Researchers Discover the Skinny Gene

For years, people have been using their crappy (ie fat) genetics as an excuse for being obese.

And for years, their fit friends have been telling them to stop eating junk and to get their butts off of the couch.

So who would have guessed that for a teeny-tiny 0.0005% of the population…there is a genetic cause for being skinny.

In a new study published in the journal Nature, researchers have found that 1 in 2000 people are born with a duplication of part of chromosome 16, making men 23x and women 5x more likely to be underweight.

Each person normally has a copy of each chromosome from each parent, so we have two copies of each gene. But sometimes sections of a chromosome can be duplicated or deleted, resulting in an abnormal ‘dosage’ of genes.

Half of all children with the duplication in this study have been diagnosed with a ‘failure to thrive’, meaning that their rate of weight gain is significantly lower than normal. A quarter of people with the duplication have microcephaly, a condition in which the head and brain are abnormally small, which is associated with neurological defects and shorter life expectancy.

Last year, the same researchers discovered that people with a missing copy of these genes are 43 times more likely to be morbidly obese.

Professor Philippe Froguel, from the School of Public Health at Imperial College London, who led the study, said: “The dogma is that we have two copies of each gene, but this isn’t really true. The genome is full of holes where genes are lost, and in other places we have extra copies of genes. In many cases, duplications and deletions have no effect, but occasionally they can lead to disease.

“So far, we have discovered a large number of genetic changes that lead to obesity. It seems that we have plenty of systems that increase appetite since eating is so important – you can suppress one and nothing happens. This is the first genetic cause of extreme thinness that has been identified.

“One reason this is important is that it shows that failure to thrive in childhood can be genetically driven. If a child is not eating, it’s not necessarily the parents’ fault.

“It’s also the first example of a deletion and a duplication of one part of the genome having opposite effects. At the moment we don’t know anything about the genes in this region. If we can work out why gene duplication in this region causes thinness, it might throw up new potential treatments for obesity and appetite disorders. We now plan to sequence these genes and find out what they do, so we can get an idea of which ones are involved in regulating appetite.”

The part of chromosome 16 identified in the study contains 28 genes. Duplications in this region have previously been linked with schizophrenia, and deletions with autism.


It may be more convenient to blame your out of shape body on your crappy (ie fat) genetics instead of owning up to your lifestyle choices, but you really, really wouldn’t want one of these genetic errors.

So, count your lucky stars that you’re healthy, download A Paleo Diet for the 21st Century and start doing my Best Body workouts.



You Are What Your Father Ate

Attention all fathers to be!!!

Researchers from the U of Mass have found that the food you eat is going to make a big difference upon the health of your future children.

So, before you inhale another bucket of popcorn chicken, be aware that your diet will influence the genetic makeup of your children.

In the UMass study, researchers found that adult mice fed a low protein diet produced offspring with an increase in the production of cholesterol synthesis genes.

And while this doesn’t mean that the wee baby mice are doomed to a lifetime of high cholesterol and prescriptions for lipitor, it does mean that a parent’s diet has a big impact on their kids –  in the form of changed epigentic information.

In the UMass experiment, scientists fed two different diets to two different groups of male mice – a standard diet and a low-protein diet. All females were fed a standard diet.

And as nature took it’s course and little mice babies were born, the researchers observed that the low-protein offspring showed an increase in the genes responsible for lipid & cholesterol production in comparison to the standard diet mice.

The observations are consistent with two human studies (1 & 2) which showed that a poor adolescent diet in one generation resulted in an increased risk of diabetes, obesity and cardiovascular disease in second-generation offspring.

However, since these previous human studies were retrospective and involved dynamic populations, they were unable to completely account for all social and economic variables.

Hence this study with lab mice.

According to lead researcher Oliver Rando, “Our study begins to rule out the possibility that social and economic factors, or differences in the DNA sequence, may be contributing to what we’re seeing. It strongly implicates epigenetic inheritance as a contributing factor to changes in gene function.”

