BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Obesity (Page 1 of 2)

Childhood Stress: Impact on Blood Pressure, Obesity, and Diabetes

Childhood stress can lead to chronic diseases? A study conducted by researchers at the Keck School of Medicine, University of Southern California, emphasizes the importance of comprehending the impact of perceived stress on cardiometabolic health factors, including obesity, Type 2 diabetes, high cholesterol, and high blood pressure. Based on data from the Southern California Children’s Health Study, the study revealed that consistently high levels of perceived stress from adolescence through adulthood were associated with a greater risk for cardiometabolic diseases in young adulthood. Individuals experiencing prolonged stress during this period exhibited worse vascular health, higher total body fat, increased abdominal fat, and a heightened risk of obesity. 

The study indicated a general association between higher perceived stress levels and elevated risks of various cardiometabolic health conditions. Those reporting higher stress levels demonstrated poorer vascular health and higher systolic and diastolic blood pressure. The findings suggest that healthcare professionals could benefit from incorporating the Perceived Stress Scale into routine clinic assessments to identify individuals with higher stress levels early, enabling timely intervention and treatment. 

While the study provides valuable insights into the long-term impact of stress on cardiometabolic health, it acknowledges the limitation of its relatively small size. The researchers recommend more extensive studies to clarify and validate the associations between perceived stress patterns and various risk factors for cardiometabolic diseases. In a study on adolescents in Louisiana, researchers found that poor diet quality during adolescence is linked to lasting health risks, according to the article Poor diet quality during adolescence is linked to serious health risks. The study focused on physical activity, sleep, and dietary patterns, aiming to improve diet and reduce health risks, including cardiometabolic risks. The findings show that not following dietary guidelines is tied to ongoing health issues in teens over two years. Ensuring adolescents maintain an active lifestyle, adopt a wholesome diet, prioritize quality sleep, and manage stress levels becomes crucial for their overall well-being.

In AP Bio’s Unit 3 on Cell Communication, we explored the endocrine system: a complex network of glands and organs that secrete hormones into the bloodstream to regulate various physiological functions and maintain homeostasis in the body. Perceived stress triggers the activation of the body’s stress response, which involves the release of stress hormones from the endocrine system, primarily cortisol and adrenaline. The prolonged exposure to high levels of stress, as indicated by the study, may lead to dysregulation in the endocrine system. This dysregulation could contribute to disturbances in metabolic processes, potentially explaining the observed associations with cardiometabolic risk factors.  Endocrine EnglishMy grandfather, Steve, was diagnosed with Type 2 diabetes in 1995. His body’s cells became resistant to the effects of insulin, a hormone produced by the pancreas that helps cells absorb glucose from the bloodstream. As a result, glucose cannot enter cells efficiently, leading to elevated blood sugar levels. As a kid, my grandfather always told me to drink water and get in those daily vegetables with every sweet I ate. As I’ve researched, diets high in refined carbohydrates, sugars, and saturated fats contribute to obesity and insulin resistance. A diet rich in processed foods and poor in fruits, vegetables, and whole grains increases the risk of type 2 diabetes. I would love to hear your thoughts and insights on childhood stress linked to chronic diseases. Please share your comments and join the conversation!

Try to eat just one potato chip – it probably won’t happen.

Potato Chips or any junk food for that matter can be very addicting after just the first bite. The high concentrations of carbohydrates, sugars, and fats commonly found in these processed foods contribute to one of America’s greatest health risks, adult obesity. Today, over 40% of America’s adult population is considered obese and in the last 20 years, the prevalence of severe obesity has almost doubled to 9.2%. A single bag of Lay’s Potato Chips contains 15g of carbohydrates and around 170mg of sodium which could take around 15 mins of very intense workout to burn off. We have learned in AP Bio that consuming many carbohydrates without burning them off through exercise results in carbs converting into fatty acids during cellular respiration. So, when looking into obesity, researchers from Osaka Metropolitan University wanted to understand why “High-calorie foods — high in fat, oil, and sugar” tend to be overeaten.

Walmart Wenatchee 2

The researchers investigated the specific gene behind overeating and linked it to one named “CREB-Regulated Transcription Coactivator 1 (CRTC1).” In the past, trials on mice have indicated that when the CRTC1 gene is removed, they become more obese indicating that it “suppresses obesity”. But, it is now known that CRTC1 is found in all neurons around the brain so, they wanted to dive deeper and find the specific mechanism or neuron within this gene that reduced obesity.
First, Associate Professor Shigenobu Matsumura, who lead the research, hypothesized that “CRTC1 expression in MC4R-expressing neurons suppressed obesity because mutations in the MC4R gene are known to cause obesity.” So, they conducted trials on mice, manipulating the MC4R-expressing neurons to test their theory. It turns out that when on a standard diet, the original mouse and the one with the manipulated MC4R gene remained the same weight. But, when put on a high-fat diet, or one more resembling junk food, the mouse that was deficient with the CRTC1 MC4R neuron became “significantly more obese than the control mice and developed diabetes.” Reflecting on this outcome, the researchers have concluded that the CRTC1 gene plays a role in controlling our portions. Looking forward, the researchers hope this will lead to a better understanding of what causes people to overeat.

Mouse Brain Cross-Section

In our current AP Biology unit, we have been learning about cell respiration and the way our body consumes both O2 and food to create ATP energy. Our body can break down glucose through glycolysis, convert it into two Pyruvate, and then Acetyl CoA, to then create NADH and FADH2 through the Citric Acid Cycle to produce about 28 ATP energy molecules through Oxidative Phosphorylation. Other nutrients we consume like fats and proteins are also converted to ATP energy when needed but, when no energy deficit is created through activity, these nutrients along with excess glycogen are bound to insulin to create fat around the body. Looking forward, it is important to understand how addictive these unhealthy foods can be on a neurological and biological level, warning us of the dangers of overconsumption.

