Posts Tagged ‘epigenetics’

Obesity: Insulin trumps Genetics

April 15th, 2009
Artist: Brian Clarke

Artist: Brian Clarke

I have said it before and I will say it again.

Genetics isn’t Destiny.

Even when it comes to obesity.

And if you don’t believe me:

Purdue University scientists have uncovered evidence that genetically identical cells store widely differing amounts of fat, depending on subtle variations in how the cells process insulin.

They said identifying the precise mechanism responsible for fat storage in cells could lead to methods for controlling obesity.

Although other studies have suggested certain “fat genes” might be associated with excessive fat storage in cells, the Purdue researchers confirmed such genes are expressed, or activated, in all of the cells. Yet those cells varied drastically — from nearly zero in some cases to pervasive in others — in how much fat they stored.

Their findings indicate that the faster a cell processes insulin, the more fat it stores.

It’s the insulin…it’s the insulin…it’s the insulin.

Just ask Jack Sprat.

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Fat Babies become Fat Kids become Fat Teenagers become Fat Adults

January 15th, 2009

fat-babies

You are not going to believe this people.

According to some startling new research, there is a direct connection between an adult’s propensity to put on weight and our early childhood diet.

I know, I know.

Who would have guessed that feeding your baby Big Macs and washing them down with Super Big Gulps could result in them having a “weight issue” as an adult?

Seriously.

Who would have guessed that?

Not his parents!

Not his parents!

and certainly not the parents of the kids in this video. (sorry about the music)

The Research

University of Calgary researcher, Dr. Raylene Reimer is a leader in the growing field of epigenetics. Her personal area of expertise is the developmental origins of health and disease. “Researchers in this area believe our pre-natal and early childhood environment influences our future risk of developing conditions like cardio-vascular disease, obesity and diabetes”.

“My research has shown that the food we eat changes how active certain genes in our body are – what we call genetic expression. In particular we believe that our diet has a direct influence on the genes that control how our bodies store and use nutrients,” says Reimer.

“There’s a growing body of work that indicates a relationship between our health as adults and our early diet, and even our mother’s diet. This research shows for the first time that our early childhood diet may have a huge impact on our health as adults.”

This research dovetails nicely with the previous studies which showed that:

  • baby_smokingBabies who smoke cigarettes are more likely to develop lung cancer
  • Babies who do shots of tequila with their parents are more likely to become alcoholics, and
  • Babies who drive automobiles without wearing a seat belt are more likely to be involved in traffic accidents

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Why Do We Get OLD?

December 1st, 2008

brad-pitt-benjamin-button-brad-ages

Harvard researchers may have just found the “root cause of aging”: A group of proteins called sirtuins.

For a decade or so, scientists have known that these sirtuins are somehow involved in the aging process.

Their interest in these sirtuins really went wild when they discovered that:

would stimulate the sirtuins into having a positive effect on aging.

So What Exactly Do Sirtuins Do?

sleeping-guardSirtuins are like a genetic watch dog.

They keep an eye on select genes to see which are turned on and which are turned off. Kind of like a security guard monitoring motion alarms and video monitors.

Here’s why:

  • While all genes are present in all cells, only a select few need to be active at any given time.
  • If the wrong genes are switched on, this can harm the cell.
  • For example, in a kidney cell, there are liver genes present, but they are switched off. If these liver genes were to become active, that could damage the kidney.

The sirtuins guard the genes that are supposed to be off and ensure that they stay that way.

To do this, they help preserve the molecular packaging—called chromatin—that shrink-wraps these genes tight and keeps them idle.

However, sirtuins have another important job.

When your DNA gets damaged by UV light or free radicals, sirtuins stop their security guard duties and rush to the site of the damaged DNA and join in on the repair.

This leads us to…

The Latest Research

In this study, the researchers found that when the sirtuins left their guard posts and rushed towards the damaged DNA, the chromatin wrapping (or shrink-wrap) covering the sleeping genes could start to unravel, and the genes that were meant to be inactive (or regulated) could in fact become active (or un-regulated).

This isn’t good.

spider-web-prey-sirtuins-genes

A Sirtuin re-wraps a Gene and puts it back to sleep

Luckily for us, the sirtuins are usually able to return to their post in time to get the awakened genes back under wraps before they cause any permanent damage.

However, the scientists found that as mice age, the rates of DNA damage increases.

This means that the sirtuins are being pulled away from their guard duties more and more often.

