9/19/14

Can Poor Sleep Cause Insulin Resistance?

Who’d ever think that poor sleep can actually cause insulin resistance? But it can. Insulin resistance is associated with obesity, even being moderately overweight, lack of exercise and poor diet. It can lead to type 2 diabetes. But a person who works out like a warrior, has a strict diet, and is a lean, mean athletic machine, can still end up with insulin resistance if he or she gets poor quality sleep.
I consulted with Dr. David Edelson, MD, board certified in internal and bariatric medicine, one of the top obesity experts in the U.S., and founder and medical director for thin-site.com and HealthBridge. He explains, “There is a strong association between sleep disorders and both obesity and insulin resistance.  When I refer to sleep disorders, I am speaking of anything that can cause either a lack of sufficient quantity of sleep (insomnia, lifestyle issues) or poor quality (sleep apnea, restless legs, fragmented REM sleep, etc.).”

Lifestyle issues include anxiety levels that keep a person tossing and turning, unable to slumber for more than several hours at a time. Dr. Edelson continues, “The basic problem is that the body requires a certain amount of deep cycle sleep to restore its normal functions after a full day of activity.”

There are two phases of restorative sleep: REM (the dream stage) and slow wave. “During these phases the body undergoes repair and rejuvenation, restoring depleted hormones and repairing damaged tissues,” says Dr. Edelson.  “If someone has poor sleep quality or quantity, these processes will not occur to a sufficient degree.  Over time this can result in a multitude of medical issues, including obesity, insulin resistance, hypertension, heart failure, arrhythmias, immune disorders, and the list goes on.”

Insulin resistance can even be caused by just one night of poor sleep, according to a study that was reported in the Journal of Endocrinology & Metabolism (2010).  “Our findings show a short night of sleep has more profound effects on metabolic regulation than previously appreciated," said Esther Donga, MD, of the Leiden University Medical Center in The Netherlands, and the study’s lead author. "Our data indicate that insulin sensitivity is not fixed in healthy subjects, but depends on the duration of sleep in the preceding night."

Millions of people have obstructive sleep apnea (OSA) and don’t even know it. Though obesity is associated with this life-threatening condition, not all patients are overweight, and it can affect children, though not commonly. If you’ve been diagnosed with OSA, you may have insulin resistance.

“As the patient falls into the deep stages of sleep, the muscles around the airway relax and the breathing becomes obstructed,” says Dr. Edelson.  “Oxygen levels fall as the patient literally is choking, and in most cases he/she snaps out of the deep stage sleep into a lighter stage.  This can happen over 100 times an hour in severe cases, with oxygen levels falling to 60 percent of normal.”

As frightening as this sounds, and as life-threatening as it is (dramatically increasing risk of heart attack and stroke), you can have this disorder and be completely unaware, especially if there’s nobody with you overnight to hear your snoring  --  a classic symptom of the condition. An overnight oxygen level test will confirm diagnosis.

A questionnaire on thin-site.com, called the Epworth Scale, can evaluate your risk of having OSA. If you turn out to be diagnosed with OSA, insist on being screened for insulin resistance.

Dr. Edelson says, “Restoring good quality sleep is often one of the most powerful things that can be done to improve a patient's overall health,” including lowering the risk of insulin resistance, or reversing it if you already have it.

Sources: 

Can Intense Exercise Prevent Insulin Resistance?

Is it really true that intense exercise can prevent you from ever getting insulin resistance? IR is when the body’s cells can no longer efficiently “take” the glucose molecules that are delivered to them via the hormone insulin. Glucose is blood sugar.
When insulin receptors on the cells can no longer receive all the sugar for energy, the body is then left with unutilized sugar, resulting in higher-than-normal blood sugar levels, and excess sugar going to the liver where it’s converted to fat.

Intuitively, it seems as though regular intense exercise should prevent insulin resistance. After all, exercise lowers blood sugar and creates more insulin receptors on cells. We’ve always heard that type 2 diabetes, of which insulin resistance can lead to, can usually be controlled with just diet and exercise. And we’ve heard that lack of exercise is strongly  --  very strongly  --  implicated in the development of insulin resistance.

