A Mechanism Behind the Yo-Yo Effect

 

The yo-yo effect in dieting is something that has been observed for a long time- someone tries to lose weight but gains it all back right after the diet. Recently, scientists have discovered a mechanism behind the yo-yo effect that could help explain why it occurs. By analyzing fat cells from overweight mice and of mice that lost weight through dieting, it was revealed that obesity leads to characteristic epigenetic changes in the nuclei of the fat cells. These changes were found to have remained even after the loss of weight, where the cells remember the overweight state and find it easier to return to it. The mice with those epigenetic markers were able to gain the weight back faster when they resumed a high fat diet. A similar study was carried out on humans and the results were found to be consistent with the mice study.

In my opinion, this is a study that has produced useful information. By discovering a mechanism for why the yo-yo effect occurs on the molecular level, we can better understand how and why it occurs in humans. We could perform more research on this topic in order to potentially develop strategies to prevent it from happening to people who are trying to lose weight and keep it off. This study could have many benefits for many of these people.

Discovering the Gene for Appetite

A recent article published in the New York Times reveals that there is a gene that plays a role in appetite suppression and predisposition to obesity. A recent study has discovered that the MC4R gene plays a vital role in hunger regulation and the feeling of fullness. There are essentially three types of possible phenotypes for this gene. The normal phenotype would be a typical appetite that signals you to eat when hungry and stop eating when you've had the correct amount of food. There is a mutation in this MC4R gene that causes some people to have this gene turned off. This causes them to never feel full and they keep eating because they never receive a signal to stop. These are the people that are at a greater genetic disposition for obesity. However, there is also another alteration to this gene that causes it to be constantly turned on. This leads to affected individuals feeling full prematurely and, as a result, they do not eat as much or desire food as much as the formerly affected individuals. This leaves this group of mutants thin and less likely to develop diseases like diabetes and heart disease. 

Like many, I have always known that predisposition for obesity was related to genetics. However, I think the vast majority of people believe this is related to metabolism, which you often inherit from your parents. To find out that this may have little to do with genetic weight gain is very interesting. It makes me wonder if the mechanism of these appetite suppressor drugs for weight loss involves turning off the MC4R gene. It also raises the question over whether as many people would look down upon these appetite pills if they knew that there was a legit genetic reasoning behind the use of the pill.

Is your physique not quite summer ready? You can blame your genes.

In January 2019, while most Americans are fulfilling their new year resolutions, U.S. News & World Report published an article which was originally composed by HealthDay News that may relieve some pressure to have that perfect beach body this summer. Robert Preidt wrote this article based on a study performed by Wellcome-MRC Institute of Metabolic Science at the University of Cambridge. Sadaf Farooqi lead the study which debunked the myth that all people who are overweight are lazy and do not care about their health. There have been similar studies done in the past which focused on obese people and how their genes may be effecting their weight. This new study differs by focusing on a broader scope of individuals and comparing their genetic make up. The group of people being analyzed included those who are underweight, healthy weight and obese. Genetic variants were discovered present in each weight category. This data was calculated to determine what impact ones genes has on the outcome of their physique. It was concluded that the individuals with specific genetic variants had a higher chance of being obese. Accordingly, thinner people showed an absence of those same genes.

We are often quick to judge others for anything and everything but most commonly their weight. People who are "too skinny" must have an eating disorder or self image issues. Those who are "overweight" must have no self control and never exercise. These thoughts are not only offensive but simply incorrect. I believe the media should focus on increasing awareness of these types of studies. This does not mean that your physique is out of your control. It just means that we all need to be a little more gracious towards one another and realize we are not all cut from the same mold.

Results of a Defect in the MC4R Gene

A study was conducted to link obese individuals with the MC4R gene. Obese individuals usually enjoy indulging in foods with high fat content. High fat content will lead to an excess in caloric intake which may lead to weight gain.A study was conducted with lean and obese individuals. However, some of the obese individuals possessed the defective MC4R gene. The individuals were taken to an open buffet. The buffet served chicken with similar tastes, but each entrée contained a different percentage of fat content. The result was that the obese individuals with the defective gene ate significantly more of the higher fat content chicken than the lean and obese individuals. The defect in the gene causes individuals to enjoy eating the higher fatty foods than an individual with an unaffected gene. Another experiment was conducted, but this time the test was sugar content. The obese individuals with the defective gene ate remarkably less of the higher sugar content in this desert. The lean and obese individuals liked the desert with the higher sugar content. The calories obtained per gram of fat is double the amount produced by carbohydrates and proteins. The individuals with the defective gene are preferring to eat foods with higher fat content which further allows for a problem with weight gain. This article was very interesting to read because obesity is such a big problem in this country. For many individuals it is difficult to lose weight and this gene is most likely the cause of the problem. It would be very interesting if the same gene in an unaffected individual was cloned and administered to the genome of an individual with the defective gene. It is possible that this would allow an obese individual with the defective gene to have less desire to eat such unhealthy, high fat content foods.

