News

GRID VIEW

No more posts
EOE.jpg

Listen to the article here:

Coming Soon

There are many ways to think of the human body. One of my favorites is that the body is like a donut. The inside of the donut is our entire body and everything that makes us what we are. The outside is our skin. The hole in the middle is made of our mouth, throat (esophagus), stomach, and intestines. The body treats the entirety of the digestive tract as the outside world. The intestines act like the skin; keeping most things out of the body and only letting specific molecules through.

This has some important implications. The whole outside of the donut – including the throat and intestines – is covered in epithelial cells. These are tight cells that interact with the outside world. When these cells determine that they are touching something dangerous they signal to get rid of it immediately. This might feel like burning or itching on the skin, and may be something like diarrhea or vomiting in the digestive tract. These may feel crummy to us, but they are very useful in keeping us safe.

The immune system is in charge of identifying and reacting to chemical and biological dangers. These can be harmful bacteria, worms, and things like splinters or some drugs. The immune system kicks into action, trying to kill or remove the dangerous particles without damaging body cells. This is a tricky dance. Antibodies will identify the dangerous particles or creatures and special B or T cells will widely sprinkle alarm particles, calling for reinforcements.

What the body does next is determined by where the danger is found. In the gut – which the body treats as the dangerous outside world – the defenses are strong. One of the biggest guns we have is a cell called an eosinophil. These are very dangerous cells. They contain highly toxic particles and proteins that aggressively dunk in on invaders. They also signal to the intestines to  contract and eject the contents. They only exist in specific parts of the body and are normally difficult to activate.

Unfortunately, sometimes our body identifies otherwise safe items as dangerous. This is called allergies, and can be very annoying. Many of us suffer from seasonal allergies, but that doesn’t mean we should glaze over the dangers of allergic reactions. One difficult condition is eosinophilic esophagitis. Eosinophilic means it is caused by the dangerous eosinophil cells. Esophagitis refers to the fact that this happens in the esophagus, the throat. Eosinophils do not normally reside in the throat at all. The throat’s main job is to move food into the stomach, so it doesn’t need to detect danger. When eosinophils mistakenly reside in the throat, however, they can misidentify otherwise safe foods before the stomach gets a chance to digest them. This can result in the eosinophils damaging the throat.

Eosinophilic esophagitis affects four in every thousand people, and can affect people of all ages. Most sufferers were diagnosed as children. In fact, it is one of the most common diagnoses for children who have trouble eating. It is chronic, or long lasting,  and symptoms are debilitating. Sufferers experience inflammation of the throat, poor food intake, vomiting, and a poor appetite. Unfortunately there are few treatments available to fix this condition. The most effective has been reducing the diet of patients. This may consist of starting with a very strict diet and reincorporating food slowly to discover triggers. Scientists are actively looking at the underlying causes of why eosinophils are in the throat to begin with. Possible future treatments would likely stop eosinophils in the throat at a cellular or genetic level.  The body may be a donut, but that doesn’t mean everything is tasty and fresh. If you are suffering from eosinophilic esophagitis or other conditions, call ENCORE Research Group and ask about studies you may qualify for.

By Benton Lowey-Ball, BS Behavioral Neuroscience



Furuta, G. T., & Katzka, D. A. (2015). Eosinophilic esophagitis. New England Journal of Medicine, 373(17), 1640-1648. https://doi.org/10.1056%2FNEJMra1502863

Janeway Jr, C. A., Travers, P., Walport, M., & Shlomchik, M. J. (2001). Effector mechanisms in allergic reactions. In Immunobiology: The Immune System in Health and Disease. 5th edition. Garland Science. https://www.ncbi.nlm.nih.gov/books/NBK27112/

Rothenberg, M. E. (2004). Eosinophilic gastrointestinal disorders (EGID). Journal of Allergy and Clinical Immunology, 113(1), 11-28. https://doi.org/10.1016/j.jaci.2003.10.047

Zuo, L., & Rothenberg, M. E. (2007). Gastrointestinal eosinophilia. Immunology and allergy clinics of North America, 27(3), 443-455.https://doi.org/10.1016%2Fj.iac.2007.06.002


Love.jpg

Listen to the article here:


In the 1990’s the philosopher Haddaway posed a critical question: What is love? This Valentine’s Day, many of us will experience love and companionship. We like to think of love as an amorphous, idealistic quality, but there are serious biological underpinnings. What is the biology behind love, and is the heart really where love lies (spoiler: maybe?)

We know that the brain directs our physical actions, but for the brain to come up with an idea, it needs input from the outside world. Interestingly, the brain can’t sense anything directly. If someone were to open up your skull and have a poke around, you would undoubtedly have a weird bit of sensation, but you wouldn’t experience the feeling of touch on the brain. We need special sensors (usually located on the skin) to feel things like touch. Indeed, our brain relies on signals coming in from all over the body to tell us about the outside world. Interestingly, we also rely on signals to tell us about the inside world – what we are experiencing. The brain interprets signals from the body, and we can experience that interpretation as an emotion.

As an example: your heart beats automatically all day, every day, at a hopefully regular interval of around once a second. When you see a scary event, such as a wild lion charging you, your brain and body respond in sync. The heart rhythm changes, beating much faster to provide your muscles, sensory organs, brain, etc., extra oxygen in order to move fast. But this effect isn’t strictly rational. After we escape from the lion, we still feel “amped up.” This effect can last for thirty minutes or so, and the reason for the long-lasting effect is complicated. Our autonomic nervous system – the one in charge of things we don’t consciously control – has kicked into action. This pathway acts like cupid, shooting cortisol through our body and activating special nervous system pathways that take a while to cool down. But our brain also looks at the state of our body to interpret our emotional state. If our palms are sweaty, we’re breathing heavily, and our heart is racing, the brain interprets that as being amped up and decides we’re still pretty excited or scared. The brain is in charge of deciphering which emotion we’re feeling, but the body lets us know how strongly we’re feeling that emotion.

This is why we sometimes still feel the need to continue an argument after the other party has conceded. It’s why telling someone to “calm down” doesn’t work – but taking some deep breaths does. Meditation, stretching, exercise, and sleep all affect our emotional state because the brain looks at the condition of the body and tries to figure out how it’s feeling. In addition, a healthy heart that can respond well to changes may increase a person’s emotional regulation. Does it do this with love as well?

According to neuroendocrinology researcher Robert Sapolsky, it does! The science may not be entirely clear, but the easiest way to be certain of this is by looking at the irrationality of love. Love doesn’t make sense, and it’s so strong that we base enormous portions of our life just on this single emotion. Love is the basis of countless pieces of art, works of literature, grand buildings, and justifications for war. When we experience love – that fluttering of the heart, the excitement and elation, the involuntary smile on our face, and the giddiness so high that our mouths stop working and we say embarrassing, cheesy things – it’s the body to blame. Our heart races when we’re in love and the brain sees this as a huge exciting event – because it is. Just seeing the person we love can change our heart rate. Physical touch from a loving partner can help lower our heart rate in response to stressful situations. And the long-term effects of companionship sometimes include a partial synchronization of our heart rhythms.

We can thank our hearts for at least some of what we call love. This Valentine’s day, get your heart racing with a partner or loved one, and keep that heart beating strong!

By Benton Lowey-Ball, BS Behavioral Neuroscience



Ditzen, B., Neumann, I. D., Bodenmann, G., von Dawans, B., Turner, R. A., Ehlert, U., & Heinrichs, M. (2007). Effects of different kinds of couple interaction on cortisol and heart rate responses to stress in women. Psychoneuroendocrinology, 32(5), 565-574. https://doi.org/10.1016/j.psyneuen.2007.03.011

Kandel, E. R., Schwartz, J. H., Jessell, T. M., Siegelbaum, S., Hudspeth, A. J., & Mack, S. (Eds.). (2000). Principles of neural science (Vol. 4, p. 980). New York: McGraw-hill.

Mather, M., & Thayer, J. F. (2018). How heart rate variability affects emotion regulation brain networks. Current opinion in behavioral sciences, 19, 98-104.

Sapolsky, RM. (various works)


The-Long-Road-of-Cholesterol-Research2.jpg

Listen to the article here:


Cardiovascular disease has remained the number one cause of death worldwide.  Multiple clinical trials have revealed that a common and modifiable risk factor for cardiovascular disease is high cholesterol, and if a person lowers their cholesterol, they can lower their risk for heart-related diseases.

Most of us have heard of cholesterol, but what is it? Why is having too much cholesterol a bad thing? How do we get cholesterol in our bodies? What can you do to lower your cholesterol to healthy levels? 

Cholesterols are a broad and useful type of fat found in the body. The body needs them to create hormones, essential vitamins (like vitamin D), and other molecules. They float on the surface of our cells, helping to maintain the structure and function of cell barriers. Cholesterols regulate cell activity and act outside of cells. They insulate the neurons in our brain, allowing us to think.  In fact, cholesterol is so important to daily function, that every cell in the body can make cholesterol from basic materials, except your eyelashes!

There are times when cholesterol is downright bad. LDL cholesterol and Lipoprotein a [Lp(a)] have some particularly sticky portions that can get stuck to the inside of our bloodstream. We call one of these portions ApoB. Sticky cholesterol obstructs blood flow in the form of plaques. Without help, this leads to atherosclerosis, scarring, and hardening of the arteries. Atherosclerosis further cascades into cardiovascular disease, clots, heart attacks, and stroke. This is very bad. Unfortunately, it is also very common; atherosclerosis in the neck is found in ¼ of people worldwide. Lowering excess cholesterol is a global health concern.

Our liver creates enough cholesterol to supply our bodies. We are also able to absorb cholesterol from our diets and make some in other cells. The most effective methods of reducing cholesterol are lifestyle and diet changes. However, for some people, diet and exercise don’t seem to budge their cholesterol numbers at all. For others, the ability to exercise and dietary restrictions may be limited. This is where medications can step in.

To understand how a medication may reduce LDL and/or Lp(a), we need to learn a bit about how the body makes things from DNA. Genes are bits of DNA that contain the blueprint for a protein. Genes provide the blueprint to messenger RNA (mRNA). The mRNA translates genetic code into proteins. The cells then fold proteins into complicated, machine-like shapes. Proteins interact with molecules and other proteins to create all sorts of things for the body – including cholesterol. Clinical research has been expanding which of these steps we can target for medications.

Statins are the first line treatment for reducing cholesterol. They target hydroxymethylglutaryl coenzyme A (HMG-CoA). HMG-CoA is a protein used to construct cholesterol molecules. Reducing HMG-CoA slows the body’s ability to create cholesterol, lowering cholesterol levels. Statins block the production of the “bad” LDL-C cholesterol and lower levels by as much as 60%. The benefits for statins to reduce cardiovascular events have been proven in multiple clinical trials over a diverse patient population.

Other oral medications, including ezetimibe and bempedoic acid, can be taken with statins. Ezetimibe can lower LDL-C levels by approximately 20% by inhibiting cholesterol absorption in the intestines, making it a useful add-on medication when statins alone are insufficient. Bempedoic acid can lower LDL-C by 15-25% by decreasing cholesterol synthesis in the liver.  Because bempedoic acid is converted to an enzyme found only in the liver and not the muscles (like statins), it is often an alternative for patients who have statin-associated muscle myalgias.    

Monoclonal antibodies (MoAbs) are a newer class of medication. MoAbs like alirocumab and evolocumab act like signaling molecules. These two stay outside of cells and tell the liver to produce less of the protein PCSK9. Controlling PCSK9 is a newer method of changing a person’s cholesterol profile. PCSK9 controls how much extra LDL cholesterol is absorbed and recycled by cells. MoAb medications affect this by targeting signaling receptors on the outside of the liver.

Even newer medications target the process by which genes get turned on inside the cells.  They are called gene silencing therapies because they aim to “silence” the gene’s effects.  Antisense oligonucleotides (ASOs) and small interfering RNA (siRNA) stop the liver from producing functional LDL or Lp(a) mRNA molecules. These act at different, very early stages of the cholesterol process. In addition, specialized packaging on the medications deliver them to the liver and not other cells. This can make for very targeted medications that (hopefully) have fewer side effects.

Inclisiran is the first FDA-approved siRNA therapy to lower LDL cholesterol.  It is a subcutaneous injection taken twice a year.  Imagine going to your physician’s office just twice a year to get your “cholesterol vaccine”!

Even more amazing, gene editing tools such as CRISPR could reduce overexpression of PCSK9 or other genes on a long-term basis. These are still in early phase trials, but the future is looking bright.

Lipoprotein a,or “L-P-little-a”,  or Lp(a), is a new target for decreasing the risk of cardiovascular disease. Lp(a) is genetically inherited and increases the risk for both heart disease and stroke because it can promote plaque buildup, blood clots, and inflammation.  New gene silencing therapies are in clinical trials right now using both ASO and siRNA technology.

Diet, lifestyle changes, and statins remain the front-line defense against high cholesterol. New medicines may work with or replace these classical defenses. As technologies move through the clinical research apparatus, we may be able to tailor custom combinations of medications for individual patients. ENCORE Research Group has been involved in every step along this path, helping to study medications in every category. Join our team and help pave the way for new medications to help combat high cholesterol! 



Sources:

Craig, M., Yarrarapu, S. N. S., & Dimri, M. (2018). Biochemistry, cholesterol. https://www.ncbi.nlm.nih.gov/books/NBK513326/

Fernandez-Prado, R., Perez-Gomez, M. V., & Ortiz, A. (2020). Pelacarsen for lowering lipoprotein (a): implications for patients with chronic kidney disease. Clinical Kidney Journal, 13(5), 753-757. https://doi.org/10.1093%2Fckj%2Fsfaa001

Prati, P., Vanuzzo, D., Casaroli, M., Di Chiara, A., De Biasi, F., Feruglio, G. A., & Touboul, P. J. (1992). Prevalence and determinants of carotid atherosclerosis in a general population. Stroke, 23(12), 1705-1711. https://doi.org/10.1161/01.str.23.12.1705

Tokgözoğlu, L., & Libby, P. (2022). The dawn of a new era of targeted lipid-lowering therapies. European Heart Journal. https://doi.org/10.1093/eurheartj/ehab841


Cholesterol-artery.jpg


The Role of Apolipoprotein C-III (apoC-III) in Atherosclerosis and Cardiovascular Disease

After we eat a meal, all that energy has to go somewhere. Body cells can use freely floating glucose sugar in the bloodstream, but fats are a bit trickier. Just like oil and water don’t mix, fats have trouble moving through the blood in our veins and arteries. They must be packaged inside special containers called lipoproteins in order to travel where they need to go. For fats that we eat, the fats (called triglycerides) are packaged into ultra-low-density chylomicrons by the digestive system. Our liver also processes and repackages fats. The liver makes very low-density lipoproteins (VLDL) out of triglycerides and ejects them into the bloodstream. VLDLs can then use the bloodstream to travel to fat cells or be converted into other forms of energy storage. The number of triglycerides in the bloodstream at once needs to be well regulated.

For adults, fasting triglyceride levels should be under 150 mg/dL. This number decreases to below 90 mg/dL for people under 19 years of age. Unfortunately, one in ten adults have high levels, called hypertriglyceridemia. When there are too many triglycerides, they can stick to the inside of the bloodstream. They can create and contribute to hard plaques, a condition called atherosclerosis. These put stress on the cardiovascular system and can lead to atherosclerotic cardiovascular disease (ASCVD). Very high triglycerides above 500 mg/dL is called severe hypertriglyceridemia. This can lead to even more problems, including chylomicronemia, pancreatitis, and death.

What contributes to high triglyceride levels? A lot, actually! A diet that is high in sugars and fats, excessive alcohol consumption, being overweight, and a sedentary lifestyle can contribute. Some conditions, such as diabetes, kidney and liver disease, and thyroid problems increase your chances. Anything that affects liver function is likely to change how the body processes fats and may increase triglycerides. This means some life-saving medications, including several cancer, hypertension, and HIV treatments may increase triglycerides. Some people have high or very high triglycerides – usually in the form of chylomicrons – even without these risk factors. This may be because of our genes.

One of the major genetic culprits for increased triglycerides is a gene called APOC-3. This gene codes for a protein of the same name: Apolipoprotein C-III (apoC-III). You can tell these apart because the gene is uppercase, italicized, and uses a (3), while the protein is mostly lowercase and uses roman numerals (III). The protein apoC-III can lead to some detrimental effects. Normal triglycerides bind to a different protein, apoC-II. This helps them get broken down in the bloodstream. ApoC-III binds to triglycerides in the same place as apoC-II but makes them less able to be processed. These triglycerides build up in the bloodstream and can cause atherosclerosis and ASCVD. Scientists also have evidence that apoC-III makes triglyceride-rich molecules stickier to the arteries. ApoC-III binds to chylomicrons very well, making these fats especially resistant to breaking down.

So why do we have apoC-III anyway? It turns out, not all of us do! Different people have different variations of the APOC-3 gene. Some people have a gene that produces excessive apoC-III protein, and a few have genes that produce none! People with defective APOC-3 genes seem to be just as healthy as everyone else. Maybe healthier, as their levels of triglycerides are very low, even after a fatty meal! Researchers consider a defective APOC-3 gene to be cardioprotective, meaning that it lowers the chances of heart disease.

Are there methods for us to lower the production of apoC-III and our triglyceride-rich chylomicrons? It looks possible. The liver produces more apoC-III in response to high levels of blood sugar and most fats, so lowering these may help. It decreases production of apoC-III when it encounters high levels of insulin or polyunsaturated fats (such as Omega-3 fatty acids). This may be helpful, but is bad news for those with type 2 diabetes. In these patients the bloodstream has extra glucose and lacks insulin.

