Simplified
Let's break things down further
The brain is an evolutionary marvel. From the simplest life forms to complex sentient beings, the nervous system (that includes the brain) serves to receive and respond to internal and external information. The central processing unit (CPU) temperature of modern-day computers can reach as high as 80°C when tasked to perform complex calculations. Yet the brain sits at around 38°C to 40°C while filtering noise and computing complex calculations on the regular - e.g., adjusting your breathing rate, heart rate and blood pressure, your posture and other housekeeping processes while you read this post with focus. It demonstrates great energy regulation efficiency while engaging in complex activities due to its exceptional filtering abilities (btw, these filtering abilities are also responsible for optical and auditory illusions).
However, the brain is not invincible. Just a few minutes of oxygen deprivation (cerebral hypoxia; cerebral: brain, hypo-: below, -oxia: oxygen) can result in irreversible damage to critical areas of the brain. Although not exhaustive, the common culprits of oxygen deprivation in the brain include blood clots due to heart attack, suffocation and traumatic brain injury. The common affected-brain regions often result in the loss of motor coordination and/or memory loss, as seen in post-stroke patients. A good number of studies have suggested an association between cerebral hypoxia and neurodegenerative diseases, of which the most notable being Alzheimer's Disease. This week we will look into uncovering the chief memory centre of the brain, how to learn and memorise better, and what happens when this memory centre starts to degenerate. Hippocampus - a campus for hippos? The Hippocampus is the chief structure of the brain involved in the encoding, storage and retrieval of memory. The hippocampus is accepted to support episodic memories (personal experiences) and, still largely debated, semantic memories (the knowledge of facts). The name Hippocampus is derived from the Greek hippos, "horse" and kampos, "sea monster", known colloquially as "seahorse". This is due to the fact that the hippocampus is a tightly rolled cinnamon roll-looking structure tucked deep inside and under each hemisphere of the brain. To the early Venetian anatomist Julius Caesar Ananzi, it looked like the rolled-up tail of a seahorse and so he named it as such. Till this day, it looks like a cinnamon roll to me but I digress... Although not a campus for hippos, it does serve as a network for making new memories and recalling old ones. There are many interpretations of how the hippocampus does this but a popular idea is that the hippocampus "communicates" bilaterally with the cortex (the outer layer of the brain). But... how? How do you know when your birthday is? You know your birthday because you have been told all your life that this particular day was the day you were born "x" number of years ago. This repetition of information coupled with yearly celebrations has encoded and cemented this idea in your brain. Every time someone asks you when is your birthday is, you immediately recall it because you "know" it so well! There is an action of memory retrieval upon stimulation! Amazingly, every time you retrieve a memory, it gets even more strengthened. How can we apply this? Let's say you need to study for an exam. Cramming all the content within a day is going to be detrimental for you. This is what we call massed learning (I have a whole section about learning in the Neuroscience category of the main blog). What we want is spaced learning, and that is equally spacing out each bout of revision with either a session of non-focused activities or sleep. Fascinatingly, adequate sleep is critical for efficient memory encoding, storage and retrieval due to memory replays happening when we snooze! Here's a simple protocol for effective learning. Start with a 90-minute session of pure focused work (no mobile phones, no distractions, nothing!). Then, couple it with a short 20-30 minutes of non-sleep deep rest meditation (link will be provided below) or go for a good nap. After the nap, try to recall what you have learnt at the start of the work session. Rinse and repeat. Now this would work perfectly for students with loads of time. What about working folks? It is unlikely appropriate the sleep on the job, so go for a stroll around the office, have a coffee (caffeine has great benefits to attention and mental acuity) or engage in social chats. As long as your mind is off the work for that short 20-30 minutes and not longer, you should be set! In the next post, we will talk about Alzheimer's Disease, a debilitating conditions that affects not only the patient but the people around them. We will also talk about caregivers and how inadequate post-mortality care great affects the mental health and livelihood of those left behind after death. Stay safe and curious! PS (13/09/23): I will update the references as soon as I get Zotero and MS Word up again... References Anand, K. S., & Dhikav, V. (2012). Hippocampus in health and disease: