Probiotic Does Not Treat Stomach Flu

Gastroenteritis(Stomach Flu) is caused by bacterial and viral infection in your gastrointestinal tract, which causes it to become inflamed and irritated. The symptoms of the disease include: watery diarrhea, vomiting, stomach pain, cramping, fever, nausea, headache, and dehydration. Dehydration can be especially dangerous in children and babies since they have so little body fluid to expel. In order to treat and cure this disease, doctors prescribe probiotics, which are live microorganisms that are intended to have health benefits. For example, yogurts are probiotics since they provide bacteria for our guts which can help us digest food easier. Therefore, probiotic medicines, such as Lactobacillus rhamnosus GG, or LGG, which is sold over the counter as Culturelle, were prescribed to restore the balance of intestinal bacteria and boost the immune system.

               However, a major U.S. study led by Washington University School of Medicine shows that a commonly used probiotic is not effective in improving symptoms in young patients with gastroenteritis. The study involved 971 children treated in the emergency departments at St. Louis Children's and nine other geographically diverse U.S. academic medical centers. Participants were eligible if they had come to the emergency room with symptoms of gastroenteritis: watery stools, vomiting, diarrhea or other signs of acute intestinal infection. They also had not taken probiotics in the preceding two weeks. The patients were prescribed either placebo or probiotic with the parents, the medical practitioners, and the patients not knowing which were probiotic. Regardless of whether they took placebo or probiotic, their symptoms and recovery were stated to be nearly identical. LGG probiotic did not help in treating gastroenteritis.

               Of course, this was only one study that was taken over 3 year period with only one type of probiotic, when there are many other types that exist to effect the microbiome of our digestive tract. However, it seems that medical practitioners have to be notified of how probiotics, by themselves without antibiotics to kill the harmful microbes, may not be a solution to treat young patients’ gastroenteritis  

Washington University in St. Louis. (2018, November 21). Probiotics no help to young kids with stomach virus: Study examined children with diarrhea in nation's emergency rooms. ScienceDaily. Retrieved November 30, 2018 from www.sciencedaily.com/releases/2018/11/181121171829.htm

David Schnadower et al. Lactobacillus rhamnosus GG versus Placebo for Acute Gastroenteritis in Children. NEJM, 2018 DOI: 10.1056/NEJMoa1802598

A Link to Decreased Magnesium in Clinical Depression

            Earlier this year, Psychology Today came out with a news story regarding the potential link to decreased magnesium and clinical depression (“Magnesium for Depression,” n.d.). This is huge news for potential treatments for depression, as despite the large amount of people that depression affects, the current treatments available are limited due to efficacy, cost, undesirable side effects, and the fact that most antidepressants only result in 50% of patients achieving remission for a short period of time (Tarleton, Littenberg, MacLean, Kennedy, & Daley, 2017). The fact that increasing magnesium levels could possibly mediate or eliminate depression symptoms at a neurologic level gives hope to the reality of establishing better and more effective treatments in the near future.

            Quite possibly the greatest link between magnesium levels and depression lies in the effects magnesium has on voltage gated Ca²⁺ channels in the presynaptic terminal. It is believed that magnesium inhibits voltage gated Ca²⁺ channels from opening which in turn decreases the amount of neurotransmitters released from the synapse (Takeda, 2003). When magnesium levels are low, voltage gated Ca²⁺ are no longer inhibited, resulting in a large influx of Ca²⁺ and an abundant release of neurotransmitters. This is specifically detrimental in the case of the neurotransmitter glutamate; if excess glutamate is released from the presynaptic terminal, this could result in over excitation of neighboring neurons that could ultimately lead to decreased synaptic function or possibly even cell death (Tarleton et al., 2017).

            The study reported by Psychology Today aimed to study the efficacy and safety of magnesium and to better understand how magnesium plays a larger role in depression (Tarleton et al., 2017). Their results indicated that the administration of magnesium supplements did have a statistically significant positive effect on depression symptoms (Tarleton et al., 2017). Over the course of the trial, average depression scores dropped significantly, bringing the mean from moderately depressed to mildly depressed. However, the positive effect felt from the magnesium supplements had completely diminished within the two weeks after stopping treatment (Tarleton et al., 2017). While this study suggests that the role of magnesium in treating depression is significant, further research should be conducted in order to fully understand the actions of  magnesium; if we can completely understand the function at a synaptic level, perhaps we could create a more effective long term treatment for depression (Takeda, 2003).