Co-author Hans Hofmann continues by saying that “the results also have implications for our understanding of evolutionary processes. It has increasingly become clear in recent years that mothers can endow their offspring with information about the environment, for instance via early experience and maternal factors, and thus make them possibly better adapted to environmental change. Our results show that offspring can inherit such acquired characters even from a parent they have never directly interacted with, which provides a novel mechanism through which natural selection could act in the course of evolution.”

So, what does this mean?

According to Dr. Rando, “we often look at a patient’s behavior and their genes to assess risk. If the patient smokes, they are going to be at an increased risk for cancer. If the family has a long history of heart disease, they might carry a gene that makes them more susceptible to heart disease. But we’re more than just our genes and our behavior. Knowing what environmental factors your parents experienced is also important.”

What’s next for this research?

Drs. Rando et al will begin to explore how and why this genetic reprogramming is being transmitted from generation to generation. “We don’t know why these genes are being reprogrammed or how, precisely, that information is being passed down to the next generation,” said Rando. “It’s consistent with the idea that when parents go hungry, it’s best for offspring to hoard calories, however, it’s not clear if these changes are advantageous in the context of a low-protein diet.”

What does this mean for you?

It means that not only will that bucket of popcorn chicken screw up your health, it will probably screw up your kid’s health as well.


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Obesity & some really cool genetic research

We all know that obesity is highly heritable – from parent to child to grandchild, etc…

And while I believe that we should be focusing our attention on the epigenetic effects of our lifestyle and environment, there is still some pretty cool genetic research going on.

And this study is definitely cool.

Using genetic resequencing, researchers have identified DNA variants in two nervous system genes that are associated with an excessively high BMI.

According to study author Kelly Frazer, “we sequenced two intervals encoding the enzymes FAAH and MGLL which modulate the levels of endocannabinoids present in the brain and peripheral tissues that are involved in the regulation of energy balance and appetite. The level of these endocannabinoids is high in obese patients, and thus these two enzymes provide strong candidates to examine for a genetic association with BMI”.

And for everybody who has ever inhaled, you know the effect that endocannabinoids can have on your appetite.

Using genetic resequencing, the researchers identified four regions associated with BMI: the FAAH promoter, MGLL promoter, MGLL intron 2, and an enhancer in the MGLL intron 3.

Further testing revealed rare variants associated with increased levels of endocannabinoids in the plasma, which is consistent with previous findings.

According to Frazer, “This is one of the first studies to use the new sequencing technologies to link rare and low frequency variants to a complex trait such as obesity and will be of particular interest to understand more comprehensively the role of inheritance in obesity, a rapidly rising serious health issue across the world”.

Or, in layman’s terms…some of us have a genetic predisposition to higher levels of endocannabinoids in our brain & nervous system. This may lead to a genetically elevated appetite…which may lead to a greater sense of hunger…which may lead to overeating….which may lead to obesity.

The operative word being may.

Because, even if you have this genetic predisposition, there’s not a darn thing you can do about it.

With our current understanding of obesity, it still comes down to lifestyle choices.


But, this genetic resequencing stuff is still pretty cool.




Can Potassium Reverse High Blood Pressure?

  • High blood pressure is a killer….we all know that
  • Eating a diet high in sodium can lead to high blood pressure….we all know that

And because we know these things, a lot of people have been told by their doctors to stop eating this…

Salty Snacks

…and to start eating this…


And they aren’t happy about it……….but maybe there is another way.

Maybe, instead of labeling salt as a BAD FOOD, and banning it from our diets altogether, we can balance out the hypertensive effect of sodium with the hypotensive effect of potassium. If only we had some proof…

The Proof

Earlier this year, researchers found that “the ratio of sodium-to-potassium was a much stronger predictor of hypertension and cardiovascular disease than sodium or potassium alone”.

“There isn’t as much focus on potassium, but potassium seems to be effective in lowering blood pressure and the combination of a higher intake of potassium and lower consumption of sodium seems to be more effective than either on its own in reducing the risk of cardiovascular disease,” said Dr. Paul Whelton, senior author of the study in the January 2009 issue of the Archives of Internal Medicine.

In this study, researchers determined average sodium and potassium intake of their test subjects.

