Life is Full of Sweet Choices: Diabetes and the Heart

Diabetes Mellitus (DM) is a very common condition with wide ranging and severe complications. DM leads to metabolic and vascular diseases including coronary artery disease (CAD), cerebrovascular disease, peripheral artery disease, eye disease and kidney disease. This can progress to heart attacks, strokes, amputations, dialysis and blindness. What is DM, how does it affect the vascular system and how do we treat it?

 

DM is common and the eighth leading cause of death in the United States (US). In 2021, 38 million Americans (16%) had diabetes and 38% of the US had prediabetes. Those numbers continue to rise. Patients with DM are five times more likely to develop heart disease then those who do not have DM. 

 

DM is diagnosed by the following criteria: a hemoglobin A1c level > 6.5 % (hemoglobin A1c is a blood test that assesses the average blood sugar over the course of a month) or a fasting blood sugar level > 126 md/dl or any random blood sugar > 200 mg/dl. Prediabetes is a hemoglobin A1c between 5.7 and 6.4% or fasting blood sugar between 100 and 125 mg/dl.

 

The pathogenesis of DM is related to the actions of insulin, which is secreted by the pancreas and regulates the body’s blood sugar. Insulin lowers sugar (glucose) level in the blood and promotes increased uptake of sugar by the muscles for energy. There are two types of DM. Type 1 DM (5.7% of all DM) is caused by destruction of the cells used by the pancreas to make insulin.  In Type 2 DM, the body is resistant to the effects of insulin. If insulin is impaired by either mechanism, the blood sugar goes up. Longstanding high levels of blood sugar leads to inflammation of the blood vessels and impaired function of the blood vessels. Two types of vascular complications ensue: microvascular and macrovascular. Microvascular complications include retinopathy (eye disease), neuropathy (nerve pain) and nephropathy (kidney damage).   Macrovascular complications refer to inflammation and blockage in the heart, brain and peripheral arteries. 

 

The goal of management of DM is to achieve a hemoglobin A1c under 7%. This can be done through diet, exercise and weight loss. Working with a dietician can help find foods that are low in sugar. Weight loss of 5 to 10% improves hemoglobin A1c and lowers cardiac risk. Other risk factors should be controlled as well. Blood pressure should be lowered to less than 130/80 mmHg. If there is concomitant kidney disease or protein in the urine, an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin-receptor blocker (ARB) should be used as first line to delay the DM related progression of kidney disease.  Cholesterol should be lowered with a statin with a goal of LDL (low density lipoprotein, the “bad” cholesterol) under 70 mg/dl. High triglycerides often accompany DM. If the triglyceride level is above 150 mg/dl, then high dose fish oil (icosapent ethyl) can reduce cardiac risk.

 

There are many medications available for control of blood sugar. Insulin injection is used to treat Type 1 DM. For Type 2 DM, especially for those with heart disease, three classes of medications are preferred.  Treatment is usually begun with metformin. Metformin decreases glucose production by the liver, reduces the uptake of sugar in the gastrointestinal system and improves insulin sensitivity by increasing glucose uptake in the muscles. Metformin can help with weight loss and improve vascular function. Sodium glucose cotransporter-2 inhibitors (SGLT2) include Jardiance and Farxiga. These agents increase the excretion of glucose by the kidneys. SGLT2 agents have been shown to reduce cardiac events, cardiac mortality, heart failure hospitalizations and slow the progression of kidney disease. Glucagon-like peptide-1 receptor agonists (GLP1) also treat Type 2 DM and have similar beneficial effects on the heart as the SGLT2 agents, lowering major cardiac events. These agents also help with congestive heart failure and delay progression of disease in chronic kidney patients. Of course, GLP1 agonists are used to treat obesity, even in patients without DM. GLP1 agents include semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro, Zepbound). They act by having the pancreas release insulin only when the blood sugar is high, stopping secretion of glucagon (which tells the liver to release sugar into the blood), slowing the movement of food from the stomach (preventing spikes in blood sugar) and controlling hunger and food craving to help lose weight.  GLP1 agents improve multiple risk factors for atherosclerosis including lowering weight, improving fat distribution (for example, decreasing waist circumference), lowering blood pressure, improving lipids and decreasing inflammation. Because of these factors, GLP1 agonists can lower the risk for major cardiac events by 20%.