Works Cited

Magnesium for Depression. (n.d.). Retrieved December 1, 2018, from

https://www.psychologytoday.com/blog/evolutionary-psychiatry/201801/magnesium-depression

Takeda, A. (2003). Manganese action in brain function. Brain Research Reviews, 41(1), 79–87.

https://doi.org/10.1016/S0165-0173(02)00234-5

Tarleton, E. K., Littenberg, B., MacLean, C. D., Kennedy, A. G., & Daley, C. (2017). Role of

magnesium supplementation in the treatment of depression: A randomized clinical trial. PLoS ONE, 12(6). https://doi.org/10.1371/journal.pone.0180067

Obamacare or Nah: discussing poverty, healthcare affordability, and ethics

Do you remember the Affordable Care Act?  Yeah.  It’s pretty controversial still.  Three years after it was approved during the Obama Administration, 54% of Americans opposed it.  Many find consolation in that President Trump and Congress have acted to try to weaken and replace it.  In fact, the recent Tax Cuts and Jobs Act repealed the tax on people who do not buy insurance, and it is estimated that millions of healthy people will drop their insurance plans when the law becomes effective in 2019.  Here is a link to a site that briefly outlines some of the pros and cons people are passionate about if you want more information on what the Act is https://www.thebalance.com/obamacare-pros-and-cons-3306059.

Part of Obamacare, the controversial healthcare reform law, stated the option to expand Medicaid to people who earn up to 138% of the federal poverty line, which addressed the gap in medical coverage for low-income families and individuals who were not eligible for Medicaid or insurance from employment.  The Affordable Care Act, in this way, increased the medication options available for patients in this low-income category who had type 2 diabetes and hyperglycemia.  The reform gave access to medications other than the normal metformin, sulfonylureas, and insulin (Brooks, Kalyanaraman, & Malek, 2018).

People who experience poverty and homelessness have benefited greatly from this aspect of the Affordable Care Act.  553,742 United States citizens, as estimated in November of 2018, experience homelessness, and if we include in our estimation the people who are in unstable housing conditions, 4.5 million people in the US experience homelessness in any given year.  To add to that altogether too high number, the rate of diabetes has been increasing among the homeless population.  And even further than that, there are many social, psychological, and physical challenges that homelessness brings people that can contribute to the rate of diabetes growth and complicate its management.  People experiencing homelessness actually report poorer health and a larger rate of early onset diabetes than people who have stable housing situations and are not experiencing poverty.

Keeping in mind all the challenges that homelessness and poverty bring to people, and remembering the health aspects that challenge these people, do healthcare providers and insurance companies have a responsibility to sustain and increase affordability of healthcare and preventative care to people who experience poverty?  Does the government have a responsibility?  Does anyone?  The Affordable Care Act has its pros and cons, and it certainly affects people all over the country in negative and positive ways economically.  But do its positive impacts on those who would not be able to afford healthcare otherwise outweigh the negatives?  As a scientist, student, and/or future healthcare provider, what do you think?

References

https://www.thebalance.com/obamacare-pros-and-cons-3306059

Brooks, L. K., Kalyanaraman, N., & Malek, R. (2018). Diabetes Care for Patients Experiencing Homelessness: Beyond Metformin and Sulfonylureas. The American Journal of Medicine. doi:10.1016/j.amjmed.2018.10.033