They collected 24-hour urine samples intermittently during an 18-month period in one trial and during a 36-month period in a second trial.

The 2,974 study participants initially aged 30-to-54 and with blood pressure readings just under levels considered high, were followed for 10-15 years to see if they would develop cardiovascular disease.

The Results

  • The highest salt consumers were 20% more likely to suffer strokes, heart attacks or other forms of cardiovascular disease when compared to the lowest of the low sodium eaters.

20% more likely to suffer a stroke. That sounds great…time to ditch that salt shaker…..right?  Maybe not…

  • The participants with the highest sodium-to-potassium ratio in urine were 50 percent more likely to experience cardiovascular disease than those with the lowest sodium-to-potassium ratios.

According to this study, the ratio of potassium to sodium in your diet is more important to the health of your heart than the overall consumption of sodium.

According to Dr. Whelton, healthy 19-to-50 year-old adults should consume no more than 2,300 milligrams of sodium per day — equivalent to one teaspoon of table salt.

NOTE: More than 95 percent of American men and 75 percent of American women in this age range exceed this amount.

What does this mean to you?

Odds are that you are part of the majority whose sodium : potassium ratio is out of whack.

  • How much potassium do you need to help balance out the salt?

To lower blood pressure and blunt the effects of salt, adults should consume 4.7 grams of potassium per day unless they have a clinical condition or medication need that is a contraindication to increased potassium intake.

Most American adults aged 31-to-50 consume only about half this amount.

  • And how do we get more potassium?
  • Good potassium sources include fruits, vegetables, dairy foods and fish.
  • Foods that are especially rich in potassium include potatoes and sweet potatoes, fat-free milk and yogurt, tuna, lima beans, bananas, tomato sauce and orange juice.
  • Potassium also is available in supplements. However, most potassium supplements come in dosages of 50mg . To get your daily 5 grams, you would need to take 100 pills.

So, maybe we should listen to the good doctor and “Let food be thy medicine and medicine be thy food”Hippocrates

Click here for the USDA’s list of foods high in Potassium..

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The status-quo is broken…We need a new model for burning fat and getting fit

For decades, we have listened to the nation’s health experts tell us:

  • what to eat,
  • what not to eat,
  • how much to eat,
  • how much exercise we need,
  • what type of exercise we need….

And, after all of that advice, we have become a nation world afflicted with runaway obesity, diabetes, heart disease, liver disease, cancer, etc…

And yet, when we want to improve our health or reduce our waistlines, we still turn to the experts.


Everyday I meet people who are trying to get into shape. For years, they have been trying to follow the rules laid down by the experts.

  • They followed the food pyramid
  • They cut the fat out of their diets
  • They did their 20 minutes of fat-burning cardio
  • They choked down their egg white omelettes
  • They ate their fiber

And they watched their backsides get wider and their blood pressure rise higher and higher.

  • It’s time for a change.
  • The status quo is broken.
  • The top-down approach doesn’t work.

But with the technology available today, we don’t need to rely solely on that expert advice from up above. We can connect those people who are desperate to transform their bodies with those people willing to help. We can create a tribe of people devoted to health, fitness and each other.

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Here's why you NEED aerobic exercise

Let’s face it. Cardio is boring. Running laps around a track or pedaling away like some spandex wearing gerbil…..Boring.

But,according to the authors of this new study, “your personal aerobic fitness is not something you will see in the mirror but it is an important predictor of your long-term health,”

“The most important part of physical activity is protecting yourself from diseases that can be fatal or play a significant role in increasing the risk factors for other metabolic diseases.”

The Study

Fatty Liver

For years, we have known that poor aerobic fitness is associated with obesity, heart disease, stroke and diabetes. This new study adds another serious condition to the list – non-alcoholic fatty liver disease (NAFLD)

The study also suggests that the resulting liver problems play a crucial step developing obesity-related illnesses. In fact, the study authors think that “Fatty liver disease will be the next big metabolic disorder associated with obesity and inactivity.”