Are You Predisposed to Being Overweight? New Genetic Variations Say Yes.

Recent studies composed by researchers from the Spanish National Cancer Research Centre and the IMDEA Food Institute show that people with a specific variation or version of a gene crucial to cell nutrition tend to accumulate less fat. This means that those with a particular change or alteration in this gene may be inclined to store less fat in their bodies. Prior research has shown that genetics only play a role in 20% of our body weight for the general population. This means that other external factors such as diet, exercise, and overall lifestyle have much more of an impact on body weight.

Past research has identified nearly 100 genetic variants which slightly increase one’s likelihood of having a high BMI. This new research identifies one additional variant. Typically genetic variations are only slightly different versions of a gene and often do not result in visible changes. But, this new variation challenges this idea. It affects the amount of fat the body stores, something which can strongly alter one’s physical appearance. What’s more, the researchers of this gene have found that it is more prevalent in Europe with just under 60% of the population having it.

Ácido desoxirribonucleico (DNA)

 

According to Alejo Efeyan, the head of CNIO’s Metabolism and Cell Signalling Group, the new research can help us to further understand the role which genes play in obesity, body weight, and fat accumulation. Efeyan says, “the finding is a step forward in the understanding of the genetic components of obesity.” Additionally, Ana Ramirez de Molina, the director of the IMDEA Food Institute, claims that a key understanding of cell pathways regarding cell nutrition may affect and spur the creation of not only obesity prevention but also personalized treatments. Essentially, understanding the new gene can help us to target obesity and body weight on an individual level rather than the population as a whole. She believes, “a deep knowledge of the involvement of the cellular nutrient-sensing pathway in obesity may have implications for the development and application of personalized strategies in the prevention and treatment of obesity.”

To find and research the genetic variant which influences fat storage and obesity a team from the IMDEA Food institute collected a variety of data from 790 healthy volunteers. This included body weight, muscle mass, genetic material, and more. The researchers found a “significant correlation between one of these variants in the FNIP2 gene and many of these obesity-related parameters.” Essentially their research proved that there is a connection between the specific gene and factors of obesity. The study has also been published in the scientific journal of Genome Biology. Although this gene may play a role in keeping body fat storage lower than others, it is important to note that it is not entirely a preventative measure against obesity or fat gain. Efeyan clarifies, “It is not at all the case that people with this genetic variant can overeat without getting fat.”

The genetic variation is present in a gene that specifically partakes in a signaling pathway that tells the cell what nutrients are available and needed. The gene signals to the cell what nutrition is necessary at a given moment. In our AP Bio class, we learned the intricacies of cell communication; how and why it can occur, the stages of it, and even the differences in the distances of communication. Connecting back to our AP Bio class, I wonder whether the gene interacts in an adjacent, paracrine, or long-distance manner. Also, how the distance can affect the communication of the gene to the cell regarding cell nutrition. We also learned about how genes in the nucleus of our cells can code for specific factors in our bodies and how they are a sort of ‘instructions’ for us to carry out. This connects to the research as we can see that a change in a gene can alter our body’s fat storage and connection to obesity. The genetic variation changed the ‘instructions’ for weight, fat storage, and obesity disposition. Additionally, the research stated that 60% percent of Europeans have genetic variation, I wonder what may have caused this. Was it a result of their diets, lineage, geography, or just a scientific anomaly? I invite any and all comments with a perspective and an idea as to what may have caused this, along with any comments regarding this research as a whole.

Obesity-waist circumference

 

 

Can Eating Late Increase the Obesity Risk in Humans?

Are you frustrated that, despite your healthy diet, you constantly feel like you are lacking energy, gaining weight, frequently hungry, and fatigued? Did you know that adjusting the time you consume meals could resolve this? Let me enlighten you on why you might be facing these symptoms!

A recent study  by Brigham’s women’s hospital orchestrated experiments to answer the following question “Does the time that we eat matter when everything else is kept consistent?”.  In the experiment, 16 patients with a BMI (body mass index) that indicated they were overweight, were examined closely. The 16 patients were on strict schedules so that their behavioral and environmental factors wouldn’t disrupt their results. They all had the same amount of sleep, the same diets, the same amount of physical activity, and the same wake up time. The only thing manipulated was the times each of them ate their meals. Each patient recorded the times they felt an increase in appetite, had their body temperature and energy levels measured and gave blood samples. The conductors of this experiment performed biopsies  of adipose tissue from the patients, to evaluate how their eating times affected how the body stores fat. 

The test results showed that the participants that were on a later eating schedule had a decrease in a hormone called leptin, which  is a hormone that regulates your appetite and energy level. The patients with a later eating scheduled were caused to feel more hungry than the group that consumed food earlier due to their body’s decrease in leptin. Eating later also had an effect on Ghrelin which is a hormone that increases your appetite.

The experiment discovered evidence that the group eating later was more at risk of obesity.  The adipose tissue gene expression revealed the pathways involved with lipid metabolism, receptor tyrosine kinases, and autophagy was altered in a way that decreased lipolysis and increased adipogenesis. Lipolysis is the process  of breaking down lipids. In our biology class, we learned how hydrolysis is the process where water is added to a molecule, which results in the molecule breaking into smaller molecules. In lipolysis, hydrolysis breaks down triacylglycerols into glycerol and free fatty acids. In biology class, we learned that lipids provide us with mass amounts of energy when they are broken down and if they aren’t being properly broken down in our body it can lead to damage in our cells and tissues. We also learned in biology class that autophagy allows your body to break down and reuse old cell parts so  that our bodies won’t work as efficiently. 