Treating high triglycerides can be complicated. A diet low in alcohol, carbs, and fats but high in omega-3 fatty acids can help. Exercise and weight loss are often helpful. Doctors may also prescribe fibrates, nicotinic acid (niacin), or statins. Unfortunately, these medications may not work if you have excessive levels of apoC-III and high chylomicrons. A diet that is very low in fats – under 20 grams a day – has been the only option for some patients. New classes of medication may be helpful as well. Antisense oligonucleotides, gene therapy, and custom antibodies can be used to target the production of specific proteins. Antisense oligonucleotides, for instance, bind to APOC-3 mRNA in the cell, preventing it from creating apoC-III proteins. They do this with extreme specificity, targeting only the gene in question. They can also do this only in liver cells by being packaged in a special way. Drugs that target apoC-III production may be able to bring down otherwise stubbornly high triglycerides without too many side effects. A side effect of being on this ENCORE Research Group mailing list is learning about these new medicines and when they may be available for you in a trial!



Sources:

Alves-Bezerra, M., & Cohen, D. E. (2017). Triglyceride metabolism in the liver. Comprehensive Physiology, 8(1), 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6376873/

Goldberg, R. B., & Chait, A. (2020). A comprehensive update on the chylomicronemia syndrome. Frontiers in endocrinology, 11, 593931. https://doi.org/10.3389/fendo.2020.593931

National Institute of Health, National Heart, Lung, and Blood Institute. (April 7, 2022). High blood triglycerides. U.S. Department of Health and Human Services. https://www.nhlbi.nih.gov/health/high-blood-triglycerides

Rahmany, S., & Jialal, I. (July 18, 2022). Biochemistry, Chylomicron. https://www.ncbi.nlm.nih.gov/books/NBK545157/

Taskinen, M. R., Packard, C. J., & Borén, J. (2019). Emerging evidence that ApoC-III inhibitors provide novel options to reduce the residual CVD. Current atherosclerosis reports, 21(8), 1-10. https://doi.org/10.1007/s11883-019-0791-9


Continuous-glucose-monitor.jpg

January 11, 2023 BlogDiabetesMedEvidence

Listen to the article here:


In fifth grade, I learned that mitochondria are the powerhouses of the cell. But what’s the fuel? The answer is carbohydrates. Big carbohydrates are broken down by digestion and converted into a couple of simple sugars. The most abundant of these simple sugars in our bodies is glucose. 

Glucose is small, simple, and packed with energy. We transport it through our bloodstream to cells in our body. Glucose levels are regulated by the liver and pancreas. Unfortunately, conditions like diabetes can result in the dysregulation of blood glucose levels. Having too much sugar in the blood is very bad over time. It can result in damage to the eyes, kidneys, nerves, and heart. On the flip side, having low blood sugar can get dangerous right away. Glucose is the fuel that powers our cells, without it the brain and other organs can’t function.

We know that glucose is critical to body function. We also know that glucose levels can get out of control. What can we do to make sure glucose levels stay safe? The most important piece of the puzzle is information. Good information on what our blood glucose levels are is critical to know what to do. We get this information by testing our blood glucose levels. There are three major ways of testing blood glucose; chemical redox reactions, color change, and enzyme-based reactions.

  • Chemical redox reaction testing works because glucose reacts with metals. By measuring how the metals react to blood, we can indirectly measure the amount of glucose. Unfortunately, other chemicals in the blood react to metal as well and can complicate the results. This method is rarely used these days.
  • The second method is through color change. This method combines blood and a special chemical called o-Toluidine. The o-Toluidine reacts to a specific part of the glucose molecule and changes it to be bright green (normally it is white or colorless). We can measure the color change visually, using test strips or with a digital glucose meter. Color change is cheap and effective, but the o-Toluidine can react to other sugars and give distorted results.
  • The industry standard for the last few decades has been enzyme-based reactions. A special enzyme, usually glucose oxidase or glucose dehydrogenase reacts with blood. This enzyme is very specific and only reacts to glucose. A result of this reaction is the production of H2O2, hydrogen peroxide. This is easily measured by digital devices. This method is inexpensive and specific, giving good results.

Now we know the chemical methods of measuring glucose, but how do we actually test our glucose level? Three broad testing types exist: oral, self-test, and continuous glucose monitors. These are differentiated mainly by the frequency and invasiveness of the test. 

  • Oral tests are a lengthy and (frankly) pretty gross affair. You fast for several hours, then drink an offensively sweet beverage and wait another hour. Blood is drawn and tested to determine how well your body can break down and clear the glucose from the bloodstream.
  • Self-tests involve drawing blood and putting it on a strip or in a digital detector. This is quick and can be done many times a day if needed. Unfortunately, repeated pricks can be annoying and you can’t test overnight unless you wake up. 
  • Continuous glucose monitors (CGMs) are worn like a patch and have a tiny sensor that goes just under the skin into the interstitial space and sends results to an external monitor. This tests blood glucose constantly, typically reporting every 1-5 minutes. CGMs can let people know their glucose via a phone app or external device. 

As the old saying goes, knowledge is power! With the help of the latest CGM technology, we are able to see information in real-time such as how food, exercise, and stress impact glucose levels. This helps us take immediate action to manage our glucose levels. So, take action to keep your blood glucose in the healthy range with your new knowledge, a good diet, and consistent exercise. Make sure it stays there by monitoring your blood glucose levels regularly. Keep your eyes open to look for new studies looking at ways to monitor your blood glucose and keep your cells powered up!



Sources:

American Diabetes Association (n.d.). Understanding A1C diagnosis. American Diabetes Association. https://diabetes.org/diabetes/a1c/diagnosis

McMILLIN, J. M. (1990). Blood glucose. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Chapter 141. https://www.ncbi.nlm.nih.gov/books/NBK248/

Wang, H. C., & Lee, A. R. (2015). Recent developments in blood glucose sensors. Journal of food and drug analysis, 23(2), 191-200. https://doi.org/10.1016/j.jfda.2014.12.001


Smoking.jpg

Listen to the article here:


Cardiovascular disease (CVD) is the leading cause of death in the United States. There are several risk factors for cardiovascular disease. This can include things you can’t change, such as sex, age, and genetics. They can also include things you can change. The WHO identifies four big behaviors that can change your risk of developing CVD:

  • Poor diet
  • Low exercise
  • Excessive alcohol consumption
  • Smoking

These behaviors generally lead to other undesirable indicators of health, including obesity, hypertension, high blood sugar, and increased cholesterol. Clearly, ceasing the behavioral risks is a high priority. Unfortunately, this is often easier said than done.

One of the most difficult habits to quit is smoking. Studies show that those attempting to quit without assistance have an over 90% relapse rate. Several medications exist to help quit smoking, including Bupropion SR (aka Wellbutrin) and Varenicline (aka Chantix). There are also nicotine-based alternatives, including gum, inhalers, lozenges, nasal sprays, and patches.  Nicotine rewires the brain as it’s consumed. It releases dopamine, the brain’s reward drug, and rewards us for smoking. Researchers think the frequency of smoking may be partially to blame for the intensity of the addiction. The amount of dopamine released is not particularly high compared with other drugs, but nicotine also causes changes to the striatum. The striatum is part of the reward circuit in the brain. Through a complicated mechanism, nicotine increases the amount of a protein called FosB, which changes the striatum’s sensitivity to dopamine. This is a change at the genetic level which makes the brain more susceptible to further reward signals. Nicotine seems to make normal activities more pleasurable. Unfortunately, as nicotine adjusts the brain’s mechanisms, the brain relies on it to get to a baseline of reward. Upon quitting smoking, the brain finds normal activities less enjoyable.

On its own, nicotine may have negative effects, and in heavy doses it has been shown to be dangerous. The biggest dangers of smoking, however, are likely in the myriad of other chemicals in tobacco and cigarettes. Though nicotine causes changes in the brain, cigarettes cause changes to the fats in your body, further increasing CVD risk. Along with this, cigarettes cause cancer, COPD, diabetes, erectile dysfunction, and immune system changes. Clearly, quitting smoking is critical to health. With the addictive nature of nicotine and the low success rate of quitting cold turkey, assistance may be needed. 

The brain gets addicted to nicotine, but we can fight back using behavior. You can actually help yourself “break the cycle” of nicotine addiction by changing your daily routines. For example if the first thing you do in the morning is reach for a cigarette, change your routine to going to the bathroom and brushing your teeth first instead. Behavioral interventions can make a significant difference. Combining behavior changes and counseling with a nicotine replacement or medication can help quit rates approach 30%. Indeed, nicotine replacements are most effective when used with behavioral interventions. 

Changing your behavior or routine can have positive impacts on your health. So next time you want to reach for a cigarette, grab your phone instead! Give us a call and discover what clinical trials you can take part in!



Sources:

Bancej, C., O’Loughlin, J., Platt, R. W., Paradis, G., & Gervais, A. (2007). Smoking cessation attempts among adolescent smokers: a systematic review of prevalence studies. Tobacco control, 16(6), e8-e8. https://doi.org/10.1136%2Ftc.2006.018853

Fiore, M. (2008). Treating tobacco use and dependence; 2008 guideline. https://stacks.cdc.gov/view/cdc/6964/cdc_6964_DS1.pdf

Garbin, U., Fratta Pasini, A., Stranieri, C., Cominacini, M., Pasini, A., Manfro, S., … & Cominacini, L. (2009). Cigarette smoking blocks the protective expression of Nrf2/ARE pathway in peripheral mononuclear cells of young heavy smokers favouring inflammation. PloS one, 4(12), e8225. https://doi.org/10.1371/journal.pone.0008225

Koren, M. (Host). (2022, May 22). Nicotine replacement therapies to help stop smoking  [Audio podcast episode]. In Medevidence! Truth behind the data. ENCORE Research Group. https://www.buzzsprout.com/1926091/10484183-nicotine-replacement-therapies-to-help-stop-smoking

Messner, B., & Bernhard, D. (2014). Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis. Arteriosclerosis, thrombosis, and vascular biology, 34(3), 509-515. https://doi.org/10.1161/ATVBAHA.113.300156

NIDA. (2018, September 28). Recent Research Sheds New Light on Why Nicotine is So Addictive. https://nida.nih.gov/about-nida/noras-blog/2018/09/recent-research-sheds-new-light-why-nicotine-so-addictive

US Department of Health and Human Services. (2014). The health consequences of smoking—50 years of progress: a report of the Surgeon General. https://www.ncbi.nlm.nih.gov/books/NBK294320/


Dont-drop-the-ball-on-your-new-years-resolution.jpg


We humans seem to like making a fresh start. Whether it’s the beginning of a semester, a month, or a week, we like having a “clean slate” to make changes. The most widely used of these fresh start times are at the beginning of the year, with a New Year’s Resolution. Over 40% of all Americans make New Year’s resolutions, but much like a firework, we make a bright claim with a loud noise, only for it to burn out quickly as the year goes on. How can we make good resolutions that we are likely to follow, and are there strategies we can use to help us follow through?

Probably the most important piece of a New Year’s Resolution is coming up with a good resolution in the first place! Surveys show that around two-thirds of all resolutions are health-oriented, including eating healthier, exercising, getting in shape, etc. Psychological studies have shown that the wording of your resolution matters. Most resolutions can be broadly lumped into either activation or avoidance goals. Activation goals are those that encourage you to do something: exercise more, eat more greens, etc. Avoidance goals are those that encourage you to not do something: watch less TV, eat less pizza, etc. Several studies have shown that activation goals are significantly more likely to be successful than avoidance goals

Sometimes our end goal is to decrease something: to lose weight, stop smoking, or eat slightly fewer cookies. In order to increase chances of success, it can be helpful to reimagine these goals as activation goals. Instead of losing weight, we can aim to exercise four days a week. Instead of stopping smoking, we can try to chew gum daily. Instead of eating fewer cookies, we can try to do some push-ups instead. When trying to avoid negative things, it can be hard to find rewards and easy to identify failures. By trying to do positive things, we can enjoy the reward of achieving our goal incrementally. Even small changes can help. Instead of “I resolve to eat no cookies this year” we can set the goal as “I resolve to do a push-up instead of eating a cookie every day.” Eventually, we will focus more on the positive action, the push-up, than the negative one, the cookie. This way our brain will spend more time focusing on the things we resolve to do!

When we follow through on a resolution, we are making a behavioral change. These changes are governed by our brain, and mimic changes within it. Some of our most popular resolutions correspond to changes in our reward pathway, called the mesocorticolimbic circuit. This contains several brain structures and is a part of the brain that is hijacked by addictive drugs. Two structures in particular, the nucleus accumbens and striatum, seem to be affected by things like resolutions. Addictive things including sugar decrease these areas’ sensitivity to naturally occurring dopamine. This makes the brain need more and more of those items to find the same level of reward. Lowering sugar, drugs, and alcohol can help restore the dopamine receptors and give your brain a fighting chance. Studies have also shown that exercise increases dopamine sensitivity of the mesocorticolimbic circuit, giving some protection against addictive undesirable behaviors. Other behaviors that we do frequently and repetitively will also make changes to the brain’s pathways, reinforcing the behaviors.

So now we know how to structure our resolutions, and how our brain responds to changes, but what can we do to make sure we don’t give up on our resolutions? The most important change is a lifestyle change. This is true with resolutions, but also with weight loss medications, smoking cessation, etc. Changing the triggers for what you want to avoid makes it easier to do the activities you desire. Even small changes – like sitting in a different chair than your preferred cookie-binge recliner – can make the process easier. Along with this, we want to make sure we have strategies to deal with tempting situations. If work has cookies on Fridays, drinking a lot of water can fill your stomach and help alleviate the temptation. Unexpected situations can also arise. If your mother invites you for afternoon tea and biscuits – only for you to learn that “biscuit” is British for “cookie”- having a plan to politely decline can be very handy. Finally, realize that resolutions aren’t all-or-nothing. If I succumb to chocolatey chip temptation and eat a cookie today, it doesn’t mean I’ve failed at my resolution and should give up. Instead of looking at hiccups as failures, look at them as learning opportunities. These are great opportunities to learn what triggered your lapse and practice a strategy to act positively and avoid this trigger in the future.

Taken together we have solid starting points for our resolutions. Resolve to do positive actions that you want to accomplish. Structure resolutions to be activation based and give yourself opportunities to celebrate success instead of regretting failure. Give yourself the advantage of changing your lifestyle to accommodate and incentivize your resolution. Give yourself a break when you miss a day and learn how to move forward better tomorrow. When we resolve to do things we want to do, we only have to countdown the days until we celebrate another New Year and a successful resolution!

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Larimer, M. E., Palmer, R. S., & Marlatt, G. A. (1999). Relapse prevention. An overview of Marlatt’s cognitive-behavioral model. Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism, 23(2), 151–160. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6760427/

Oscarsson, M., Carlbring, P., Andersson, G., & Rozental, A. (2020). A large-scale experiment on New Year’s resolutions: Approach-oriented goals are more successful than avoidance-oriented goals. PLoS One, 15(12), e0234097. https://doi.org/10.1371/journal.pone.0234097

Trifilieff, P., & Martinez, D. (2014). Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity. Neuropharmacology, 76 Pt B(0 0), 498–509. https://doi.org/10.1016/j.neuropharm.2013.06.031

Wimmer, S., Lackner, H. K., Papousek, I., & Paechter, M. (2018). Goal orientations and activation of approach versus avoidance motivation while awaiting an achievement situation in the laboratory. Frontiers in psychology, 9, 1552. https://doi.org/10.3389/fpsyg.2018.01552


Does-Chocolate-Really-Have-Health-Benefits.jpg

Listen to the article here:


Most of us have heard by now that chocolate is healthy, or that a small amount is healthy, or that you can eat an infinite amount of chocolate and it will be healthy forever. Where do these claims come from, and do they add up? 

There is evidence of people consuming chocolate up to 1600 years ago. It is native to the Americas and was said to be the “food of the gods” in mesoamerica. Today we think of chocolate as sweet and delicious and the perfect food, but this was not always the case. Chocolate is thought to have originally been mixed with water and drunk as a bitter, spiced beverage. During the 1500’s chocolate was brought to Europe, where it was considered as exotic as Mars. Healers claimed chocolate healed diseases of the liver and stomach, and that it could help with fever.

By 1631, chocolate had changed. Adding sugar was now typical, and the prescriptions for chocolate had changed as well. Chocolate in this era was used to help gain weight (likely due to sugar), stimulate the brain (likely due to caffeine), and aid in digestion.

Ironically, the same benefits chocolate seemingly presented to chronically underweight pre-industrial people has become a bit of a problem for us. By the mid to late 1800’s there were investigations into the health problems associated with chocolate’s additives – milk and sugar. They found that regularly eating fatty, sugary foods might not be healthy. By the 1900’s chocolate began to be associated with obesity, tooth decay, gum disease, etc. The “dark” chocolate age had begun.

By the early 2000’s, the opinion pendulum on chocolate had begun to swing back. Individual components of chocolate, such as flavanols, methylxanthines (Methyl-zan-theens) and polyphenols were shown to be beneficial to heart function in a lab. Since then there have been claims that chocolate helps everything from cardiovascular problems to metabolic ones and even cancer. It looked like chocolate was on a holiday high in medical opinion.

Unfortunately, these results may have been candy-coated. Research trials haven’t shown as much benefit as in the lab. One sweet spot picked up by newspapers was an observational meta-study which looked at over 300,000 participants. This study looked for an association between chocolate consumption and coronary artery disease (CAD). They found that people who ate chocolate more than once a week (or more than 3½ times a month) had a significantly lower incidence of CAD, heart attack, heart failure, and acute coronary syndrome. It is important to note that this was not an interventional study, and only looked at associations. Additionally, this didn’t take into account the type of chocolate eaten. Finally, this study found that some negative indicators actually rose, likely due to the extra calories from fats and sugars added to chocolates.

