It wasn't just a preference for metrosexuals in SoCal tv studios.
On the basis of recent research, some fat people
are destined to be so by genes, and others because
of an invasion of a particular microbe. It's not
certain what came first, the obesity or the microbe,
but if they can find it, they can eradicate it. Same
could happen for the genetic problem, at some
point in the future.
For the rest of us, cut the soft drinks. The average
half litre of their goop has over 10 teaspoons of
sugar, and apparently that does a number on
your tongue and then your liver.
This is why, if you get my point about futurism, is
why there are likely no fat people on Star Trek.
They'll have been fixed, if you understand.
If Star Trek is seen as a
show of futuristic world, you would expect to
see some signs of what the future might be like.
They had pieces of plastic to hold data. they
talked to computers. They had bio-readers. they
had mobile phones with skype.
All of these things have come to pass.
The show broke the tv race barrier.
Uhuru, Chekov and Spock
Maybe they boldly went where nobody
else had dared. To dream of the
the end of Fatness.
[not an ounce of fat, and the green chicks are even better]
If it were only about self-
control, I think fat would be a personal problem.
I don't think it is strictly personal, as you'll see
below. This is a semi-scientific article, but he's
on the right track about the complexity of
what people eat.
I think a lot of it is about not being tempted by
agri-biz, and trying out new theories about
diet. enjoy.
checkit: Ted
How
microbes define, shape — and might even heal us
Rob
Knight
As both
a scientist and a human being, I am continually awestruck by discoveries about
the power of the microbiome to define and shape us. But what excites me most is
the very real prospect that, as we come to better understand and even influence
the microbiome, it could have the power to heal us.
We’re
already starting to link our microbes to
a wide spectrum of specific diseases, from the obvious — like infectious
diseases and inflammatory bowel disease — to surprising ones such as multiple sclerosis, autism, and depression.
It’s
worth noting that just because we know a microbe is involved in a specific
disease, it doesn’t mean the answer — or
the cure — is to eliminate that microbe. In fact, doing so might cause
irreversible damage. It may turn out that targeting diet or inhibiting an enzyme (that’s a protein that speeds up
a particular chemical reaction) might be more effective than attacking the
microbes directly. And yet the reason there is so much excitement about the
microbiome is the prospect of discovering entirely new mechanisms to treat
conditions that have resisted existing therapies.
susceptibility to essentially every kind of
infection hinges greatly on genetics.
But
first, let’s ask: How is it we know that certain microbes are associated with
particular diseases?
The
easiest cases to make are those where one particular microbe has a significant
impact on health, which essentially describes the last 150 years of infectious
disease research. If you get exposed to a microbe such as Salmonella, or Giardia,
or Mycobacterium tuberculosis (the bacterium that causes tuberculosis), you
expect to get sick. And then, if you treat it with the right antibiotic (or other drug), you expect
to get better.
But
wait: Do you always get sick just because you’re exposed?
Actually,
our risk of sickness depends on a combination of exposure, genetic makeup, and
other factors. Some people are born with resistance
to certain diseases. You’ve probably heard of Typhoid Mary, a New York cook in the early twentieth century who carried
the bacteria that causes the disease typhoid fever. She infected family after family with her excellent cooking that was
laced with a dose of her not-so-excellent microbes. But Mary was never
sick. She was naturally immune to the fever she carried inside her. Where does
such resistance come from? Well, it’s these questions that make mouse studies
popular with researchers: besides the fact that we can more ethically give a
mouse an infection, we can also manipulate the mouse’s genome. From these studies,
we’ve learned that susceptibility to
essentially every kind of infection hinges greatly on genetics. And mouse
versions of Typhoid Mary are easy to create in the lab — not just for typhoid
fever but also for a whole range of other infections. It’s proof that our genes
influence which microbes make each of us sick.
We’re
beginning to realize that there may be many more diseases where we’re all
exposed to the same microbe, but it’s dangerous only to some of us. We still
need more research to explain why.
