bouchard was leader of the HERITAGE Family Study which, during its first phase, took 481 healthy but sedentary Caucasian
subjects from 98 separate families and tested their aerobic capacity, put them on a lab-supervised training regimen for the
next 20 weeks, and then re-tested them.3
The
study tested for VO2 max, which is the maximum capacity of a person to transport and utilize
oxygen during incremental exercise: a reflection of the person’s level of fitness. The study found that trainability
is a heritable trait, up to 47%. It is also not surprising that there were some people who responded to training much better
than others, representing a typical bell curve of results. The surprising data come from what I already discussed, which is
that some people appeared to be “untrainable.” The normative prediction for expected VO2
max improvement for the group was 400 ml/min, but in actuality the range was from 0 ml/min to >1000 ml/min, with about
10% falling into the “non-responder” category.4
There
is no question that some people will respond better to training than others. You may discover that working hard gets great
results. You may start running and find that you suck at first, but after a few weeks you can go further and faster than when
you started. Conversely, you could be a low responder and have to work at it for a long time before you see improvements in
your aerobic ability.
Vassilis Klissouras, in an article
in the European Journal of Sport Science disagreed with some of Bouchard’s findings in regards to trainability.
According to Klissouras, “Scrutinization of the available evidence does not support the contention
that trainability of VO2max is genotype-dependent, nor does it warrant the inference that superior athletes are more sensitive
to training.”5
Are you a high or a low responder? You’ll never know unless you try. Even if you find that you are
slow to respond to training, improvements can be made. Even if the assessments in the HERITAGE study of 10% of people being
non-responders is true (which, as Klissouras pointed out, is debateable), the study was of short duration, and only measured
VO2 max as an indicator, whereas in real life there are many other variables in which to evaluate fitness and responsiveness
to training. Bouchard’s work didn’t address issues like improvements in strength, metabolic changes, fat loss,
increases in overall muscularity, cholesterol levels etc.
Genetic Influences on Longevity
There is a definite
connection between genetics and living longer, but not in the way you may think. There do not appear to be any specific genes
that are directly associated with longevity, rather the opposite is true. Some unfortunate people have deleterious heritable
traits that lead to premature death from any number of diseases or detrimental effects such as high cholesterol or a tendency
towards obesity or cancer.6 This provides confirmation to what I wrote in Chapter 3 – that people who
die at an earlier age usually do so because of disease (or an accident), but those who live significantly longer than the
average life expectancy remain disease free until they near the end of their lives. Regarding cancer, a 2008 review determined that only 5 – 10% of cancers are related to
genetics. The study reported that: “The evidence indicates that of all cancer-related deaths, almost 25–30% are
due to tobacco, as many as 30–35% are linked to diet, about 15–20% are due to infections, and the remaining percentage
are due to other factors like radiation, stress, physical activity, environmental pollutants etc.”7
I should note that the majority of the cancers caused by infection are related to sexual activity (HPV and HIV/AIDS),
so be careful where you stick it.
Although
the vast majority of cancers are lifestyle related, there may be some diseases that you are at a much higher
risk for because they’re hard-coded into your DNA. You might be a ticking time bomb, but if there is any hope to delay
things going boom it is living a healthy lifestyle. As I’ve already shown, even if you have preprogrammed susceptibility
to something like heart disease you can extend your life by keeping your weight at a healthy level, controlling cholesterol
(with pharmaceutical help, if necessary), exercising regularly and intensely, avoiding smoking, limiting alcohol intake and
consuming a healthy diet. You may be programmed to die early, but you can fight a valiant delaying action and stretch out
the time you have left, probably by a long time.
I’ve already explained how exercise staves off heart disease, stroke, type 2 diabetes and a number of cancers, but
there is another interesting example of how high levels of physical activity can mitigate a genetic time bomb, and that is
cognitive decline. Albertine Schuit et al. studied the effects of a nasty genetic trait called the e4 allele which dramatically
increases the risk of going batshit senile when you get older. However, if these carriers are moderately physically active
they reduce their risk of Alzheimer’s by almost 80% compared to sedentary e4 carriers8 In short, if you let genetically programmed
diseases have their way with you, they will.
Caloric Intake and Taste Preferences
A 1988 article published in the American
Journal of Clinical Nutrition found that heredity had negligible effect on overall caloric intake. This means the total
amount of Calories you take in aren’t genetically predetermined. However, the study did find that there is a 20% degree
of heredity when it comes to percentage of carbohydrates and fat in a person’s diet, and an 11% genetic effect on protein
intake.9 In other words, from a genetic perspective you have
complete control over how much food you eat, and a large degree of control over what kind of food you eat.