The Role of Vitamin D in Diabetes and Other Metabolic Disorders

According to the physiological and biochemical make up of the human body, we were meant to live with some exposure to sunlight. Due to increased amounts of employment opportunities requiring our society to earn their living indoors behind a computer, inside a restaurant, or in a factory to name a few, people are not absorbing the vitamin D they need daily. Therefore, vitamin D deficiency, along with other metabolic disorders are becoming increasingly more prevalent and more severe. However, with high prevalence comes an increase in awareness. Today new discoveries have shown those with low vitamin D levels are more likely to have diabetes. In addition, calcium plays a large role in the body to maintain bone and muscle health (Clemente et al., 2015). In a recent study published in Science Daily®, participants had their vitamin D levels checked via blood testing and measured the expression of the vitamin D receptor gene in adipose. Diabetic subjects were found to have lower levels of vitamin D in their system compared to those who had not been diagnosed with glucose metabolism disorder (Clemente et al., 2015). Vitamin D is vital in the body to help absorb calcium in the gastrointestinal tract. Vitamin D is first biologically inert and needs to be hydroxylated in the liver by an enzyme called vitamin D-25-hydroxylase. Vitamin D becomes 25(OH)D, but this form of vitamin D needs further hydroxylation in the kidneys by another enzyme 25(OH)-1-OHase to finally form the biologically active form of vitamin D, which is vitamin D 1,25(OH)2D. This form allows for intestinal calcium absorption. Without vitamin D, only ten to fifteen percent of dietary calcium can be absorbed (Nair & Maseeh, 2012). Vitamin D receptors on most cell surfaces in most tissues in the body does a wide variety of things inside the body. First, it inhibits cellular proliferation and angiogenesis. Second, it stimulates insulin production, but prevents renin production. Regarding genetic affects, the 1,25(OH)2D is potentially responsible for regulating up to two hundred genes that can have pleiotropic health benefits. Pleiotropy means that a single gene can have multiple, unrelated genetic affects (Nair & Maseeh, 2012). It is apparent vitamin D plays a large biochemical role in calcium absorption, which is vital for bone and muscle health. Overall, it makes sense that low levels of vitamin D can be correlated with glucose metabolism disorders because vitamin D receptors play a crucial role in stimulating insulin production. Resources: Clemente-Postigo, M., Muñoz-Garach A., Serrano, M., Garrido-Sánchez, L., Bernal-López, M., Fernández-García, D., Moreno-Santos, I., Garriga, N., Castellano-Castillo, D., Camargo, A., Fernández-Real, J., Cardona, F., Tinahones, F., Macías-González M. (2015, April). Serum 25-Hydroxyvitamin D and Adipose Tissue Vitamin D Receptor Gene Expression: Relationship With Obesity and Type 2 Diabetes, The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 4, 1, Pages E591–E595, https://doi.org/10.1210/jc.2014-3016 Nair, R., & Maseeh, A. (2012). Vitamin D: The "sunshine" vitamin. Journal of pharmacology & pharmacotherapeutics, 3(2), 118-26. https://www.blogger.com/blogger.g?blogID=4842520274317742324#

Navigating the Facts About Gluten

In general, there has been a shift in the Western diet towards an increase in the consumption of gluten, which is the pain protein in wheat products. Subsequently, recently, there has been a call for gluten-free diets or an overall decrease in gluten intake. Many of those who endorse a gluten-free diet often cite health benefits from cutting out gluten from their diet. In general, most of the studies surrounding gluten-free diets have revolved around celiac disease, which is an immune reaction that causes inflammation in the lining of the small intestine and malabsorption due to consumption of gluten. Increased incidence of celiac disease has been linked to the increase in glucose consumption and a small number of other studies suggests that gluten consumption might also be linked to other autoimmune disorders because the increase in autoimmune disorders coincides with a societal increase in gluten consumption. Recently, reports have shown that gluten consumption might have detrimental effects on health in general, with possible symptoms such as inflammation, increased apoptosis in the cells of the small intestine, a decrease in DNA and glycoprotein synthesis, and many more (all of which can be summarized in figure 1 below). However, as mentioned before, most of the research about the effects of gluten has surrounded those with celiac disease and is not representative of the population as a whole. Moreover, there is a lack of research on the effects of gluten in controlled human studies; most of the evidence of the detrimental effects of gluten is limited to several in vitro studies in model organisms. Thus, further clinical trials are required before people can begin to claim that cutting out gluten can be advantageous. In light of the current debate about gluten and the possible benefits of a gluten-free diet, I would argue that there simply isn’t enough research supporting the supposed benefits of a gluten-free diet (excluding those with celiac disease). Thus, popular opinions surrounding gluten should be taken with some skepticism!  

Source:

Lerner, Aaron, et al. “Adverse Effects of Gluten Ingestion and Advantages of Gluten Withdrawal

in Nonceliac Autoimmune Disease.” Nutrition Reviews, vol. 75, no. 12, 2017, pp.

1046–1058., doi:10.1093/nutrit/nux054.

Enough Vitamin B?

The presence of vitamins, particularly vitamin B, is important for maintaining control of our metabolic processes. Many of these vitamins act as cofactors for different enzymes in the body, and a deficiency in these compound can lead to many different diseases including anemia. As it turns out, vitamins are also extremely important for pregnant women.

Prenatal supplements often include vitamins to ensure that metabolism for both the mother and the child runs smoothly. Particularly, folate (vitamin B-9) has been established as a protective factor against neural tube defects in the fetus. Reports have also shown that low folate levels during pregnancy increase the risk of preterm birth and preeclampsia. In the United States, mandatory fortification of cereal-based products to prevent folic acid deficiency in women of fertile age in order to decrease the rates of neural tube defects in fetuses.