But in
the meantime, what follows is a roundup of the key diseases in which we now
suspect that microbes may play a part.
Inflammatory
Bowel Disease
Inflammatory
bowel disease (IBD) is a catch-all diagnosis for inflammation of the digestive
tract. The big illnesses that fall under the IBD label are ulcerative colitis
and Crohn’s disease. What these diseases have in common is an altered relationship between intestinal
microbes and the immune system. In an attempt to target the pathogens
afflicting you, your body goes to war
with all the creatures in your intestines, and the intense pain, bleeding,
and all-too frequent trips to the toilet are the collateral damage.
One
typical sign of these diseases is an increase in the abundance of certain bacteria. What’s particularly interesting is
that the microbes in patients do not appear to be behaving normally: their
metabolism is off; they’re eating and secreting different chemicals. We
don’t yet know if this altered behavior is caused by the body’s immune response or if microbes are at fault.
Your immune system does not so much keep lists of good and bad microbes as it
concerns itself with good and bad microbe behavior. Your immune system is not
the FBI conducting a manhunt for John Dillinger. Instead, it’s the guard in the bank who freaks out and opens
fire when somebody leaps the counter and starts stuffing money into a sack.
It’s
also not clear yet if these inflammatory bowel diseases are caused by a change
in the microbiome or if there is something in the genes of the afflicted that
causes the body’s normal relationship with gut microbes to go awry, and the
changes in the microbial population are merely a response. Perhaps it is some
combination of both factors?
Celiac
disease is related to inflammatory bowel disease and also involves an immune
system component: when celiac sufferers eat wheat products, the natural gluten
proteins in wheat activate the immune
system, which attacks the lining of the gut, shredding it. Celiac was
originally identified and named by the
Greek physician Aretaeus of Cappadocia in the first or second century AD.
But it wasn’t as widely known until Dutch
physician Willem-Karel Dicke observed in the “Hunger Winter” of 1944–45 during
World War II that when wheat was unavailable, his celiac patients survived
much better. (Dicke would go on to pioneer the gluten-free diet.) There has been intense interest in whether
celiac is linked to the microbiome, but at this point, the dozen or so studies
have found essentially no consistent trends associating microbes with celiac.
Although many studies are able to find differences between the microbiomes of
celiac patients and healthy people, the bacteria in the celiac patients differ
from study to study. Clearly the pattern is complex, and more work is needed to
understand whether gut bacteria contribute to celiac or simply respond to the
altered, gluten-free diets of celiac patients.
Obesity
Until
a trip to Peru in 2008, I used to
weigh quite a bit more. My wife Amanda and I hiked the Inca Trail and then spent
a week in the Amazon, where we both came down with really nasty diarrhea — not
what you want when you’re in a tent. We recovered, only to both have it flare
up again. To treat it, we both took doses of the same antibiotic. When we got home, we resumed more or less the same
diets and exercise patterns we’d had before we left for the trip. However, I
lost about eighty pounds in a few months, going from obese to a healthy body weight.
The
difference was remarkable. I had to buy new pants, and colleagues took me aside
to ask if I had cancer or if there was something else they should know about.
In contrast, Amanda lost no weight at all. I believe that the difference was
related to a radical change in my microbes:
we each responded differently to the same disease and the same course of
treatment.
there’s a strong microbial component to
obesity.
While
we can’t, of course, draw scientific conclusions from a study of one couple, my
experience here mirrors what published studies are increasingly showing. We’re
learning that there’s a strong microbial component to obesity. Normal-sized,
germ-free mice that receive a fecal
transplant from an obese mouse become fatter themselves. And the experiment
works regardless of whether that first mouse was fat because it had been
overfed an unhealthy diet or because it had a genetic mutation that made it
fat.