So, to test the link between aerobic fitness and fatty liver disease, the researcher bred a strain of genetically unfit rats. These couch-potato rats could only run an average of 200m compared to over 1500m for the average fit rat.

Leaving both strains of rats to their own devices, the researchers noticed that at 25 weeks, the unfit rats showed clear signs of fatty liver. “By the end of their natural lives, the rats’ livers had sustained damage including fibrosis (the precursor to cirrhosis) and unexpected cell death”.

In contrast, the ‘fit’ group enjoyed heathy livers throughout their lifespans – despite the fact that neither group was getting any real exercise.

The team’s findings provide the first biochemical links between low aerobic fitness and fatty liver disease, and have lead the authors to suggest that NAFLD could potentially be treated or prevented by a suitable exercise program.


  • Aerobic exercise is boring
  • Aerobic exercise prevents fatty liver disease
  • You don’t want fatty liver disease, so
  • Get movin’

Obesity: Insulin trumps Genetics

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.

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The Cure for Cancer: Prevention?


Earlier today, researchers from the American Institute for Cancer Research and the U.K.-based World Cancer Research Fund released their report:

Policy and Action for Cancer Prevention

Food, Nutrition, and Physical Activity:
A Global Perspective

A few days ago, I talked about the strong link between obesity and cancer that the AICR/WCRF has identified.

With this new report, the AICR/WCRF builds upon that research and makes a strong argument for diet and exercise as the key to fighting cancer.

It calls research and spending on the treatment of cancer “necessary but not sufficient,” and contends that a far better strategy for reducing the world’s annual tally of 11 million cancer cases would be to develop a public-health policy aimed at preventing people from getting the disease in the first place.

Their findings are based on an a review of the nearly 7,000 scientific studies into whether cancer rates are influenced by diet, obesity and exercise.

In their report, they conclude that cancer “is mostly preventable.”

They estimate that about one-third of all cases in advanced countries like the U.S., Canada, Australia and Europe could be eliminated by diets that aren’t loaded with fatty, sugary foods, by people exercising regularly and, if they are obese, by slimming down to an appropriate weight.

And considering that another 1/3 of all cancer cases are due to smoking, the folks over at the AICR/WCRF believe that 2/3 of all cancers are preventable.

But What about Genetics?

For years and years, scientists have looked towards the genome for answers to the mystery of cancer. And since we began mapping out the human genome, that research has intensified.

This report attempts to throw cold water on the genetic hypothesis for cancer.

One of the study’s lead researchers,Dr. Kumanyika said studies tracking immigrants and their children who move from areas of low cancer incidence, such as Asia, to countries with high rates, such as the United States, suggest the genetic factor may be overrated.

Over time, cancer rates among migrants and their children rise toward the levels prevalent in their adopted countries, suggesting that something common to everyone in the new environment is the cause.

So, what do we do now?

According to AICR/WCRF, the short answer to that question is cooperation.

They envision an approach which combines the efforts of 9 separate “actors”. Their hope/belief is that the combined and coordinated efforts of those 9 actors will create a synergistic weapon in the fight against preventable cancers.


And what are role are we, the people, expected to play in this noble fight against cancer?


So, what do you think?

Still not convinced?

Maybe Dr. Marmot can convince you.

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Fat Babies become Fat Kids become Fat Teenagers become Fat Adults

You are not going to believe this but, 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?

Who could have guessed that?

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?

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. But their interest in these sirtuins only took off 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 keeping an eye of the security 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.

But that’s not all. 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.

All of this leads us to…

The Latest Research

In this stnew udy, 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).

Apparently, this isn’t a good thing to have happen.

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, in this latest study, the researchers found that as their little lab mice age, their 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 a good to have happen. 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, my news eventually 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.


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 little lab mice. Tests on humans have yet to be scheduled.

So, for now, you can either wait for the science to come to a proper conclusion, or you can load up on some resveratrol.

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Genetics Isn't Destiny

  • 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?

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.


Genetics isn’t Destiny

Being born with a FTO gene variant does not guarantee a lifetime of obesity and diabetes. Your health and physical appearance is up to you and the lifestyle choices you make.