I consulted with Dr. David Edelson, MD, board certified in internal and bariatric medicine, one of the top obesity experts in the U.S., and founder and medical director for thin-site.com and HealthBridge. He explains, “Insulin resistance is a genetic trait ... you either have it or you don't.  However, much like a pendulum, it must be pushed to be set into motion.  The ‘push’ could be bad diet, lack of exercise, poor sleep, aging, medications or some other external environmental force.”

Think of it this way: Genetics load the gun, but lifestyle habits pull the trigger. Dr. Edelson continues: “Conversely, exercise acts like a ballast providing extra weight to a pendulum, making it require more force to set into motion.  So while in a strict sense exercise will not prevent insulin resistance, it will make it much harder to turn on the gene and set the wheels in motion.”

This is why exercise is one of the major forces that physicians urge their IR patients to undertake to reverse the condition. Inactivity is a leading cause of IR, which affects about one out of every five American adults.

Dr. Edelson explains, “Exercise has definitely been proven in several clinical studies to reduce insulin resistance.  First of all, it burns up excess circulating blood sugar, preventing the pancreas from having to secrete too much insulin. Persistently high levels of insulin in the bloodstream cause reduction in the amount of insulin receptors, the first stage of manifesting IR.”  

“Secondly, regular exercise causes increased production of insulin receptors on the muscle cells.  More receptors means better response to the effects of insulin, resulting in lowering blood sugar and triglyceride levels, less hunger and prevention of weight gain.”

By the way, you can have a normal fasting blood sugar value and still have IR (too much of the hormone in the bloodstream because the pancreas has to over-secrete it in order to lower blood sugar). Hardcore, intense exercise, though not capable of outright preventing insulin resistance, is a formidable tyrant at minimizing your odds of ever developing IR, not to mention so many other medical conditions.

Sources
"Exercise-Induced Transcription of the Muscle Glucose Transporter (BLUT4) Gene"; Biochemical and Biophysical Research Communications, Volume 292, Issue 2, 29 March 2002, Pages 409-414
 "Acarbose with Exercise Improves Metabolic Control and Cardiovascular Risk Factor"; Diabetes Care 2006 29:1471-1477
www.healthbridgeinfo.com

Diagnosed with Prediabetes? How to Prevent Diabetes

You don’t have to get diabetes if you have prediabetes.

If you’ve been diagnosed with prediabetes, the steps you take now can prevent you from getting diabetes. Amazingly, only nearly half of American adults with prediabetes made attempts to reverse this condition and thereby prevent diabetes, says a study that was reported in the American Journal of Preventive Medicine (April 2010).

Exercising and losing weight are the key lifestyle habits to adapt. If you have prediabetes (you may not even know it, actually), it should scare the dickens out of you that this can eventually develop into type 2 diabetes.

If you haven’t been making efforts to lose weight, exercise more and improve your eating habits, then think about what a royal pain in the neck it would be to live with diabetes  --  all that finger pricking for blood sugar tests every day; keeping track of the numbers; having to keep track of how many carbohydrates you eat; when you eat; when you exercise; worrying if your blood sugar will plummet while you’re asleep… not to mention the increased risk for stroke, heart attack, some cancers and Alzheimer’s!

The study was carried out by researchers from Emory University, the Division of Diabetes Translation of the CDC, and the National Institute of Diabetes and Digestive and Kidney Diseases. Over 1,400 survey participants reported whether or not they had, in the past 12 months, increased exercise, cut calories or fat, and tried to lose weight. They also responded to other relevant questions. The study investigators reported that in 2005-2006, nearly 30 percent of American adults (at least age 20) had prediabetes.

It is estimated that 90 percent of people in the U.S., who have prediabetes, don’t even know it. This condition often has no symptoms. However, symptoms can be overlooked as well. Classic warning signs are: unexplained fatigue; increased thirst; frequent urination; blurry vision.