The best way to look for health benefits or drawbacks of any medicine is to do an interventional experiment – a clinical trial. This is where you compare groups randomly assigned to take chocolate or a placebo. An examination of 15 such studies where chocolate was the medicine sadly found few benefits. These studies looked for changes in:

  • Skin condition
  • Weight / BMI
  • Blood glucose
  • Blood pressure
  • Cholesterol
  • Cognitive function

When looking at all 15 studies, there was no significant change in any of these indicators. The only significant change across studies was a decrease in triglycerides. This can be helpful, as high triglycerides can be a risk factor for CAD, stroke, and pancreatitis. Overall, however, chocolate doesn’t appear to be the miracle drug it’s been touted as for the last millennium and a half. As we have learned countless times, using randomized clinical (interventional) trials is the best and often only way to discover if medicines have the effects people claim!

Interventional trials are conducted at clinical research organizations such as ours, ENCORE Research Group. We are a premier clinical research organization that has conducted more than 2,500 clinical trials over 25 years and has worldwide recognition for providing patients access to cutting edge medical research.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Krittanawong, C., Narasimhan, B., Wang, Z., Hahn, J., Virk, H. U. H., Farrell, A. M., … & Tang, W. W. (2021). Association between chocolate consumption and risk of coronary artery disease: a systematic review and meta-analysis. European journal of preventive cardiology, 28(12), e33-e35.https://doi.org/10.1177/2047487320936787

Lippi, D. (2015). Sin and pleasure: the history of chocolate in medicine. Journal of agricultural and food chemistry, 63(45), 9936-9941.

Montagna, M. T., Diella, G., Triggiano, F., Caponio, G. R., Giglio, O. D., Caggiano, G., … & Portincasa, P. (2019). Chocolate,“food of the gods”: History, science, and human health. International Journal of Environmental Research and Public Health, 16(24), 4960. https://doi.org/10.3390/ijerph16244960

Tan, T. Y. C., Lim, X. Y., Yeo, J. H. H., Lee, S. W. H., & Lai, N. M. (2021). The health effects of chocolate and cocoa: A systematic review. Nutrients, 13(9), 2909. https://doi.org/10.3390/nu13092909


The-Science-of-Gift-Giving.jpg

December 12, 2022 BlogMedEvidence

Listen to the article here:


With the onset of frosty weather and short days, we can all use a boost. Luckily, giving gifts can produce a “warm glow” to help out. This isn’t just decorative talk, giving gifts has been shown to increase well-being in people across the globe. In study after study, psychologists have found that acts of kindness, such as giving gifts, have positive results on both the receiver and the giver.

In one study, scientists gave children treats while measuring happiness. The children were then asked to give treats to a puppet. These could be their own treats or ones from a researcher’s supply. The data showed the children were happier to give a treat to the puppet than to receive one for themselves and were happiest when they gave their own treat to the puppet. Overall, the cheer of giving seemed maximized when giving away more important gifts.

Why could this be, though? Why would gift giving be beneficial for the person losing something? Could it be that giving a gift clears your already extremely crowded gingerbread house and increases your Feng shui? The real answer is that gift giving is a prosocial behavior. This means that it promotes social acceptance and friendship. This is a positive behavior in social contexts. Prosocial behaviors are seen in several social animals, including apes and dogs.

Scientists have shown that giving gifts can increase synchronization between friends. In two studies, scientists hooked pairs of friends up to brain scanning devices. The friends performed cognitive tasks, then one would give the other a gift (at a random time), and they would perform the task again. The scientists found that accuracy on the tasks increased. In addition, activity increased in the dorsolateral prefrontal cortex (DLPFC). This is part of the brain located beneath the hairline (assuming you have hair). It is associated with decision making and memory, and is also implicated in suppressing selfishness and building relationships. This helps with cognitive tasks, but also with forming and maintaining friendships. Even more interesting, they found that the brain waves of friends were synchronizing! The brainwaves measured in the DLPFC would “sync up” and produce similar patterns after gift giving! Giving a gift doesn’t just increase friendship, it helps you think like your friends too!

The DLPFC isn’t the only section of the brain that’s active when giving. When giving to charity, people’s mesolimbic reward system and subgenual areas activate. The mesolimbic reward system is a general reinforcement pathway in the brain, and also rewards for things like food, sex, and drugs.  The subgenual area releases important hormones such as oxytocin (the love hormone) and vasopressin. These make us feel good and increase our social happiness.

So this winter, give gifts to keep yourself warm inside and out. By giving gifts you can increase your own happiness, strengthen bonds with friends, and release dessert-like chemicals in the brain. Also, consider giving the gift of health to others by volunteering for a clinical trial at one of our ENCORE Research Group locations. 

By Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Aknin, L. B., Barrington-Leigh, C. P., Dunn, E. W., Helliwell, J. F., Burns, J., Biswas-Diener, R., … & Norton, M. I. Prosocial Spending and Well-Being: Cross-Cultural Evidence for a Psychological Universal.https://doi.org/10.1037/a0031578

Aknin, L. B., Hamlin, J. K., & Dunn, E. W. (2012). Giving leads to happiness in young children. PLoS one, 7(6), e39211. https://doi.org/10.1371/journal.pone.0039211

Balconi, M., Fronda, G., & Vanutelli, M. E. (2019). A gift for gratitude and cooperative behavior: brain and cognitive effects. Social cognitive and affective neuroscience, 14(12), 1317-1327. https://doi.org/10.1093/scan/nsaa003

Balconi, M., Fronda, G., & Vanutelli, M. E. (2020). When gratitude and cooperation between friends affect inter-brain connectivity for EEG. BMC neuroscience, 21(1), 1-12.

Curry, O. S., Rowland, L. A., Van Lissa, C. J., Zlotowitz, S., McAlaney, J., & Whitehouse, H. (2018). Happy to help? A systematic review and meta-analysis of the effects of performing acts of kindness on the well-being of the actor. Journal of Experimental Social Psychology, 76, 320-329. https://doi.org/10.1016/j.jesp.2018.02.014

Moll, J., Krueger, F., Zahn, R., Pardini, M., de Oliveira-Souza, R., & Grafman, J. (2006). Human fronto–mesolimbic networks guide decisions about charitable donation. Proceedings of the National Academy of Sciences, 103(42), 15623-15628. https://doi.org/10.1073/pnas.0604475103


atrial-fibrillation-afib.jpg

Listen to the article here:


The familiar wub-dub of the heart accompanies us throughout our lives, providing a gentle beat that keeps us alive. But for some of us, the beat might not be so steady. For 33 million people worldwide, the heartbeat lacks a rhythm at all. It sounds like shoes in a clothes dryer and gets progressively worse. This is called Atrial Fibrillation, or AFib for short. The risks of AFib increase with age, and there is a genetic component as well. Other risk factors include:

  • Heart failure
  • Ischemic (low blood flow) heart disease
  • High blood pressure
  • Diabetes
  • Obesity
  • Sleep Apnea

In order for AFib to occur, doctors believe there needs to be a trigger and a substrate. A trigger, or driver, is the electric signal that travels to the heart and initiates an arrhythmic event. This can be from several areas, but is frequently from one of the big pulmonary veins that carry oxygen to the heart. A substrate is the underlying condition that makes a sustained event possible and could be structural or electrical. Common substrates include the electrical system of the heart, dilation (or stretching) of the atrium, cellular-molecular changes, and/or an increase in disruptive cells called fibroblasts. In general, many or all of these changes would occur, leading to constant AFib.

AFib is very dangerous. Other than a wonky pulse, there are three major complications: heart failure, stroke, and myocardial infarction (a heart attack). Heart failure is when the heart can’t pump enough blood, while stroke and myocardial infarction can be caused by stray blood clots. Heart failure is both a risk and a symptom, which illustrates one way in which AFib is a progressive disease. Through complicated electric and biocellular mechanisms, long term AFib seems to cause more AFib.

Treating AFib has proven difficult. It is effective to treat the underlying risk factors, such as obesity and diabetes, but this is difficult and the actual cause of AFib isn’t always clear. Controlling the rhythm of the heart is also tough and risky, as messing with heart rhythm can easily lead to big problems. Atrial fibrillation ablation is an effective treatment. It is an intensive surgical procedure where doctors scar problem areas to reduce electrical activity. Even with this method, the risk of resurgence is over 30% after 5 years.

Two of the biggest complications of AFib are related to blood clots. Because of this – and the difficulty of other treatments – major pharmaceuticals often target thromboembolisms, or clots. The clotting system itself is very complicated. A simple version is that platelets activate and produce several enzymes. These enzymes make thrombin, which makes a big mesh-like protein called fibrin. This would be a slow process, except that thrombin also activates amplifier enzymes, which makes this process very fast. The fibrin then catches red blood cells and blocks wounds – or blood vessels. When these clots travel to the brain they can cause a stroke. When they restrict blood flow to the heart they can cause a myocardial infarction – a heart attack.

Classic anticoagulants, such as Warfarin (also called Jantoven and Coumadin) work by stopping the clots before they start. These are Vitamin K dependent anticoagulants and can be effective at reducing clots. Unfortunately, they are occasionally too effective. The biggest side effect of Vitamin K dependent anticoagulants is increased bleeding. This can be a serious problem for several patients, including high-risk older patients. 

Doctors are investigating new classes of medications which do not depend on vitamin K. These are called Non-vitamin K oral anticoagulants (NOACs) and some target the amplification pathway of clotting instead. There are  currently four FDA-approved NOAC drugs on the market; dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa). Thrombin and fibrin still get produced and some clotting can occur, but the rapid amplification is shut down. The hope is that this can allow the body to repair trauma and stop external bleeds without building internal clots from AFib. With your help and participation in clinical trials, we can push science without pushing clots.

By Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Iwasaki, Y. K., Nishida, K., Kato, T., & Nattel, S. (2011). Atrial fibrillation pathophysiology: implications for management. Circulation, 124(20), 2264-2274. https://doi.org/10.1161/CIRCULATIONAHA.111.019893

Wijesurendra, R. S., & Casadei, B. (2019). Mechanisms of atrial fibrillation. Heart, 105(24), 1860-1867. http://dx.doi.org/10.1136/heartjnl-2018-314267

Vann, M. R. (May 10, 2013) The Sound of an Afib Heartbeat. Everyday Health. https://www.everydayhealth.com/heart-health/sound-of-afib-heartbeat.aspx


C.-diff-stomach-pain.jpg

Listen to the article here:


Clostridioides difficile, C. difficile, or just C. diff is a particularly nasty bacteria that can make us very sick. The bacteria itself has the name difficile because it was difficult to isolate and study when it was first discovered. Forms of the problem bacteria are found all over the environment, but most can’t make us sick. The organism itself doesn’t kill cells like a virus; instead, it can produce toxins that can kill cells in the gut. C. diff has over 800 different strains, but only a few produce dangerous toxins. Overall, C. diff causes dangerous infections in hundreds of thousands of patients each year.

Several people have C. diff inside their gut already, but it doesn’t cause them problems. Other bacteria in our gut can outcompete C. diff and keep it from causing damage. Unfortunately, one of the biggest medical breakthroughs, antibiotics, can destroy these helpful bacteria and allow C. diff to start running amok. In fact, any kind of immunosuppression can increase your risk of developing C. diff, including HIV/AIDS medications and those used after organ transplants. Being above 65 years old is another large risk factor. Close contact with some animals, like pigs, can also pose a risk. The most dangerous forms of C. diff are spread from person to person. This occurs with our most vulnerable populations: those in hospitals and those in elderly care. Due to the innate nature of care, people in hospitals and care homes can be exposed to C. diff unknowingly.

How does C. diff survive in the notoriously clean hospital environment? The bacteria has a special trick up its sleeve; it can become dormant – and almost invincible. C. diff has two life cycle stages, the spore and vegetative stage. While in the spore stage, C. diff is inactive. It doesn’t need to eat or breathe. While in this stage it can survive in the environment, the stomach, through most antibiotics, and through alcohol washes. When a C. diff spore makes it into our gut, however, trouble can begin. It germinates in the duodenum – the part of the intestine connected to the stomach. Here it transforms into the vegetative stage. In the vegetative stage, C. diff is active. It can’t survive the stomach or in oxygen, but thrives in the intestines. Here it grows and reproduces. This is also where some strains produce dangerous toxins.

The toxins of C. diff can produce a host of issues. The toxins can degrade and kill intestinal cells and cause inflammation of the intestines. Major symptoms are diarrhea, inflammation of the gut, and tissue necrosis (cell death). Other symptoms can include:

  • Fever
  • Tenderness and pain in the stomach
  • Loss of appetite and nausea
  • A severely dilated colon (toxic megacolon)
  • Sepsis (severe infection response)
  • Death

So what can be done to fight C. diff? The first line of defense is the simplest: wash your hands! Prevention is the strongest barrier: avoid close contact with people who have an active infection and wash clothes and linens regularly. A medical professional (who should be wearing gloves!) can monitor any antibiotics an infected person is currently taking and might suggest probiotics. Some specific antibiotics target C. diff, including Metronidazole, Vancomycin, and Fidaxomicin. These may have unpleasant side effects, but can be effective. Treatments available include fecal microbiota transplantation (FMT), antitoxins, new antibiotics, and injectable antibodies. Additionally, prophylactics that can help protect the gut and vaccines against the dangerous toxins are in development. Keep an eye out, and with your participation in clinical trials, we can help protect those at the highest risk from  C. diff!

By Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Dayananda, P., & Wilcox, M. H. (2019). A review of mixed strain Clostridium difficile colonization and infection. Frontiers in microbiology, 10, 692.https://doi.org/10.3389/fmicb.2019.00692

Smits, W. K., Lyras, D., Lacy, D. B., Wilcox, M. H., & Kuijper, E. J. (2016). Clostridium difficile infection. Nature reviews Disease primers, 2(1), 1-20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5453186/

U.S. Department of Health & Human Services/Centers for Disease Control and Prevention (September 7, 2022). What is C. diff  https://www.cdc.gov/cdiff/what-is.html


Heart-Failure.jpg

Listen to the article here:


When EMTs arrive on the scene of an emergency, they have to remember their ABCs. These are Airway, Breathing, and Circulation. The absolute top priority for any patient is to ensure they have an open airway to breathe, that air is entering the lungs, and that the heart is pumping blood to the brain and other organs. This is also the most important thing our body does in daily life as well. We can go weeks without food, days without water, hours without ice cream, and minutes without oxygen.

In order to get oxygen from the lungs to our brain and organs, we rely on one of the most remarkable organs in our body: the heart. The heart pumps automatically, nonstop, 24/7, from womb to grave. It consists of four chambers, two on top, and two on the bottom. Each heartbeat pulls blood into the top two chambers and pumps it out of the bottom two. The bottom two are more muscular and do the heavy lifting. Unfortunately, the heart can deteriorate and lead to heart failure. 

Heart failure is a condition where the heart can’t pump well enough to deliver oxygen to the organs effectively. The heart is still pumping, but organs are not receiving enough oxygen to function. This is not good. Heart failure affects over six million Americans and ten times as many people worldwide. Risk factors for heart failure include:

  • Heart disease, including Coronary Artery Disease
  • High Blood pressure
  • Tobacco
  • Excessive alcohol
  • Poor diet
  • Lack of exercise
  • Obesity
  • Diabetes

Heart failure has several signs and symptoms. Some of the most consistent are edema and shortness of breath. Edema is fluid trapped in the body’s tissues and most often pools in the lower extremities and the abdomen. Shortness of breath is due to the heart failing to deliver enough oxygen. This is particularly prevalent when trying to do activities or when lying down. Shortness of breath can keep patients from exercising or sleeping, which only exacerbates problems. Patients who have limited exercise in their routine may not be aware of progressive difficulty, masking this important symptom.

Other symptoms can be broad and nonspecific. They include:

  • Sudden weight gain
  • Persistent coughing or wheezing
  • Lightheadedness and fainting
  • Depression
  • Nausea and loss of appetite
  • Irregular heartbeat, high pulse, and palpitations
  • Fatigue

If you have heart failure and find yourself experiencing several of these conditions simultaneously, especially with edema and shortness of breath, we urge you to contact your physician immediately. Additionally, you may want to keep track of your level of fatigue because this symptom increases as the heart failure progresses. The excellent news is that new and exciting monitoring devices are currently being developed to help patients manage their heart failure and determine if their condition is deteriorating.

Check out clinical research options available to you with ENCORE Research Group on our enrolling studies page. 

By Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Albert, N., Trochelman, K., Li, J., & Lin, S. (2010). Signs and symptoms of heart failure: are you asking the right questions?. American Journal of Critical Care, 19(5), 443-452. https://doi.org/ajcc2009314

Groenewegen, A., Rutten, F. H., Mosterd, A., & Hoes, A. W. (2020). Epidemiology of heart failure. European journal of heart failure, 22(8), 1342-1356. https://doi.org/10.1002/ejhf.1858

U.S. Department of Health & Human Services/Centers for Disease Control and Prevention (October 14, 2022). Heart failure  https://www.cdc.gov/heartdisease/heart_failure.htm


Turkey-and-Tryptophan.jpg

November 16, 2022 BlogMedEvidence

We all know how Thanksgiving works. A giant meal with a giant turkey followed by tasty desserts. Then, after the meal, sleepiness sets in. But why? We usually blame the turkey and the tryptophan in the protein. But I’m a vegetarian, and I still get the post-thanksgiving snoozies. So, what is tryptophan, and does it make us tired, or is there something else to blame? This article contains a cornucopia of information to help answer these questions.