You
might wonder if it’s the microbes that are doing this or if it’s something else
in the stool? Good question. To answer it, Jeffrey Gordon, a biologist who
directs the Center for Genome Sciences and Systems Biology at the Washington
University School of Medicine in Saint Louis, and a team of researchers in his
lab, asked whether you could isolate hundreds of individual strains of bacteria
from an individual person, grow each strain in the lab (without the rest of the
fecal matter), mix them together in similar proportions as in the original
sample, and then transfer the differences in weight by transferring those
bacteria to a new host. Indeed they could, proving that it was the microbes
responsible for the weight gain — not a virus, an antibody, a chemical, or
anything else in the stool. Even more remarkably, by isolating bacteria from
lean people, we could design a microbial
community that prevented a mouse from gaining the weight it would normally
gain when housed with an obese mouse and exposed to its new roommate’s chubby
microbes.
My lab
and others haven’t been able yet to design a microbe community that actually
slims down a mouse (or a person), although that’s certainly the goal. But in
yet-unpublished research, other groups have reported using antibiotics to
target the bacteria that proliferate on a high-fat diet, successfully slimming
down the mice even if they still ate unhealthily.
It’s exciting to think that we could grow
ourselves healthier and leaner microbiomes by altering our diets.
Many
fad diets for humans are now targeted at improving your microbiome. But the evidence that these actually work is limited. We just don’t know enough
about the ways in which particular microbes affect digestion and absorption to
make a targeted intervention. In 2011, researchers at Harvard University
published a study in the New England Journal
of Medicine that found some foods are associated with weight gain, and others with
weight loss. It won’t shock you to hear that fat-rich French fries are
associated with weight gain, more so than any other food. But oddly, the two foods most associated with weight
loss are yogurt and nuts, even though both can be high in fat. What exactly
is going on? Well, microbes might play a role here. We know from studies in
mice that particular microbes, or combinations of microbes, are associated with
weight gain or weight loss. Could there be a connection between specific foods
and the microbes that make us slimmer?
There
is plenty of evidence that what you eat
alters your microbiome, making it more habitable for some species and less so
for others. Gary Wu, a professor of gastroenterology at the University of
Pennsylvania, has shown that diet over the long term — a year or more —
correlated very strongly with the overall microbiome. It was his team that
demonstrated that people who ate a lot of
carbohydrates (pasta, potatoes, sugars) tended to have a lot of Prevotella.
In contrast, people who ate a lot of protein, especially meat (a la the Western
diet), tended to have a lot of Bacteroides.
These two genera of bacteria help us digest and metabolize our food, but they thrive on different foods. We’ve yet to
untangle what influence Bacteroides species have on such typically Western
diseases as obesity and diabetes,
but there are some suggestive correlations. It’s exciting to think that we
could grow ourselves healthier and leaner microbiomes by altering our diets.
Some
dietary changes can rapidly alter our microbes. Peter Turnbaugh, a systems
biologist then at Harvard University, and his colleagues got some hardy
volunteers to either go vegan or to eat essentially a meat-and-cheese diet. Veganism caused little immediate change to
their gut microbes. But the meat-and-cheese diet caused big changes overnight, increasing the kinds of bacteria linked to
cardiovascular disease, such as Bilophila wadsworthia. So a sufficiently
extreme diet can have bad effects quickly: an open question is whether there’s one
that exerts good effects that fast.
Allergies
and Asthma
The
idea that reduced microbial
diversity leads to asthma and
allergies dates back to the work of David Strachan at St. George’s Hospital
Medical School at the University of London. In the late 1980s, Strachan noticed that later siblings in
larger families tended to have lower rates of hay fever and related
allergies, and he suggested that catching infections from older siblings
(especially classic childhood diseases) might help train the immune system to target real invaders, not dust mites.
This idea, known as the “hygiene hypothesis,” essentially suggests that keeping
ourselves too clean can lead to
immunological problems, as our idle immune systems — unchallenged by the
bacterial and viral pathogens that humans co-evolved with — get restless.
you still shouldn’t challenge your kid’s
immune system by encouraging them to eat tainted meat or lick a hospital floor.