As a result, more and more sleeping genes wake up, break out of their shrink-wrap and break free before the sirtuins can return and put them back to sleep.

Once again, not good.

pod-people-invasion-of-the-bodysnatchersIn fact, it’s really starting to sound a lot like the Pod People from that movie, The Invasion of the Bodysnatchers.

And it gets even worse,

  • Scientists found that many of these haplessly activated genes are directly linked with aging, and that
  • They also found that older mice had higher numbers of these unregulated genes.

But don’t despair, it gets better:

The Good News

Discovery of the mechanism behind all of this bad news has led to a hypothesis on how to reverse this action and potentially reverse signs of aging.

Scientists began wondering what would happen if they put more of the sirtuin back into their aging test mice.

They believed that with more sirtuins on the job, DNA repair would be more efficient, and the aging mouse would maintain a youthful pattern of gene expression into old age.

And that’s precisely what happened.

Using a mouse genetically altered to model lymphoma, researcher Philipp Oberdoerffer administered extra copies of the sirtuin gene, or fed them the sirtuin activator resveratrol, which in turn extended their lifespan by 24 to 46 percent.

Conclusions

Because of this research, we now know that while DNA damage increases the rate of aging, it isn’t the actual cause of aging.

  • Un-regulated genes are the cause of aging.

And, because of this research, we also know that if we can help the sirtuins keep regulated genes from becoming un-regulated, the elements of aging can be reversed.

Big news people, big news.

.At least for the mice.

Tests on humans are yet to be scheduled.

Paul Giamatti (Sideways) loads up on his Resveratrol

Paul Giamatti (Sideways) loads up on his Resveratrol

So, for now, loading up on some resveratrol may be a good idea.

And if you have any questions….hang on for another 24 hours; tomorrow’s post will be dedicated to everything resveratrol.

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Genetics Isn't Destiny

September 9th, 2008

  • You’re 20 pounds overweight.
  • You have been trying to lose that weight for years and years.
  • Not matter how hard you try, the weight just won’t come off.

Sound familiar?

You bet.

Maybe it’s your genetics?

In the last few years, study after study has have linked genetics to obesity. Here are just a few of the studies:

And here’s the latest scientific gem:

In this latest study, scientists from the University of maryland looked at the common FTO (fat mass and obesity associated) gene variants that have recently been associated with high Body Mass Index (BMI) and obesity in several large studies.

Specifically, they investigated the effect that physical activity can have in those people born with the FTO gene variant.

Can Exercise Trump Genetics?

A little background on the FTO gene variant:

  • Carriers of this gene variant are more likely to be obese.
  • In fact, people with two copies of the FTO variant are on average 7 pounds heavier and 67 percent more likely to be obese than those who don’t have it.
  • Carriers also have higher rates of type 2 Diabetes.
  • The International HapMap Project estimates the number of FTO carriers as:
  • 45% in the West/Central Europeans population
  • 52% in Yorubans (West African natives) population
  • 14% in Chinese/Japanese population

The Study

Researchers looked at a population of Old Order Amish in conducting this study.

The Amish were used because:

  • Their day to day activities provide a high level of physical exercise. This is due to the fact that the Amish don’t drive cars or have electricity in their homes, eschewing many of the trappings of modern life. Most Amish men are farmers or work in physically demanding occupations such as blacksmithing or carpentry. Women are homemakers who work without the aid of modern appliances and often care for many children.

The researchers tested the particpants for:

  • The presence of the FTO gene variant
  • Their BMI scores
  • Their levels of physical activity

The participants’ activity levels were measured with the aid of accelerometers, worn on the participants’ hips.

The researchers gathered measurements of their physical activity over seven consecutive days.

Participants were classified as “high activity” or “low activity” depending upon their accelerometer readings.

The “high activity” group burned 900 more calories per day than the “low activity” group. This total translates into 3 to 4 hours of moderate intensity activity, such as brisk walking, housecleaning or gardening.

The Results

The researchers found that the Amish people with the FTO variant were no more likely to be overweight than their non-FTO carrying cousins….as long as they got their three to four hours of moderate activity every day.

Conclusion

Genetics isn’t Destiny

Being born with a FTO gene variant does not guarantee a lifetime of obesity and diabetes.

The choice is up to you.

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Epigenetics & Obesity – Obesity Research Update #3

July 16th, 2008

Researchers at Baylor College of Medicine have made a groundbreaking discovery – Overweight moms give birth to children who become even more overweight and who in turn have children who become even more overweight and so on and so on.