 

Type 2 DM is preventable with lifestyle modifications. Effective lifestyle management includes watching calorie, carbohydrate and fat intake in the diet, maintaining a good body weight and exercising.  In patients with obesity and high risk for DM, these lifestyle changes lowered the risk for DM by 34% over a ten-year period. If lifestyle isn’t working, the use of the GLP1 agonist semaglutide lowered the risk for DM by 73% in obese patients.

 

Life is full of sweet choices. One choice you should make is to try to avoid Type 2 DM and its myriad complications. So, choose to exercise regularly, watch your weight and keep the sweets to a minimum.

What Can a Reverend Who Lived in the 1700’s Teach Us About Heart Artery Disease Today?

 

 

“It’s tough to make predictions, especially about the future”

 

The quote about predictions is from noted philosopher (and Yankees Hall of Famer) Yogi Berra. One person who can help us make predictions, Thomas Bayes, was a Presbyterian minister.  He was born in 1701 in England and studied theology and logic at the University of Edinburgh. He worked as a minister but continued to dabble in questions of logic until he died in 1761. After he passed away, his family found a paper that he wrote and brought it to the attention of the Royal Society. The paper described what came to be known as Bayes Theorem. Bayes Theorem launched a new way of thinking and Bayesian probability has become the core of modern statistics. In 2018, the University of Edinburgh dedicated their informatics department to Reverend Thomas Bayes. Bayes Theorem gives a way to work out conditional probabilities. A conditional probably is the probability of an event A, given that condition B is true; what is the probability of A given B.  In other words, it takes a belief, evaluates new evidence and gives a new, improved belief.  Scientists believe that human brains use a type of Bayesian thinking to deliberate and decide. Bayesian reasoning has exploded with uses in many diverse areas including physics, ecology, psychology, artificial intelligence and even self-driving cars. One of the fields where Bayes Theorem is most useful is in medicine. 

 

Consider the case of a 50-year-old man who comes to his doctor’s office for evaluation. What is the probability of coronary artery disease (CAD) for this man? In 1979, the New England Journal of Medicine published a landmark study introducing Bayes Theorem to the medical community. The article asked exactly this question; how can the probability of CAD be calculated in a 50-year-old male patient? From population studies and autopsies, the probability of CAD for a 50-year-old male is 7% (for comparison the probability of CAD in a 50-year-old woman is 1.6%, for a 65-year-old man it is 12%). Next, we learn of a new finding, our 50-year-old man has been having chest pain. Suppose he is having symptoms that are typical of angina pectoris. We know that being 50 years old and a male he has a probability of CAD of 7%. Now we have new information, he has chest pain, typical angina.  We can evaluate with Bayes equation and find that his probability of CAD is now 90%. If his symptoms are more atypical, then his probability of CAD is only 53%. If he has atypical chest pain, but has a positive stress test, then his probability goes back up to 70%. Contrast that with a 30-year-old man who has a low baseline probability (0.03%). Even if the 30-year-old has typical chest pain, his probability of CAD is only 26%.  This is the power of Bayes, the probability of a disease can be revised up and down based on each piece of new information. 

 

The most important factor in determining the risk for CAD is baseline characteristics (pre-test probability). Age and sex give a crude estimate. More sophisticated calculators have been developed that incorporate more variables (for example diabetes, blood pressure, cholesterol, smoking, family history). These include the Framingham risk score, the American College of Cardiology (ACC) risk calculator, the Pooled Cohort equations and the most recent iteration, the PREVENT equations. These tools are accurate but they have drawbacks. They give a 10-year estimate for the risk for a heart attack (rather than providing a risk for CAD right now) and are not useful in all populations (for example, they are less accurate in lower socioeconomic groups). In addition, they may not be able to predict a first heart attack.  A study analyzed 465 patients under 65 years old without known CAD who presented with a heart attack. The patients’ information was entered into the ACC risk estimator and the PREVENT calculator. The researchers found that 45% of the patients would have classified as low risk with ACC calculator, meaning no further testing or statin advised. For the PREVENT calculator, 61% would have been classified as low risk. Predicting the future is hard.