An overview. Annals of Indian Academy of Neurology, 15(4), 239. https://doi.org/10.4103/0972-2327.104323 Rolls, E. T. (2018). The storage and recall of memories in the hippocampo-cortical system. Cell and Tissue Research, 373(3), 577–604. https://doi.org/10.1007/s00441-017-2744-3 Rzechorzek, N. M., Thrippleton, M. J., Chappell, F. M., Mair, G., Ercole, A., Cabeleira, M., Rhodes, J., Marshall, I., & O’Neill, J. S. (2022). A daily temperature rhythm in the human brain predicts survival after brain injury. Brain, 145(6), 2031–2048. https://doi.org/10.1093/brain/awab466 Wang, H., Wang, B., Normoyle, K. P., Jackson, K., Spitler, K., Sharrock, M. F., Miller, C. M., Best, C., Llano, D., & Du, R. (2014). Brain temperature and its fundamental properties: A review for clinical neuroscientists. Frontiers in Neuroscience, 8, 307. https://doi.org/10.3389/fnins.2014.00307
1 Comment
PART III
Yerba Máte is a popular South American tea beverage that has recently come under the spotlight of health and weight loss influencers, and even fans of Lionel Messi as he is often seen drinking the beverage. It was estimated that the global market sales of Yerba Máte will hit a total of USD$2 billion in 2023 as the demand for the drink continues to skyrocket. Why is Yerba Máte so popular? Is it truly a great coffee alternative and a possible weight loss tool? Let’s take. Closer look at this ancient tea beverage and how it has influenced the world today. History of Yerba Máte Yerba Máte (Ilex paraguariensis) is believed to have been cultivated by the early indigenous Guaraní people of South America. It was seen as both a medicinal and social drink, often being passed around in a gourd and sipped through a specialised straw – more colloquially known as a bombilla. Early Spanish colonisers of South America were introduced to the drink by the Guaraní and were instantly hooked on this stimulating drink. It gave them a boost similar to the already-popular café or coffee back in Europe. Early Jesuit missionaries further expanded the supply and exposure of this energy-boosting tea through mass cultivation – usually involving the inhumane and involuntary labour of the native people. In modern times, the beverage is seen as a natural health product and are often marketed as an immunity booster and great weight loss tool. Preparing Yerba Máte Frequent consumers of Yerba Máte often describe a strong stimulatory effect followed by a disinterest in consuming food. This sounds familiar doesn’t it! Yerba Máte contains a plethora of polyphenols (an antioxidant chemical often found in teas) and three xanthines, of which the main constituent is caffeine. Depending on the method of brewing, Yerba Máte can contain as much as one to two times more caffeine than coffee. A common method of brewing starts with the creation of the slope of tea leaves otherwise known as la montaña (the mountain). Temperate water is then added away from the leaves, leaving the top of the mountain dry and ready for another pour. This helps prolong the drink as not all leaves are steeped at one go unlike coffee. Yerba Máte is consumed throughout the day or until all the leaves are wet. We’ve all had good and bad coffee drinks. Likewise, when Yerba Máte is not prepared properly it can give off a very off-putting bitter taste. A common mistake is pouring boiling water all over the leaves or steeping the drink for too long. This extracts too much caffeine and other bitter alkaloids found in the leaves. However, when brewed at an optimal temperature (~65-80°C), it produces a much richer and earthy flavour. Potential of Yerba Máte So, what is this hype on Yerba Máte being a potential weight loss tool? Remember GLP-1 from Part II of this series? Although earlier studies on Yerba Máte proved inconclusion, more recent studies have suggested that the beverage (in either tea or extract form),
Wow! Isn’t it such a powerful drink? Well… Most of these over-the-top studies were conducted using mice and rat models that were consuming a high-fat diet (ketogenic). Although these models may display similar outcomes in humans, it remains inconclusive. The available human studies that were reported had patients suffering from specific forms of diabetes or at different intensities of lipidemia (at content in blood). More importantly, the administration of Yerba Máte were either pure extracts or at unrealistically high concentrations that may not be found in the natural plant. This part remains inconclusive, however the most powerful aspect of Yerba Máte is its anorexigenic effect, or an increased satiety effect. The common problem with most patients suffering from obesity and other preventable chronic metabolic diseases is their control over food. If there was a way to reduce their intake of food, perhaps their medication may have a much stronger effect. Weight loss programs often come with diet and exercise plans. Once the program is over, these patients often relapse as their control over food is no longer moderated. Remember our dear friend, GLP-1? It turns out, Yerba Máte stimulates a significant amount of satiety markers like GLP-1 and