Tryptophan is an essential amino acid. Amino acids are the building blocks of proteins and are baked into many of the body’s needs. Being an “essential” amino acid means that we can’t create our own tryptophan and must instead gather it from the foods we gobble up. We need some tryptophan in our diet because it is used to create some critical molecules our body uses.

Two of these important molecules are the neurotransmitter serotonin and the hormone melatonin. These are critical little molecules derived from tryptophan and – interestingly, both interact with our sleep cycle. Serotonin acts on parts of the brain involved with learning, pain, social behavior, and sleep, among many others. Melatonin is like turkey dressing; it’s harvested further from serotonin and can increase sleepiness. Neither of these gets produced in large quantities after eating turkey, however. The large amount of other amino acids found in turkey protein keep tryptophan from making a pilgrimage to the brain after a meal because the amino acids compete for rides on the path to our brain.

So then, why do we feel tired after a big Thanksgiving meal? Well, one reason might be linking carbs (sugars) to tryptophan. Some carbohydrates can increase the ability of tryptophan to cross into the brain and get serotonin and melatonin cooking. Additionally, heavy carbohydrate intake has been associated with higher levels of tiredness and lower levels of alertness. This can be attributed to the rise in blood sugar from the heavy carbohydrates which is followed by release of insulin to lower the blood sugar.  The lower blood sugar causes you to feel tired.  So too much dessert might be resulting in a blood sugar crash after the meal.

In fact, too much of everything may be making you tired. When we eat large meals, the body activates the parasympathetic nervous system. This is also known as the “rest and digest” pathway, and does exactly what it sounds like. After a large meal, the body focuses on relaxation and digestion. This can cause extra blood flow into the stomach and can make you less alert and awake.

Turkey may get too much blame for our tiredness. As my sweet tooth will attest, the desserts may be a bigger culprit. So, this Thanksgiving, feel free to gather the family to feast (and nap) as you please, but squash the blame on the turkey!

Written by: Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Ballantyne, C. (2007). Does Turkey Make You Sleepy? Scientific American. https://www.scientificamerican.com/article/fact-or-fiction-does-turkey-make-you-sleepy/

Høst, U., Kelbaek, H., Rasmusen, H., Court-Payen, M., Christensen, N. J., Pedersen-Bjergaard, U., & Lorenzen, T. (1996). Haemodynamic effects of eating: the role of meal composition. Clinical Science, 90(4), 269-276.

Mantantzis, K., Schlaghecken, F., Sünram-Lea, S. I., & Maylor, E. A. (2019). Sugar rush or sugar crash? A meta-analysis of carbohydrate effects on mood. Neuroscience & Biobehavioral Reviews, 101, 45-67.

Vreeman, R. C., & Carroll, A. E. (2007). Medical myths. Bmj, 335(7633), 1288-1289.


Hawthorne-Effect-Lightbulb.jpg

Listen to the article here:


Several of my friends hate flossing their teeth. They go months without flossing, which I think is pretty gross. But then an odd thing happens. About a week before their dental appointment, these same friends will start flossing. By the time they reach their appointment, they have unusually clean gums (though dentists can see through this fairly well, I’m told). On a different tone, some family members have a condition called White Coat Syndrome. When they go to the doctor’s office, their nervousness causes a spike in blood pressure or heart rate, giving deceptively high readings. What’s going on? Can psychological effects like these be used to our advantage?


The Hawthorne Effect is a term used to describe a very beneficial effect seen in clinical trials. This is named after a productivity study in Hawthorne Works, a Western Electric factory in the 1920s and 30s. The study was attempting to discover a link between the amount of light and productivity of workers. When increasing the amount of light, productivity increased. Strangely, when lowering the amount of light, productivity also increased! Researchers attributed the increase in productivity to the workers simply being observed. In research, we tend to see increased positive results for patients simply because we are observing them in a study.


Hawthorne Works


Let’s analyze a 2014 sleep study. Researchers measured 195 patients’ amount and quality of sleep at night. 81 days later, before any medical intervention, researchers measured the patients again. They found that patients slept an average of 30 minutes longer per night and had an increased quality of sleep. This was before any medication or intervention! The change was attributed to the Hawthorne Effect.

Patients at ENCORE Research Group comment on the excellent quality of care they receive during clinical trials. Instead of seeing a doctor for a few minutes once a year, patients see doctors and medical staff for much longer and are encouraged or required to call and report changes in health. Quality of care is increased and makes for a pleasant and healthful patient experience. Patients in clinical trials may also experience more observation time from medical professionals due to the attention to detail that clinical trials require for data integrity in studies.

Finally, patients are found to have better adherence to medication requirements while undergoing clinical trials. The increased emphasis on accuracy and adherence results in better patient outcomes, even when they are part of a placebo or standard-of-care group.

In clinical trials, we see these benefits and must account for them. Randomization of patients helps spread the effect. Everyone sees increased baseline results on average; we are interested to find out if those receiving investigational treatment do even better. Join a clinical trial today and experience the Hawthorne Effect for yourself… and floss your teeth!

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Benedetti, F., Carlino, E., & Piedimonte, A. (2016). Increasing uncertainty in CNS clinical trials: the role of placebo, nocebo, and Hawthorne effects. Lancet Neurol, 15, 736-47. http://dx.doi.org/10.1016/S1474-4422(16)00066-1

Cizza, G., Piaggi, P., Rother, K. I., Csako, G., & Sleep Extension Study Group. (2014). Hawthorne effect with transient behavioral and biochemical changes in a randomized controlled sleep extension trial of chronically short-sleeping obese adults: implications for the design and interpretation of clinical studies. PLoS One, 9(8), e104176. https://doi.org/10.1371/journal.pone.0104176

ENCORE Research Group. (2020, October 14). Hawthorne effect.[Video]. Youtube. https://www.youtube.com/watch?v=1DH7jwqFlyw

Mayo, E. (1993). The human problems of an industrial civilization. The Macmillan Company. 

McCarney, R., Warner, J., Iliffe, S., Van Haselen, R., Griffin, M., & Fisher, P. (2007). The Hawthorne Effect: a randomised, controlled trial. BMC medical research methodology, 7(1), 1-8. https://doi.org/10.1186/1471-2288-7-30


Cirrhosis-Hepatic-Encephalopathy.jpg


The liver is critical to maintain body function. Unfortunately, millions of Americans suffer from liver disease. When the liver suffers prolonged damage, scarring can form. This scarring, called cirrhosis, is debilitating and reduces liver function. Cirrhosis is sometimes called end stage liver disease, and is irreversible. On its own, cirrhosis can be painful and cause suffering, but is frequently made worse through complications. One of these is encephalopathy.

Encephalopathy is a broad term used to describe several diseases and disorders. The unifying concept is that these diseases change the brain’s structure or function. When the cause of this change is through cirrhosis, the condition is called hepatic encephalopathy. This is the condition caused by cirrhosis of the liver, and can be horrible. It comes with a high mortality rate, over 25%, and affects over 30% of people with cirrhosis.

The full mechanism of how hepatic encephalopathy works isn’t fully known. The most likely candidate for hepatic encephalopathy is a buildup of ammonia in the bloodstream. Ammonia is a common waste product for many cells. A damaged liver has trouble filtering ammonia from the blood. The ammonia accumulates in the blood where it can travel to the brain and cause confusion and disorientation at first. Additionally, liver damage can result in reduced muscle mass and immunosuppression. Muscles can remove excess ammonia from the blood, but may become damaged without a functional liver and be unable to help. A reduced immune system can lead to a buildup of harmful bacteria that produce excess ammonia. These combine to create excess toxic levels of ammonia in the bloodstream that make their way to the brain.

The brain is normally protected from toxins in the blood through the blood brain barrier. Astrocytes are special cells in the brain that surround blood vessels and help filter the blood, letting only specific nutrients and particles through. Excess ammonia in the blood appears to damage astrocytes, with wide ranging effects on the brain. When the blood-brain barrier is reduced, toxins can enter the brain. This can lead to damage in neurotransmission, meaning the brain cannot function effectively. There is also an increased chance of infection in the brain and alterations to brain metabolism.

This is a devastating compilation which can drastically reduce quality of life. In the early stages of hepatic encephalopathy, people may experience a general slowing of the brain. This is noticeable in attention, some motor response, and other vague areas. As the encephalopathy progresses, people experience more severe symptoms. Changes in personality have been reported, such as irritability and impulsivity. They may angrily buy m&ms in the checkout line. It also slows the brain and reduces its ability to function. People may become disoriented, experience distortions of time and space, become excessively sleepy, and descend into a coma. Clearly this condition needs medical attention!

Luckily, hepatic encephalopathy can be reversible in many patients! The most important short-term treatment is to get rid of excess blood ammonia. The current standard of care is lactulose, a chemical that binds to ammonia and expels it rectally. This helps in the short term, and can also be recommended to help reduce recurrence. Though effective, lactulose is a laxative and can cause bloating, cramping, and other undesirable side effects. Because of this, many patients don’t like using this drug long term. Since the immune system is suppressed with cirrhosis, antibiotics may help as well. In fact, antibiotics may be helpful in preventing hepatic encephalopathy in the first place by eliminating harmful, ammonia producing bacteria before they can produce too much ammonia. Used with or without probiotics and drugs that help restore normal brain chemistry, we may be able to lower the burden of hepatic encephalopathy for those who suffer.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Bustamante, J., Rimola, A., Ventura, P. J., Navasa, M., Cirera, I., Reggiardo, V., & Rodés, J. (1999). Prognostic significance of hepatic encephalopathy in patients with cirrhosis. Journal of hepatology, 30(5), 890-895. https://doi.org/10.1016/s0168-8278(99)80144-5

Ferenci, P. (2017). Hepatic encephalopathy. Gastroenterology report, 5(2), 138-147. https://doi.org/10.1093/gastro/gox013


Variables-independent-dependent.jpg


In science and medicine we measure if and how well things work using measurements. This idea may sound simple, but it’s often a challenge to find out exactly what to measure – and how. We typically measure things that can change – things that can vary. We call these things variables. Variables can be broadly split into two major categories: dependent and independent. Either type of variable can change, the difference is what changes them.

Independent variables are changed by researchers, particularly in clinical (patient) research. This variable in a medical research study is what we are testing. The changes to an independent variable may include dose, length, and method of drug delivery. We evaluate independent variables that may change outcomes of the people in a study – but sometimes they do not. In order to understand the effect of medicines, researchers test the medicine against a control. The control could be a placebo (something that has no effect) or a standard of care (the current normal medicine).

Dependent variables are what we expect to change during a trial. In a clinical research, we may expect changes in blood pressure, cholesterol levels, disease symptoms, mortality, and other categories. In a well designed study, we assess changes in the dependent variables related to changes in the independent variables. There is always the chance that the dependent variables are changed by other things, however. A patient might take a new blood pressure medicine but retire from their job. The reduced stress could decrease their blood pressure even if the medicine did not. 

Because of individual changes in people’s circumstances, researchers use statistics to find trends. If your blood pressure medicine was only studied on the one person above, you might have erroneous results. Instead clinical trials have dozens, hundreds, or even thousands of participants. With large populations these little differences get figured out. One person might retire, but another might get fired, having an opposite effect. Altogether, statistical analysis can help discover if any changes in the dependent variable are due to the effects of the independent ones.

Chart 1. Each amount of Rosuvastatin on the left corresponds to an amount of LDL on the right. The dependent variable (LDL levels) change in proportion to the amount of independent variable (rosuvastatin) taken by the patient.


Other variables exist in a study. The most concerning of these variables is known as a confounding variable. This is a variable that can undermine the study at a fundamental level. A confounding variable can be introduced by researchers and might include things like placing all overweight patients in the 10 mg group and all underweight people in the placebo group. ENCORE Research Group (and any legitimate clinical research group) avoids confounding variables and bias by randomizing patients. Patients are randomized through an impartial method (usually a computer program) which will randomly place patients into any of the test groups. By randomizing patients, we can avoid the most concerning confounding variables and make sure we are studying what we intend to!

To learn more about the clinical trial process, call our Recruitment Team at (904) 730-0166.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Schweiger, C. (2003). Clinical trials with rosuvastatin: efficacy and safety of its use. Italian Heart Journal: Official Journal of the Italian Federation of Cardiology, 4, 33S-46S. https://pubmed.ncbi.nlm.nih.gov/14983745/

Stewart, P. A. (1978). Independent and dependent variables of acid-base control. Respiration physiology, 33(1), 9-26. https://www.nlm.nih.gov/nichsr/stats_tutorial/section2/mod4_variables.html


1918-Influenza-Article.jpg

Listen to the article here:


A pandemic spread around the planet in the first quarter of the century. Not this century, however, but the last. The 1918 Flu Pandemic was the largest and deadliest outbreak of disease since the bubonic plague in the 1300s. The first official reported case was in Kansas in 1918. This gives the disease its proper name, the 1918 Influenza Pandemic. A much more common name, however, is the Spanish Flu.           

The name Spanish Flu is an unfair name. Spain lost around a quarter million people to the 1918 Influenza. This is less than half as many as the USA, and fewer than Afghanistan, Mexico, Russia, Italy, and Japan. On top of that, India lost somewhere above 18 million people, and China between four and nine million. The big difference in losses was due to Spain being neutral during World War I. Because of this, they weren’t shy about publishing accurate data. Spain was the first country to publicly disclose that the pandemic was real, and other countries underreported or lied about numbers for years. This may strike some as familiar; during the COVID-19 pandemic, several national and local governments around the world tried to downplay the severity of COVID for political gain.           

But what is influenza? Influenza, known as the flu, is very similar to COVID-19 in many ways. It is a viral infection, and its primary symptoms are cough, fever, joint pain, headache, body aches, and others. However, more serious complications such as pneumonia, liver damage, or brain problems can be triggered by influenza. It spreads through the air and can survive in water. Soap, changes in pH, and heat can destroy the influenza virus. The most dangerous part of influenza is how variable it is.  

The influenza virus has several subtypes, and each of these mutates constantly.  This makes it hard for the immune system to detect and fight new forms of the virus. It also means the specific symptoms of infections can change. In the 1918 influenza pandemic, the strain of influenza was particularly deadly for young, healthy people. This resulted in a lot of excess deaths compared to other strains. 

The 1918 Influenza Pandemic was made much worse because of World War I. The war resulted in overcrowded barracks, troops stuffed in ships, and people crowding in shelters. Additionally, it spread wide and far as governments deployed troops around the world. A lack of accurate reporting and proactive measures certainly didn’t help. The biggest difference between then and now was medicine. 

1918 was over a hundred years ago, but in the realm of medicine, it may as well have been much longer. Viruses were only discovered around 20 years prior, and there were no effective ways to fight them. There were no antiviral medications. For patients that developed pneumonia, there were no ventilators and no antibiotics. On top of this, there was no influenza vaccine. 

The “Spanish flu” of 1918 helped refocus medical attention around pandemics – particularly influenza. In the early 1930s new vaccines were being developed from chicken eggs, and less than ten years later, the first experimental influenza vaccines were developed. Today, our yearly flu shots come from a direct line of response from the 1918 influenza pandemic. A century later, we have come a long way with medical advances, and since we know the influenza virus mutates regularly, the best way to help continue the fight against it is to participate in a clinical trial for the latest flu vaccines.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Hayden, F. G., & Palese, P. (2009). Influenza virus. Clinical virology, 943-976.

Jester, B., Uyeki, T. M., Jernigan, D. B., & Tumpey, T. M. (2019). Historical and clinical aspects of the 1918 H1N1 pandemic in the United States. Virology, 527, 32-37.

Johnson, N. P., & Mueller, J. (2002). Updating the accounts: global mortality of the 1918-1920″ Spanish” influenza pandemic. Bulletin of the History of Medicine, 105-115.

Knobler, S. L., Mack, A., Mahmoud, A., & Lemon, S. M. (2005). The threat of pandemic influenza: are we ready? workshop summary.

Mayer, J. (29 January 2019). “The Origin Of The Name ‘Spanish Flu’”. Science Friday. Retrieved 30 July 2021. https://www.sciencefriday.com/articles/the-origin-of-the-spanish-flu/

CDC, National Center for Immunization and Respiratory Diseases. (September 28, 2022). Similarities and Differences between Flu and COVID-19​. https://www.cdc.gov/flu/symptoms/flu-vs-covid19.htm


Insulin-Resistance-The-Darkside-of-Diabetes.jpg

September 27, 2022 BlogDiabetesMedEvidence

How does the body use energy? After we eat, most food is broken down into parts that cells can use for energy. The bloodstream carries these pieces through the bloodstream to our cells, which let them in and convert food to energy. In some cases, the cells don’t let food particles in. In these cases, the problem may be diabetes.

Cells need to separate their insides from the environment around them. Cells only let in specific molecules at specific times. Insulin is the molecule that tells cells to let in sugars in the form of glucose. It is produced by the pancreas and is released when the pancreas detects high levels of sugars in the blood. In some cases, such as with obesity, fatty acids can disrupt how cells absorb and use sugar in the blood. When this happens, cells are less sensitive to insulin and absorb less blood sugar per unit of insulin in the blood. Since blood sugar stays high, the pancreas produces more and more insulin, which has less and less effect. Cells can’t respond to all the excess insulin and are increasingly resistant to its effects.

Insulin is also the hormone the pancreas uses to communicate with the liver about blood sugar. When the liver detects insulin it converts blood glucose into glycogen, a short term storage molecule. When high levels of insulin persist, the liver sends extra energy to fat cells.

