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Posts Tagged ‘genetics’

Can Potassium Reverse High Blood Pressure?

May 20th, 2009

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…

…and to start eating this…

And they aren’t happy about it.

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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.

Better 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.

That doesn’t mean you should go crazy with the double bacon cheeseburgers.

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.

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

So, it’s probably safe to assume that you are part of the majority. 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

May 11th, 2009

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.

Why?

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

April 19th, 2009

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.

Conclusion

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

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Obesity: Insulin trumps Genetics

April 15th, 2009

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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The Cure for Cancer: Prevention?

February 26th, 2009

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

January 15th, 2009

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!

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:

Babies 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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Posted in Diet/Nutrition, Research, health

Tags: childhood obesity epigenetics fat fitness genetics health obese obesity pediatric obesity weight loss

Why Do We Get OLD?

December 1st, 2008

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:

a low calorie diet, or
the red wine super chemical resveratrol

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

So What Exactly Do Sirtuins Do?

Sirtuins 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.

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.

In 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

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:

Physical Activity and the Association of Common FTO Gene Variants with Body Mass Index and Obesity

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:

They are a genetically homogeneous population.

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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Scientists Discover New Obesity Gene – Obesity Research Update #4

July 18th, 2008

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?

NO.

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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Posted in Diet/Nutrition, Exercise, Research, health

Tags: diet Exercise fitness genetics health life obesity Research science weight loss

Scientists discover the Couch Potato gene

July 17th, 2008

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.

Success!

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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Tags: Exercise fitness genetics health life obesity Research science sloth