The next most important factor is symptoms (for example, chest pain).  Remember that our 50-year-old man (baseline 7%) having typical chest pain, has a probability of CAD of 90%.  The characterization of the chest pain is vitally important as it will shift the probability (and therefore the work up and treatment) of CAD significantly. Typical angina pectoris (chest pain) is exertional, described as a tightness or squeezing or pressure or heaviness or dull aching located in the area of the breast bone. The pain can radiate to the left arm, neck, jaw or back. It will usually last a few minutes and be relieved by rest. Atypical pain is sharp or stabbing, located on the right side and brought on by deep breathing or change in position.  There is a substantial population of patients who continue to have typical angina despite having no severe blockage on heart catheterization. This problem has vexed clinicians for more than 40 years. After years of research, we now have a better understanding of this syndrome (microvascular dysfunction) and a catchy moniker, ANOCA (Angina, NOrmal Coronary Arteries). Catheterization will evaluate for blockage in the main heart arteries, but catheterization only shows about 10% of the total heart circulation. The rest consists of small vessels, the microvasculature. The small vessels are the primary site of regulation of blood flow to the heart muscle. When the heart needs more oxygen (for example while running) the microvasculature dilates and the flow increases. With ANOCA, that regulation is abnormal and patients will have classic chest pain when the demand is greater than the supply. ANOCA patients have predictable triggers of chest pain such as exertion or emotional stress. It is more common in women, in smokers, and people with hypertension or high cholesterol. ANOCA is common, occurring in about 25% of all heart catheterizations and affecting about 3 to 4 million Americans. It is diagnosed after the large heart arteries are found to be normal. A stress test with PET imaging or heart catheterization with specialized testing will diagnose ANOCA. 

 

So, if you have chest pain, you can calculate your probability of CAD by entering your variables into Bayes equation, or enter the data into a Bayes app (it does exist!) or checking a table. However, the prudent course would be to call your doctor and ask what tests are necessary. If you continue to have classic angina despite normal arteries on heart catheterization, then seek out a cardiologist specializing in ANOCA (they do exist!).

 

 

 

Packing in the Protein

 

Everyone is talking about increasing protein, from dieticians to athletes to social media influencers. Now, the United States (US) government is weighing in. The Dietary Guidelines for Americans is released every five years by the US Department of Health and Human Services to provide advice on what to eat. In January 2026, a new guideline was released and caused a major stir. The new food pyramid was inverted, with protein on top and animal sources of protein (for example, red meat) placed above plant proteins. In addition, the amount of protein to be eaten each day was doubled compared to prior guidelines. This prompted many questions. Should dietary protein be increased? Are high protein diets good or bad for overall health?  What are sources of good protein? What is dietary protein anyway?

 

Protein is an essential nutrient made of amino acids. The body needs protein to grow, repair cells, and build muscles, bones, skin and hair. Protein is important for metabolism and to make enzymes, hormones and antibodies. The body uses 20 different amino acids. Nine amino acids are deemed essential because the body can’t make them; they are obtained only in the diet. The other 11 non-essential amino acids are ones the body can synthesize. A food item is considered a complete protein if it contains all nine essential amino acids (for example, pistachio nuts). It is important to understand that there is no way to store protein in the body (unlike carbohydrates and fat). It is also essential to realize that proteins are not peptides (which have been in the news recently). A peptide is a compound of two or more amino acids linked by a chemical bond (a peptide). 

 

Prior to January 2026, the Dietary Guidelines recommended 0.8 grams per kilogram per day (g/kg/d) of protein intake. The new guidelines ask us to aim for 1.2 to 1.6 g/kg/d. What kind of numbers are we talking about? A 150-pound man weighs 68 kg (150 divided by 2.2). The old recommendation had our man ingesting 54 grams per day of protein (0.8 x 68). The new guidelines have him increase that to 82 grams (1.2 g/kg/d) to 108 grams per day (1.6 g/kg/d). Are there harms in ingesting that much protein? The popular theory is that by increasing protein intake, you could lose weight and gain muscle.  To do that, you need to exercise, specifically doing resistance exercises. If not, then the extra calories that usually accompany extra protein will be turned into fat, increasing the risk for obesity and type 2 diabetes. People with chronic kidney disease shouldn’t increase protein in their diet. Metabolizing the extra protein could worsen kidney disease and lead to dialysis. Increased protein is also associated with an increased risk for colon cancer. Multiple studies have shown no benefit for ingesting more than 1.6 g/kg/d. The beneficial effects plateau around this level. There is no increase in muscle strength or mass and no weight loss above that number. For perspective, less than 25% of the population ingest above 1.5 g/kg/d of protein.