After long periods of insulin resistance, the pancreas itself stops working properly. Pancreatic cells become damaged and unable to produce insulin. This is called Type 2 Diabetes (T2D). With T2Ds, blood sugar stays high, insulin stops being produced, any produced insulin is less effective, and cells stop metabolizing properly. On top of this, the body gains excess weight which can stress the pancreas further. Other symptoms include cardiovascular disease, nerve dysfunction in the extremities (called neuropathy), and increased chance of death.

Diabetes is very common in the United States. Tens of millions of Americans have T2D. Type 1 diabetes is an autoimmune disorder which results in pancreatic damage. Type 2 diabetes is an insulin resistance disorder and can have a slow onset.  Major risk factors are obesity and lack of exercise. These should be the first steps to managing T2D as well.

When a healthy diet and exercise aren’t enough to manage healthy blood sugars, or aren’t an option, several key medications exist to help with type 2 diabetes:

  • Insulin: By injecting insulin with meals, the effects of a compromised pancreas can be reduced. Synthetic insulin, such as glargine, is in wide use.
  • Glucagon-like peptide-1 receptor agonists (GLP-1 RA): These stimulate the pancreas and coerce it into properly releasing the correct amounts of insulin. It slows some pancreatic cells and helps restore the pancreas-liver communication lines. One generic name for GLP-1 RA drugs is semaglutide, often branded as Ozempic and Rybelsus. A benefit of these drugs is that a common side effect is weight loss, one of the drivers of type 2 diabetes.
  • Metformin: Originally inspired by the French Lilac plant, metformin lowers blood sugar levels by acting on the liver, bloodstream, intestinal tract, and even the gut microbiome! The complex action on different areas of the body results in overall lower blood sugar levels.
  • SGLT2 Inhibitors: These act on the kidneys, changing the threshold of reabsorption of sugar so they excrete more than usual removing blood sugar through the urine. 

Altogether, there are several medications which may be helpful for controlling type 2 diabetes. Discovering how these medications interact, lowering side effects,  and finding treatments that are easy and straightforward is key. If you have type 2 diabetes, look for enrolling studies soon and improve your diet and exercise if possible!

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Berg, J. M., Tymoczko, J. L., & Stryer, L. (2012). Biochemistry (7th Ed., pp 798-803). New York: W. H. Freeman and Company

DeFronzo, R. A., Ferrannini, E., Groop, L., Henry, R. R., Herman, W. H., Holst, J. J., … & Weiss, R. (2015). Type 2 diabetes mellitus. Nature reviews Disease primers, 1(1), 1-22. https://www.nature.com/articles/nrdp201519

Olokoba, A. B., Obateru, O. A., & Olokoba, L. B. (2012). Type 2 diabetes mellitus: a review of current trends. Oman medical journal, 27(4), 269. http://doi.org/10.5001/omj.2012.68

Rena, G., Hardie, D. G., & Pearson, E. R. (2017). The mechanisms of action of metformin. Diabetologia, 60(9), 1577-1585. https://doi.org/10.1007%2Fs00125-017-4342-z

U.S. Department of Health & Human Services/Centers for Disease Control and Prevention (August 10, 2021). Insulin Resistance and Diabetes https://www.cdc.gov/diabetes/basics/insulin-resistance.html

U.S. Department of Health & Human Services/Centers for Disease Control and Prevention (December 16, 2021). Type 2 Diabetes https://www.cdc.gov/diabetes/basics/type2.html

Witters, L. A. (2001). The blooming of the French lilac. The Journal of clinical investigation, 108(8), 1105-1107.https://doi.org/10.1172%2FJCI14178


Alzheimers-disease-Pathological-Tau-protein.jpg

Listen to the article here:


Methods used to diagnose Alzheimer’s disease are changing. In the past, the only definitive way to diagnose Alzheimer’s disease was after death, by an autopsy, which is not exactly helpful for treatment. The autopsy would reveal both amyloid plaques and tau tangles in the brain; these are hallmarks that characterize Alzheimer’s disease. Thankfully, science has drastically improved over the years. We currently have spinal fluid tests that look for these two key biomarkers and imaging tests that show changes in the brain.

A recent example of other evolving diagnosis methods is COVID-19. Early in the pandemic, when there were no COVID-19 tests, the only way to know if someone might have the virus was to check for a fever. Nowadays, we look for biomarkers – such as with a rapid antigen test – which can detect antigens to the virus even in asymptomatic people. 

We now understand that a person can be suffering from the progressive nature of Alzheimer’s even if they do not yet show signs of cognitive impairment. Without biomarker testing, most patients’ first symptoms are memory loss, including long and short-term. Alzheimer’s is usually associated with increased age because the biological underpinnings of the disease accumulate over time. Diagnosis can be made by using something called the ATN framework. This framework describes the two major proteins involved, amyloid plaques and tau tangles, and the associated neurodegeneration – changes in the brain structure.


Let’s discuss the AT part of ATN: the two protein accumulations called amyloid plaques and tau tangles. It is no coincidence that these are also the biomarkers sought by scientists and doctors when diagnosing Alzheimer’s. Amyloid plaques are bundles of protein that build up outside of cells in the brain. They disrupt how cells connect and communicate with each other. Tau tangles are proteins found inside the neurons. In a healthy neuron, tau proteins help stabilize the microtubule that transfers nutrients. In Alzheimer’s patients, the tau proteins become corrupted and tangled, blocking the neuron’s transport system. This leads to cell death. As more cells die and neural network connections break down, areas in the brain begin to shrink.  In the late stages of Alzheimer’s disease, there is widespread loss of brain volume.


The N of ATN is neurodegeneration which is the deterioration of neurons causing specific structural changes to the brain. A structural MRI and a radioactive PET scan are two classic methods of determining neurodegeneration. These are effective as staging tools, discovering how far along the disease has progressed. They are effective but can be expensive and time-consuming.

The good news is that researchers are currently working on blood tests that will hopefully be able to detect tau biomarkers quickly and easily. A blood test should be easy, cheap, and relatively simple. With luck, these early biomarker findings will also help drive the effectiveness of clinical therapies, paving the way for better Alzheimer’s treatments in the years to come.

By Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Kandel, E. R., Schwartz, J. H., Jessell, T. M., Siegelbaum, S., Hudspeth, A. J., & Mack, S. (Eds.). (2000). Principles of neural science (Vol. 4, pp. 1149-1159). New York: McGraw-hill.

Largent, E. A., Wexler, A., & Karlawish, J. (2021). The Future Is P-Tau—Anticipating Direct-to-Consumer Alzheimer Disease Blood Tests. JAMA neurology, 78(4), 379-380. https://doi.org/10.1001/jamaneurol.2020.4835

Ossenkoppele, R., Reimand, J., Smith, R., Leuzy, A., Strandberg, O., Palmqvist, S., … & Hansson, O. (2021). Tau PET correlates with different Alzheimer’s disease‐related features compared to CSF and plasma p‐tau biomarkers. EMBO molecular medicine, 13(8), e14398. https://doi.org/10.15252/emmm.202114398

Peterson, R. C. [UCI MIND] (2019, April 3).  Diagnosis of Alzheimer’s disease in the era of biomarkers – Ronald C. Petersen, MD, PhD [Video]. Youtube. https://www.youtube.com/watch?v=KtS5xynes2M

What Happens to the Brain in Alzheimer’s Disease? (2017, May 16) National Institute on Aging. https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease


Kidney-Impariment.jpg

Listen to the article here:


Imagine if your plumbing stopped up. Not your toilets, but your sink and shower. How would you get rid of the dirt and junk off your skin? How would you make sure you stay clean? Our kidneys ask this question every day. The blood in our body travels around and around, including the critical filtration stage of the kidneys. The kidneys act as a big two-way filter. Impurities and excess minerals or water are extracted from the blood, and necessary minerals or water are added as needed. The kidneys keep the ingredients of blood at healthy levels. Finally, kidneys get rid of waste products and extra water by producing urine. When this goes wrong, your blood can’t function properly and waste products can build up.

When dealing with the kidneys, you may see three terms thrown about. The origin of “kidney” is unknown, but likely English. “Renal” is the Latin word for kidneys, and the prefix “nephro-” is Greek in origin. If you see any of these terms you can bet we’re dealing with the kidneys. With this in mind, when the kidneys fail to perform their job, we call it renal insufficiency.

There are two major divisions in how the kidneys fail, based on the amount of time. 

  • Acute kidney injury (AKI) has a sudden onset. It may affect 100,000 people a year in the United States, with a higher proportion of sufferers being Black or African American than White.
  • Chronic kidney disease (CKD) is the long term degradation of the kidneys.  It is harder to measure, as the kidneys do a pretty good job compensating: until they don’t. It is estimated that around 2 million Americans may be suffering from CKD, with the majority being men.

There are several possible causes of renal impairment. The vast majority of causes are “upstream,” meaning something affects the blood before it gets to the kidneys.

In acute cases, this can be hypotension – not enough fluid, some drugs, such as NSAIDs, or organ failure. When there isn’t enough fluid in the bloodstream, the kidneys compensate by releasing more water, which can deplete the kidney’s reserves and cause failure.

In chronic kidney disease, the most frequent cause is diabetes, especially type 2. Prolonged hypertension, and vascular diseases can also be the culprit. With chronic cases, the kidneys will do their best to compensate – constantly filtering out excess blood sugar, for instance. Over time, the excess sugar damages the blood vessels in the kidneys.  Some parts of the kidneys may fail and the remaining portions get stressed and eventually decompensate. This is when the kidney fails as an organ.

Other possible causes of renal impairment are contained in the kidneys and “downstream” blockages. The kidneys themselve can be the victim of disease or injury, possibly due to long term upstream stress. The ability of the kidney to release urine can also -in rare cases – be disrupted.

Regardless of the cause, renal impairment is very dangerous. The kidneys are responsible for keeping blood healthy. A failure of the renal system can result in a need for dialysis or transplant. Dialysis is when external technology filters blood and maintains levels. This is uncomfortable, cumbersome, and expensive.

Fixing renal impairment can be a tall order. The most important step is usually treating the underlying cause. Since the kidneys filter several drugs out of the bloodstream, stopping or replacing them may be key. Fluids may need to be replaced in acute cases, and lifestyle changes may be needed in chronic ones. Maintaining healthy blood sugar levels can be key if the root cause is diabetes. For heavily progressed chronic renal impairment, dialysis or transplant may be the only options.

Transplant and dialysis are not fun, so we should try to avoid renal impairment before it starts. Many of the tactics to keep your kidneys healthy are the same to keep the rest of your body healthy. Exercise, not overindulging on sugar, and keeping your diet under control can help. Additionally, maintaining a healthy blood pressure is vital. Finally, lowering or cutting out tobacco and alcohol can help keep your kidneys healthy.  When it comes to filtering your blood, give your kidneys every advantage you can!

By Benton Lowey-Ball, BS Behavioral Neuroscience



Adapted from:

Bindroo, S., & Rodriguez, Q. BS; Challa, HJ Renal Failure. (February 24, 2022). StatPearls; StatPearls Publishing: Treasure Island, FL, USA. https://www.ncbi.nlm.nih.gov/books/NBK519012/


Human-Heart-EKG.jpg


Heart failure is quite frankly, a terrifying sounding condition. It is severe, but not as immediately drastic as it sounds. Put simply, heart failure is when the heart fails to pump as much blood as the body will need long-term. The heart works like a balloon, filling with blood and contracting to pump it out. Ejection fraction is a term used to describe the amount of blood pumped out compared with the total the heart can hold. In a normal heart, 50-70% of blood is ejected with each heartbeat. When this amount falls below 40%, a person has a reduced Ejection Fraction (the rEF of HFrEF). This is a serious condition.

The heart pumps blood to every cell in the body. This is how cells receive oxygen and nutrients, and how they get rid of waste products. Without enough blood, cells suffocate. Oxygen isn’t reaching cells and the brain interprets this as being short of breath. Common symptoms of HFrEF include:

  • Fatigue
  • Difficulty breathing, especially when lying down or sleeping
  • Inability to exercise
  • Ankle swelling

Inside the body, doctors can also look for diagnostic markers. These may include structural changes to the heart and increased natriuretic peptides. Natriuretic peptides are hormones that regulate the amount of salt and water in the blood. They act as vasodilators, opening blood vessels which can be helpful in compensating for heart failure. The body attempts to compensate for the loss of oxygen and nutrients in the blood in many ways, but long term the body has trouble sustaining with heart failure.

Who is at risk of developing HFrEF? Unfortunately, it is more prevalent in the United States than almost anywhere else, affecting 6.5 million Americans each year. Risk factors include age, being male, obesity, and smoking. Additionally, other medical conditions increase your risk of developing Heart Failure with reduced Ejection Fraction. Previous heart attacks, coronary heart disease, diabetes, and hypertension are some associated conditions. All told, HFrEF leads to around a million hospitalizations every year, and being hospitalized for HFrEF comes with a low 5-year survival rate.

What can be done? There are several methods of dealing with a reduced ejection fraction. Some methods treat symptoms, such as diuretics, and others can help reduce mortality, such as beta-blockers. There are several other medications and even some implantable devices that can help with HFrEF. These can help improve your ejection fraction or health outcomes but are not yet a silver bullet. New medications with increased outcomes and fewer side effects are entering clinical trials and may help with the underlying condition. To learn more about current heart failure research options, call our office today.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Bloom, M. W., Greenberg, B., Jaarsma, T., Januzzi, J. L., Lam, C. S., Maggioni, A. P., … & Butler, J. (2017). Heart failure with reduced ejection fraction. Nature reviews Disease primers, 3(1), 1-19. https://www.nature.com/articles/nrdp201758

Martinez-Rumayor, A., Richards, A. M., Burnett, J. C., & Januzzi Jr, J. L. (2008). Biology of the natriuretic peptides. The American journal of cardiology, 101(3), S3-S8. https://doi.org/10.1016/j.amjcard.2007.11.012

Murphy, S. P., Ibrahim, N. E., & Januzzi, J. L. (2020). Heart failure with reduced ejection fraction: a review. Jama, 324(5), 488-504. https://doi.org/10.1001/jama.2020.10262


Diet-and-Exercise-May-Not-Be-Able-to-Help-With-This-Inherited-Cardiovascular-Risk-Factor.jpg


If someone in your family had a heart attack or stroke before the age of 60, you could be at risk and might want to have your blood tested for this little-known hereditary risk factor, Lp(a). Cardiovascular disease remains the leading cause of death in the United States, even during the COVID-19 pandemic. Determining and reducing the risk factors for cardiovascular disease is critical. 

Lipoprotein(a), also called Lp(a), pronounced “LP Little a” is a particularly dangerous culprit.  Its levels are controlled by a single gene, and a single genetic variation in this gene is enough to drastically change Lp(a) levels. Unfortunately, since it is genetically determined, diet, exercise, and lifestyle have little or no effect on Lp(a) levels. High Lp(a) can contribute to several cardiovascular conditions. These include a two to three times increase in the risk of developing:

  • Coronary heart disease
  • Peripheral heart disease
  • Aortic valve stenosis
  • Ischemic stroke

Lp(a) has been referred to as the evil twin of the more familiar LDL (bad) cholesterol and is a triple threat because it is:

  1. Pro-atherogenic:  higher risk fatty deposits in the walls of arteries
  2. Pro-thrombotic:  promotes blood clots
  3. Pro-inflammatory:  inflammation is an important risk of cardiovascular disease

There are two methods of measuring Lp(a).  The most common method of measuring Lp(a) is by mass, in mg/dL. Measuring how many individual particles, regardless of size, is another method and is measured in nmol/L. It is important to know which method was used when understanding your numbers. If you have never had your Lp(a) level checked, we offer Lp(a) testing to our ENCORE community for those who pre-qualify (call for details). 

Currently, there are no approved therapies to lower Lp(a) levels and reduce one’s risk.  However, three exciting therapies are currently being studied in clinical trials at ENCORE Research Group sites across Florida. The good news is that because of clinical research and your involvement, we have new treatments for elevated Lp(a) on the horizon!

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Sources:

Kamstrup, P. R. (2021). Lipoprotein (a) and cardiovascular disease. Clinical chemistry, 67(1), 154-166. https://doi.org/10.1093/clinchem/hvaa247

Miksenas, H., Januzzi, J. L., & Natarajan, P. (2021). Lipoprotein (a) and cardiovascular diseases. JAMA, 326(4), 352-353. doi:10.1001/jama.2021.3632

Health.harvard.edu

Amgenscience.com


Why-you-should-cosider-getting-a-fibroscan.jpg


Fatty liver disease is incredibly prevalent in the United States. Some estimates place the number of Americans with non-alcoholic fatty liver at over 30%, that’s around 100 million people in this country! Liver diseases are deadly serious; the liver is a critical organ and without it we cannot survive. The biggest problem with all liver diseases is that they frequently progress without symptoms. Because of this, the disease may progress to a dangerous or irreversible stage before it is even detected. Clearly, early, and routine testing for people at risk is critical.

We can’t see the liver from the outside, so the only way to learn about how it is doing is by looking at it. We can look through the skin using technology or under a microscope using a biopsy.

A biopsy – looking at a section of the liver under the microscope – is the “gold standard” of liver diagnostic techniques. This has drawbacks, however. Patients typically need to dedicate half a day to the procedure, and there can be rare complications. A biopsy is an invasive procedure requiring a piece of the liver be taken and examined. It is a critical piece of the liver diagnosis pie but is not a routine procedure to be done without cause.

Imagining techniques can be very effective in diagnosing a fatty liver. Some techniques, such as a CAT scan and ultrasound, can’t diagnose the amount of scarring on the liver but can give an indication that there is fat present. CAT scans use x-rays, but imaging is otherwise safe. An ultrasound is fast and non-invasive. It is an excellent first step that many doctors use when they suspect a fatty liver. Magnetic Resonance Imaging (MRI) is the next best diagnostic procedure to a liver biopsy. With an MRI, doctors can clearly see the state of the liver. They are expensive, however. This again means they are an excellent tool for those who are known to have fatty liver but may not be an option for all patients to use regularly.