Folate is also implicated in 1-Carbon metabolism; folic acid activates the oxidation/reduction of single carbons. This process is important for amino acid metabolism and synthesis of DNA, RNA, membrane lipids, and neurotransmitters. Interestingly, maternal pregnancy folate levels have been associated with insulin resistance in children of 6 years old and greater adiposity in their offspring. Moreover, folic acid appears to play a role in the prevention of congenital heart disease and oral clefts. The fortification of cereals in the U.S. has been shown to significantly reduce the instances of spinal cord defects, which is a prime example of how public health initiatives can drastically change health outcomes.

Citation:

Greenberg, J. A., Bell, S. J., Guan, Y., & Yu, Y. (2011). Folic Acid Supplementation and Pregnancy: More Than Just Neural Tube Defect Prevention. Reviews in Obstetrics and Gynecology, 4(2), 52–59.

Solé-Navais, Pol, et al. “Early Pregnancy B Vitamin Status, One Carbon Metabolism, Pregnancy

Outcome and Child Development.” Biochimie, vol. 126, 2016, pp. 91–96., doi:10.1016/j.biochi.2015.12.003.

HIV-resistant babies using CRISPR to edit the genome

Yesterday, it was announced that a Chinese scientist claimed that he has created the world's first genetically-edited babies.  The scientist, He Jiankui, stated that he altered the twins' genes before implanting them in the mother to make them resistant to Human Immunodeficiency Virus (HIV).  He reported that he recruited couples where the male was infected with HIV, and used in-vitro fertilization to create embryos and used CRISPR-Cas9 to disable the CCR5 gene that creates the proteins that HIV needs to enter the cells (source).  However, he didn't publish his work anywhere and didn't provide evidence to show that his attempt was successful.

HIV works by attacking CD4 cells, which are a type of T cell.  The virus binds to receptors on the surface of the cell and its RNA enters the cell.  From there, reverse transcriptase converts the HIV RNA into HIV DNA.  That DNA inserts into the nucleus and replicates.  The cell is able to create and push out HIV proteins and RNA (it is noninfectious at this point), a protease cleaves the protein chains, and then the chains can combine to form infectious HIV (source).  HIV is able to evade the immune system because the proteins on the surface of the cells are constantly mutating and changing shape, and this is what antibodies latch onto (source).

Globally, ~37 million people have HIV, and 1% of people aged 15-49 live with HIV (source).  People with HIV initially experience flu-like symptoms, such as fevers, muscle aches, and swollen lymph nodes.  If left untreated by anti-retroviral therapy (ART), it can progress to Acquired Immunodeficiency Syndrome (AIDS).  People with AIDS often have an immune system that is so destroyed by the virus that they frequently get opportunistic infections and infection-related cancers, which is why HIV/AIDS is so dangerous, especially since HIV does not have a cure (source).

Conceptually, it makes sense that CRISPR-Cas9 could be used to solve this problem.  The CRISPR mechanism was discovered in E. coli, which uses it as an immune response to defend against viral infection by cutting up viral DNA and storing it so that it can recognize it if it appears again (source). It’s been described as a “ninja-assassin-meets-DNA-editing-tool” because CRISPR turns the immune response process that the bacteria utilize as a defense mechanism into a repair mechanism (source). A cell is transfected with DNA matching the gene of interest, the Cas9 cuts the matching DNA sequence in the host cell, resulting in the host cell beginning the process of DNA repair, effectively correcting the targeted gene sequence (source).

While this might sound like a good thing, many people were outraged by it.  There is a possibility that there was an off-target cleavage, and the effects of that might not arise for several years (source).  From an ethical standpoint, many people think that this could lead to a slippery slope of people creating "designer babies" (source).

Is it the right thing to do to attempt to eradicate HIV via genome editing, especially given that now people being actively treated for HIV have a near-normal life expectancy (source)?  What do you think?

P.S.  The first source I used to describe CRISPR is one of the coolest podcasts ever (Radiolab).  I highly recommend giving it a listen!

Cancer is nuts...but eating nuts might really help prevent cancer!

Recently I have been reading up on colon cancer because my dad was diagnosed with it almost two years ago.  He, like so many others, is battling cancer, a disease that his own body feeds and grows from.  Learning of his diagnosis piqued my interest and has held it for a while, and in my research, I came across an interesting article that looks at the relationship between nut intake and colorectal cancer risk (Lee, Shin, Oh, & Kim, 2018).  It describes a case control study on nut intake, which is fascinating to me because I would have thought it was nuts (pun intended) to put so much weight on, well, nuts when it came to diet and its effects on cancer growth.