Cholesterol
and Genetics In
tackling the data for this subject the best assessment I can come up with regarding genetics and cholesterol is that the link
is significant. According to Claude Bouchard, “it has long been recognized that there are considerable differences among
individuals in response of serum cholesterol to dietary cholesterol.”10 Some people can eat piles of butter
fried shrimp battered in egg yolks and served with a side of bacon and have minimal impact on their serum cholesterol levels.
Some others catch a whiff of sizzling bacon and their level spikes. I’m closer to the latter. Right now I keep my cholesterol
levels in a safe range by getting a crapload of aerobic exercise and watching my diet. That may not always be the case. I
get it checked annually to keep on top of it because high cholesterol can lead to heart disease, and it can be treated with
drugs. Just because there are good drugs, however, doesn’t
give you license to scarf loads of high-cholesterol food. First off, food that is high cholesterol is higher in fat and higher
in caloric content, so limiting these types of foods makes sense from a fat loss perspective. Secondly, the drugs are not
a magical cure all. They are intended to work in conjunction with a healthy diet and exercise to lower overall serum cholesterol.
Somatotypes
Question: What
is a somatotype?
Answer: Who gives a shit?
Seriously,
these are vague labels that don’t mean bugger all in real life. I’ve been working out for fifteen years and couldn’t
say for sure what mine is. I don’t burn fat easily; I have to monitor Calories and do lots of aerobic exercise to stay
slim. I don’t build muscle effortlessly either. I’ve worked my ass off to get the moderate amount of muscle I
have. I’m not genetically programmed to be a bodybuilder (like I care).
Anyway,
I’ll relay the theory, but in my opinion somatotype is something that you shouldn’t worry about because your body
type is what it is.
- Ectomorph: “characterized by linearity and fragility, along with poor
muscle development and a predominance of surface area over body mass.”11 Linearity and fragility? I guess
that’s the scientific term for “pencil neck.”
- Mesomorph: Allegedly these folks are the genetic lottery
winners. I’ll admit that I look like one if you go by the definition, but I don’t think I am a natural meso because
my body resists fat burning like a mofo and I don’t build muscle without serious effort. I look like this because of
hard work and that’s it. Mesos are “characterized by the predominance of muscle, bone, and connective tissues,
so that muscles are prominent with sharp definition.”12 Uh, that description may fit me now, but it sure
didn’t when I was a fat ass at 25-years old.
- Endomorph: Also known as “Sucks to be you.” The text book
description is: “characterized by the predominance of the digestive organs [WTF?] and by roundness and softness of contours
throughout the body.”13
Knowing your somatotype isn’t necessary
in the grander scheme of getting in shape. It’s just a scientific label so I advise you to care less. It’s like
body fat percentage; a member of my advisory committee asked me if I wanted to get a hyper-accurate body fat measurement using
the university’s underwater weighing tank, but I declined because it’s not a number I care about. Cholesterol
levels are numbers I care about. BMI is a number I care about. How many abdominal muscles I can see when I look in the mirror
is a number I really care about.
Think about it. A couple of years from
now when you’re strolling down the beach and some babe checks out your six pack she’s not thinking, Wow. Check
out that mesomorph. I bet his body fat is below seven percent.
No, she’s thinking something else: Nice abs.
Heritability of BMI
When it comes to the question of whether or
not BMI is a heritable trait, we are one-hundred percent certain that we’re just not sure. Estimates range from as high
as 90% heritability to almost zero.14 Yeah, whatever.
The problem is that most studies have
a hard time separating the effect of genes and environment. Nevertheless, some determined researchers have utilized twin and
adoption studies to try and get to the bottom of it. Comparing MZ twins (monozygotic, which means identical) raised apart
with MZ twins reared together allows for some measure of control over confounding influences of a shared family home.
The results suggest that sharing a family home didn’t contribute much to
BMI variation of MZ twins, but that there shared genes might. I wrote “might” because the genetic effect presumes
that the MZ twins who were raised apart did not grow up in a similar home environment. Considering that many families have
low activity levels and poor eating habits, the same type of upbringing is entirely possible. Making some best guesses, some
early studies conducted in the 1990s found that genetic effect of MZ twins on BMI falls into the 40-70% range.15
More recent research backs up these earlier findings that genetics can have a moderate to strong effect on BMI.