Ultrasonic elastography is a different technique. It is commonly called Fibroscan, after the manufacturer of the diagnostic tool. Fibroscan uses sound waves to gently shake the liver and measure how it responds. The liver will stretch slightly. In a healthy liver, the tissue stretches more, but hard scar tissue is less elastic. The fibroscan can interpret the difference and determine how much fat and scar tissue is present. The test is very similar to an ultrasound; it is painless, fast, and safe. The fibroscan does not replace other imaging techniques but is cheap and effective at determining the stage of fatty liver present. Unlike other techniques, a Fibroscan can be done routinely for anyone who is at risk of having fatty liver.

Fibroscans are very popular around the world, including in Europe, Asia, South America, and Canada. It is a cheap procedure with little reimbursement for practitioners, which unfortunately prevents widespread use in the USA. Risk factors for non-alcoholic fatty liver include being overweight or obese, being prediabetic or having diabetes, and eating a high-fat diet. If you are concerned about fatty liver, talk to your primary care physician and/or contact ENCORE Research Group for a complimentary Fibroscan.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



Afdhal, N. H. (2012). Fibroscan (transient elastography) for the measurement of liver fibrosis. Gastroenterology & hepatology, 8(9), 605.

Koren, M. (Host). (2022, July 20). Common fibroscan technology questions [Audio podcast episode]. In Medevidence! Truth behind the data. ENCORE Research Group. https://encoredocs.com/medevidence/

Koren, M. (Host). (2022, July 13). You cannot live without your liver [Audio podcast episode]. In Medevidence! Truth behind the data. ENCORE Research Group. https://encoredocs.com/medevidence


Metabolic-Syndrome-When-Fat-Fights-Back.jpg


Metabolic syndrome is a cluster of conditions which have been slowly rising in people in the United States. It is also known as insulin resistance syndrome.

It is currently defined as three of the following conditions:

  • Excess fat around the waist
  • High plasma glucose concentration
  • High blood pressure
  • High triglycerides
  • Low levels of good cholesterol or HDL 

Having one of these conditions does not mean that you have metabolic syndrome. Having three or more of these conditions will result in a diagnosis of metabolic syndrome and will increase your risk of health complications.  If left untreated, metabolic syndrome can lead to heart disease, Type 2 diabetes, and stroke. 

Metabolic syndrome is incredibly prevalent – affecting over one-third of Americans. Hispanic adults are at the highest risk. Among non-Hispanic adults, white men and black women are at higher risk than other groups. Other risk factors include lifestyle, age, family history, and use of some medications. Similar conditions may increase the chances of getting metabolic syndrome. These include being overweight or obese, immune system and sleep problems, and PCOS. Unfortunately, these risk factors overlap with the symptoms. This implies that metabolic syndrome may spiral and get worse over time.

The exact mechanism of metabolic syndrome is unknown, but scientists have an idea of what is to blame. It may be insulin resistance, dysfunctional fat cells, inflammation, and oxidative stress. Insulin resistance causes the cells to store sugars instead of using them. This makes cells (and people) tired and increases fat. Fat cells may become overactive and grow so large that they die, prompting an immune response. The immune system may cause inflammation and plaque build ups in the bloodstream. Inflammation can further cause skin problems and long-term damage.

While it sounds like this is all the fault of insulin resistance, it is not that clear cut. There may be many pathways into metabolic syndrome. Inflammation can be caused directly through a dysfunctional molecule responsible for fighting tumors. The liver has an important role in guiding the insulin response of the body. Obesity can cause oxidative stress that damages fat cells. Several other processes can interrupt these systems. Additionally, each symptom can increase the risk of developing others.

So what can we do about metabolic syndrome? There are no approved medications to cure the underlying condition. For medical solutions, doctors may prescribe symptomatic treatments. These treat the parts of metabolic syndrome that we can diagnose: high triglycerides, cholesterol, and hypertension. 

Currently, our best way to fight metabolic syndrome is through diet and exercise. This may seem overwhelming to some people and making solid changes takes time. Instead of exercise, many need to think of movement.  Movement can look like walking in the neighborhood, gardening, housecleaning, or anything that gets you moving, gets your heart rate up and is something you enjoy. 

Changes in other lifestyle choices may include consuming less sugar and sugary drinks, cutting out smoking and drinking, and getting regular sleep! Lack of appropriate sleep can increase your appetite for high-calorie foods due to hormonal changes.  There are two hormones that make you hungry or full.  Ghrelin is the hormone that increases your appetite and makes you crave food.  Leptin is the hormone that makes you feel full with little appetite.  These hormones can become unbalanced with lack of sleep, leading to negative changes in appetite.

There is no silver bullet for everyone, but it’s a good start to take steps towards healthier lifestyle changes.

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



References:

McCracken, E., Monaghan, M., & Sreenivasan, S. (2018). Pathophysiology of the metabolic syndrome. Clinics in dermatology, 36(1), 14-20. https://doi.org/10.1016/j.clindermatol.2017.09.004

Moore, J. X., Chaudhary, N., & Akinyemiju, T. (2017). Peer reviewed: Metabolic syndrome prevalence by race/ethnicity and sex in the United States, National Health and Nutrition Examination Survey, 1988–2012. Preventing chronic disease, 14.

Zimmet, P., Alberti, K. G. M. M., Stern, N., Bilu, C., El‐Osta, A., Einat, H., & Kronfeld‐Schor, N. (2019). The Circadian Syndrome: is the Metabolic Syndrome and much more!. Journal of internal medicine, 286(2), 181-191. https://onlinelibrary.wiley.com/doi/full/10.1111/joim.12924


vaccines-2.jpg

Listen to the article here:


With flu season on the horizon, reviewing the vaccine pathway and how we got to where is worthwhile. We have an amazing and complex immune system. It has several specialized cells, but detection is the first line of an immune response. Detecting a harmful organism that has invaded the body can be surprisingly tricky. This is because cells have to chemically discover specific proteins or sugars on the outside of pathogens. These proteins or sugars can (and do) mutate in quickly-replicating pathogens. Luckily, our immune system can learn the danger of closely-related pathogens. 

Vaccines have a long and storied history. From the first records of vaccines in China hundreds of years ago to the first inoculation against smallpox (using cowpox) to today’s cutting-edge mRNA vaccines, the technology is constantly improving. Here are some of the major ways vaccines are made:

Use a weak virus

The cowpox-smallpox vaccine was an example of a live, whole-pathogen vaccine. This is a type of vaccine where doctors inject small amounts of live viruses into the body. The body responds and becomes inoculated against large doses of the virus in the wild. In the 1950’s live-attenuated vaccines became available. In these, the virus is weakened in a lab so it does not cause serious disease in people. This type of vaccine provides a strong and long-lasting response. Examples of live attenuated vaccines include measles, mumps, and rubella vaccine (MMR), smallpox, chickenpox, and yellow fever. 

Use a dead pathogen

There are other methods to mitigate the problems of live viruses. An inactivated vaccine uses dead virus or bacteria. This makes the vaccine much safer and comes with fewer side effects, but is less effective. The current yearly flu vaccines are inactivated vaccines. Some manufacturers use hen’s eggs to grow the vaccine before inactivation. The resulting vaccine can contain very small amounts of egg protein as a result. The CDC still recommends those with egg allergies get the flu vaccine.

Use part of a virus or bacteria

Subunit vaccines are pieces of a pathogen – generally protein or sugar pieces. These aren’t whole viruses and have fewer side effects as a result. Additionally, these subunits may be able to grant protection against many forms of a pathogen. The Hepatitis B vaccine is an example of a protein subunit vaccine.

Target a dangerous product

Toxoid vaccines such as DPT can help lessen the damage of infection because some bacteria do their damage by releasing dangerous toxins instead of attacking cells. Toxoid vaccines train the body to recognize these toxins as dangerous. Diphtheria and tetanus vaccines are examples of toxoid vaccines. 

Get the body to do the work

Nucleic acid vaccines are a new and different approach that has many benefits. Instead of using a weakened or inactivated pathogen to trigger our immune system, nucleic acid vaccines employ the body to make the vaccines in house. DNA, mRNA, and vector virus vaccines use genetic code created in a laboratory; there is no virus needed to develop the vaccine. Messenger RNA (mRNA) vaccines are the best known and use mRNA, a blueprint for creating specific proteins. When injected into the body, they provide the instructions for our body to produce antigens (proteins) that trigger an immune response. The T-cell and antibody response that follows can fight the disease. This can provide long-lasting, stable, relatively low symptom responses. The real benefit, however, is the time it takes to develop a new vaccine is drastically reduced. This was evident with COVID-19, when researchers created a brand-new vaccine in less than a year. Equally important was distributing it to hundreds of millions of people one year after. A typical vaccine takes 10-15 years to develop – and even longer to scale production.

New studies are coming to compare the effectiveness of mRNA-based vaccines to inactivated vaccines for viruses and diseases beyond covid. Keep a lookout to join this new and developing vaccine research. 

Written by Benton Lowey-Ball, BS Behavioral Neuroscience



References:

NIH, National Institute of Allergy and Infectious Diseases. (2021). Flu vaccine and people with egg allergies. https://www.cdc.gov/flu/prevent/egg-allergies.htm

NIH, National Institute of Allergy and Infectious Diseases. (2019). Vaccine types. https://www.niaid.nih.gov/research/vaccine-types

Greenwood, B. (2014). The contribution of vaccination to global health: past, present and future. Philosophical Transactions of the Royal Society B: Biological Sciences, 369(1645), 20130433.

Boylston, A. (2012). The origins of inoculation. Journal of the Royal Society of Medicine, 105(7), 309-313.


Whats-Being-Done-to-Increase-Clinical-Trial-Diversity.jpg


Earlier this year, a bipartisan bill was introduced in the US congress to increase diversity in clinical research trials. The DEPICT act, as it’s called, has many major changes to how clinical trials would be conducted. These changes would affect sponsors, the government, and clinical research sites. Sponsors are the companies which develop new drugs and devices in clinical trials.

The bill would require new demographic analyses for drug and device trials by sponsors. Demographic data includes age, sex, race, and ethnicity. Sponsors would investigate the rates of a disease among demographic groups before starting a trial. They would then devise a diversity action plan. This ensures the clinical trial includes a representative sample of the affected population. Let’s say a drug targeted lung cancer, for example. The sponsor would have to find out who has increased chances of getting lung cancer. If they found that Black Americans were at higher risk, they would make a plan to ensure this group was included in any research trials. Plans could include community outreach, specific site selection, and diversity training.

A key aspect of the bill is discovering how to best reach diverse communities. Research sponsors would need to submit annual reports. These would outline how successful their studies were at reaching the demographic goals. If they failed to meet goals, they would give possible reasons they did not. The Food and Drug Administration (FDA) would compile and analyze the reports. The FDA would issue public reports on diversity and enrollment targets. They would also publish justifications for failure to meet targets and recommendations to solve this. Additionally, the National Institute of Health (NIH) would provide outreach. For sponsors, they would issue best practices for increasing diversity. They would engage with minorities to bring awareness of clinical research trials. They would also help local organizations inform their community about research trials.

The final piece of the bill is increasing access. The bill would enhance clinical research infrastructure in underserved communities. The bill provides grants to expand clinical research facilities. These would be in rural areas, on Indian tribal lands, and in federally recognized underserved communities. The grants would help facilities conduct research trials in these areas.

Altogether, this bill addresses the shortcomings of clinical trials in diverse communities. It closes the gap between who suffers from medical conditions and who participates in clinical research trials. It helps find out which methods increase clinical trial diversity. It also helps expand access to clinical trials in underserved communities. There is still a long way to go before this bill makes it to the voting floor, but it’s a good step.

Written by: Benton Lowey-Ball, B.S. Behavioral Neuroscience



Source:

Text – H.R.6584 – 117th Congress (2021-2022): DEPICT Act. (2022, February 3). https://www.congress.gov/bill/117th-congress/house-bill/6584/text


The-Fight-Against-Hypertension.jpg

Listen to the article here:


Hypertension is one of the most prevalent conditions on the planet. Scientists estimate that it affects 30-45% of adults, somewhere over a billion people! Hypertension is the chronic elevation of blood pressure. The CDC defines it as above 130 mmHg systolic or above 80 mmHg diastolic. For short periods of time, elevated blood pressure can be useful – for exercise, say. People can have high blood pressure for years without symptoms. For long periods of time, however, hypertension is deadly serious. Unfortunately, living with high blood pressure can lead to a host of problems. Hypertension can lead to heart attack and stroke, and damage to the heart, brain, kidneys, and even eyes!       

Everyone is at risk of high blood pressure. In America, men have a higher likelihood of hypertension. There are also differences in ethnicity and race, non-Hispanic Black or African American adults are at the highest risk. Unfortunately, even the lowest risk categories still have around a 40% prevalence of high blood pressure. Clearly this is a large issue in America and around the world.           

The big culprit behind hypertension is the Renin–angiotensin–aldosterone system (RAAS). RAAS is a critical system for maintaining blood pressure. It regulates two primary factors: the amount of blood and how constricted blood vessels are. It does this through the kidney, liver, and adrenal gland (just above the kidneys). In response to body signals, the kidneys release an enzyme to the liver. In response, the liver produces the hormone angiotensin I. Another enzyme, angiotensin-converting enzyme (ACE) converts this to angiotensin II, which goes to work.  

Angiotensin II has wide-ranging effects to increase sodium and water retention. It also causes blood vessels to constrict. Angiotensin II is very short-lived, only lasting 1-2 minutes. One of its many effects is to get the adrenal gland to produce aldosterone. Aldosterone has similar effects as angiotensin II, but instead of a few minutes, it takes hours or days to take effect. The end result is that two major hormones – one fast-acting and one slow-acting – cause high blood pressure.          

There are many medications available to fight hypertension. Most of these, such as diuretics or beta-blockers, have wide-ranging side effects. This is because they are system-wide, indiscriminate actors on the body. Beta-blockers, for instance, slow the heart. This is helpful in lowering blood pressure but obviously leads to other effects on the body. RAAS-acting specific medications may be more helpful in combating hypertension with minimal side effects. ACE inhibitors, for instance, stop the fast-acting angiotensin II from having its effect on the body. This targeted approach to hypertension can lead to fewer side effects in some patients. Unfortunately, by acting on only the fast-acting portion of RAAS, they must be taken daily. Even worse, a few missed doses can have longer-term effects on blood pressure. Luckily, researchers are investigating other targeted methods of reducing the effect of RAAS, and blood pressure! Keep an eye out for a clinical research study to help investigate this exciting part of the fight against hypertension.

Written by: Benton Lowey-Ball, B.S. Behavioral Neuroscience



Sources

Fountain, J. H., & Lappin, S. L. (2017). Physiology, renin angiotensin system.

National Center for Chronic Disease Prevention and Health Promotion, Division for Heart Disease and Stroke Prevention. (September 27, 2027). Facts about hypertension. U.S. Department of Health and Human Services. https://www.cdc.gov/bloodpressure/facts.htm


Celiac-Disease-Article.jpg


Celiac disease is one of the major health issues on our planet, affecting around 1% of the population (that’s about 80 million people!). Celiac disease is more likely to occur in females. Though onset can occur at any age, it is most likely to be discovered around age two or during young adulthood.

Celiac disease is commonly known as gluten intolerance and is classically characterized by its gastrointestinal symptoms including diarrhea, loss of appetite, weight loss, and other digestive issues. Additionally, there are other symptoms that are unrelated to the digestive system. These include anemia, bone density issues, neurological symptoms, skin rash, and more. Together these make for a severe detriment in the quality of life of most celiac sufferers.

Like most autoimmune disorders, the leading symptoms come from the body’s immune system overreacting and causing damage. Celiac disease is unusual in that the reason for the immune response is gluten, which we eat. Gluten is a structural protein found in wheat, rye, barley, spelt, and kamut. Gluten isn’t fully digestible, and some intact protein pieces make it through the stomach into the intestines. In celiac patients, the protein pieces cross the intestinal lining and are mistaken for dangerous particles or microorganisms. This can trick the immune system into action, causing inflammation and damage.

The number of people with celiac disease has been growing significantly. Five times as many people had the condition in 2000, compared with 1975. Scientists are still unsure why the disease has been growing worldwide. Better clinical testing, a spread of high gluten Mediterranean diets, and new varieties of grain are leading theories. Scientists have been able to discover much of the underlying mechanism of how celiac disease occurs, thankfully. It is genetic, and the key player appears to be HLA-DQ2 or HLA-DQ8 antigens which mistake gluten for danger. The presence of HLA-DQ2/DQ8 isn’t enough to guarantee celiac disease, but it is required. Additional contributors are thought to be other genes, environmental factors, and gut microbiota. Regardless, 95% of celiac patients have one of these dangerous antigens.

Currently, the only treatment for celiac is a strict gluten-free diet. This can be difficult to maintain, and even with a gluten-free diet, some patients continue to have symptoms. Additionally, contaminants can be unknowingly present in food and even low amounts of gluten can cause a resurgence of symptoms. Scientists are looking for new ways to combat this disease and participating in clinical trials is the best way that you can help move celiac disease medicine forward.

Written by: Benton Lowey-Ball, B.S. Behavioral Neuroscience



Source:

Caio, G., Volta, U., Sapone, A., Leffler, D. A., De Giorgio, R., Catassi, C., & Fasano, A. (2019). Celiac disease: a comprehensive current review. BMC medicine, 17(1), 1-20.




