Mayo Clinic researchers found that the genetic mutation, alpha-1 antitrypsin deficiency (Ą1ATD), could explain up to about 12 percent of lung cancer patients in this study and likely represents the same widespread risk in the general population. The World Health Organization estimates that at least 120 million people worldwide are Ą1ATD carriers.
A normal Ą1AT gene produces a protein that stops enzymes from breaking down elastin, which keeps lung tissue elastic for normal function. However, the mutated gene produced less of the lung-protecting chemical from the protein, increasing the odds of developing lung cancer.
In the particular study, a team of 12 researchers looked at three different groups: 1,443 patients with lung cancer treated at Mayo Clinic from 1997 to 2003; a control group of 797 residents in the community; and a second control group of 902 siblings of the lung cancer patients. They found that:The Ą1ATD carrier rate among 1,443 genotyped patients with lung cancer was 13.4 percent, compared to 7.8 percent among unrelated control participants.
All Ą1ATD gene carriers were at a similarly greater risk of developing lung cancer, regardless of smoking status. Also, the estimated attributable risk for Ą1ATD carriers in this study among those who never smoked and among heavy smokers was 11 percent to 12 percent, suggesting that the genetic disorder might explain a significant proportion of lung cancer in the general population.
Although the study helps explain why people who have never smoked can develop lung cancer, it doesn't mean that people who don't have the gene won't develop lung cancer. "Smoking remains the overwhelming risk factor for lung cancer development."
Reference
Mayo Clinic (2008). Common Gene Disorder Doubles Risk Of Lung Cancer, Even Among Nonsmokers. ScienceDaily. Retrieved May 28, 2008, from http://www.sciencedaily.com /releases/2008/05/080526171349.htm
Leigh Frazer 4143927
Wednesday, May 28, 2008
Genetics, Playing a Key Role in Obesity
A recent study conducted at Brigham Young University in Utah, USA has found new evidence to suggest that obesity may be linked to genetics. The study involved examining evolutionary selection on Pima Indians, indigenous to the Sonora Desert of Arizona and New Mexico. It is known that there is a high rate of obesity among the modern Pima Indians and this is thought to be due to their fast metabolism which was advantageous during times when food was scarce. However problems arise when food is in abundance, leading to high rates of obesity in modern Pima communities. Two hundred obese Pima individuals were included in the study, with their metabolic rates being measured. With the researchers focusing on changes in their mitochondrial DNA or SNP’s (single nucleotide polymorphisms) they found that two of the three known SNP’s influence metabolic efficiency. The researchers then used software to analyze and track these variations across a number of different mammals leading to their proposal that variations in these SNP’s affect the mitochondrial respiration chain and consequently causes change in metabolic rate. Although the study focused primarily on the Pima Indians, similar variations in SNP’s can be found in other populations. Where a high metabolic rate was an advantage in the past, it can now be seen as detrimental as there is an abundance of food leading to high and increasing rates of obesity in populations all around the world. This study found evidence to suggest that genetics play a key role in obesity. http://www.sciencedaily.com/releases/2007/10/071016074958.htm
Genetic Mutation Causes Lung Cancer In Non-smokers!
Mayo Clinic researchers found that the genetic mutation, alpha-1 antitrypsin deficiency (Ą1ATD), could explain up to about 12 percent of lung cancer patients in this study and likely represents the same widespread risk in the general population. The World Health Organization estimates that at least 120 million people worldwide are Ą1ATD carriers.
A normal Ą1AT gene produces a protein that stops enzymes from breaking down elastin, which keeps lung tissue elastic for normal function. However, the mutated gene produced less of the lung-protecting chemical from the protein, increasing the odds of developing lung cancer.
In the particular study, a team of 12 researchers looked at three different groups: 1,443 patients with lung cancer treated at Mayo Clinic from 1997 to 2003; a control group of 797 residents in the community; and a second control group of 902 siblings of the lung cancer patients. They found that:The Ą1ATD carrier rate among 1,443 genotyped patients with lung cancer was 13.4 percent, compared to 7.8 percent among unrelated control participants.
All Ą1ATD gene carriers were at a similarly greater risk of developing lung cancer, regardless of smoking status. Also, the estimated attributable risk for Ą1ATD carriers in this study among those who never smoked and among heavy smokers was 11 percent to 12 percent, suggesting that the genetic disorder might explain a significant proportion of lung cancer in the general population.
Although the study helps explain why people who have never smoked can develop lung cancer, it doesn't mean that people who don't have the gene won't develop lung cancer. "Smoking remains the overwhelming risk factor for lung cancer development."
Reference
Mayo Clinic (2008). Common Gene Disorder Doubles Risk Of Lung Cancer, Even Among Nonsmokers. ScienceDaily. Retrieved May 28, 2008, from http://www.sciencedaily.com /releases/2008/05/080526171349.htm
Mayo Clinic (2008). Common Gene Disorder Doubles Risk Of Lung Cancer, Even Among Nonsmokers. ScienceDaily. Retrieved May 28, 2008, from http://www.sciencedaily.com /releases/2008/05/080526171349.htm
Leigh Frazer 4143927
Genetic Mutation Causes Lung Cancer In Non-smokers!
Mayo Clinic researchers found that the genetic mutation, alpha-1 antitrypsin deficiency (Ą1ATD), could explain up to about 12 percent of lung cancer patients in this study and likely represents the same widespread risk in the general population. The World Health Organization estimates that at least 120 million people worldwide are Ą1ATD carriers.
