Wanna Blame Your Genes For Your Size? This Might Be Your Big Break…

After all these years, people have still not figured out that being healthy in the long-term includes having a strong mind, a good diet and a proper exercise regimen. As humans, we are still inclined to think of shortcuts to success. What do we do when the shortcuts do not yield success? We find a way to put the blame on something rather than take responsibility.

It is therefore no surprise that in this day and age, when being overweight is touted as a negative trait, many people would rather blame their genes and metabolism than take responsibility, cultivate a plan, put it into action and work their way to better health. I’m not saying that genetics does not play a part in body size, or that metabolic syndromes don’t exist, but I am saying that it is often used as an excuse because of its convenience.

With that being said, it is also not surprising that millions of dollars are being fuelled towards research about the genetics of obesity. To the governments, it is an investment to save them the billions that obesity-related illnesses cost to the healthcare system. At the individual level, people who don’t want to take responsibility for their laziness would be licking their lips at the prospect of yet another excuse about their lack of success. Now onto the research:

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Scientists in Milwaukee, Wisconsin have allegedly found how the “key gene” associated with obesity works in making people fat. Of course, this could lead to wider implications as to how obesity is treated. To hell with diet and exercise, they imply. On this note, I understand that scientists need to be competitive to win research grants by publishing, but c’mon, isn’t this stooping to a new low?

Anyways, this gene has been called “FTO” and research began on it in 2007. It was recently found that when it does not function properly, the energy from food would have a tendency to be stored in the body as body fat. However, genetic intervention in mice and human cells has shown that this process can be reversed.  Yes, because experiments done in mice and human cells in controlled environments totally mimic our human bodies in real life. Science!

So now the next phase would be to come up with a drug or treatment that can fix errors in this particular gene. And the leader of the study says that this genetic discovery challenges the idea that peoples’ obesity is due to their choice of poor diets and a lack of exercise. Gee, how very convenient. A new drug like this can add to the repertoire of existing drugs that target the brain and appetite.

Other scientists have praised the research and stated that other genes play a role, citing that 44% of Europeans are obese while the figure stands at 5% for Africans. Right- because there are no social factors to be considered apart from genetics. Anyways, the people in charge of this project are seeking a patent related to the work, because clearly science is about peoples’ well-being, and not about making a boatload of money, right?

So what other shortcuts will we take? We already have liposuction and gastric band therapy, both of which do not have any side effects at all, as we are well aware of. Then there are protein powders and pills, which of course also have no side effects and will even boost your kidney and liver by stimulating them to work harder. Productivity oooh yea!

Alright, if you haven’t discovered already, it is uncommon to find a Granite Fitness blog post that drips with as much sarcasm as this one. It is because as a person, I, the writer, am generally not a sarcastic person. But as a fitness motivator who wants the best for you, I have to be honest and slap you with the reality that long-term weight loss and maintenance will require effort on your part. The earlier you realise this, the better!

I hope this injects some sense into you. For something reasonable that would require some effort and patience, but has a much higher chance of success in the long-term, grab the Granite Fitness Solution or the Granite Fitness Masterclass.

Mark

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