Lypolosis

Overall, the time of our eating has many effects on our appetite, body temperature, weight fluctuation, number of calories we burn, energy level, and risk of obesity, and can even cause  molecular changes in our fat tissue. In the future, Brigham and Women’s Hospital, hope to perform more related experiments to discover further information about this topic and specifically the relationship between meal time and bedtime on energy balance.

I have always tried to be the healthiest version of myself, which will make me feel like my best self. I remember telling my brother that I was feeling sick because I ate really late at night and he laughed at me and said I was being dramatic. It is really interesting to learn the science behind eating late at night and how it can affect how you look and feel. I especially liked gaining a better understanding of this topic because now I know the factors that cause my body to not feel as great when I eat later than usual! 

How CRISPR Can Help Individuals Overcome Obesity

Fat, which is made up of cells that have been distended with greasy or oily materials, or triglycerides, is required for the body to function, but it may also be hazardous if consumed in excess. Fat cells are distinct from other cells such that they lack surface receptors and constitute only a small percentage of the cells in fat tissue. While restricting diets can assist those who are obese lose weight, the results are typically solely temporary. If only there were a way to target fat cells specifically… Well, there just might be!

Breast tissue showing fat necrosis 4X

A group of doctors discuss a potential prospective breakthrough utilizing CRISPR-Cas9, a technology that has proven particularly elusive in the study of adipose tissue, in a recent publication published in the Journal of Biological Chemistry. Their study was tested on mice, in order to see how it worked and what it targeted. The gene-editing technology CRISPR-Cas9 changes genes by precisely cutting DNA and then allowing natural DNA repair mechanisms to take charge. This technology has changed the ability of deleting or inserting certain genes of interest into an organism. Cas9, an enzyme that can break DNA strands as well as a piece of RNA that directs the Cas9 enzyme to a specific location in the genome for modification, is encased in a non-harmful virus and supplied to the cells being studied. The equipment has also been used to study the heart, liver, neurons, and skin cells, to name a few. However, brown fat adipose cells have never been studied.

Brown fat cell

Using CRISPR-Cas9 components, the physicians were eventually able to target brown fat adipose cells. In mature mice, they were able to knock off the UCP1 gene, which specifies brown adipose tissue and allows it to generate heat. They discovered that knockout mice were able to adjust to the absence of the gene and maintain their body temperature under freezing settings, indicating the existence of additional mechanisms involved in temperature regulation. Overall, the CRISPR interference system assisted mice in losing about twenty percent of their body weight, proving that CRISPR can accurately target fat cells.

3LFM FAT Mass and Obesity Associated (Fto) Protein

Genetics can have a significant impact on the quantity of fat cells you are born with. However, the proportion of tendency to becoming overweight differs by individual. For example, in some people, genes account for just 25 percent of the tendency, but in others, the genetic effect might be as high as 70 percent to 80 percent. Obesity is most commonly associated with the FTO gene. This FTO gene is not found in everyone. For example, around 20 percent of white people have a variation of the gene that increases their risk of obesity. The FTO gene is located on chromosome 16, which is one of the 23 pairs of chromosomes in humans. While this chromosome pair represents under 3 percent of the total DNA in cells, if FTO is present, it can affect whether if one is obese or not, depending on the alleles of the gene. CRISPR has the potential to target this gene as well as other genes that affect body weight, such as brown fat adipose cells.

Diagram of Chromosome 16

Your health is essential for the rest of your life! A healthy lifestyle can aid in the prevention of chronic diseases and long-term ailments. The alleles on the FTO gene can have an impact on your health and are linked to type 2 diabetes, obesity, and other health concerns.

Snacks That Smile Back…No More!

Throughout the world, child obesity is a global issue that has gone on for many years. With very few signs of progress, many people around the world are struggling to find innovative ways to save this worldwide problem. As more and more kids interact with many of these social media platforms including: Snapchat, Instagram, Facebook, Twitter, and Youtube, many fast food chains use this as an opportunity to spread the word about their food. Disregarding the foods and beverages of high fat, sugar, and salt(HFSS) could be one of the leading factors to the growing percentage with children who suffer with obesity. As part of U.K. government’s plan to limit child obesity through 2030, the article states that the government is “considering limitations on television advertising for HFSS products between the hours of 5:30 a.m. and 9 p.m.”.

This picture displays common junk food found in commercials.
This picture displays common junk food found in commercials.

The Study

Throughout this study, researchers used data on children’s exposure to HFSS advertising during the controlled hours(5:30 a.m.— 9 p.m.), as well as previously published information on the association between exposure to HFSS and children’s calorie intake in order to trigger a decrease in children being exposed to HFSS food. As the experiment was conducted, the ending results concluded that if all advertising containing foods with HFSS were to be limited or even terminated, 3.7 million children in the U.K. would experience on average 1.5 fewer advertisements per day, as well as decrease there calorie intake by an average of 9.1 kcal. The article states that these findings “would reduce the number of children aged 5 through 17 with obesity by 4.6% and the number of children overweight by 3.6%”. This data is equivalent to 40,000 fewer U.K. children who struggle with obesity and over 120,000 fewer children who classify as overweight. It it important to keep in mind that this study only focuses on the direct impact of HFSS advertising on children’s calorie intake and not the changing of children dietary preferences and habits.