A normal Ą1AT gene produces a protein that stops enzymes from breaking down elastin, which keeps lung tissue elastic for normal function. However, the mutated gene produced less of the lung-protecting chemical from the protein, increasing the odds of developing lung cancer.
In the particular study, a team of 12 researchers looked at three different groups: 1,443 patients with lung cancer treated at Mayo Clinic from 1997 to 2003; a control group of 797 residents in the community; and a second control group of 902 siblings of the lung cancer patients. They found that:The Ą1ATD carrier rate among 1,443 genotyped patients with lung cancer was 13.4 percent, compared to 7.8 percent among unrelated control participants.
All Ą1ATD gene carriers were at a similarly greater risk of developing lung cancer, regardless of smoking status. Also, the estimated attributable risk for Ą1ATD carriers in this study among those who never smoked and among heavy smokers was 11 percent to 12 percent, suggesting that the genetic disorder might explain a significant proportion of lung cancer in the general population.
Although the study helps explain why people who have never smoked can develop lung cancer, it doesn't mean that people who don't have the gene won't develop lung cancer. "Smoking remains the overwhelming risk factor for lung cancer development."
Reference
Mayo Clinic (2008). Common Gene Disorder Doubles Risk Of Lung Cancer, Even Among Nonsmokers. ScienceDaily. Retrieved May 28, 2008, from http://www.sciencedaily.com /releases/2008/05/080526171349.htm
Leigh Frazer 4143927
Are Elite Athletes Genetically Pre-disposed?
“A fast, simple and painless genetic test can identify whether you may be naturally geared toward sprint/power events, or towards endurance sporting ability.”1 This test is known as the “ACTN3 Sports Gene Test®”, it is a simple genetic analysis of an individual’s DNA. The ACTN3 test analyses the DNA sample to determine which genotype of the “α-actinin-3” gene an individual posses. What is the ACTN3 Gene?
“The ACTN3 gene instructs our body to produce a protein called alpha-actinin-3. This protein contributes to the muscle’s ability to generate forceful, repetitive muscle contraction.”1 The α-actinin-3 gene has two alleles ‘R’ and ‘X’, “Scientists have found a variant (known as R577X) in the ACTN3 gene that alters the way the body reads the ACTN3 gene instruction.”
Studies of elite athletes from the Australian Institute of Sport (AIS) have shown that an individual’s ACTN3 genotype can influence their ability to perform at different types of sports 2. Results of this study showed athletes specialising in endurance events had a higher frequency of both alleles as X (R577X). Respectively athletes whom specialised in sprint/power events had a higher frequency of the genotype RR (the absence in both alleles of R577X)2.
From this it can be inferred that athletes who posses both alleles as R577X are more likely to perform well in endurance events and athletes who have both alleles as R-type ACTN3 genes perform better in sprint and power style events.
References:
- YOUR GENETIC SPORTS ADVANTAGE. http://www.gtg.com.au/archives/migration/2/110/383/ACTN3%20web%20brochure.pdf
- ACTN3 Genotype Is Associated with Human Elite Athletic Performance. http://esvc001057.wic005u.server-web.com/archives/2/110.040/700/ACTN3%20Am%20J%20Hum%20Gen%2073(3).pdf
By: Alex Stevenson – 41744026
Tuesday, May 27, 2008
Diet choices 'written in genes'
Experts from Kings College London believe our genes may play a key role in our food likes and dislikes. They compared the eating habits of thousands of pairs of twins and then find out that identical twins were far more likely to share the same dietary patterns suggesting tastes may be inherited.
Identical twins means that have exactly the same genetic make-up as each other, so scientists, by comparing them to non-identical twins, can work out the likelihood that their characteristics are due to “nature” or “nurture”.
By looking at a total of more than 3,000 female twins aged between 18 to 79, working out their broad preferences using five different dietary “groups” Their results, published in the journal Twin Research and Human Genetics, suggested that between 41% and 48% of a person's leaning towards one of the food groups was influenced by genetics.
For example, the strongest link between individual liking and genes involved a taste for garlic and coffee. Professor Tim Spector, who led the research, said: "For so long we have assumed that our upbringing and social environment determine what we like to eat. This has blown that theory out of the water - more often than not, our genetic make-up influences our dietary patterns." Furthermore there is some supporting findings. Professor Jane Wardle, from University College, said that the findings, and other similar research, pointed to genetics playing a "moderate" part in the development of preferred foods. She said that it was possible that genes involved with taste, or the "reward" chemicals released by the body in response to certain foods, might play a role.
Identical twins means that have exactly the same genetic make-up as each other, so scientists, by comparing them to non-identical twins, can work out the likelihood that their characteristics are due to “nature” or “nurture”.
By looking at a total of more than 3,000 female twins aged between 18 to 79, working out their broad preferences using five different dietary “groups” Their results, published in the journal Twin Research and Human Genetics, suggested that between 41% and 48% of a person's leaning towards one of the food groups was influenced by genetics.
For example, the strongest link between individual liking and genes involved a taste for garlic and coffee. Professor Tim Spector, who led the research, said: "For so long we have assumed that our upbringing and social environment determine what we like to eat. This has blown that theory out of the water - more often than not, our genetic make-up influences our dietary patterns." Furthermore there is some supporting findings. Professor Jane Wardle, from University College, said that the findings, and other similar research, pointed to genetics playing a "moderate" part in the development of preferred foods. She said that it was possible that genes involved with taste, or the "reward" chemicals released by the body in response to certain foods, might play a role.
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