leptin in mice fed on a high fat diet. Can we translate this into humans? Although high fat foods (ketogenic diet, yoghurt, etc.) can also improve satiety, they often pose additional risk factors on other health conditions. Therefore, it still remains inconclusive if Yerba Máte or its extract can be an alternative to Semaglutide. Let’s assume Yerba Máte does enhance GLP-1 secretion and has all the powerful positive effects on health. Are there still risks? Cancer Risks In association studies, long-term Yerba Máte consumption was shown to be associated with an increased risk for mouth, throat, lung and bladder cancers. It was suggested that perhaps long-term Máte consumption at high temperatures can continuously damage the mucous linings of our digestive tracts, increasing our risk of cancer. However, cancers to the lungs and bladder are unlikely to be attributed to this effect. Polycyclic aromatic hydrocarbons (PAHs) are carcinogenic (cancer-causing) substances often found in cigarette smoke. The most common method of drying Yerba Máte leaves is over an open flame and/or smoking. The smoked variety of Yerba Máte contains an immense amount of PAHs that may be substantially extracted with repeated brewing of the same leaves. However, different methods of brewing can result in varied PAH extractions in the tea. More work has to be done in order to fully understand the risk and implications of Máte brewing methods Conclusion So, is Yerba Máte truly a powerful weight loss tool? Maybe, it does result in many positive outcomes albeit mostly in animal models. Does it come with carcinogenic risks? Likely but many other foods and drinks we consume are also carcinogenic, yet we continue to consume them frequently. Is it a suitable alternative to Semaglutide? That remains uncertain for now, but we can continue to enjoy this drink and the benefits it appears to impart to us. Until next time, this is your friendly scientist signing off! Summary
References Gambero, A., & Ribeiro, M. L. (2015). The Positive Effects of Yerba Maté (Ilex paraguariensis) in Obesity. Nutrients, 7(2), 730–750. https://doi.org/10.3390/nu7020730 Gawron-Gzella, A., Chanaj-Kaczmarek, J., & Cielecka-Piontek, J. (2021). Yerba Mate—A Long but Current History. Nutrients, 13(11), 3706. https://doi.org/10.3390/nu13113706 Hussein, G. M. E., Matsuda, H., Nakamura, S., Hamao, M., Akiyama, T., Tamura, K., & Yoshikawa, M. (2011). Mate tea (Ilex paraguariensis) promotes satiety and body weight lowering in mice: Involvement of glucagon-like peptide-1. Biological & Pharmaceutical Bulletin, 34(12), 1849–1855. https://doi.org/10.1248/bpb.34.1849 Loria, D., Barrios, E., & Zanetti, R. (2009). Cancer and yerba mate consumption: A review of possible associations. Revista Panamericana De Salud Publica = Pan American Journal of Public Health, 25(6), 530–539. https://doi.org/10.1590/s1020-49892009000600010 Silverman, L. (2023). The Coffee Alternative Americans Just Can’t Get Behind. The Atlantic. https://www.theatlantic.com/health/archive/2023/01/yerba-mate-consumption-caffeine-coffee-alternative/672820/ WTN Editor. (2023). Yerba Mate Market and Consumer Demand Is on The Rise, According to New Research. World Tea News. https://www.worldteanews.com/issues-trends/yerba-mate-market-and-consumer-demand-rise-according-new-research PART II
Chronic obesity is a public health concern as it is often accompanied with an increased risk of insulin resistance, cardiovascular diseases and liver-related diseases. It affects mobility and therefore the quality of life. This results in social and economic complications as family members have to care for these immobile patients, many even having to quit their jobs to provide care full-time. Recall that chronic hyperglycemia is both the cause and effect of insulin resistance. What if there was a way to reduce our intake of food such that we do not put ourselves in deeper risk of T2DM and obesity? Semaglutide is a glucagon-like peptide-1 (GLP-1) analog recently approved for controlling blood sugar levels in adult T2DM patients by the Food & Drug Administration (FDA). What is GLP-1? How is Semaglutide revolutionary? Glucagon-like peptide-1 (GLP-1) What does it mean to be Glucagon-like? Let’s break down each word and compare with insulin. Insulin and glucagon are both part of a feedback system to ensure our blood glucose levels are balanced. Glucagon raises blood glucose by using up our stored glucose (glycogen) and fatty acids. Both glucose and fatty acids can be used as energy sources to keep us running. This is what happens when we are in a starving state, our body literally eats itself up as it tries to use up stored energy! It’ll be easier to think of fats as your body’s bank of energy that stores our weekly savings and fat burning as “cash” withdrawals for use. GLP-1 is also produced by the body and behaves somewhat similar to glucagon but not exactly the same. It is derived from the same “precursor” protein (proglucagon) as glucagon and acts to maintain homeostasis in the system. Homeostasis is just a process of self-regulation to maintain balance in the body! As such, Glucagon raises blood glucose while GLP-1 reduces blood glucose by promoting insulin release. Let’s look at some of its functions. 