 

Is a high protein diet associated with heart disease? The excess calories consumed with more protein increases the risk for weight gain, diabetes and subsequent heart disease. Red and processed meats have high levels of saturated fats. Increasing their intake will increase low density lipoprotein (LDL) and increase inflammation. This increases the risk for heart artery disease. Studies have shown an association of high protein diets with increased risk for heart failure, all cause death and a shortened lifespan. Excess protein intake can accelerate blockages in the heart arteries, especially at levels above 1.5 g/kg/d. On the other hand, these studies mostly were of people who had high consumption of animal protein, especially red and processed meats. Other sources of protein such as chicken, seafood, low-fat dairy and soy have not been associated with increased cardiac risk. 

 

Here are some important protein points:

-It seems that protein intake follows the old adage that if something in moderate amounts is good for you, more of something isn’t necessarily better and can be harmful.

-Eating protein doesn’t build muscle. Protein plus exercise, especially resistance exercise, builds muscle 

-Remember that protein is not stored in the body. Eating more than you need only results in the excess being eliminated.

 

What is the best recommendation for protein? It seems prudent to follow the journalist Michael Pollan’s famous advice: “Eat food, not too much, mostly plants”. “Eat food” means ingesting whole foods, not processed or packaged foods. “Not too much” means moderation. For protein, that means eating between 0.8 and 1.6 g/kg/d. Protein intake closer to the higher level can be recommended for older people (over age 65) to prevent age-related muscle loss (along with resistance exercise). “Mostly plants” emphasizes plant-based proteins over animal-based proteins (especially red and processed meats). Two good types of protein are nuts and Greek yogurt. Nuts are an excellent source of plant-based protein (see table below) with known cardioprotective characteristics. Following a Mediterranean diet supplemented with nuts (walnuts, almonds, hazelnuts) reduces the risk for heart attack, stroke and cardiovascular death by 28%. Similarly, Greek yogurt has plenty of protein and has been shown to help with blood pressure reduction, lowering LDL and reducing cardiac risk.

 

 

Item	Serving	Protein (grams)	Calories
Plain, regular, nonfat yogurt	6 ounces	7	85
Plain, Greek, nonfat yogurt	6 ounces	18	189
Frozen Greek yogurt bar	2.2 ounces	4	80
Walnuts	¼ cup	4.5
Pine nuts	¼ cup	4.5
Cashews	¼ cup	5
Pistachios	¼ cup	6
Almonds	¼ cup	7
Hazelnuts	¼ cup	5

 

Can Sitting and Watching World Cup Soccer Cause Heart Disease?

 

                                            Google Images

The World Cup has taken the United States by storm with hordes of fans traveling to see their teams in action. In addition, there are hours and hours of television (TV) coverage of the event with as many as six games per day. One could easily watch nine to twelve hours of soccer. Is all of that soccer watching good for you? Is the World Cup detrimental to cardiovascular health? We know that watching soccer can cause a high degree of emotional stress.  A study compared heart attacks among German fans during the 2006 World Cup tournament with cardiac emergencies in Germany at other times the same year. When the German team played, acute cardiac events were 2.6 times more likely to occur. Similarly, the risk for hospital admission for heart attack increased 25% in England on the day in 1998 that England lost to Argentina on a penalty shoot-out. A more recent study showed that acute mental stress (such as watching a tense soccer match) induced inflammation in the heart arteries, increasing the risk for cardiac events. We can see that mental stress worsens heart outcomes, but how about sitting and watching television for prolonged periods? How dangerous is that?