Why is this Important?

This study proved that implementing a certain time frame throughout the day(5:30 a.m. -9 p.m.) to potentially reduce the exposure of less-healthy food(HFSS) advertising could provoke a valuable contribution towards not only protecting the future health of children who live in the U.K., but children all over the world. As children are becoming more connected with social media, it’s hard to avoid the mass amount of advertisements displayed throughout all these sites. “children now consume media from a range of sources, and increasingly from online and on-demand services,” says Dr. Oliver Mytton, researcher at the Centre for Diet and Activity Research (CEDAR) at Cambridge University.

Many of these less-healthy food options contain saturated Fats. These fats have fatty acid chains with “single-bonds” between carbons. This allows chains to pack closely together forming a solid, which are less healthy to consume due to the formation of plaques in blood vessels. These fatty foods also contain lots of carbohydrates as well. When consuming an excessive amount of carbs, your blood sugar levels can get too high. This leads to your body creating more insulin, which tells your body to store extra glucose as fat, making the person gain more weight, as well as lead to other major health issues.

I believe that obesity is a prevalent issue throughout our world, and the more studies and experiments we conduct to try and prevent this condition, the more healthy our world can become. What do you think? Leave a comment below!

Yes, Some of Us Have Different Human Ecosystems.

Our human ecosystems inside of us are composed of countless quantities of cells. However, only 10% of those cells are human cells.  Jeroen Raes , a Biologist based in Belgium, made a vital and fascinating discovery about the other 90%. He discovered that there are three different possible ecosystems inside individual humans. Each person has one of these three ecosystems: bacteriode, prevotella or ruminococcus. These ecosystems are composed of hundreds of trillions of harmless bacteria. One could explain our relationship with these bacteria as symbiotic, as we give them a share of food and they return the favor by helping us digest food and convert it to energy. Furthermore, these bacteria help us fight disease, and can even make us happier by triggering our neurons to release more serotonin. Raes’ experiment tested people from the US, Japan, and Denmark. Despite each regions unique diets, Raes claims to have found no correlation between diets and their individual ecosystems. Furthermore, Raes found no correlation between their age/genetic makeup and individual ecosystems.

People who have the bacteriode system “have a bias” toward bacteria that get most of their energy from proteins and carbohydrates. Bacteriode ecosystems also have more bacteria that make greater quantities of vitamins C, B2, B5, and H. On the contrary, both prevotella and ruminococcus ecosystems mostly digest proteins that are sugar coated. Both of these ecosystems also have more bacteria that create vitamin B1 and folic acid.

Raes’ findings have yielded very confusing results. Even Raes has conceded that he is unsure as to why only three total human ecosystems exist. Moreover, Raes admits his sample size of only a few hundred people will increase with more time and funding. Raes hopes to further his research on these unique human ecosystems, and potentially find links to obesity, diabetes, Crohn’s disease, and autism.

 

Cellular Roadblocks for Immigrants: The Loss of Gut Microbe Diversity

Recent evidence from the University of Minnesota in conjunction with the Somali, Latino, and Hmong Partnership for Health and Wellness suggested that immigrants and refugees moving to the United States were likely to experience a rapid change in their gut microbes. Described as “westernizing” to their environment, immigrants tended to lose their diverse, native microbes in favor of microbes that are common to European Americans.

The participants of this study originated from Southeast Asia, specifically the ethnic minorities of Hmong and Karen from China, Burma, and Thailand. The study used ethnic minority communities from both Southeast Asia as well as those living in Minnesota as a comparison, analyzing the gut microbes in these participants and using Caucasian American people as controls. The researchers also looked into the first generation children of these immigrants. Additionally, the study was able to follow a group of nineteen Karen refugees, tracking the changes in their gut microbes as they traveled to the United States.

The study discovered that the gut microbes in these participants changed rapidly. Particularly, in the group of Karen refugees, the Western strain of Bacteriodes replaced the non-Western strain of Prevotella in the matter of less than a year. Furthermore, the overall gut microbe diversity continued to decrease in all participants in the United States in relation to the length of their stay. Likewise, the children of immigrants had a more profound decrease in diversity. Researchers in this study suggested that this decrease in microbe diversity may have been a result of a Western diet, or for the children, growing up in the United States.

Image result for bacteroides

Closeup of Bacteroides biacutis(Image Credit: CDC/Dr. V.R. Dowell)

 

So why does this matter? Well, the study established a correlation: the greater the “westernization” of gut microbes, the greater obesity in immigrants. This obesity problem appeared to be more prevalent in immigrants, and the study had discovered a key piece of evidence for why.

“When you move to a new country, you pick up a new microbiome.” Dan Knights, one of the key authors of the study as well as a quantitative biologist at the University of Minnesota, says. “…What enzymes they carry…may affect the kinds of food you can digest and how your diet affects your health. This may not be a bad thing, but we do see that Westernization of the microbiome is associated with obesity in immigrants.”

 

The United States Plays a Role in Changing our Bodies

Researchers at the University of Minnesota and the Somali, Latino, and Hmong Partnership for Health and Wellness have new evidence that the gut microbiota of immigrants and refugees rapidly Westernize after their arrival in the United States.

In order to accomplish this research, the researchers used a community-based participatory research approach from Minnesota’s large community of refugees and immigrants from Southeast Asian (particularly the Hmong and Karen people, ethnic minorities originally from China and Burma that mostly now live in Thailand). These immigrants and refugees were involved with designing the study.

A concern that has been relevant in the communities of refugees and immigrants was obesity. With this in mind, the researchers wanted to see if there is a relationship with immigrants and obesity.