1. Reduces gastric emptying = you feel full for a longer time 2. Reduces gut motility = food takes longer to move through your digestive tract 3. Reduces appetite and increases satiety = you don’t feel like eating much 4. Increases fat break down = this is a plus! 5. Increases muscle glucose uptake = more energy for when you exercise The list goes on, but one thing is for sure. It seems… too good to be true. We must preface that these functions of GLP-1 are mostly associative and not completely known to result in these effects. One thing to note is that although GLP-1 is made in our bodies, they are released at very low levels and only rise 2-3x when we consume food – a sufficient amount for satiety. Other food groups like fat, protein and dietary fibre were also shown to promote GLP1 secretion. Talk about a well-balanced diet! Since Semaglutide is a GLP1- analog, meaning it is structurally similar, it should affect similar targets of GLP1! Let’s take a look. Semaglutide A double-blinded, randomized controlled phase 3 clinical trial conducted in 2018 showed that administration of 2.4mg Semaglutide once a week for 68 weeks resulted in almost 15% reduction in body weight for the treated group compared to the control group. Further body scans revealed that the treated group also lost a significant amount of total body fat compared to the controls. Remarkably, the control group also lost weight but at a lower rate. This could open up a new market for weight loss therapies but more has to be done to validate these effects. However, as of this post, there is a global shortage of Semaglutide as the demand for this drug has increased with “off-label” usage. This means that the drug is not used for its intended purpose of aiding diabetics but is used for other purposes than its intended approval – e.g., a “miracle weight-loss drug”. However, all drugs come with some risk and adverse effects. The majority of adverse events in the study were related to gastrointestinal complications like diarrhea, vomiting, headache and gastrointestinal disorders. Only a handful of patients suffered from hypoglycemia (very low blood glucose). This is a great thing as most anti-diabetic drugs (e.g., sulfonylureas, biguanides, etc.) leave patients with severe hypoglycemia that could lead to fainting and even death. So, is Semaglutide a great alternative for treating T2DM? The answer, as with many new drugs, remains uncertain until more work is done. Being FDA-approved is only one step towards understanding the power and risk of Semaglutide. There are still many years of post-market surveillance and diligent adverse drug reporting (pharmacovigilance) to account for before we can truly put our faith in Semaglutide. Until then, this is your friendly scientist signing off! Summary
References Barnes, A. S. (2011). The Epidemic of Obesity and Diabetes. Texas Heart Institute Journal, 38(2), 142–144. Goyal, R., & Jialal, I. (2023). Type 2 Diabetes. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK513253/ Klein, B. E., Klein, R., Moss, S. E., & Cruickshanks, K. J. (1996). Parental history of diabetes in a population-based study. Diabetes Care, 19(8), 827–830. https://doi.org/10.2337/diacare.19.8.827 Mahapatra, M. K., Karuppasamy, M., & Sahoo, B. M. (2022). Semaglutide, a glucagon like peptide-1 receptor agonist with cardiovascular benefits for management of type 2 diabetes. Reviews in Endocrine & Metabolic Disorders, 23(3), 521–539. https://doi.org/10.1007/s11154-021-09699-1 Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., & Kushner, R. F. (2021). Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine, 384(11), 989–1002. https://doi.org/10.1056/NEJMoa2032183 Diabetes mellitus (DM) affects hundreds of millions of people as of 2023. It is a major health concern as DM increases the risk of developing other comorbidities (>2 chronic conditions) like cardiovascular disease, obesity, cancer and hypertension. In 2021 alone, an estimated USD 966 million was allocated for diabetes-related healthcare expenditures - an over 300% increase from 2006. The term diabetes mellitus can be broken down into the Greek diabainein for "to flow through" and Greek/Latin mellītus for "sweet". Together, they suggest something sweet flowing through. This characterisation stems from the observation that DM patients urinate a lot and sometimes when they forget to flush, ants can be seem scurrying around the toilet. Doctors commonly use the term "hyperglycemia" when describing persistently high blood sugar levels in suspected DM patients. In most sciences, we name phenomena based on symptoms and observations. In this case, we can break up the word "hyperglycemia" into hyper-: high, glyc-: glucose (sugar), -emia: presence in the blood. Add the word "chronic", from the Greek chronos for time, and you get chronic hyperglycemia or long-term high blood sugar. This quickly describes chronic hyperglycemia in DM patients as having "sweet" blood flowing throughout the entire body for a long time.