For example, a 2007 Danish twin study of 625 MZ and DZ twin pairs (DZ refers to dizygotic, which are non-identical) reported
that “The genetic correlations between the traits
for overall fatness… were 0.94 in men…”16 Although 94% seems shockingly high, it is important
to note that these twins were in the same family; it did not utilize twins reared in separate homes. Therefore, at least some
of the correlation can be attributed to shared familial environment. Also note that these are identical twin studies.
The correlations are for people who are 100% genetically identical.
A
more comprehensive review of 25,000 MZ and DZ twin pairs and 50,000 biological and adoptive family members revealed the following
regarding genetic and environmental factors and their contribution to BMI:
- Correlation
for MZ twins is 74%
- Correlation for DZ twins is 32%
- Correlation for non-twin siblings is 25%
- Correlation for parent
to offspring is 19%
- Correlation for adoptive relatives is 6%17
The
interesting note here is that DZ twins have a 7% higher correlation than do non-twin siblings. DZ twins have no more shared
genes than do siblings born years apart, yet the influence of a shared womb and being the same age growing up together has
influence on BMI.
If you have a fat identical twin I could see how this information
might be depressing. Otherwise, the news is pretty good because the parent to offspring correlation is only 19%. You a not
a clone of any one parent, but a mixture of the two, and genes have a way of mixing in unexpected ways, sometimes to your
benefit. Every male I know of in both of my parents families is balder than Captain Picard, yet I still have my hair.
Can Obesity be Inherited?
Obesity is a complex trait. According to Dr. Stephen Roth:
“The bottom line is that both genetic and environmental factors (and their interactions) are likely
to explain obesity in any one person… the human genome is not adapted to a sedentary environment, having evolved over
centuries of hunter-gatherer living, so that low levels of physical activity are harmful…”18
And Dr. Bouchard had this to say (in PhD speak) about whether or not obesity is inherited:
“Excessive body fat content or obesity is a complex multifactorial trait that
develops under the interactive influences of many affectors from the social, behavioral, physiological, metabolic, cellular,
and molecular domains. Segregation of genes for obesity is not easily detected in familial or pedigree studies; whatever the
influence of genotype on the etiology of obesity, it is generally attenuated or exacerbated by nongenetic factors.”19
As I mentioned at the beginning of this chapter, the epidemic of obesity in the developed world
has nothing to do with genetics. Only a small portion of the populace is genetically challenged when it comes to maintaining
a healthy body weight, and these genes haven’t changed in millennia. If I wanted to be nasty I could say it’s
your fault that you’re fat, but that isn’t entirely true. Genetics may play a role, but what is more likely is
the role played by our changing society. We have machines to do the vast majority of our labor and easy access to an overabundance
of highly palatable food. No wonder so many people are overweight when we don’t have to do anything physical and there’s
lots of yummy chow to be had.
Prior to the 20th century people didn’t
have a choice but to be thin because of the amount of daily labor required just to survive, and the fact that food was in
shorter supply. There was a direct relationship between the amount of food people consumed and the amount of work they had
to do to obtain that food. Not only that, but the food they did have didn’t taste as good and took a lot more preparation
than going through the McDonald’s drive-through or hitting the convenience store for a bag of potato chips and a pint
of ice cream. Our ancestors didn’t have to think about watching their weight because circumstances watched it for them.
Well, circumstances have changed, and so must you.
A prime example of how circumstances affect BMI is that of the Pima Indians. A group
of Pima Indians in Arizona were compared with Pima in an impoverished and remote area of Mexico.
The two groups have a shared genetic background (a background that in theory is programmed to gain weight easily), but their
circumstances are not at all alike. The Arizona Pima have a lifestyle that requires far less manual labor and provides access
to ample high-Calorie foods. As a result, the Arizona tribe has one of the highest rates of obesity
and type 2 diabetes in the world. By contrast, the Mexican Pima tribe had an average BMI of 25.9 for women (just barely “overweight,”
and far from “obese”) and 23.6 for men (well within the “normal” range). The Mexican Pima live a spartan
existence with high levels of physical activity and modest caloric intakes. As a result, they are proof that even though programmed
to be overweight (a “thrifty gene” survival response developed over thousands of years of living through lean
times),20 these Pima remain at healthy BMI levels because of their lifestyle. Granted, that lifestyle is one of
poverty and wasn’t made by choice, but from a genetic perspective it provides proof that no one is destined to be fat,
some people just have to work harder at controlling their weight. For an unlucky portion, they have to work exceptionally
hard.