According to the study, there is a “favorable association” between consuming a high frequency of nuts and a lowered risk of colorectal cancer in both women and men (Lee, Shin, Oh, & Kim, 2018).  For the highest category of nut consumption, there was a 24% decrease in cancer risk!  This decrease might be explained by analyzing multiple biological pathways.  Apparently, peanuts are rich in things like isoflavones, phytosterols, resveratrols, and phenolic acid, all of which may have anti-cancerous effects including the normalization of hyper-proliferative cells or decreasing D1 and D2 cyclins to regulate the cell cycle.  Almonds and pine nuts are rich in fibers, resveratrol, selenium, flavonoids, polyphenols, and folic acid, which might help prevent cancer through antioxidants, regulation of cell differentiation and proliferation, reduction of DNA damages, regulation of inflammatory response, and immunological activity (Lee, Shin, Oh, & Kim, 2018).  In addition to this, high nut intake is associated with a decreased risk of obesity and diabetes mellitus, which are both risk factors for colorectal cancer.

Looking at these possible anti-cancerous effects, I think that nuts are definitely good options for dieting.  It is a shame that I am not very fond of the taste of them.  But I urge you all to make it a habit to eat nuts more often.  Apparently they are more healthy than most people realize.

References

Lee, J., Shin, A., Oh, J. H., & Kim, J. (2018). The relationship between nut intake and risk of colorectal cancer: a case control study. Nutrition Journal, 17(1). doi:10.1186/s12937-018-0345-y

What is happening in 35 million brains across the globe because of Alzheimer's Disease?

While brainstorming what to research for a blog post, I tried to focus on diseases that interested me but also those with which I had personal connections to.  So I came across an article that talked about Alzheimer’s disease (AD) called “Brain insulin signaling, glucose metabolism and female’s reproductive aging: A dangerous triad in Alzheimer’s disease.”  According to this article, AD is the main cause of dementia and impacts approximately thirty-five million people across the globe, and ⅔ of these are women (Duarte, Santos, Oliveira, & Moreira, 2018).  After the age of sixty-five, women are much more likely to develop behavioral and cognitive changes than men.  This means that old age and being female are two risk factors for AD, which is slightly terrifying since I am a female and will (hopefully) continue to age for a while.  Alzheimer’s is a neurodegenerative disease that beings with “subtle decline in the ability to encode new memories,” then progresses towards profound behavioral, cognitive, personality, and adaptive deterioration (Duarte, Santos, Oliveira, & Moreira, 2018).  Sooner or later, those with Alzheimer’s forget what they ate for breakfast the previous day, who they live with, and even their families.

Here is a little background on Alzheimer’s disease and its characterizations.  AD is characterized mainly by extracellular senile plaques (SPs) formed by amyloid build-up in the brain.  These plaques mostly contain amyloid-beta (AB), which has 40-42 amino acids.  This amyloid-beta comes from the processing of the amyloid-beta precursor protein (ABPP), which is then catalyzed by aspartic protease beta-site ABPP cleaving enzyme-1 and then by gamma-secretase complex.  Interestingly, AB impairs hormone-mediated signaling (including estrogen and insulin), mitochondrial metabolism, and calcium homeostasis, which leads to stress laid on the endoplasmic reticulum, microglia activation and inflammation, and endothelial dysfunction.  This all leads to synaptic and cognitive loss (Duarte, Santos, Oliveira, & Moreira, 2018).  But AB that has yet to aggregate may also act as an infectious agent and can move in neurons and across synapses from the neocortex to other regions in the brain, allowing the plaque-forming ability to spread as well (Duarte, Santos, Oliveira, & Moreira, 2018).

            AD is also characterized by intracellular neurofibrillary tangles (NFTs).  NFTs are composed of helical filaments that contain the aggregated hyperphosphorylated Tau protein.  The Tau protein is of the family of microtubule-associated proteins (MAPs) that interact with tubulin.  They help maintain the axonal diameter and the stability of the microtubules to essentially maintain the structure of the neurons and the transport of the synapses.  If Tau aggregates in neuronal perikaryal, it interferes with the network of microtubules and induces stress on oxidation and causes the mitochondria to malfunction, which can cause neurodegeneration and neural death.  AB, the amyloid-beta, can induce Tau to aggregate, which only causes these negative effects to worsen (Duarte, Santos, Oliveira, & Moreira, 2018).