The team of researchers compared the gut microbiota of Hmong and Karen people still living in Thailand; Hmong and Karen people who had immigrated to the U.S.; the children of those immigrants; and Caucasian American controls.

With this, the researchers found that there were significant changes in just the first six to nine months! The Western strain bacteroids began to displace the non-Western bacteria strain Prevotella. The more interesting part is that this Westernization continued to happen in the next decade, and so on. Overall, as the immigrants and refugees spent more time in the U.S., the diversity in the microbiome started to decrease. Indeed, the changes were even more pronounced in their children.

Overall, participants’ food logs suggested that eating more Western food played a role in changing the microbiome, but could not explain changes in the body, like obesity. So, we are still left with some wonder, but scientists will soon put our wondering to an end!

 

Welcome to America, here is a risk of obesity?

Each individual has a personalized micro-biome with trillions of bacteria weighing about half a pound. We receive this microbiome at birth as a departing gift from our mothers, but this microbiome does not remain the same through the years. Studies by Dan Knights from the University of Minnesota have shown, however, that geographic location and diet results in shifts in our gut microbiota.

         Figure 1

 

So what does this mean?

The study by Dan Knight shows that immigration is causing dramatic shifts in new arrivals to the country. These new arrivals surveyed through stool samples are from places in Southeast Asia including 500 women of Hmong and Karen descent. These 500 women varied from individuals remaining in Thailand where most Hmong and Karen people live currently, first- and second-generation U.S. immigrants, and even included 19 Karen women followed through their first six to nine months in their new nation. All of these samples were then compared to 36 European Americans born in the United States.

On the microscopic level, the aforementioned immigrants are facing a shift in the gut microbiota from Prevotella bacteria to Bacteroides. “Prevotella bacteria produce enzymes that digest fibrous foods more common in Asia than the United States. In Thailand, the women ate more palm, coconut, a fruit called tamarind and the bulbous part of a plant named konjac.” This shift in bacteria causes a loss of 15% of microbiome diversity and furthermore does not shows signs of compensating for the loss of native microbes.

As the diversity shifts towards that of European American, obesity rates seem to spike among the population. The immigrants’ obesity rates increased by nearly six times, which is a drastic shift for the immigrants who held an originally low risk of metabolic disease. This shift, however, is still a complete mystery. The researchers cannot pinpoint the true cause as diet, location, medicines, water composition, or an unknown but there is a clear correlation between obesity and the lessened diversity in the gut microbiota. This correlation was discovered through an experiment involving mice injected with germs from obese women. These mice subsequently became heavier despite having the same food as their lean equivalents. Knight and his colleges plan to continue their studies in hope to possibly provide a solution to obesity through the injection of Prevotella, as they are driven by the intense sensitivity and stake of their subjects’ health.

File:Gut microbiota and obesity.png

Figure 2: Experiment on Obesity with Mice

 

 

While immigration to the United States, a place of opportunity, may appear a blessing it does not come without risks. As the leading nation in obesity, it comes as no surprise that something is causing a drastic shifting in newly immigrated individuals’ gut microbiota and larger micro-biomes resulting in a higher risk of obesity. A gift and a curse, however, this phenomena has resulted in research that could possibly grant new insight on how to prevent obesity.

 

 

Can Bacteria in Your Gut Cause Obesity?

Bacteria in your gut, aka gut microbiota, is made up of tens of trillions of microorganism, including 1000 different species of known bacteria. Although scientists are currently not incredibly knowledgeable on gut microbiota, an increasing amount of research has shown that it is plays a significant role in our health.

https://pixabay.com/en/anatomy-bacteria-bacterium-bowels-160524/

In a recent study at Lund University in Sweden, researchers have found correlation between gut bacteria and obesity. The purpose of the study was to identify metabolites in the blood that can be linked to obesity and see if they affect the composition of the gut microbiota in stool samples. The researchers studied blood plasma and stool samples from 674 participants and found 19 different metabolites that could be linked to the person’s BMI. Their data showed that Glutamine and BCAA (branched-chain and aromatic amino acids) had the strongest connection to obesity and that four different intestinal bacteria, Blautia, Dorea, Ruminococcus, and SHA98, were linked to the obesity related metabolites. Glutamine, “the strongest risk factor in the study”, has been linked with obesity in previous studies as well. Marju Orho-Melander, professor of genetic epidemiology at Lund University, summed up the study by stating, “The differences in BMI were largely explained by the differences in the levels of glutamate and BCAA. This indicates that the metabolites and gut bacteria interact, rather than being independent of each other.” Therefore, the metabolites they found are potential mediators between gut microbiota and obesity, and may be consequential in ultimately preventing obesity.

Does Immigration Alter the Microbiome?

Each human has our own microbiome; one that is unique to us. However, recent research has shown that the microbiome of someone’s body is not static, but highly subject to alteration. Microbiomes change depending on the atmosphere you are in- and they change very quickly, taking only nine months in the U.S. The University of Minnesota has found that, in people emigrating to the US, microbiomes “rapidly westernize”; aka, their native microbes are replaced with new ones. However, this shift in microbes is not equal- there aren’t enough new microbes to replace the old, resulting in a harsh decline in diversity; diversity that stimulates metabolism, digestion, and immune system development.