 

There is always lots of discussion about exercise and its benefits, but its polar opposite, a sedentary lifestyle, doesn’t get as much press. It is well known that sedentary individuals are at higher risk for heart disease. One study showed that sedentary individuals have a 30% greater risk for heart disease than active people. For each hour per day spent sedentary, the risk for cardiovascular disease rises by 5%. If sedentary time is greater than 10 hours per day, the risk for heart failure and cardiac death increase. In addition, a sedentary lifestyle increases the risk for diabetes, obesity, Alzheimer’s disease, Parkinson’s disease, dementia, depression, and cancer. The reason for this may be found at the level of the cell.  A recent study found that the cells of sedentary people produced 30% less energy than in people who are active. The cells can’t metabolize fat and produce more damaging byproducts. So, if the demand for energy rises (such as going out for a walk), the cells are inefficient and can’t meet the demand. This starts the body on the path to metabolic disease (for example obesity or diabetes). Sedentary behavior is defined as any activity that is less than 1.5 metabolic equivalents (METs). The MET is the energy cost of doing any activity such as walking the dog (3.0 METs). Examples of low energy activities include eating (1.5 METs), washing hands (1.5 METs) and sitting (1.0 METs). Someone who runs for 60 minutes each morning then sits for eight hours working is considered both active and sedentary. It can be difficult to gauge how much sedentary activity any individual accumulates. One proxy for sedentary behavior is television viewing time (sitting and watching TV, 1.0 METs). 

 

Many studies have shown that television viewing time is associated with an increased risk for high blood pressure, diabetes, obesity, inflammation, high triglycerides, heart artery disease, heart failure, cardiac death and stroke. Increased TV viewing time at a young age (younger than 23) translates into higher risk for cardiovascular events as an adult, independent of TV viewing as an adult. How much TV time is associated with heart disease? For perspective, the average daily time watching TV in the United States is 5 hours while Europe, Australia and Japan average three to four hours per day. Several studies have correlated the amount of time watching TV with the development of heart disease. One study showed that watching more than 2 hours per day increased the risk of heart disease by 12% compared to watching less than one hour per day. Another study found an 80% increased risk of cardiac death watching more than 4 hours of TV per day versus less than 2 hours. A third study found that watching more than 6 hours per day increased the risk of dying from heart disease. Several studies show a dose response to TV watching; the more sitting and watching, the higher the risk. Each one hour per day increase in watching TV increased the risk of cardiac mortality by 4% to 8%. Does exercise offset the risk of watching TV for many hours?  Some studies show that moderate exercise can eliminate the risk of cardiac disease associated with TV watching, while others have not shown the same effect. One recent study found that 150 minutes per week of exercise reduced the risk for heart failure by 15% and cardiac death by 10%. Therefore, a winning strategy would be to increase the amount of exercise each week (no harm in doing that), while decreasing the amount of time sitting and watching TV (a definite benefit).

 

Enjoy the rest of the tournament. However, instead of sitting and watching the rest of the matches, consider walking on a treadmill or riding a stationary bike instead. Or do a Viking Row.

 

Novel Ways To Improve Brain Connectivity

 

It is universal. Everyone wants to slow cognitive decline and stay sharp as they age. It used to be taught that the brain could not generate new neurons, we are stuck with the brain cells we were born with and they would atrophy over time. This turns out not to be true. Animal models have shown that new neurons are produced throughout life. In addition to the ability to make new cells, the brain is constantly making new connections among its existing neurons. Brain connectivity helps with learning and memory.  Here are three novel ideas on how to promote the generation of new brain cells, increase creativity and improve connectivity in the brain.  