            The last characterization of AD is a downregulation of both pre- and post-synaptic proteins.  This causes neurodegeneration and neural death, which causes cognitive deficiencies as well (Duarte, Santos, Oliveira, & Moreira, 2018).

AD is extremely interesting, but is such an awful, heartbreaking disease.  My father’s grandmother, who is still alive and kicking at 101 years old, has AD, and she has no idea who any of her five children are.  If I went to visit her today, she would not remember me or my family, and that saddens me.  I cannot imagine not remembering my family, and watching my grandfather talk to his mother and seeing how she does not know who he is is tragic.  I never want to become part of the 35 million people in the world that gets AD, but I know how it feels to have a family member go through the loss of memory, cognition, and relationships.  So while AD is extremely interesting, it is not something I hope to become more personally familiar with.

References

Duarte, A., Santos, M., Oliveira, C., & Moreira, P. (2018). Brain insulin signaling, glucose metabolism and females reproductive aging: A dangerous triad in Alzheimer’s disease. Neuropharmacology. doi:10.1016/j.neuropharm.2018.01.044

Should Matilda quit smoking?

We all know that quitting smoking has tons of health benefits, right? People who quit smoking have more energy, better circulation, and stronger immune system, among other considerations. In the long term, smoking cessation lowers the risk of heart disease, COPD, and cancer, increasing life expectancy. Recently, the New England Journal of Medicine published an interesting article that used 3 cohort studies in the U.S. to prospectively assess changes in smoking status. Basically, the analysis found that smoking cessation is associated with an increase risk of type 2 diabetes compared with continuing to smoke. Not the first thing you’d expect, right? 

Although quitters do experience a lower risk of developing type 2 diabetes over the long-term, recent quitters within 2-6 years of cessation are actually at a higher risk. This is primarily due to the weight gain many experience after cessation, and was found to be directly related. The weight gain is generally due to increased appetite, decreased physical activity, and decreased metabolic rate. However, the increased risk of type 2 diabetes after smoking cessation doesn’t outweigh the overall benefits of giving up smoking on reducing total and cardiovascular mortality. Better tell Matilda from Wednesday night crochet class to kick that cigarette habit, Campisi!

https://www-nejm-org.dml.regis.edu/doi/10.1056/NEJMoa1803626

Sleep deprivation and obesity

I know I'm not the only one that has stayed up later than I've intended to do homework or go out with my friends.  But did you know that getting less than the recommended amount of sleep is linked to obesity?

The CDC estimates that 1 in 3 U.S. Americans aren't getting the recommended 7 hours of sleep each night (CDC.gov, 2016).  The link between obesity and sleep deprivation comes in with the hormones ghrelin (which increases hunger) and leptin (which decreases hunger).  A decrease in sleep is linked to an increase in ghrelin and a decrease in leptin.  Additionally, sleep deprivation is thought to increase cortisol release, which increases eating behavior (St-Onge et al., 2011).  Additionally, short sleep duration, poor sleep quality, and late bedtimes are all associated with excess food intake, poor diet quality, and obesity in adolescents (Chaput & Dutil, 2016).

There is also a link between brain response to food stimuli and limited sleep.  One study found that a group of people with limited sleep had greater food intake and higher brain activity in areas linked to desire and motivation (St-Onge et al., 2012).

With the rising obesity epidemic in the United States among all age groups, it seems that in addition to decreasing food intake and increasing physical activity, another feasible (and arguably easier) way to combat obesity is to go to bed earlier.

Moral of the story: get some sleep.

Citations:
Chaput, J-P. & Dutil, C. (2016). Lack of sleep as a contributor to obesity in adolescents: impacts on eating and activity behaviors. International Journal of Behavioral Nutrition and Physical Activity, 13(103). DOI 10.1186/s12966-016-0428-0.

CDC.gov. (2016). 1 in 3 adults don't get enough sleep. Retrieved from https://www.cdc.gov/media/releases/2016/p0215-enough-sleep.html.

St-Onge, M., McReynolds, A., Trivedi, Z., Roberts, A., Sy, M., & Hirsch, J. (2012) Sleep restriction leads to increased activation of brain regions sensitive to food stimuli. American Journal of Clinical Nutrition, 95, 818-824.

St-Onge, M., Roberts, A., Chen, J., Kelleman, M., O'Keefe, R., Choudhury, A., & Jones, P. Short sleep duration increases energy intake but does not change energy expenditure in normal-weight individuals. American Journal of Clinical Nutrition, 94, 410-416.