Dan Knights, a computational microbiologist at the University of Minnesota, states that in moving to another country, you pick up new microbes native to that country, and new disease risks as well. In this case, the shift in the microbiome makeup can be beneficial, as the new microbes may aid in defense against new disease. However, it has also been found that “Obesity rates among many of the study immigrants increased sixfold. Those who became obese also lost an additional 10 percent of their diversity.” This fact links diet shifts to microbiome shifts, yet Knights states that “diet alone wasn’t enough to explain the rapid Westernization of the microbiome,” and that other things such as water and antibiotic use factor in as well. However, diet is still an important part in microbiome health and diversity. Knights studied microbiota of Hmong and Karen women who had immigrated to the U.S., these immigrants’ American-born children, and white American controls. Their microbiomes shifted to Prevotella to Bacteroides, coming to resemble those of the white Americans who acted as the control. The immigrants’ children were even more susceptible to changes in and loss of microbial diversity.

Obesity statistics worldwide from the years 1996-2003.

We as Americans are highly aware of our obesity epidemic and are doing all we can to find a way to fix it. Research that links it to a cause relieves people- it provides hope that there is a way to change it. Knights remarks that “we do see that Westernization of the microbiome is associated with obesity in immigrants, so this could an interesting avenue for future research into treatment of obesity, both in immigrants and potentially in the broader population.” However, it cannot be used as an excuse for our problem as Americans- it is simply a breakthrough in a long journey that may help us in the long run.

The Behavioral Causes of Obesity

Obesity is a big issue that is affecting the world today. Obesity is mostly caused by abnormal eating habits, which include overeating, but little is known about what causes overeating. To further understand the behaviors that lead to overeating and obesity, scientists from the Centre for Genomic Regulation and the Pompeu Fabra University in Barcelona, Spain conducted research on mice. There findings were published in Addiction Biology.

The scientists put the mice in an environment where they are only fed high calorie foods. Their diet consisted of chocolate bars and their normal food. As the mice started to gain more weight, they started to become addicted to chocolate and started binge-eating it. They would eat the chocolate over their normal food, even though they were more full from eating their own food. Their new binge eating habits also changed their eating schedule. They started eating during the day, rather than at night.

In conclusion, this research made scientists aware that some people can be trapped in a binge eating state which can lead to obesity. Obesity is not just a metabolic disease, but is caused by behavioral issues. This research is helpful because people can now take preventative measures and go to therapy to change these eating habits. This research is very interesting because it can help solve obesity issues. To learn more about obesity behaviors and treatment, click here and here. 

Striped Field Mouse

 

What You Eat Now Matters Later!

 

Researchers from the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen have potentially uncovered the cause for developing obesity. This process involves precursor cells, the fatty acid palmitate and the hormone TNF-alpha.

^Above is a photo of fat tissue

What are precursor cells and how does it work? 

A precursor cell is an immature cell that has not undertaken a specific role in the body yet, for example a mature cell would be considered a muscle cell. When this cell comes in contact with the fatty acid palmitate and the hormone TNF-alpha it is disrupted. This interaction will cause future damage; it causes the cell to develop into a dysfunctional fat cell. Obese patients with type two diabetes will often contain these types of reprogramed cells.

How were these cells discovered?

The researchers collected physical data from multiple types of patients with 43 planned opporations. They retrieved fat tissue from 15 lean patients, 14 obese patients, and 14 obese patients with type two diabetes. When they compared the data from the three groups of patients they noticed that the fat cells from the obese patients with type two diabetes were not normal fat cells, they were reprogrammed cells that did not function like normal fat cells. Once they realized this, the researchers were able to recreate the reprogrammed cells by exposing precursor cells to the palmitate and hormone TNF-alpha. In just 24 hours they were able to complete the process successfully!

What can I do with this information?

These results illustrate how essential it is for you to maintain a healthy diet and lifestyle. It proves that your habits now will affect you in the future. This is why people should learn about how to live a healthy lifestyle at a young age. The younger the better, because it would decrease the chances of precursor cells to be transformed into abnormal fat cells for your future life.

The future:

Hopefully, this study sparks new ideas and discoveries regarding preventative obesity tactics. The researchers hope to discover a way to reverse the abnormal programing of the fat precursor cells. If researchers could figure out a way to reverse this programing how much safer could obese patients become? Could this research impact the education systems, forcing health classes earlier in students lives? This article interested me because I am always focused on how my decisions will affect me in my future, however I never thought of this with my eating habits.

Possible Links Between Gut Microbes and Obesity, Cancer & Autism

While the bacteria in our gut play a vital role in the digestion process, recent findings have suggested that it could effect much more in our bodies. New studies have found possible links between the bacteria in our gut and obesity, cancer and autism.

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A study done by Cornell University and King’s College London revealed that Christensenellaceae minuta, a strain of gut bacteria, was found more often and in larger quantities in people with lower body masses. To investigate whether the bacteria is actually linked with obesity, researchers added the same bacteria into the guts of mice and compared their weight gain to mice lacking the bacteria. The research showed that the mice with Christensenellaceae minuta gained noticeably less weight than the mice lacking the bacteria. While research is still in its early stages, these results have made an exciting connection between bacteria in our gut and weight gain, which could dramatically impact the future of our health.

In addition to obesity, the bacteria in our gut has also been linked to cancer- in both beneficial and detrimental aspects. Researchers from the National Cancer Institute tested the effect of gut bacteria on chemotherapy in mice and found that the chemotherapy was significantly less effective in the mice lacking the bacteria. Similarly, another study found that cyclophosphamide, an antitumor drug, was less effective in mice with insufficient gut bacteria compared to those with normal levels. While these studies showed positive links between gut bacteria and cancer, other studies have found adverse effects of gut bacteria.