MedEvidence! Radio is a monthly live broadcast from WSOS 103.9 FM / 1170 AM with Kevin Geddings and Dr. Michael Koren. This month’s MedEvidence Radio discusses Damar Hamlin’s cardiac event during a football game on January 2, 2023.

We will dive into the following:
🩺 Commotio cordis
🩺 Hypertrophic Cardiomyopathy
🩺 Atrial Fibrillation
❤️ Cardiovascular Health
🔬 Clinical Research Trials

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals.  Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.  On a personal note, Dr. Koren has a lifelong interest in history, technology, Public Health, and music. He has written two musical plays.


Listen to the full episode here:




MedEvidence! Radio is a monthly live broadcast from WSOS 103.9 FM / 1170 AM with Kevin Geddings and Dr. Michael Koren from St. Augustine, Florida. This month’s MedEvidence Radio discusses the diabetic epidemic in the US.

We will dive into:
💉GLP-1 Drug Class
💉SGLT2i Drug Class
💉Newer Class of Diabetic Drugs
❤️Cardiovascular Safety
🔬 Past and New Clinical Research Trials

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals.  Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.  On a personal note, Dr. Koren has a lifelong interest in history, technology, Public Health, and music. He has written two musical plays.


Listen to the full episode here:




On this month’s MedEvidence radio episode, Doctors Michael Koren, MD, Matthew Todd Braddock, DO, Jackson Downey, MD, Albert Lopez, DO and WSOS Radio Host Kevin Geddings discuss NASH, Fatty Liver, and Fibroscans.

This month’s MedEvidence! Radio will answer:

  • What is NASH?
  • What are the stages of NASH?
  • How do you treat NASH?
  • Is NASH reversible?
  • Is NASH related to cholesterol problems?

MedEvidence! Radio is a monthly live broadcast from WSOS 103.9 FM / 1170 AM with Kevin Geddings from St. Augustine, Florida. Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals.  Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.  On a personal note, Dr. Koren has a lifelong interest in history, technology, Public Health, and music. He has written two musical plays.


Listen to the full episode here:




Clinical Trials Day is celebrated around the world in May to recognize the day that James Lind started what is often considered the first clinical trial aboard a ship on May 20, 1747.

Here’s the story…

Also included in this month’s MedEvidence! Radio

  • Why we do Clinical Trials
  • Phases of Clinical Trials
  • Why you may want to participate in clinical trials

MedEvidence! Radio is a monthly live broadcast from WSOS 103.9 FM / 1170 AM with Kevin Geddings from St. Augustine, Florida. Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals.  Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.  On a personal note, Dr. Koren has a life-long interest in history, technology, Public Health, and music. He has written two musical plays.


Listen to the full episode here:





Dr. Michael Koren sits down with his middle school buddy, Mick LaSalle, a well-known film critic, to discuss changes in the direction of medicine & media. Their “Staten Island humor” is evident as they talk about how the media markets medicine from aspirin to covid, what the media says vs. what the medical data proves.

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Mick LaSalle, film critic for The San Francisco Chronicle and former on-air film critic for the ABC-TV affiliate in San Francisco, KGO. He is the author of Complicated Women: Sex and Power in Pre-Code Hollywood (2000), Dangerous Men: Pre-Code Hollywood and the Birth of the Modern Man (2002); The Beauty of the Real: What Hollywood Can Learn from Contemporary French Actresses (2012); and Dream State: California in the Movies (2021).  With Leba Hertz, he hosted the Mick LaSalle podcast between 2005 and 2010. He wrote and co-produced the Complicated Women documentary for Turner Classic Movies, which Jane Fonda narrated. He has also written introductions to several books, including The Enduring Star, Peter Cowie’s biography of Joan Crawford (Rizzoli, 2009). He met Dr. Michael Koren in Middle School during the 1970s.


Prefer to listen to the podcast without video? You can do that below!








Brad Hightower, the founder of Hightower Clinical, clinical research professional, and host of the Note to File podcast, sits down with Dr. Michael Koren to discuss clinical research as a care option, decentralized clinical trials, and clinical research technology and data collection using EMRs and CTMS such as Clinasyst.

Michael J. Koren, MD, is a practicing cardiologist and Chief Executive Officer at Jacksonville Center for Clinical Research, which conducts clinical trials at 7 locations in Florida. He received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine and fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.

He is a fellow of the American College of Cardiology, fellow and two-time president of the Academy of Physicians in Clinical Research, and the regional chapter of the American Heart Association.

Dr. Koren has served as an Investigator in over 2,000 trials and as the international lead investigator for many multi-centered trials, including ALLIANCE, ROLE, TREAT to TARGET, OSLER, and MENDEL studies. He has written and co-authored over 100 peer-reviewed articles and been published in the most prestigious medical journals. Dr. Koren has also designed a research training course for physicians, now in its 20th year.

On a personal note, Dr. Koren developed a lifelong interest in technology and Public Health during his time at The Massachusetts Institute of Technology and The Harvard School of Public Health. He also loves music. He has written two musical plays.

Brad Hightower, founder of Hightower Clinical, clinical research professional, and host of the Note to File podcast. Brad lives, works, and podcasts from Oklahoma City, OK.  He has worked at the site level in clinical research for ten years and is the former Executive Director of the Oklahoma Heart Hospital Research Foundation.  Brad has since started his own integrated site network, Hightower Clinical.
To learn more about Hightower Clinical, please visit hightowerclinical.com.
To connect with Brad, please reach out on LinkedIn.





The Next Generation of Clinical Researchers series concludes with a discussion of research outreach, research ambassadors, and the value of educating the community about clinical research to help advance medicine and healthcare for all.

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Adrian Rowda, a second-generation clinical researcher, graduated from Jacksonville University in 2008 with a BSN. Followed by working as a nurse in Mayo Clinic’s Surgical Intensive Care Unit and ED for 6 years.  In 2014 she graduated from Jacksonville University with her MSN as a Family Nurse Practitioner and began working at UF Health in their Trauma/Surgical Intensive Care Unit for 3 years.  Since 2017 she has been with Baptist Medical Center in their Neuro Intensive Care Unit.


Prefer to listen to the podcast without video? You can do that below!







Episode three in the MedEvidence series, The Next Generation of Clinical Researchers discusses patients’ value propositions for the next generation as spoken by a second-generation researcher.

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Adrian Rowda, a second-generation clinical researcher, graduated from Jacksonville University in 2008 with a BSN. Followed by working as a nurse in Mayo Clinic’s Surgical Intensive Care Unit and ED for 6 years.  In 2014 she graduated from Jacksonville University with her MSN as a Family Nurse Practitioner and began working at UF Health in their Trauma/Surgical Intensive Care Unit for 3 years.  Since 2017 she has been with Baptist Medical Center in their Neuro Intensive Care Unit.


Prefer to listen to the podcast without video? You can do that below!







What characteristics, quality & attributes are needed for the Next Generation of Clinical Researchers? Listen in as the current, future & second-generation of researchers discuss this topic and share personal stories.

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Adrian Rowda, a second-generation clinical researcher, graduated from Jacksonville University in 2008 with a BSN. Followed by working as a nurse in Mayo Clinic’s Surgical Intensive Care Unit and ED for 6 years.  In 2014 she graduated from Jacksonville University with her MSN as a Family Nurse Practitioner and began working at UF Health in their Trauma/Surgical Intensive Care Unit for 3 years.  Since 2017 she has been with Baptist Medical Center in their Neuro Intensive Care Unit.


Prefer to listen to the podcast without video? You can do that below!







Listen in on the new MedEvidence series, The Next Generation of Clinical Researchers, to learn how research transfers knowledge from generation to generation as spoken by a second-generation researcher.

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Adrian Rowda, a second-generation clinical researcher, graduated from Jacksonville University in 2008 with a BSN. Followed by working as a nurse in Mayo Clinic’s Surgical Intensive Care Unit and ED for 6 years.  In 2014 she graduated from Jacksonville University with her MSN as a Family Nurse Practitioner and began working at UF Health in their Trauma/Surgical Intensive Care Unit for 3 years.  Since 2017 she has been with Baptist Medical Center in their Neuro Intensive Care Unit.


Prefer to listen to the podcast without video? You can do that below!







The MedEvidence Diabetes series concludes with managing individual patients’ diabetic needs with anecdotes and stories by Dr. Koren and Sharon Smith.

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Sharon Smith, RN, CDCES, is the VP of Recruitment at ENCORE Research Group and a Diabetic Educational Nurse with a passion for educating patients as well as staff on healthy lifestyle options without giving up on special treats.


Prefer to listen to the podcast without video? You can do that below!







In part 3 of the MedEvidence Diabetes series Dr. Koren and Sharon Smith discuss choosing drug classes for diabetes, weight loss and cardiovascular health.

💉GLP-1 Drug Class
💉SGLT2i Drug Class
🔬 Past and New Clinical Research Trials

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Sharon Smith, RN, CDCES, is the VP of Recruitment at ENCORE Research Group and a Diabetic Educational Nurse with a passion for educating patients as well as staff on healthy lifestyle options without giving up on special treats.


Prefer to listen to the podcast without video? You can do that below!







What does a diabetic educational nurse want you to know about blood sugars, and what is a cardiovascular doctor doing in the diabetes space? Let’s find out! In part 2 of the MedEvidence diabetes series, Dr. Michael Koren and Sharon Smith will discuss:

🩺  4 Main Components of Type 2 Diabetes Care
💉  Newer Classes of Diabetic Drugs
❤️  Cardiovascular Safety
🔬  New and Past Clinical Research Trials

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Sharon Smith, RN, CDCES, is the VP of Recruitment at ENCORE Research Group and a Diabetic Educational Nurse with a passion for educating patients as well as staff on healthy lifestyle options without giving up on special treats.


Prefer to listen to the podcast without video? You can do that below!







In honor of American Diabetes Month, we are releasing the MedEvidence! Diabetes series. In this episode, Dr. Michael Koren and Diabetic Nurse Educator, Sharon Smith explain the basics of diabetes and the history of diabetic drugs.

In this issue, you will learn:
🩺Type 1 vs Type 2

💉History of Diabetic Drugs

❤️Cardiovascular Safety

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!






MedEvidence Radio is a monthly live broadcast from WSOS 103.9 FM / 1170 AM with Kevin Geddings and Dr. Michael Koren from St. Augustine, Florida. This month’s MedEvidence Radio discusses all the various viruses coming our way this season.

We will dive into:

  • RSV – Respiratory Syncytial Virus
  • COVID
  • Flu
  • Developing a virus strategy plan
  • Vaccine effects
  • Antibody levels

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!





MedEvidence! Radio is a monthly live broadcast from WSOS 103.9 FM / 1170 AM with Kevin Geddings and Dr. Michael Koren from St. Augustine, Florida. This month, Dr. Erich Schramm joins the conversation in discussing whether patients benefit from clinical research and, if so how?

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Erich Schramm, MD, is a board-certified family physician in Ponte Vedra, Florida, with 22 years of experience. He is currently a principal investigator with ENCORE Research Group.


Prefer to listen to the podcast without video? You can do that below!





This week’s MedEvidence podcast concludes with episode 4 of our series about MedEvidence. Dr. Koren explains the passion, goals, and need for MedEvidence a trusted resource at a time when the world is filled with misinformation.  Meet the team behind MedEvidence, where we learn how medical truths are found. What hypothesis testing is, the history of finding truth through research, and Dr. Koren’s founding of  Jacksonville Center for Clinical Research.

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.




This week’s MedEvidence podcast continues with episode 3, where we learn how medical truths are found. What hypothesis testing is, the history of finding truth through research, and Dr. Koren’s founding of  Jacksonville Center for Clinical Research.

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.




This week’s MedEvidence podcast continues with episode 2, where we learn a little personal history about our founder, Dr. Michael Koren. From the gas attendant’s son to Harvard Medical School to ENCORE Research Group, who is the man behind the white coat?

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.




This MedEvidence podcast is a four-part series. MedEvidence, What Is It and Why Does the World Need It?  Michelle McCormick asked Dr. Michael Koren why he created MedEvidence and why it’s so important in a world filled with misinformation.

You will learn how MedEvidence will:

  • MedEvidence is a truth-based interface to help people make medical decisions
  • How MedEvidence will help you understand confusing claims in medical news
  • Help you decipher medical scenarios that are difficult to sort through
  • Learn more about Clinical Research

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.




This week’s MedEvidence podcast is on Medical Marijuana. Meet Dr. Charlie Booras, former Principal Investigator at Jacksonville Center of Clinical Research, and Baptist Primary Care physician who grew his practice into Booras MD as a tribute to his father after treating his ALS with medical cannabis as a medication. Dr. Michael Koren and Dr. Booras dive into the scientific basis for the efficacy of medical cannabis.

You will learn:

        • Florida Medical Marijuana Law and Process
        • THC vs. CBD
        • Health Benefits for Medical Marijuana
        • History of Marijuana
        • Learn more about Clinical Research
        • Learn more about BoorasMD

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!






This week’s MedEvidence podcast is the second episode in a two-part series on Liquid Biopsy.

In this 24-minute episode Doctors, Michael Koren and Bharat Misra discuss liquid biopsy usage now & in the future of medical evaluations.

You will learn:

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Bharat Misra is the Medical Director of ENCORE Borland Groover Clinical Research and has been a Principal Investigator of numerous clinical trials. He also serves on the board of directors at Memorial Hospital and Jacksonville Center for Clinical Research in Jacksonville, Florida. He completed his residency in internal medicine and fellowship in gastroenterology at the Nassau University Medical Center, State University of New York, and his Bachelor of Medicine and Bachelor of Surgery from Gandhi Medical College in India.


Prefer to listen to the podcast without video? You can do that below!





This week’s MedEvidence podcast is a two-part series on Liquid Biopsy: What is it & Do I Need One?

In this 22-minute episode Doctors, Michael Koren and Bharat Misra explain liquid biopsies and conditions that are subject to evaluations with liquid biopsies.

You will learn

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Bharat Misra is the Medical Director of ENCORE Borland Groover Clinical Research and has been a Principal Investigator of numerous clinical trials. He also serves on the board of directors at Memorial Hospital and Jacksonville Center for Clinical Research in Jacksonville, Florida. He completed his residency in internal medicine and fellowship in gastroenterology at the Nassau University Medical Center, State University of New York, and his Bachelor of Medicine and Bachelor of Surgery from Gandhi Medical College in India.


Prefer to listen to the podcast without video? You can do that below!





“What’s New with the Flu?”  Dr. Michael Koren, Dr. Victoria Helow, and Michelle McCormick discuss Flu and COVID.

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Victoria Helow, is a well-respected pediatrician, clinical research investigator at ENCORE Research Group, and practicing emergency room physician.


Prefer to listen to the podcast without video? You can do that below!





Wrapping up this month’s MedEvidence! podcast series on “What to do after a Heart Attack or Stroke?”  Doctors, Michael Koren and Albert Lopez, DO discuss treatments, medications, and clinical research you need to know as a post-heart event patient.

You will learn:

  • Treatment therapies to use after a heart attack or stroke
  • What is Lp(a)
  • Male vs Female Symptoms
  • Cardiovascular Disease Research

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Albert Lopez, DO practices Internal Medicine with Millennium Physician Group in Jacksonville, Florida. He is also a Principal Investigator with ENCORE Research Group specializing in lipid clinical trials. Dr. Lopez, DO completed his residency at the University of Pennsylvania and his Doctor of Osteopathic Medicine at Nova Southeastern University in Miami, Florida. He is known as one of the earliest evidence-based physicians in Jacksonville utilizing nutrition and lifestyle for disease prevention.
I believe in “N” of one” because “N of one” is about the patient. If it is not about the patient, then it is about nothing. – Dr. Albert Lopez, DO


Prefer to listen to the podcast without video? You can do that below!





This month’s MedEvidence! podcast is a three-part series on “What to do after a Heart Attack or Stroke?” In the first MedEvidence segment we established that people who have had either a heart attack or stroke have a high risk for a repeat procedure or event. We also discussed knowing who’s on your Heart Health Team, PCP, specialist, and family. What’s abnormal, normal, and what to do when symptoms last greater than 20 minutes? In this 15-minute episode, Doctors, Michael Koren and Albert Lopez DO discuss the Risk Factors You Need to know for your heart health.

You will learn:

      • What modifiable risk factors are
      • What non-modifiable risk factors are
      •  What you can do to help your risk factors
      • How clinical trials and research find other drug benefits
      • How to be involved in a clinical trial

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Albert Lopez, DO practices Internal Medicine with Millennium Physician Group in Jacksonville, Florida. He is also a Principal Investigator with ENCORE Research Group specializing in lipid clinical trials. Dr. Lopez, DO completed his residency at the University of Pennsylvania and his Doctor of Osteopathic Medicine at Nova Southeastern University in Miami, Florida. He is known as one of the earliest evidence-based physicians in Jacksonville utilizing nutrition and lifestyle for disease prevention.
I believe in “N” of one” because “N of one” is about the patient. If it is not about the patient, then it is about nothing. – Dr. Albert Lopez, DO


Prefer to listen to the podcast without video? You can do that below!





This MedEvidence! podcast is a three-part series on “What to do after a Heart Attack or Stroke?” In this episode, Doctors, Michael Koren and Albert Lopez, DO help you identify your heart health team.