Scientists Discover New Obesity Gene – Obesity Research Update #4

Obesity researcher, Professor Philippe Froguel and his team have discovered a new obesity gene.

Apparently, this gene ( PCSK1 ) plays a part in the maturation of various hormones that control food intake.

This means that if you have a mutated version of this gene, you are predisposed to severe obesity. Severe obesity, not just regular, run of the mill obesity.

The Details

PCSK1 produces an enzyme called proconvertase 1.

Proconvertase 1 activates several hormones and circulating peptides that are involved in controlling appetite – insulin, glucagon, GLP1, and pro-opiomelanocortin (POMC).

The conclusion of this study is that even apparently minor abnormalities in a proconvertase 1 are enough to significantly increase the risk of severe obesity and to lead to excessive weight in the general population.

So what does this mean?

This means that if your PCSK1 gene is mutated, you are probably obese. Just like if your were born with a congenital leptin deficiency.

So, what percentage of the population is walking around with a deformed PCSK1 gene.

We don’t know, and neither do the scientists.

What causes this gene mutation?

We don’t know, and neither do the scientists.

Can this mutation be corrected?

We don’t know, and neither do the scientists.

Should obese individuals rely on science to provide them with a treatment for a potentially rare genetic mutation that most likely did not cause their obesity in the first place?


oops, sorry, my objectiveness slipped a little..

We don’t know, and neither do the scientists.

The study is published in the journal, Nature Genetics.


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Scientists discover the Couch Potato gene

A group of researchers, from the University of North Carolina at Charlotte, have mapped out 23 specific chromosomal locations that account for 84% of the behavioral differences between low activity (see lazy) mice and high activity mice (see type A super achievers) – sorry, no human tests yet.

Link to Study # 1

Link to Study # 2

Initially, the researchers thought that the difference between the lazy and active mice was due to a genetic effect on the way energy is used by the muscle tissue.

This was proven false. Okay then, moving on.

This led the researchers to look at how genetic differences in brain chemistry might be causing this propensity towards laziness.


The Studies

The first thing the researchers did was to interbreed the active mice with the lazy mice. Then, they tested the offspring of this ‘unholy union’ for activity using three measurements – speed, endurance and distance.

Genetic tests were performed on the mice and strong correlations were found between the differences in the their genomes and their test results. In fact, the scientists identified 23 genes that were shown to affect activity levels.

While, the scientists have no idea what these genes are doing to cause these differences in activity level, they know that there is a link.

So what does this mean?

This may mean that while some people may be genetically predisposed to enjoy exercise, others may be genetically predisposed to glue their butts to the couch and watch re-runs of Murder She Wrote until they fall asleep in a Doritos induced slumber.

How depressing.


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Epigenetics & Obesity

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.

And as we know, you can’t beat bad genetics. Those pudgy little kids are doomed.

Or, maybe not. 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.

With this special diet, they were attempting 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”.

In layman’s terms, obese mothers who supplement with folic acid, vitamin B12, betaine and choline before & during their pregnancy might help their kids resist the scourge of childhood obesity.

NOTE:  This is only one study, performed on mice. There is more work to be done and just because this study is positive, moms-to-be should check in with their doctors before they start mega-dosing supplements in order to produce babies with six packs.

Why is America so Fat

Why is America so Fat? – In Utero Big Macs

Q:  Why is America so fat?

A:  New research shows that moms who eat junk food (a diet high in sugar, fat and salt) are dooming their kids to a life of obesity, high blood sugar, high levels of circulating insulin, high triglycerides and/or cholesterol.

Why is America so Fat

This study showed that a “maternal junk food diet promotes adiposity in offspring and brings on the earlier onset of hyperglycemia, hyperinsulinemia and/or hyperlipidemia”.

Even when the little lab rats were switched over to the “healthy” rat chow, they still had excess body-fat and enlarged fat cells. Unluckiest of all were the Big Mac eating girl rats, who showed significantly higher levels of…

  • IGF-1,
  • IRS-1,
  • VEGF-A,
  • PPARã,
  • leptin,
  • adiponectin,
  • adipsin,
  • LPL,
  • Glut 1,
  • and Glut 3 mRNAexpression than their non-twinkie eating sisters.