Unfortunately, a study published in The Journal of Cancer Research in 2012 has made a possible connection between Lactobacillus johnsonii, a strain of gut bacteria, and lymphoma, cancer of the white blood cells. The study claims that the presence of this specific strain of bacteria could lead to the development of lymphoma. Another study done in the UK in 2013 found that a specific gut bacterium, Helicobacter pylori, has the ability to deactivate the part of our immune system responsible for regulating inflammation. In effect, this could cause stomach cancer and ulcers.

While it may seem like a stretch, numerous studies have found a possible link to autism and the bacteria in our gut. A study done in 2013 by Arizona State University found that compared to children without autism, children suffering from autism had lower levels of Prevotella, Coprococcus and Veillonellaceae, three strains of gut bacteria. Even more surprisingly, another study revealed that the presence of Bacteroides fragilis in the gut reduced autism-like symptoms in mice. Research in this field is still in its primary stages, as researchers are trying to figure out if these connection are in fact related, and if so, how the bacteria directly effects these conditions.

 

Obesity Related to the Brain

Lauri Nummenmaa has done research the connects obesity to the brain.  This research shows that people struggling with obesity have a lower amount of μ-opioid receptors available for binding in the brain.  (To learn more about μ-opioid receptors click here.)  Due to evolution, our brains are still “wired” to search for food and nutrients.  Since eating gives off a sensation in the brain, related to the opioid receptors, people with fewer receptors that are able to bind will therefore eat more to make up for the loss in sensation.  This reaction is the same as a reaction to an addiction would be, causing more neurotransmitters to be secreted.  The next step that scientists are taking is to discover whether being obese causes a lack in opioid receptors, or if a lack in opioid receptors, caused by another source, is what causes obesity.  One test that scientists did was testing μ-opioid receptors in people that had bariatric surgery.  Bariatric surgery causes more receptors to work again, shown by the fact that scientists could not distinguish between the μ-opioid receptors or healthy people and the μ-opioid receptors of people who had the surgery.

Some body fat, however, is helpful to the brain.  This article describes that “fat tissue in the bodies of mice releases an extracellular form of nicotinamide phosphoribosyltransferase (eNAMPT), an enzyme that travels to the hypothalamus, and gives animals energy during fasting.”  (To learn more about eNAMPT click here.)

This photo shows how a neurotransmitter is sent from neuron to neuron generally.

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The Relationship Between Girls and Their “Skinny Jeans”

New findings suggest that the dynamic between a girl’s gene and her early socio-economic environment can dictate if they have a larger fat intake or healthier consumption in relation to others within the same class background. The gene variant is called the DRD4 repeat 7 (7 repeats). According to the McGill Centre for the Convergence of Health and Economics, girls from poorer families with DRD4 repeat 7 have an increased fat intake than other girls from the same socio-economic environment. However, girls with the gene variant from wealthier families and backgrounds have a lower fat intake. These studies portray how it isn’t solely the gene that determines an individual but how the gene influences an individuals sensitivity to environmental factors that contribute to a child’s preference to fat.

This research was done by collecting diaries by parents of 200 Canadian children (about 4 years old). Their fat, protein, and carbohydrate percentages were all measured along with their BMI and also saliva tests to see who are carries of the DRD4 repeat 7 gene. To categorize the children in their socio-economic environment, the family income was used while acknowledging the food environment (what type of foods are available in that neighborhood).

Plasticity genes,” where carriers of gene variants might be more “open” to their environment rather than those who are not carries of gene variants, is a term used to describe the DRD4 repeat 7 gene. Researchers realized that the fat intake has a direct correlation with any modification of the girls social environment and how they are raised. Therefore, the gene itself is not to blame for a high fat intake.

The data had only shown to be consistent with girls, not boys. From an evolutionary perspective, in order to sustain hard conditions and be able to reproduce, girls had to have more weight on them. Another reason may be because the age four is not old enough to measure the gene’s activity in boys because boys can gain weight at different stages than girls.

Furthermore, this research contributes to the idea that preventing childhood obesity cannot have a general and “one size fits all” type of approach. Instead, specific approaches for certain populations is what’s needed. Especially populations that are vulnerable in adverse conditions because they are more likely to respond better if their conditions improve.

 

Original article can be found here.

Is it Really Your Choice to Make Better Choices?

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Obesity has become an increasingly prevalent epidemic around the globe and especially in the United States. Obesity has numerous roots. Recently, researchers from the McGill Centre for the Convergence of Health and Economics found that in some circumstances, it is possible to blame obesity not solely on genetic make-up, but rather on genetic make-up and socio-economic background combined. The McGill researchers discovered that the fat intake of a female who is a carrier of DRD4 VNTR with 7 repeats, a specific gene variant, is determined by the interaction of the female’s socio-economic environment with the gene. This gene variant affects about 20% of the population and is commonly related to obesity, especially in females. Males are typically not as affected by the gene because when comparing males and females at the same age, males do not typically show the same pattern of food preferences.

In order to research this topic, McGill researchers randomly selected about 200 Canadian children with an average age of 4 from the MAVAN birth cohort in Montreal, Quebec and Hamilton, Ontario to take place in the experiment. The McGill researchers used food diaries kept by the parents of every child in order to determine what was being eaten and how often the child was fed. The researchers were able to calculate the percentages of fat, protein, and carbohydrates the children were consuming, as well as the BMI of every child. Since the children were selected at random, the researchers tested every child for the gene variant using a saliva test. The researchers also analyzed the socio-economic background of every child and availability of particular foods based off of the family’s income.