You will learn:

    • Who do I call if I think I’m having a heart attack?
    • What are my risks for another event?
    • How can my family help?
    • How to find a clinical trial

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Albert Lopez, DO practices Internal Medicine with Millennium Physician Group in Jacksonville, Florida. He is also a Principal Investigator with ENCORE Research Group specializing in lipid clinical trials. Dr. Lopez, DO completed his residency at the University of Pennsylvania and his Doctor of Osteopathic Medicine at Nova Southeastern University in Miami, Florida. He is known as one of the earliest evidence-based physicians in Jacksonville utilizing nutrition and lifestyle for disease prevention.
I believe in “N” of one” because “N of one” is about the patient. If it is not about the patient, then it is about nothing. – Dr. Albert Lopez, DO


Prefer to listen to the podcast without video? You can do that below!





In this final 30-minute episode Doctors, Michael Koren and Bharat Misra dive into new treatments in clinical trials for Fatty Liver Disease and NASH.

You will learn

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Bharat Misra is the Medical Director of ENCORE Borland Groover Clinical Research and has been a Principal Investigator of numerous clinical trials. He also serves on the board of directors at Memorial Hospital and Jacksonville Center for Clinical Research in Jacksonville, Florida. He completed his residency in internal medicine and fellowship in gastroenterology at the Nassau University Medical Center, State University of New York, and his Bachelor of Medicine and Bachelor of Surgery from Gandhi Medical College in India.


Prefer to listen to the podcast without video? You can do that below!





This month’s MedEvidence! Hour is a three-part series on You Cannot Live without Your Liver.   In this 14-minute Part 2 episode Doctors, Michael Koren and Bharat Misra answer your questions on Fibroscans.

  • Who should receive a Fibroscan
  • How often should I get a Fibroscan
  • Should I ask my primary doctor for a Fibroscan
  • Liver Biopsy vs. Fibroscan
  • Insurance and Fibroscan
  • What should I do after my Fibroscan
  • How to find a free Fibroscan

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Bharat Misra is the Medical Director of ENCORE Borland Groover Clinical Research and has been a Principal Investigator of numerous clinical trials. He also serves on the board of directors at Memorial Hospital and Jacksonville Center for Clinical Research in Jacksonville, Florida. He completed his residency in internal medicine and fellowship in gastroenterology at the Nassau University Medical Center, State University of New York, and his Bachelor of Medicine and Bachelor of Surgery from Gandhi Medical College in India.


Prefer to listen to the podcast without video? You can do that below!





This month’s MedEvidence is a three-part series on the liver.   In this 12-minute episode Doctors, Michael Koren and Bharat Misra discuss technologies to diagnose dysfunctions of the liver.

You will learn:

  • Technologies in clinical research
  • What a fibroscan is
  • Why your doctor may not be offering you a fibroscan
  • Liver biopsy vs. MRI vs. fibroscan

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.

Dr. Bharat Misra is the Medical Director of ENCORE Borland Groover Clinical Research and has been a Principal Investigator of numerous clinical trials. He also serves on the board of directors at Memorial Hospital and Jacksonville Center for Clinical Research in Jacksonville, Florida. He completed his residency in internal medicine and fellowship in gastroenterology at the Nassau University Medical Center, State University of New York, and his Bachelor of Medicine and Bachelor of Surgery from Gandhi Medical College in India.


Prefer to listen to the podcast without video? You can do that below!





In this episode, Dr. Michael Koren and Michelle McCormick wrap up their discussion on how clinical trials find the truth as well as truth vs. faith and the conclusion of lady tasting tea. Could she actually tell whether the milk or tea was put in first?

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!





In this episode, Dr. Michael Koren and Michelle McCormick walk through the history of Clinical Trials. From Biblical stories of Daniel through the smallpox pandemic to our present COVID pandemic. How far have we come and where do we go from here?

Some of what you will learn:

  • History of Clinical Research
    • Daniel and King Nebuchadnezzar
    • Newgate Prison
    • Cotton Mather & Onesimus
  • Current Vaccine Trials
    • Chickenpox
    • Shingles
    • Covid
    • Flu
    • RSV
  • Future of COVID

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!





In this second episode, Dr. Michael Koren, New York Central High School alumni, and Michelle McCormick take us back to high school minus having that awkward conversation about asking your date to prom.  Listen to find out what your high school classes have to do with clinical trials.

Some of what you will learn:

  • What makes a good hypothesis
  • Statistical concepts
  • Statistical methods involved in carrying out a study
  • The vocabulary of clinical research
  • History of clinical research
    • Newgate Prison
    • Daniel and King Nebuchadnezzar
    • Pepsi vs. Coke

Dr. Michael Koren is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!





In a four-part series on What are Clinical Trials & Why are they important, in this first episode Dr. Michael Koren and Michelle McCormick talk about The Science of Clinical Trials, What makes a good Clinical Trial, good?

What do these things have in common?

  • R.A. Fisher
  • Lady Tasting Tea
  • Truth vs Faith
  • Experiments
  • Clinical Trials

Dr. Michael Koren, is a practicing cardiologist and CEO at ENCORE Research Group. He has been the principal investigator of 2000+ clinical trials while being published in the most prestigious medical journals. Dr. Koren received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine with a fellowship in cardiology at New York Hospital / Memorial Sloan-Kettering Cancer Center/ Cornell Medical Center.


Prefer to listen to the podcast without video? You can do that below!





In the final episode of Kicking the Nicotine Habit, It’s a Brain Thing. The MedEvidence! doctors roll out the clinical trials on Cytisinicline, an approved therapy in central and Eastern West Europe for the past 20 years.

This month Dr. Michael Koren and Michelle McCormick talk with Dr. Mitchell Rothstein, a clinical Pulmonary and Sleep Medicine physician for 30 years in the Jacksonville, Florida area.  Dr. Rothstein is the Medical Director of the Phase 1 unit at Jacksonville Center for Clinical Research.

Inside this episode:

  • Cytisinicline
  • Alpha4beta2 Nicotine Receptor
  • Clinical Trials to help quit smoking

Prefer to listen to the podcast without video? You can do that below!





Part 3 in a 4 part series on Kicking the Nicotine Habit, It’s a Brain Thing. The MedEvidence doctors continue their discussion on smoking while diving into nicotine replacement therapies.

This month Dr. Michael Koren and Michelle McCormick talk with Dr. Mitchell Rothstein, a clinical Pulmonary and Sleep Medicine physician for 30 years in the Jacksonville, Florida area.  Dr. Rothstein is the Medical Director of the Phase 1 unit at Jacksonville Center for Clinical Research.

Inside this episode:

  • Nicotine Replacement Therapies
  • Quit smoking medications
  • E-cigarettes & Vaping
  • IQOS – heated tobacco products

Prefer to listen to the podcast without video? You can do that below!





Part 2 in a 4 part series on Kicking the Nicotine Habit, It’s a Brain Thing. Today the doctors dive into the behavioral habits of smoking and give you 5 strategies you can start NOW.

This month Dr. Michael Koren and Michelle McCormick talk with Dr. Mitchell Rothstein, a clinical Pulmonary and Sleep Medicine physician for 30 years in the Jacksonville, Florida area.  Dr. Rothstein is the Medical Director of the Phase 1 unit at Jacksonville Center for Clinical Research.

Inside this episode:

  • Do you want to stop smoking?
  • How do you get to that point?
  • Behavioral Modification strategies
  • 5 Things you can do today to stop smoking

Prefer to listen to the podcast without video? You can do that below!





Part 1 in a 4 part series on Kicking the Nicotine Habit, It’s a Brain Thing.

This month Dr. Michael Koren and Michelle McCormick talk with Dr. Mitchell Rothstein, a clinical Pulmonary and Sleep Medicine physician for 30 years in the Jacksonville, Florida area.  Dr. Rothstein is the Medical Director of the Phase 1 unit at Jacksonville Center for Clinical Research.

Inside this episode:

  • What makes smoking harmful?
  • What makes smoking so addictive?
  • Preventable form of Cardiovascular factors

Prefer to listen to the podcast without video? You can do that below!





This month’s MedEvidence guest, Dr. Steven Toenjes, MD, a board-certified neurologist, former staff neurologist in the U.S. Navy, and an award-winning director of neurology residents at the Uniformed Services University of Health Sciences and decorated Navy veteran, joins Dr. Michael Koren and Michelle McCormick to discuss the future of Alzheimer’s research and what your gut has to do with Alzheimer’s.


Prefer to listen to the podcast without video? You can do that below!





What are all the hullabaloos about Aduhelm, the first new Alzheimer’s drug approval since 2003? This month’s MedEvidence guest, Dr. Steven Toenjes, MD, a board-certified neurologist, former staff neurologist in the U.S. Navy, and an award-winning director of neurology residents at the Uniformed Services University of Health Sciences and decorated Navy veteran joins Dr. Michael Koren and Michelle McCormick to discuss the first new Alzheimer’s drug approval since 2003 and the controversy over FDA’s approval of Biogen’s Aducanumab (Aduhelm).


Prefer to listen to the podcast without video? You can do that below!





In Part 2: Is it Alzheimer’s or Something Else? Drs. Toenjes and Koren begin by answering the popular question, “When do you know something is wrong? Followed by explaining amyloid proteins, DNA structure, Alzheimer’s therapy, and the research behind it.

Dr. Steven Toenjes, MD, a board-certified neurologist, former staff neurologist in the U.S. Navy, and an award-winning director of neurology residents at the Uniformed Services University of Health Sciences and decorated Navy veteran, joins Dr. Michael Koren and Michelle McCormick to discuss Alzheimer’s disease in a four-part series.


Prefer to listen to the podcast without video? You can do that below!





This month’s MedEvidence guest, Dr. Steven Toenjes, MD, a board-certified neurologist, former staff neurologist in the U.S. Navy, and an award-winning director of neurology residents at the Uniformed Services University of Health Sciences and decorated Navy veteran joins Dr. Michael Koren and Michelle McCormick to discuss Alzheimer’s disease in a four-part series.

With over six million Americans believed to have Alzheimer’s disease and the sixth leading cause of death in the United States, MedEvidence breaks down Dementia vs. Alzheimer’s, including diagnosis and treatments.


Prefer to listen to the podcast without video? You can do that below!





In this final episode on longevity, Dr. Michael Koren, Dr. Victoria Helow, and Michelle McCormick talk about medical research and apply its wisdom to maximize a healthy lifestyle. Topics discussed:

  • Aspirin: Doses, Purposes & Populations
  • Types of anti-inflammatories
  • Importance of Cholesterol numbers
  • RNA Technology
  • Viruses
  • Vaccines
  • Hugging vs. Handshake
  • Becoming Part of Advancing Science

Related articles:


Prefer to listen to the podcast without video? You can do that below!





What is the formula to living longer? In this third episode in our four-part series Dr. Michael Koren, Dr. Victoria Helow, and Michelle McCormick apply medical research to fish, nuts, sex, sunscreen, and more.

Related articles:


Prefer to listen to the podcast without video? You can do that below!





Can medical research help us live longer? In this four-part series Dr. Michael Koren, Dr. Victoria Helow, and Michelle McCormick discuss the relevant medical evidence and apply its wisdom to discover the secrets to longevity.

Related articles:


Prefer to listen to the podcast without video? You can do that below!





Can medical research help us live longer? In this four-part series Dr. Michael Koren, Dr. Victoria Helow, and Michelle McCormick discuss the relevant medical evidence and apply its wisdom to discover the secrets to longevity.

Related articles:


Prefer to listen to the podcast without video? You can do that below!



10-Early-Signs-of-Alzheimers-Disease.jpg

Alzheimer’s Disease is devastating. An estimated 6.2 million Americans age 65 and older are living with Alzheimer’s dementia in 2021. Alzheimer’s is a brain disease that causes a slow memory decline. It can also affect your thinking, problem-solving, and reasoning skills. There are ten signs that you or a loved one may be experiencing early stages of Alzheimer’s Disease. If any of these signs persist, you should schedule an appointment with your doctor and come in for a free memory screening at Jacksonville Center for Clinical Research (JCCR).

1.Memory Loss that Disrupts Daily Life 

A critical factor in spotting Alzheimer’s Disease’s early stages is noticing the memory loss of recently learned information. The memory loss examples include forgetting dates and events and asking the same questions multiple times. 

2. Difficulty Completing Normal, Daily Tasks

It can be difficult for a person in the early stages of Alzheimer’s to complete daily tasks. For example, they may find it difficult to find familiar locations or do simple things such as making a grocery list or remembering the rules to a favorite game.

3. Trouble with Planning or Problem Solving 

It can sometimes become difficult for those with Alzheimer’s to work with numbers. Tasks such as paying bills may get swept under the rug or have excessive errors. They also have difficulty planning things as simple as everyday errands.

4. Confused about the Current Time or Place

Alzheimer’s Disease can cause confusion and result in anxiety or panic. Frequently, they can forget where they are or how they got there. 

5. Trouble with Vision and Depth Perception 

Alzheimer’s Disease and vision issues can go hand-in-hand. For example, they may show difficulty reading, balancing, or distinguishing the depth and color of objects. 

6. Difficulty Pronouncing Words or Writing 

It can be difficult for someone with Alzheimer’s to join a conversation. They may stumble on their words. They may have trouble remembering names and often repeat themselves. 

7. Losing Important Items Often

Everyone loses their keys, remote, or wallet every once in a while. However, someone suffering from the early stages of Alzheimer’s may often lose these things or put them in strange places. For example, they are putting their keys in the fridge. 

8. Poor Judgement

Someone who has Alzheimer’s Disease may have poor judgment. Examples of this can be poor hygiene, trouble dealing with money, or acting irrationally.

9. Becoming Socially Distant

It can become difficult for people with Alzheimer’s to work or interact socially. You may notice them pulling away from normal social activities. They may start to have trouble keeping up with their favorite activity. 

10. Mood Swings 

Suffering from Alzheimer’s Disease can be extremely frustrating. It is common to experience sudden mood changes and sometimes act irrationally. They can quickly become confused, suspicious, depressed, or even fearful.

It is important to remember that we can have a natural decline in cognitive ability as we age. However, when that decline disrupts daily life, it is time to see a doctor for a memory screening. 

Thankfully, there have been many breakthroughs in memory research, although there is still no cure for Alzheimer’s. Clinical trial studies are the only way to continue to learn about this disease in hopes of and finding a cure. If you or a loved one is currently experiencing any of these early symptoms of Alzheimer’s Disease, we encourage you to get a memory screening. ENCORE Research Group offers free memory screenings at our Jacksonville Center for Clinical Research location and has several studies enrolling for Alzheimer’s Disease.

For more information, visit encoredocs.com or call 904-730-0166.


The-Hawthorne-Effect-Facebook-Cover-1200x676.jpg

November 17, 2021 BlogClinical Trials

The Hawthorne Effect is an interesting phenomenon where people alter their behavior due to the awareness of being observed. This effect was first discovered in the 1950s outside of Chicago. The experiment was done on factory workers, and it found that workers had a positive response to the extra attention given by managers who cared about them.

This same phenomenon has been noticed in clinical trials as well. “When you’re doing a clinical trial, and you’re involved with something that is being observed, your patients tend to do better regardless of how they are being medically treated.” Dr. Michael Koren, CEO of ENCORE Research Group, says. For example, if a patient is in a clinical trial for weight management, they may be more likely to lose weight if they must keep a log of everything they eat and present it to their study coordinator. 

So what does that mean for you? It means that you have the chance to improve your health just by participating in a clinical trial, even if you happen to be on a placebo. Studies have shown that patients in clinical studies are more adamant and knowledgeable about their health in the first place. It is safe to say your health will likely improve no matter what study you participate in! To see what studies are available right now, visit our enrolling studies page!


Research-Participation-Survey.png

We asked, “What motivates you to participate in clinical trials?” With over 160 responses, the answer is clear. People who participate in clinical trials are dedicated to helping others by improving medicine for future generations.

We also found that very few were participating in order to receive the stipend for time and travel. This says a lot about the type of people who are willing to participate in clinical trials. They are in it for the cutting edge treatment, and the need to help others.

There is truly only one way to improve healthcare, and that is to participate in clinical trials. Thank you to everyone who responded to our survey, and everyone who participates in these trials.


Limey.jpg

On a sailing ship in 1747, twelve sailors who had begun the voyage feeling fine were overcome with fatigue.  Their gums were swollen and sore, making it difficult to eat.  Their teeth were falling out.  Their legs were swollen and purple from bruising.

 

Dr. James Lind was a passenger on that ship, and he set out to find the cause.  He set up what may have been the first clinical nutrition experiment.  He decided on six groups of treatments, 2 sailors in each group:

 

  1. drank one quart of cider a day
  2. gargled with sulfuric acid
  3. had two spoonfuls of vinegar, 3 times a day
  4. drank ½ pint seawater a day
  5. drank barley water
  6. ate two oranges and 1 lemon a day

 

Within six days, the sailors who ate the oranges and lemon felt better and were able to work again.  The other sailors in the experiment felt worse.  The ill sailors were suffering from a lack of vitamin C, now known as Scurvy. They had plenty of fresh fruits and vegetables when they first set out on the voyage.  But fresh foods ran out on the long voyage, and they suffered symptoms from this lack. After this finding, sailors often brought lime juice aboard ship because it could be stored longer. This is how sailors earned the nickname “limey”.

 

1747 was well before the requirement of informed consent of the patient, detailed eligibility criteria, protocols and regulations, which are a foundation of today’s clinical research.  Nevertheless, it is an interesting example of a method of discovering the best treatment for a disabling condition.

 

Scientific minds are still seeking solutions for medical problems.  Modern clinical research is strictly regulated for the safety and well-being of the research volunteer.  Great progress has been made in medical science over the last decades.  This progress could not happen without dedicated volunteers. Participation in clinical trials can be a rewarding endeavor for both investigators and volunteers alike.

 

Written by: Julia Baker, RN, CCRC

Resources:
https://askabiologist.asu.edu
https://www.umass.edu/nibble/infofile/limey.html