The male rats got off a little bit easier. They showed elevated levels of only IRS-1, VEGF-A, Glut 4 and LPL, when compared to their carrot eating brothers. No idea why there was a difference between the males and females.

The study’s authors concluded that, “a maternal junk food diet promotes adiposity in offspring and the earlier onset of hyperglycemia, hyperinsulinemia and/orhyperlipidemia. Male and female offspring also display a different metabolic, cellular and molecular response to junk-food-diet induced adiposity”.

Why is America so Fat

What does this mean?

First off, let’s not blame it all on Mom – Mom has it hard enough without this kind of guilt being dumped in their laps.

However, this study does show that the 9 month gestational period has an enormous effect on the rest of the baby’s life. When a mom-to-be succumbs to the lure of the Golden Arches, she may be setting her unborn child up for a lifetime of obesity, health problems, societal stigma, stress, depression, etc…

The list goes on and on.

To avoid these problems, Mom NEEDS to eat healthy if she wants healthy babies.

apple vs pear-health-obesity-appearance-bodyfat-fitness-healthhabits

The Science behind Spare Tires and Thunder Thighs

Why is it that some people store their body-fat around their middle while others store it on their thighs and bottom?

According to the medical community, your genetic makeup predisposes you to be either an “apple” or a “pear” when it comes to your body-fat distribution.

So what kind of fruit are you?

  • Generally speaking, women typically collect fat in their hips and buttocks, giving their figures a “pear” shape. In medical terms, this fat distribution pattern is referred to as gynecoid.
  • Men, on the other hand, usually collect fat around the belly, giving them more of an “apple” shape. In medical terms, this fat distribution pattern is referred to as android.


Keep in mind, this is not an absolute. Some men are pear-shaped and some women become apple-shaped, particularly after menopause.

Health Effects of Fat Distribution Patterns

To put it bluntly, apple-shaped people are more likely to develop many of the health problems associated with obesity. They are at increased health risk because of their fat distribution. While obesity of any kind is a health risk, it is better to be a pear than an apple.

Note: For a more thorough discussion of the health implications of being an apple or a pear, click here.

So What Makes Someone an Apple or a Pear?

  • Attached to all of your fat cells, you have hormone receptors which are designed to accept specific types of hormones.

When it comes to weight loss and your fat cells, we are concerned with the adrenoreceptors designed to accept adrenaline and noradrenaline. Think of the receptor as a lock and the hormone as a key. Only specific hormones can “unlock” the receptor and open up the fat cell membrane to allow for body-fat storage or release.

Of all of the different types of hormone receptors, fat cells have only two – Alpha 2 (A2) and Beta 1 (B1).

  • B1s are the good guys.

B1 receptors activate lipase (the enzyme that breaks down fat). Lipase causes your fat cells to break down the stored fat into fatty acids and glycerol to be used as energy throughout your body. This fat breakdown procedure is initiated when B1s hormone receptors link up with the key hormone nor-adrenaline.

Note: Adrenaline could also set off this procedure, but your body-fat lacks the major arteries and veins that adrenaline needs to travel in.

  • On the other hand, your A2 receptors are the bad guys.

Their job is not only to keep fat inside the cell, but to encourage the formation of new fat into the cell. As a special bonus, they decrease the body’s generation of nor-adrenaline. Making things even worse, when you go on a low calorie diet, you are increasing the number of A2 receptors.

Doesn’t sound good does it?

But this still doesn’t answer why my love handles / butt / etc… is fatter than the rest of my body. Hopefully this does:

Why Apples are Apples and Pears are Pears

  • Problem area fat cells have very few B1 receptors. This means they do not release much stored fat – diet or not.
  • Problem area fat cells have lots of A2 receptors. And that number grows when you diet.

This means that a typical yo-yo dieter is actually making their problem areas much more stubborn every time he/she jumps on and off the diet bandwagon.

So what do I do NOW?