 

What do these famous folks have in common? Aristotle, Alexander Hamilton, Henry David Thoreau, Ludwig Van Beethoven, Friedrich Nietzsche, Immanuel Kant, Virginia Woolf, Steve Jobs, Charles Darwin. All of these luminaries were known for their great creativity, their great thinking and all were obsessive walkers. Charles Dickens mentally composed most of A Christmas Carol while on his nighttime walks.  The poet William Wordsworth felt that walking “was indivisible from the act of writing”. How does walking promote the thought process?  Does exercise increase brain connectivity? We know that walking and exercise have many beneficial effects, including improving memory and protecting against cognitive decline. Add to the list generating new brain cells and promoting creativity. Neuroscientists agree that only one activity can trigger the birth of new brain cells, vigorous exercise. Many studies have shown that exercising followed by sitting down to work increases creativity versus just sitting and trying to think and write.  For example, a classic experiment asks students to come up with creative ideas for common objects (such as a hat, a plate, or a shovel). The students who thought while walking on a treadmill had higher creativity scores than students who sat at a desk. It may be the mind freeing effect of exercise, rather than the exercise itself, which promotes this deep thinking. When exercising, a rhythm, a cadence, is produced. Once in that rhythm, the body works, it is on autopilot, but the mind is free to wander and ponder. It is a quiet time for reflection. Walking, running or biking can produce this cadence. This kind of thinking likely can’t occur while playing team sports, or tennis, or pickleball as the brain is otherwise occupied by the chess match of competition. However, there is a physiologic basis for why exercise improves thinking. Neuroscientists have shown that exercise promotes new connections between different parts of the brain and stimulates the growth of new brain cells. These two processes help to stem the atrophy that occurs with age. Where the connections are made is also interesting. One area is the hippocampus, the area of the brain associated with learning and memory. The other is the frontal cortex, where executive function is located. After vigorous exercise, studies have shown that exercise increased blood flow to these regions, resulting in new neurons and new connections. One study looked at sedentary people aged 55 to 80. Half started walking 40 minutes three times per week. A magnetic resonance image (MRI) was done before and after the study period on each participant. The MRIs showed improved connectivity in the walker’s brains, but not the people who remained sedentary. How else can brain function be improved?

 

Which is better for the brain: handwriting or typewriting? An intriguing study showed that handwriting and typing used different brain networks. Handwriting improved brain connectivity, as well as memory and learning, while none of these things were true for typing. Handwriting requires the fine motor skills of the hand, so one must pay greater attention when writing. Typing is more mechanical and repetitive. More of the brain is used, stimulated and connections made, when handwriting. The authors concluded that handwriting is beneficial when taking lecture notes (to increase understanding) or when writing longer pieces (such as an essay or a novel). 

 

Which is better for the brain: speaking one language or being multilingual? Studies have shown that speaking two or more languages confers multiple benefits. For example, multilingual people experience a later onset of dementia than those who speak one tongue. In addition to more years of healthy aging, multilingual people live longer. Lastly, studies show that learning a second language, especially at a younger age, increases the brain’s neuroplasticity (more connections) and increases the grey matter in the brain (more brain cells). Grey matter is located in the cerebral cortex and is responsible for processing information, storing memories and making decisions.

 

If you want to increase brain connectivity, slow cognitive decline and live longer, go for a long walk and craft a novel. Then go home and hand write the plot. After it is done, translate your work into another language. Not interested in writing a novel? This information can still be useful. If you are stuck on a particularly vexing problem, or have to make a big decision, go for a walk or a bike ride. Clear your head and think through the issues.

Congestive Heart Failure Enters the Space Age

 

In the original Star Trek series, if a crew member became ill, they would visit Dr Leonard “Bones” McCoy. Dr McCoy would wave his medical tricorder over his stricken colleague and have a diagnosis. The tricorder was hand-held, noninvasive, did not require an intravenous catheter, did not use radiation and was risk free. How close are we to developing and implementing a medical tricorder type of device in our world?

 

Shortness of breath is one of the most common complaints when a patient presents to an emergency room. In general, shortness of breath can be due to anemia (low blood count), lung disease or heart disease. One of the most common heart causes of shortness of breath is congestive heart failure (CHF), fluid building up in the lungs. CHF is extremely common and carries high morbidity and mortality. CHF affects more than 60 million people worldwide. In people over the age of 55 in the United States, there are 1 million new cases of CHF diagnosed each year. In 2016, there were 1.9 million doctor visits due to CHF and more than 400,000 emergency room visits for CHF. CHF is the most common diagnosis for hospital admission. After a hospital admission for CHF, 83% of patients will be readmitted with CHF. Considering all of the doctor visits, emergency room evaluations, hospital admissions and readmissions, CHF exacts an enormous economic toll. More Medicare dollars are spent on CHF than any other diagnosis. In 2020, 32 billion dollars were spent on CHF. CHF exacts another high toll, mortality. After a patient develops CHF, the prognosis is poor as 42% will die within 5 years.