There are several types of DM but we will only look at Type II Diabetes Mellitus (T2DM) as it comprises around 90% of all DM cases. T2DM is commonly characterised by chronic hyperglycemia, insulin insensitivity/resistance and subsequently insulin deficiency as the pancreas begins to fail. Do you remember the times when our parents nagged at us for consuming too much sugar, "you're gonna lose your sight or leg like uncle/auntie so-and-so if you do not control yourself!". Ever wondered why? Chronic hyperglycemia can actually cause sugars in our blood to coat proteins and lipids (fat molecules), leading to fat deposition and the scarring of our blood vessels. If these damages occur in narrow blood vessels (microvascular damage), the cells that those blood vessels supply to will be deprived of nutrients and die. This causes blindness (diabetic retinopathy), chronic kidney disease, cardiovascular disease and risks amputation due to gangrene. Imagine if you stepped on a pin but did not feel it because the nerve cells under your feet have died. You wouldn't take necessary action to remove the pin because you don't feel it! This can develop into an infection that goes unbeknownst until the infected part becomes gangrenous. Doctors would have to make the tough decision to amputate the dead infected limb or risk spreading the infection further. As you can tell, this drastically affects their mobility and quality of life which exacerbates an already debilitating condition in an endless loop. This sounds really scary, doesn't it? Thankfully, T2DM is the mostly preventable as changes to diet and lifestyle can greatly restore insulin sensitivity and stop/slow down the disease progression to a more severe stage. Before someone is considered a T2DM patient, they are categorised under the prediabetic stage. At this point, they have lost some degree of insulin sensitivity and are asymptomatic (not experiencing any complications) but still able to cope. Many a times, people would start to look after their health and try to push themselves back towards a more stable and healthier state. Those who do not would most likely progress to T2DM (Stage 3 and 4). What is important is that at every stage of T2DM progression, there are primary, secondary and tertiary prevention measures that can be taken. Before we dive into preventive measures, let's talk about insulin first. Insulin is a small peptide molecule made and released by specialised cells in the pancreas. It acts like a keycard for our cells to have access to sugar in our blood. In a healthy person, insulin efficiently reduces blood sugar levels after a meal. However, in prediabetic/T2DM patients, their cells become less responsive to insulin, leaving their blood sugar levels high even hours after a meal. Recall, what happens to your blood vessels when your blood sugar level is high for too long? What preventive measures do prediabetic/T2DM patients have today? Metformin is a drug commonly prescribed to prediabetics and T2DM patients by doctors. It works to reduce blood sugar by slowing down the absorption of sugar from our food and increasing insulin sensitivity. It also tells our liver to stop producing glucose. Yes! Our livers actually store glucose in a more compact form (glycogen) like a food bank and uses this extra sugar to support us when our blood sugar is low. However, for prediabetics and T2DM, we do not want this to happen because their blood sugar is already high! Metformin is a great first line of defence against T2DM with minimal side effects but there are other emerging drugs that may possess superior protection from high-risk T2DM patients (e.g., T2DM patients with chronic kidney problems). Herein lies the bigger question, "If there are already drugs that can help diabetic patients, why are there still so many?". It is a very complex question with an answer containing many contextual factors, one of which is lifestyle. If we can stop ourselves from over-consuming food, perhaps we can really win the war against diabetes. What if there was a drug that could seemingly solve this altogether? Summary
References Baker, C., Retzik-Stahr, C., Singh, V., Plomondon, R., Anderson, V., & Rasouli, N. (2021). Should metformin remain the first-line therapy for treatment of type 2 diabetes? Therapeutic Advances in Endocrinology and Metabolism, 12, 2042018820980225. https://doi.org/10.1177/2042018820980225 Barnes, A. S. (2011). The Epidemic of Obesity and Diabetes. Texas Heart Institute Journal, 38(2), 142–144. Goyal, R., & Jialal, I. (2023). Type 2 Diabetes. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK513253/ IDF (n.d.) IDF Diabetes Atlas | Tenth Edition. Retrieved 11 August 2023, from https://diabetesatlas.org/ Klein, B. E., Klein, R., Moss, S. E., & Cruickshanks, K. J. (1996). Parental history of diabetes in a population-based study. Diabetes Care, 19(8), 827–830. https://doi.org/10.2337/diacare.19.8.827 Liu, R., Li, L., Shao, C., Cai, H., & Wang, Z. (2022). The Impact of Diabetes on Vascular Disease: Progress from the Perspective of Epidemics and Treatments. Journal of Diabetes Research, 2022, 1531289. https://doi.org/10.1155/2022/1531289 |
More About This Page
To make scientific concepts more digestible, simplified versions of the deep dive blog posts are posted here. I hope to be able to further simplify content for the everyday Joe/Jody to appreciate science and the world we live in. The artwork in the banner above was drawn by me. It symbolises how small we are in the grand scheme of things yet without the little things no beauty can shine out from the void. ArchivesCategories |