  1. STOP DIETING – Microwaved diet entrees are not the answer.
  2. START EATING HEALTHY… Fruits…Vegetables…Lean Protein…Nuts & Seeds…Fish

More info on eating healthy

More info on exercising for health

In the meantime, be aware that lots and lots of lab coat wearing scientists are working night and day to discover the perfect A2 receptor antagonist – that perfect pill that will block the Noradrenaline key from fitting into the A2 receptor lock. And when they do, you can go back to eating cheesecake.

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Health, Fitness, Obesity and Genetics

Health, Fitness, Obesity and Genetics

As a kid, I was always ‘husky’.

Growing up , I threw myself head first into a hardcore fitness lifestyle… involving a ton of research, sweat, discipline and hard work. With all of this, I was able to transform my body from fat to fit. And since 1989, I have passed on my knowledge and perhaps more importantly, my confidence to hundreds of people that came to me and asked me to help them re-shape their bodies.

Not too surprisingly, while most of these people already had a pretty good idea of what they had to do to become lean, fit & healthy; they had never been able to turn their goals into reality.

It took the experience of seeing their friends transform their bodies with the help of a “personal trainer” to truly believe that this magical “personal trainer” was the solution to all their health and fitness dreams. Even after they had done all the hard work, all of them believed that I was responsible for their transformations.

An example of “stick” motivation

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.

  • They believed that their obesity and genetics were inextricably linked and had doomed them to a life of obesity and poor physical fitness.
  • How wrong they were.

While it is true that our genetic makeup does have a profound effect on every aspect of our lives, we still have a role to play in how our genetic potential is expressed.

  • Where we live
  • How much money we make
  • What food we eat and which food we don’t eat
  • Our relationships with family and friends
  • Etc, etc, etc…

The impact that our environment has upon our genetic coding is currently being researched by a branch of science called Epigenetics.

  • 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.

Genetics isn’t Destiny. We have the power to make the best or the worst with what we have been given.

Believe that.


  • 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.

The Link Between Genetics and Obesity

The American Society for Addiction Medicine held their annual conference in Toronto this past weekend. One of the attendees, Dr. Carolyn Ross spoke about the link between human genetics and obesity. In an interview with a local radio station, 680 News, Dr. Ross said that “70 per cent of obesity is genetic”.

Dr. Ross hopes that this linkage between obesity and genetics will ‘take away some of the stigma and shame associated with obesity’.

A related newspaper article appeared in this past Sunday’s Toronto Star. In this article, the link between anorexia nervosa and human genetics was discussed. In this article, the point was made that over the past 30 years, the rate of anorexia has remained unchanged while the rate of bulimia has risen sharply. The point being made here is that while bulimia may indeed be driven by a societal demand for thinness, anorexia may be driven by a genetic flaw.

While research into a genetic cause of anorexia (or bulimia, binge eating, etc) is only in it’s infancy, “results of the first genetic studies, released in the past five years, reveal that genetic vulnerability for anorexia nervosa lies on chromosome 1 of the 24 chromosomes that make up the human genome”.

So what do we take from this?

If Dr. Ross is correct and genetics has a huge impact on obesity, do we ignore the smaller role of our own behaviour? If you knew that you had inherited a genetic propensity towards obesity, do you give up trying to eat a healthy diet and engage in physical exercise? Do you wait for science to come up with a genetic cure?

While I agree with Dr. Ross that the social stigma attached to obesity is cruel and thoughtless ( if there is a genetic component to both obesity & cancer, why is it acceptable to mock the obese but not a cancer patient?), obese individuals still have to accept responsibility for their own health.

For every person who was born with a congenital leptin deficiency, there are thousands upon thousands of obese individuals who have a simple genetic predisposition towards obesity. A PREDISPOSITION.

Genetics is not Destiny.

Learn how to keep your body healthy, learn how to train your body to overcome cravings, eat well, exercise, and make the most with the genetic hand that you were dealt.

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If you like this article, don’t forget to subscribe to @healthhabits. When you subscribe, my friends at MailChimp will make sure to send you an email every time I post something new here at the blog.

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