Damn!

Maybe I have been wrong all these years. Maybe our body composition is determined by our DNA.

Nope.

According to this study, researchers found that by supplementing an obese mother’s diet with folic acid and other methyl supplements, they were able to reverse this form of inherited obesity.”

The Hypothesis

Lead researcher, Dr. Robert Waterland, designed this study to test the hypothesis that maternal obesity before and during pregnancy affects the body weight regulatory mechanisms in her offspring.

In layman’s terms, does a fat mom produce fat babies?

In regards to reversing this cycle of inherited obesity, Dr. Waterland believes that “DNA methylation may play an important role in the development of the hypothalamus (the region of the brain that regulates appetite).”

The Method

Waterland et al tested this hypothesis on three generations of genetically identical mice, all with the same genetic tendency to overeat. (agouti viable yellow [Avy] mice)

The mice were divided into two groups:

  1. Standard diet group
  2. Standard diet supplemented with folic acid, vitamin B12, betaine and choline. This special ‘methyl supplemented’ diet enhances DNA methylation.

Sorry about that. You don’t have to worry about nerd terms like DNA methylation, there won’t be a test at the end of this post.

What they were attempting to do was to reduce or silence the effect that the inherited gene had over the development of the baby mice.

Can mice that are genetically predisposed to obesity be spared from a life of stretchy pants and motorized scooters?

The Results

The mice on the standard diet piled on the body-fat, as expected, and subsequent generations were progressively more obese.

Those on the methyl supplemented diet did not gain weight through successive generations.

So what does this mean to me?

Well, according to Dr. Waterland, “the effect of methyl supplementation on body weight was independent of epigenetic changes at the Avy locus, indicating this model may have direct relevance to human transgenerational obesity”.

OR

This treatment could be safely adapted for human trials and could potentially provide a cure for inherited pediatric obesity.

Please note that this is one study, performed on mice. This doesn’t mean that moms-to-be should start mega-dosing supplements in order to produce babies with six packs.

Let the geeks do their work.

First come the scientific human trials. Then come the drug company trials. Then come the drugs and/or supplements.

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Nutrition, Environment and Epigenetics

May 5th, 2008

Genetics is Not Destiny.

I truly believe that. I have to believe that.

As a kid, I was always ‘husky’.

Through research, discipline and hard work, I was able to transform my body from fat to fit.

During the past 19 years, I have given my knowledge and perhaps more importantly, my confidence in that knowledge to the people that came to me and asked me to help them re-shape their bodies.

While most of them already knew what they had to do to become physically fit; they just couldn’t do it.

But they had seen their friends / my clients sculpt lean, strong, fit bodies out of the over-sized lumps of clay that they had previously called home.

So they came to me for the secret. Even after I told them there was no secret, and even after I had helped them transform their own bodies, most of them believed that I was responsible for their transformations.

Years of being fat and out of shape had become normal for them. They were fat. Even when they had lost the weight, there was still this little voice in the back of their heads telling them that this was just temporary. If they stopped working with me, they would re-gain their original shape.

It was their genetics.

How wrong they may have been.

Ever since Darwin’s Survival of the Fittest theory of evolution became accepted as truth, genetics and in particular our DNA has shaped the progress of human biology.

Science searched for a genetic answer to every human ailment. It even spawned a genetic ‘gold rush’ called the Human Genome Project.

But recently, that absolute faith in genetics as fate has been shaken. So

Epigenetics.

Epigenetics looks at the impact our environment has upon our genetic coding.

How is it that one identical twin can develop cancer while the other twin does not?

Was the life-long smoking habit of one of the identical twins responsible for their diagnosis of cancer? Did the healthy lifestyle of the second twin prevent their potential diagnosis of cancer?

While the science is still new, I think down deep, we all know that how we live our lives has a strong impact on our health.

Where we live. Our friendships, or lack thereof. The air we breathe. The water we drink. The amount and type of exercise we perform. The food we eat.

Nature v.s. Nurture.

Bruce Lipton is currently the biggest ‘name’ in Epigenetics. The following two video clips serve as an introduction to Lipton and the science behind Epigenetics.

Like most scientific endeavours, epigentics seems to result in more questions being raised rather than answering the ones that we already have.

For those interested, I will report back with new & interesting research into this field of science and how it applies to health & nutrition.

Remember, genetics is not destiny.

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