 

When a patient with shortness of breath comes to the emergency room, the physical examination, chest X Ray and lab tests can help determine if there is CHF. However, in many cases, the diagnosis is still uncertain with the basic evaluation. It would be great if there was a hand-held, noninvasive device that could be brought to the bedside and reliably diagnose CHF without risk to the patient. A device like McCoy’s tricorder.  Such a device exists and is currently in use in emergency rooms. The device, Point of Care Ultrasound (POCUS), consists of a wand with an ultrasound probe that connects to a portable console or a cell phone. POCUS can distinguish CHF from other causes of shortness of breath with great accuracy. POCUS can determine if there is fluid in the lungs, the body’s overall volume status (excess volume means CHF) and can assess the heart’s function (if the heart muscle is weakened, the diagnosis of CHF is highly likely).

 

POCUS is very neat space age technology, but it is not available to everybody. Smartphone apps would give the general public the ability to diagnose CHF. Currently, two apps are being developed and tested. One app detects changes in the motion of the heart. Heart motion is transmitted throughout the chest and these vibrations can be picked up on the skin. Using commercially available smartphones, with sensors already present as part of their technology, these heart vibrations can be assessed. The smartphone is placed on a person’s sternum (breast bone) and subtle changes in cardiac motion can differentiate between a patient in CHF and someone who is not in CHF with great accuracy. Another app uses speech recognition technology. Changes in a person’s voice can determine if someone is in CHF. The app can tell if the person has a “wet’ voice, signaling fluid overload, or a “dry” voice consistent with normal fluid levels. The apps will be important because they will be widely available and will allow early detection and early administration of medications, to prevent CHF from happening. This will alleviate symptoms from occurring and avoid hospitalizations. The voice app was able to detect CHF 20 days before hospitalization became necessary.

 

While waiting for the apps to become available, what can be done to prevent CHF? There are four modifiable risk factors for CHF, hypertension, diabetes, obesity and diet. With hypertension, each 20 mmHg increase in systolic blood pressure increases the risk for CHF by 28%. Lowering the blood pressure by 10 mmHg wipes out that 28% increase. Obesity is another major risk factor. In patients with CHF and normal heart function, more than 80% are overweight or obese. A body mass index (BMI) greater than 30 kg/m2 (normal 18-25, overweight 25-30, obese > 30) doubles the risk for CHF. A 10% reduction in fat mass reduces the CHF risk by about 20%. A sedentary lifestyle puts a person at risk for CHF. A high amount of physical activity decreases the risk for CHF by 23%. Lastly, treating diabetes will decrease the risk for CHF. Treatment with a glucagon-like peptide 1 receptor agonist (GLP1 agonist, for example Ozempic, Zebound or Mounjaro) reduces the risk for CHF by 18%. Similarly, treatment with a sodium glucose cotransporter 2 inhibitor (SGLT2, for example Jardiance or Farxiga) reduces the risk for CHF by 30%. What type of diet is best to avoid CHF? A plant-based, Mediterranean style diet is associated with a 41% lower risk for CHF hospitalization, while a Southern diet increased the risk for CHF. Other modifiable factors include low alcohol consumption and keeping sodium (salt) in the diet to a low level. The prevention of CHF doesn’t involve space age technology, but relies on good old fashioned hard work and perseverance.

 

In the near future, if you have shortness of breath, you’ll be able to talk into the phone tricorder resting on your chest and know if you have CHF. Until then, manage the modifiable risk factors noted above to avoid being a CHF statistic.

 

 

Plastic or Metal: Which Water Bottle is Best?

 

In ancient times, the philosophers would gather and walk around the marketplace, the agora, and contemplate the weighty matters of the world such as the nature of justice, the ideal city, distinguishing the good from opinion, and seeking truth and knowledge.  All of that walking, talking and thinking in the hot sun can make a scholar dehydrated. So, naturally, the first question these great minds would tackle is: plastic or metal? Which water bottle is best for walking and thinking?