Laurette Dubé, Scientific Director at this particular Centre at McGill and lead researcher on the study, analyzed the results. Dubé found that when comparing two females from the same socio-economic background, one with the gene variant and one without, the female with the gene variant had a higher fat intake, even though the two females came from the same socio-economic background. She also discovered that when comparing two females with the gene variant, one coming from a wealthy family and one coming from a poor family, the female coming from the poorer family had a higher fat intake, despite the fact the two females were both carriers of the gene variant. This newly found research led the McGill research team to believe that the gene alone does not determine an individual’s fat intake, but instead the gene causes an individual to be more sensitive to his or typically her environmental conditions that determine what are “good” eating patterns and what are “bad” eating patterns. Dr. Robert Levitan, co-invesitgator on the project, leader of the childhood obesity program of the MAVAN cohort, and Senior Scientist at the Centre for Addiction and Mental Health (CAMH), is an expert on the DRD4 gene in adult female “overeaters”. Levitan said, “We previously assumed that the 7-repeat variant caused weight gain in these patients by increasing the rewarding aspects of certain foods. These new results suggest a different way that the gene might affect food choices” (Biology News).

In certain cases, obesity isn’t all about genetic make-up, but the likeliness of obesity is determined by the socio-economic background of an individual as well! So, if you are a carrier of the DRD4 VNTR with 7 repeats gene variant, which, because of your environment, impacts your decisions, is it really your choice to make better choices?

Source: Biology News 

 

Have No Fear, Gut Microbes Are Here!

Ever dream about being a real life Captain America? Well, with the help of microbes, we are one step closer to achieving a “super soldier.” Microbes might not make a soldier muscular, but they can help with soldiers’ health and versatility. Scientist Jeff Tabor is working on engineering a probiotic organism that can help humans easily fight diseases, prevent obesity, and change their body’s ability to adapt to certain environments.

The gut bacteria affects many functions of the human body. The digestive system, immune system, and nervous system are all influenced by gut bacteria. Disrupting these microorganisms can cause indigestion, a weak immune system, depression, insomnia, and affect other cognitive abilities. Tabor’s goal is simply to create a microbe that can be consumed to prevent these problems.

Gut Microbe

Gut Microbe

Initially, Tabor wanted to use these microbes to target obesity because scientists have abundant knowledge of obesity at the molecular level. He recently succeeded in genetically modifying E.Coli to detect chemicals in the body that carry disease in mice guts. He hopes to use this modified E.Coli to sense chemicals in the gut that are connected to obesity and then use other molecules to prevent this obesity. The creation of a microbe that can control weight can be extremely helpful for the U.S. armed forces. For example, soldiers going from sea level to the top of a mountain way above sea level experience changes in temperature and pressure. Using this engineered gut microbe, the soldiers can put on weight to help them keep warm on top of the mountain and then lose weight to keep cool at sea level.

Another military benefit that these microbes can provide is to help soldiers operate effectively on little to no sleep or to help soldiers adapt to changes in their circadian rhythms, either from time change or going below sea level in a submarine. Scientists are interested in experimenting with the gut microbe to be able to achieve these goals in the future.

Some people might be afraid of the possible affects that these genetically modified bacteria might have on the human body. However, Tabor’s goal is for the bacteria to stay in the gut for about six hours to do its job and then self-destruct or die naturally to prevent the bacteria for staying in the body too long. There are other concerning issues about creating a microbe that can help prevent obesity. The creation would take away any incentive for humans to eat healthy and focus on their diets because they could just use the microbe to prevent gaining weight. Any new scientific experiment comes with its pros and cons, but using gut microbes for human health, especially for the military, can be a big step in the right direction.

Source Article

Sewage Does More than Just Gross You Out… It Carries a Signal For the Microbiomes of Humans

Who knew that sewage would ever be useful. Well, it is a successful way to collect fecal bacteria from people. It can monitor, through gut microbes, the public health of a population without invading people’s privacy. The human gut microbiome consists of huge amounts of bacteria in the gastrointestinal tract. This gut bacteria has important functions in a healthy human. Recently, there has been much attention to the human microbiome, and more specifically, finding a “healthy microbiome” by identifying which bacterial communities are associated with healthy individuals. What has been hindering this experiment are financial concerns but also privacy concerns in terms of the individuals that can be screened.

Researchers from MBL (Marine Biological Laboratory) and the UWM (University of Wisconsin-Milwaukee) School of Freshwater Sciences proposed the idea of using sewage as a population that consists of a signal for human microbiomes. The scientists used oligotyping to compare 137 healthy people’s gut bacteria (provided by the Human Microbiome Project) to the bacterial communities of more than 200 sewage samples from 71 different U.S. cities. Researchers realized that geographically distributed populations consists of a similar core set of bacteria and its members symbolize many different communities within U.S. adults. The percent of obese people in a city is used by the study as a measure of a lifestyle difference which indicates that this bacteria community structure is accurate in detecting obesity in a city. Lifestyle differences are important because they can change the human gut microbiome and an indicator of obesity is the microbial community composition. This process of working with microbiomes of individuals is similar to drawing a map of a specific geographical area and fishing out new understandings and patterns. If it weren’t for the sewage, the scientists wouldn’t have been able to differentiate the cities based on their level of obesity. This type of approach can be effective when it comes to answering concerns about public health, without undermining the privacy of individuals.

I found it interesting how this profound yet relatively small experiment is even part of a bigger plan to create better water pollution and public health assessments. Do you think it can lead a better water pollution and efficient public health assessments? Overall, it’s amazing how new technologies can aid in decrypting information from complicated environments. I’m excited to see where this experiment takes us as it leads researchers and scientists in a more knowledgeable outlook on our environment and in public health.

The original article can be found here.

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