Since
Strachan’s time, the focus has shifted away from common infections such as measles, colds, and flu, which are now believed
to be strictly harmful. Instead, the
modern hygiene hypothesis centers on our squeakyclean
childhoods, which keep us insulated from diverse microbes from healthy sources, ranging from soil to leaf
surfaces to domestic or wild animals. To understand how this works, think
of your immune system as a radio: if you’re dialed into a specific station you
can hear the music crystal-clear, but if you’re between stations then random
signals can cause loud and unpleasant static. In a similar way, the immune system may find something else
to latch onto if there is no signal. If you’re lucky it’ll be pollen or
peanut butter that spikes through the “static,” causing allergies, but if
you’re unlucky the immune system might latch onto your own cells, causing diabetes, multiple sclerosis, or other
autoimmune diseases.
Translation
for parents: you still shouldn’t challenge your kid’s immune system by
encouraging them to eat tainted meat, lick a hospital floor, approach a rabid
bat, or otherwise expose themselves to likely harmful microbes — but the modern
hygiene hypothesis says encountering good
microbes via dirt and contact with healthy, diverse people and animals may be
good preventive medicine.
What’s
the evidence for this? Well, it’s been growing rapidly, with more than one in
four of the articles on record
published just in 2014. Erika von Mutius at the Children’s Hospital of the
University of Munich is a pioneer in this area. She has showed that exposure to
farming in early life reduces the
risk of allergies and asthma substantially, and that some of this effect can be
explained by children coming in contact with straw, cows, farm milk, and
certain bacteria and fungi. What
about the impact of our invariably dusty
homes, which seem to harbor all sorts of nasal irritants despite our best
efforts with the mop? Contrary to expectations, von Mutius and others have
demonstrated that exposure to allergens
such as dust mites and cat hair does not explain the incidence of asthma.
Some intriguing
recent findings suggest that microbial exposure
during pregnancy, not just during childhood, may be important for reducing
allergic diseases (although some caution is warranted here because in mice, viral attack or even simulated viral
attack during pregnancy can trigger symptoms resembling autism).
Other promising, yet still preliminary, results show that:
several probiotics can relieve atopic
disease and asthma (Lactobacillus salivarius LS01, in particular, can reverse
atopic dermatitis symptoms in some children).
changing animals’ microbiota with
antibiotics can induce allergic diseases.
certain microbe species can reverse food
allergies in mice or prevent the food allergies from developing in the first place — while others can cause them.
exposure to diverse microbes, whether
through older siblings, pets, or through good old-fashioned playing outdoors,
seems to help.
The
data on whether breast milk can
reduce the incidence of these diseases is somewhat equivocal: the few robust studies
that have been done tend to show modest if any effects. Interestingly, simply living in a setting with more diverse
microbes (say, a home with a backyard garden rather than an urban apartment far
from any parks) seems to decrease risk of allergic disease. And it’s clear that
one’s setting exists indoors, not just outdoors. Early exposure to dogs, especially prenatally and in the first year of life, appears to decrease
allergy risks later. Surprisingly, we showed that having dogs, but not having
kids, increased human microbial diversity for couples living together. However,
exposure to dogs and cats in adolescence
increases the risks of asthma and eczema.
It’s
tricky to add up all this early evidence into a prescription for lowering your
child’s risk of asthma and allergies. I’d sum up the recommendations like this:
have a dog (but make sure you start early, ideally prenatally), live on a farm
where your kids are exposed to cows and straw, avoid antibiotics early in life,
and perhaps take probiotics and breastfeed (although the evidence for those
last two is preliminary at present). In general, exposure to diverse microbes,
whether through older siblings, pets, or livestock — or through good
old-fashioned playing outdoors — seems to help, even if scientists are still
sorting out the specific microbes involved. It may be that diversity itself is
most important.
This
text is taken from Follow Your Gut: The Enormous Impact of Tiny Microbes, by
Rob Knight, with Brendan Buhler (TED Books/Simon & Schuster), available
now. Illustrations by Olivia de Salve Villedieu.