 

Plastics are everywhere. The worldwide production of plastic has exploded from less than 2 million tons in 1950 to about 400 million tons in 2020. Once a plastic item has been used, it tends to stick around for a while. Plastic takes a long time to break down. For example, a plastic water bottle may take 450 years to decompose! Due to this phenomenon, plastic waste is everywhere. Only 10-15% of plastic is recycled. The rest ends up in a landfill or the ocean or is burned off. As the plastic in landfills or in the ocean breaks down, smaller particles called microplastics are produced. When plastic is burned, microplastics are released into the air. Microplastics have been found everywhere including on remote islands, in Antarctica, deep in the ocean and, increasingly, in human tissue and organs. Microplastics enter the body by two routes. Microplastics in the air are inhaled. They also enter by ingestion, for example by eating microplastic laden sea fish or drinking from plastic water bottles (even reusable water bottles). Microplastics have been found throughout the human body. They are present in high concentrations in the liver and kidneys and to lesser degrees in the hair, saliva, blood, colon and lung. Aside from just being present, do microplastics cause human disease? An important study found microplastics in atherosclerotic plaque. In the study, 58% of patients undergoing surgery for blockage in their carotid (neck) arteries had microplastics in their arteries. These patients were 4 times more likely to die, have a heart attack or stroke over the next three years compared to patients without microplastics. Another study found that coastline counties in the United States (where there is a higher exposure to ocean microplastics) had higher risks for diabetes, heart artery disease and stroke. We now know that the brain is full of microplastics as well. It was found that the level of microplastics in the brain increased by 50% from 2016 to 2024. In addition, people with higher levels of brain microplastics had more dementia and Alzheimer’s disease. 

 

Like plastics, metals are everywhere. However, unlike plastics, our bodies require small amounts of certain metals, called essential metals, for normal metabolism. Essential metals include copper, manganese, cobalt and zinc. Small amounts of these metals are needed, but larger quantities can be toxic as are nonessential metals, such as cadmium, arsenic, lead, tungsten, uranium and mercury. Cadmium is present in tobacco smoke, meats, shellfish, and vegetables. Cadmium, tungsten, uranium, cobalt, copper and zinc come from industrial emissions, electric batteries, oil production, welding, and mining. Arsenic is found in the water and some foods. What are the health effects of metals? It has been shown that with high urinary concentrations of cadmium, tungsten, uranium and the essential metal zinc, there is an increased risk for dementia. There is no association of high urinary lead levels and dementia. In addition, there is an association between high urinary levels of cadmium, tungsten, uranium, and the essential metal cobalt and coronary calcification, a measure of plaque in the heart arteries. It is felt that these metals promote atherosclerosis through inflammation. A recent study proved the concept by showing that lead and cadmium exposure leads to increased blood levels of troponin (a measure of heart damage), proBNP (a measure of heart strain) and C reactive protein (a measure of inflammation). Lastly, a study from China showed that long-term exposure to high levels of copper, manganese, aluminum, zinc and cadmium in the drinking water increased the risk for major cardiac events (heart attacks, cardiac deaths). 

 

What should our philosophers choose, a plastic or metal water bottle?  Which one is the healthier choice? Reusable plastic water bottles add to the microplastic load. Wear and tear, repeated washing and exposure to heat damages the inner surface of the bottle, releasing microplastics into the water that is drunk. The concentration of microplastics in reusable bottles is higher than single use water bottles. Most bottles are made of polyethelene terephthalate (PET). Bisphenol A (BPA) is another chemical used to make plastic bottles. BPA has multiple adverse health effects including endocrine problems, diabetes, high blood pressure.  It is best avoided. Most metal water bottles are made of stainless-steel. Stainless-steel does not wear down and release metal into the water. In addition, there are no known adverse health effects of stainless steel. When choosing a stainless-steel water bottle, make sure there is no aluminum and no lead-based solder used to seal the bottle. Lastly, make sure the plastic cap does not contain BPA.

 

So, don your toga, grab your stainless-steel water bottle and head to the agora to think those heavy thoughts.