Rats Beat Aging

Did you ever wonder of you can beat the effects of aging? Well, a new study showed that mice can. Scientists at Washington University School of Medicine gave healthy mice a natural compound called NMN. Tests have shown that these mice had more energy and reduced typical signs of aging. For example, weight gain, decrease in physical activity and loss of insulin sensitivity. Thus, older rats act like younger ones. Scientists believe that this can help humans remain healthier as they age since mice cells and human cells rely on the same process for energy production. When one ages, they lose the ability to produce NAD (nicotinamide adenine dinucleotide). Studies have shown that this tissue decreases in mice as they age. However, giving NAD to mice is ineffective. Therefore, scientists looked one step earlier in the NAD supply chain to find NMN (nicotinamide mononucleotide). This method can potentially reduce aging in humans and/or allow aging to occur in a more healthy way.

Bacteria's Affect on Weight

Many people are completely ignoring a part of their body that plays a huge factor in their health. There are 10 x more bacterial cells in a human body than their own cells. These bacteria play many different beneficial roles such as immunity and nutrients. Therefore, it’s logical to think that bacteria can determine with how much weight we gain from the foods we eat. The bacteria in our guts play a major role in how we store fat and what are the glucose levels in our blood. So, people with different concentration of bacteria will have different reactions to the same food.

Scientist performed an experiment with genetically identical mice. These mice were given the same amount of food in a sterile environment. However, some mice received gut bacteria from an obese person while the others received gut bacteria from a lean person. As a result, the mice that received bacteria from the obese person gained more weight than the others even though they received the same amount of food. I believe more research needs to be done to really identify how the bacteria manipulate weight gain in people. However, I am very excited to learn how much bacteria manipulate our bodies and what new methods can be done to improve health.

New "Obesity Gene" Found

Researchers from the University of Chicago have said that they have found a gene that is associated to obesity. They have said that they think that the gene IRX3 controls body mass and regulates body composition. Although the research showed an association between the gene and obesity, it did not prove a cause-and-effect link. The IRX3 gene was first found though the analysis if 150 samples of DNA from people of European descent. To verify the role of IRX3 in obesity, the researchers created mice without the gene and found that they weighed about 30 percent less than normal mice. Most of the weight difference were due to the lack of body fat of these altered mice. These new rats were completely resistant to high-fat diet-induced obesity. The only problem with this research is that animal studies cannot often be replicated in humans. Previous studies have said that mutations of the gene FTO has a significant role in determining the risk of obesity in people. But this new study shows that this obesity mutation in FTO interacts with the IRX3 gene and alone the FTO mutation has only a minor effect on obesity risk.
          It is interesting that certain genes increases the risk in obesity in people. But the final deciding factor whether someone will be obese or not is that person. It is up to the individual to determine whether they will either exercise and eat healthy, or be lazy and eat McDonald's every day.

Link Between Fat Cells and Brain Clock Molecules Shown

In a new study in Nature Medicine shows that the deletion of the clock gene in fat cells caused mice to become obese.  The clock gene is known as Arntl or Bmal1.  The recent findings shed light on the causes of obesity in humans.  The study was conducted by Georgios Paschos PhD, a research associate in the lab of Garret FitzGerald, MD, FRS director of the Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania.  The studies show that food consumption during what is considered the rest period for mice favored energy storage.  This caused the mice to become obese without consuming more calories.  This behavioral change in mice is similar to night-eating syndrome in humans, which is also associated with obesity.

[caption id="" align="aligncenter" width="480" caption="Mice with a broken clock in their fat get fat as they eat when they should be sleeping. (Credit: Georgios Paschos PhD, Perelman School of Medicine, University of Pennsylvania)"][/caption]

When the clock was broken in fat cells, the hypothalamic rhythm was disrupted to favor food consumption at inappropriate times.  This means the mice would get the urge to eat in the daytime when they should be asleep.  The change in daily rhythm caused changes in metabolism.  The Penn team also found a handful of genes that were altered by the broken clock in the fat cells.  Those genes governed how unsaturated fatty acids, such as EPA and DHA were released into the blood stream.  The Penn team found that EPA and DHA levels were low at the time of inappropriate feeding.  Interestingly enough, Paschos states that the team supplemented EPA and DHA to the knockout mice, which "rescued the entire phenotype".  The findings show that show-term changes have an immediate effect on the rhythm of eating.  These changes lead to an increase in body weight.  I really enjoyed this study.  I think it should be brought to the attention of others about the importance of not eating past a certain time.  I know there has been conflicting reports regarding nighttime eating and weight gain.  Some say it doesn't matter when you eat, while we hear sayings like, "Eat breakfast like a king, lunch like a prince, and dinner like a pauper" all of the time.  This study seems like it supports the latter opinion.