Genetics of Where Fat is Stored Yes, genetics can influence where fat gets stored on your body,21
but do you really care? I’m getting tired of writing this chapter so let’s just say that guys mostly store it
in their gut, which as I pointed out in the previous chapter, is bad. Rather than dwell on this point, let’s just focus
on burning it off.
Genetics
of Physical Activity
Genetics can play an influential role in a person’s level of physical
activity. The important thing to note here is that physical activity, technically speaking, is not the same thing as exercise.
Nevertheless, if you have the genes they can be of tremendous benefit.
My daughter is a twitchy little
thing. At seven-years old she has impressive muscularity and visible abdominals. I’m not sure where these genes came
from, but it might just be one of those odd mixings that is akin to me still having hair. I can tell just by living with her
that she is genetically programmed to be active because she prefers to be mobile as much as possible (No, she doesn’t
have ADHD – she can concentrate just fine when she wants to and does well in school). Anyway, there are many people
who are “fidgeters” and this is largely an inherited trait. They have a difficult time sitting still and as a
result can burn hundreds of more Calories per day over a non-fidgeter (studies have measured this difference in a respiratory
chamber).22 Any time my daughter comes to sit on my lap to watch TV within about three minutes it turns into a
wrestling match.
I’m not a fidgeter; I can
happily glue my ass to the couch and watch a Lord of the Rings marathon getting up only to grab another beer, dial
for pizza, or get rid of some processed beer. I rarely have a burning desire to jump up and go to the gym or go for a run
– I have to consciously decide to do it. High-energy fidgeters are more likely to be active because they don’t
like sitting still.23
Now either you are a fidgeter (or hyper, on-the-go,
vigorous etc.) or you aren’t. I’m guessing you fall into the “aren’t” category, which makes
motivation to exercise and careful planning of activity that much more important.
Genetics and Physical Performance
Like obesity, muscularity, trainability and performance can be inherited
traits. Heredity plays a significant role in the amount of fat-free mass (FFM) you have. High percentage of FFM is a good
thing because it means that you have a lower percentage body fat. Being that muscle tissue makes up the majority of FFM, then
a genetic connection is easily made. In fact, studies have shown a higher genetic correlation to FFM than to fat mass and
percentage body fat.24
Your body has a definite set point of how much muscle
you can potentially build, both cleanly and using anabolic steroids (which I strongly discourage). There is an upper performance
limit for just about anything you try to do with your body. Gold medal Olympians train rigorously, but also have superior
genetic abilities that help make them better than everyone else at their sport. They are genetically programmed to be high
responders to training and to excel in a specific area or areas of sport. The marathoners can’t lift heavy weights and
the powerlifters can’t run all that far. Although their training plays a role, genetics are the key factor in these
types of differences. According to Vassilis Klissouras, “Training can not modify a phenotype [a trait that is expressed
as a result of both genetic and non-genetic factors] beyond a limit set by the genotype and will never erase individual differences
due to innate ability.”25
That “innate
ability” comes from certain fitness oriented genes. Thus far researchers have identified approximately 200 such genes.
For example, there is ACE gene which is believed to promote endurance by having an effect on cellular energy, MSTN which makes
people more muscular, and EPOR which increases endurance via improving the blood’s oxygen carrying capacity.26
If I had to guess, I’d say I’m pretty middle of the road between an endurance athlete
and a power athlete. I’ve trained myself to be pretty good at both (not in real competition, but compared to the typical
middle-aged guy). I can run a half marathon in about an hour a fifty minutes, which isn’t bad, and my highest one-rep
max on bench press is 315 pounds. I’ve never yet run a marathon, and I don’t plan to in the near future because
it goes against my visual goals of having high muscle mass. If I decided that marathons were my thing then to get good at
it I’d need to drop a bunch of muscle because the extra weight would slow me down. If I trained hard for a couple of
years I think I could get my time to about three hours and thirty minutes, and for my age group this still isn’t fast
enough to qualify for the Boston Marathon.
Conversely,
I can’t see getting much stronger without ‘roids. Benching 315 is a milestone for a lot of gym rats because it
is six 45 pound plates on the 45 pound bar. In a “regular” health club type gym there aren’t a lot of guys
who can do it. I set it as a personal goal and spent two months changing my program just to be able to say I did it. At any
given time I can bench about 290, but adding 25 pounds to my bench was friggin’ hard. I barely did it and probably never
will again. If I spent the next two years training my ass off for bench press power I might get it as high as 350
or 360. I can’t see it ever getting higher than that. Like I said, I’m pretty good at both endurance and strength,
but not exceptional at either one. As I mentioned near the beginning of this book, I sucked at every sport I tried growing
up. I am not a natural athlete. I have painful memories from gym class and to this day I hate basketball.
The type of athlete you can become is determined partially by your muscle fiber distribution.
There are two types of muscle fibers: Type I and Type II (Type II is divided into two subtypes, but the difference isn’t
significant enough to warrant exploration in a “getting in shape” book).
Type I Muscle Fibers
These are also known as slow-twitch fibers (ST), a name I will use from now on. These are small in size
and programmed for endurance. They are the aerobic muscle fibers that, in a manner of speaking, don’t reach exhaustion
– at least not for a long time. These are the ones you use when you walk, run, swim, bike etc.27
The fact that they are small is significant. Endurance athletes who don’t strength train are slim and wirey. They
have muscular definition, but their muscles lack much bulk. They also have less short-burst power.
Type II Muscle Fibers
These ones are the fast-twitch fibers (FT), are larger in size and quickly
exhausted of their energy because they are used for short-burst power. While you can run for a while (well, maybe not yet,
but we’ll get you there), the FT fibers have little stamina. These are the ones you are using while weightlifting, and
the dynamics of FT fibers is the reason why you can only lift heavy weights just a few times.28
But they’re big, and when you work them, they grow bigger. Hoo-raa.
There
is a moderate heritability factor to muscle fiber distribution, and I could relay a bunch of percentages pulled from a text
book, but I’m not sure there is much point in doing that anymore. After all, I didn’t know any of this stuff when
I got in shape, and I’m not so sure you need to either. The fact is that when it comes to muscle fibers, what you’ve
got is what you’ve got and who cares how that came to be?
However, your own past can give you
a clue as to your future. Were you a good athlete in your high school days, but then let yourself go after graduation? Were
you more of a sprinter or a distance runner? What kind of sports were you good at as a teenager? Were you good at short-burst
power sports, or endurance sports, or perhaps both? Or were you like me and sucked at everything?
Back when you could see your muscles, how did they compare to other guys your age? If you looked pretty good at 18 then
you can reclaim that physique and build on it. If you struggled with your weight even as a child then your challenges with
fat loss will be greater. If you were thin as a rail then you likely will burn fat easier than you will build muscle.
It
sounds lame and cliché to say so, but you’ll never know what you’re capable of until you try. Conclusion
Okay, that was indeed
painful. If you thought it was hard to read, imagine what it was like for a non-geneticist to write. I had to slog through
some of the most academic-oriented geek speak and then translate it into normal English. Did you note in the section on trainability
that I mentioned Vassilis Klissouras refuted claims about a segment of the population being untrainable, but I didn’t
provide details regarding his arguments as to why? Well, here are his exact words: “This postulate was based on the observation that 10 MZ twin pairs submitted to endurance training demonstrate a close
intrapair resemblance in the magnitude of change in VO2max (r = 0.74) and that the variation in training response
was six to nine times larger between pairs than within pairs (35). However, in other co-twin training studies, the intraclass
coefficient for aerobic and anaerobic power was considerably lower (9, 15), or the contribution of genotype-training interaction
to the total variance was negligible (42), while in the HERITAGE Family Study the correlation between VO2max and the VO2max
change response to training ranged from 0.03 to –0.16 (2). Neither was there any evidence of genotype-training interaction
for muscle cross-sectional area (41) nor key enzyme activity and fiber type composition of human skeletal muscle (36). In
addition, sedentary individuals were used as subjects in all these studies, and hence the focus had been centered on the etiology
of individual differences in the normal range of the distribution curve and can hardly be applied to athletes of the upper
end of the distribution. Furthermore and most important, reanalysis of Prud’ Houme’s data (35) by separating the
twins into distinct categories, those with a low and those with a high genotype, shows that the improvement of VO2max is almost
identical in both groups (23).”29
Now I can understand and appreciate what his point is, but after 90
minutes of trying to translate it into English I finally said to hell with it, grabbed a beer out of the fridge and sat down
to watch The Simpsons in an effort to return my brain to a state of normalcy. I hope you appreciate the
effort.
I digress. The point is that genetics can play an influential
role in body type, trainability, predisposition towards exercise and eating habits, as well as overall obesity risk.
Notice that I wrote “can play an influential role.” This is far from being an absolute.
Because you are now aware of how genetics can affect your efforts to get in shape, you can use that information to your
benefit. The primary takeaway from this chapter is: be adaptable. Pay close attention to what works and what doesn’t
and work on improving in areas that you are weak while taking advantage of areas in which you are strong.
It can be hard to determine exactly what genes you have. Even men who are programmed to lose fat and build muscle easily
can look like blobs if they are donut-loving couch potatoes. Maybe your genes will be your friend and maybe they won’t
be. Like most things in life, the variety of expression of the human genome distributes people along the bell curve. All men
are NOT created equal. Maybe you are programmed for power over endurance or maybe the other way around. Maybe you have potential
to be good at both. Maybe you suck at both. Not everyone gets to be an astronaut when they grow up, or an Olympic athlete.
As I wrote at the beginning, it is all about achieving your maximum genetic potential, no matter what that potential may
be, and you won’t find out what it is while watching TV. Remember that heritability is not a prison sentence unless
you decide to make it one.
Go to the Next Section
Previous Section
Notes
- Katherine Flegel et al., “Prevalence and Trends in Obesity among U.S Adults, 1999-2000,” Journal
of the American Medical Association, 288 (14), October 9, 2002, p. 1724.
- Claude Bouchard,
(Ed.), “Introduction,” Physical Activity and Obesity, (Champaign, IL:
Human Kinetics, 2000), p. 13; Stephen Roth, Genetics Primer for Exercise Science and Health, (Champaign,
IL: Human Kinetics, 2007), p. 57.
- Claude Bouchard et al., “Familial
aggregation of VO2 max response to exercise training: results from the HERITAGE Family Study,” Journal
of Applied Physiology, 87, 1999, p. 1003.
- Ibid., pp. 105-107.
- Vassilis Klissouras,
“The Nature and Nurture of Human Performance,” European Journal of Sport Science, 1 (2), June
1, 2001, p. 1.
- Claude Bouchard et al., Genetics of Fitness and Physical Performance, (Champaign, IL:
Human Kinetics, 1997), pp. 110-111.
- Preetha Anand et al., “Cancer is a Preventable Disease that Requires
Major Lifestyle Changes,” Pharmaceutical Research, 25 (9), September, 2008, p. 2097.
- Albertine Schuit,
et al., “Physical Activity and Cognitive Decline, the Role of the Apoliproprotein e4 Allele,” Medicine &
Science in Sports & Exercise, 33 (5), May 2001, p. 775.
- Louis Pérusse et al., “Familial
Resemblance in Energy Intake: Contribution of Genetic and Environmental Factors,” American Journal of Clinical Nutrition,
47 (4), April 1, 1988, p. 633.
- Bouchard et al., Genetics of Fitness,
p. 141.
- Ibid., pp. 153-154.
- Ibid., p. 153.
- Ibid., p.
153.
- Ibid., p. 182.
- Ibid., p. 183.
- Ann Hasselbalch
et al., “Common Genetic Components of Obesity Traits and Serum Leptin,” Obesity, October
16, 2008, p. 1.
- Hermine Maes, et al., “Genetic and Environmental Factors in Human Body Weight and Relative
Adiposity,” Behavior Genetics, 27 (4), July, 1997, p. 325.
- Roth, Genetics Primer, p. 57.
- Bouchard et
al., Genetics of Fitness, p. 206.
- Caroline Fox et al., “Is a low leptin concentration,
a low resting metabolic rate, or both the expression of the ‘thrifty genotype’? Results from Mexican
Pima Indians,” American Journal of Clinical Nutrition, 68, 1998, p. 1053; Bouchard
(Ed.), Physical Activity and Obesity, p. 13.
- Bouchard et al., Genetics of Fitness, p. 190.
- Ibid.,
p. 124.
- Ibid., pp. 124-125.
- Ibid., pp. 226-227.
- Klissouras,
“The Nature and Nuture,” p. 1.
- Craig Sharp, “The Human Genome and Sport, Including Epigenetics
and Athleticogenomics: A Brief Look at a Rapidly Changing Field,” Journal of Sports Sciences, 26 (11), September,
2008, pp. 1129-1130.
- Bouchard et al., Genetics of Fitness, p. 224-227.
- Ibid.
- Klissouras,
“The Nature and Nuture,” p. 7.
|