It’s important to realize that the frequent urination is what leads to the increased thirst, not the other way around. In other words, don’t think that it goes in this sequence: 1) Increased thirst, 2) Drinking more water, 3) Increased urination.

No. The proper sequence in prediabetes and diabetes is: 1) Frequent urination, 2) Increased thirst, and 3) Drinking more water. However, the actual sequence might not be easy to keep track of.

If you’ve been diagnosed with prediabetes, stop making excuses and start exercising. Join a gym. Buy a home gym or at least a few sets of dumbbells to get started. Knock out the high fructose corn syrup and white sugar, fried foods and heavily processed foods. These changes alone will cause weight loss.  
  

Source: http://www.news-medical.net/news/20100302/Majority-of-prediabetic-patients-are-not-adopting-preventive-measures-to-avoid-diabetes.aspx

Cymbalta for Depression Saved My Mother’s Life

Cymbalta snuffed out my mother’s crippling depression.

Yes, the antidepressant Cymbalta literally saved my mother’s life. Cymbalta wiped out my mother’s depression and panic attacks, with no side effects save for a few brief dizzy spells at the beginning.

My mother became disabled from depression, which included a weight loss of 12 pounds (mostly muscle) from refusing to eat, and reverted to weeping over the tiniest issues. I didn’t need medical training to recognize a textbook case of clinical depression, and I recommended an antidepressant (though not naming Cymbalta specifically). 

It all began when I planned on living with my parents for about three days, to help my mother recover from knee arthroscopic surgery. Little did I know that a power-hungry depression awaited me and would hold me hostage there for over two months.

In hindsight, I realize that subtle signs of depression had been present for several weeks preceding the surgery. However, the depression began stomping its feet the morning of the knee surgery, and had an unforgiving accomplice: panic attacks. My mother had had orthopedic surgeries before, but never sobbed or was convinced she was dying like this time. The problem was merely a meniscus tear in the knee. She also complained that the fingers of both hands were tingly.

Several days after the surgery, I suspected clinical depression and I began urging my father for “psychiatric intervention,” and that “she needs an antidepressant!”

Both my mother and father adamantly opposed antidepressants. My mother denied having depression, and attributed her apathy, overall weakness, inability to hold herself together while doing simple shopping, comments about wanting to die, excessive crying, loss of appetite and withdrawal from daily activities to 1) post-surgical knee discomfort, and then 2) a developing pain in both hands and arms, along with continuing tingling in the fingers.

My father admitted something was wrong, but attributed it to “lingering effects of anesthesia” (even five days out from surgery), and then to the hand pain (eventually diagnosed as carpal tunnel syndrome). Meanwhile my mother often talked about her funeral, gave us “If I die…” talks, and often said her entire body hurt.

“She has depression!” I kept harping to my father, who still opposed antidepressants and accused me of trying to play doctor.

After six weeks of taking care of my mother, including daily battles to get her to eat, I finally convinced my exhausted father to embrace an antidepressant. I chose Cymbalta because at the time, we thought that her frequent shoulder pain (which would trigger hard sobbing) was residual nerve pain from the double carpal tunnel syndrome surgery. In addition to nerve pain, Cymbalta is prescribed for panic attacks, and my mother often felt as though death were imminent.

I showed my father information from a Web site about how major depression can cause whole-body pain and amplify pre-existing joint pain by heightening a person’s perception of pain. I just had a gut feeling that the Cymbalta would take out the depression like a tank. That evening my mother took one 30 mg Cymbalta capsule. “I don’t know how long it will take before it kicks in,” I told her, “But believe me, this is the RIGHT thing to do.”

Next morning, my mother awakened feeling vibrant, pain-free, and eager for a big breakfast. Absent was the scene for the past six weeks: a withered, crying, wasted-looking stranger. My mother’s eyes were alive, voice robust. She said, “I feel GREAT!”

I said, “It’s the drug, the Cymbalta, it worked!”

My mother needed no help sitting upright; she popped right up and got ready for the day as though nothing were wrong. “For the first time in weeks, I feel human!” she said. And for the first time in seven weeks, she washed her hair. My father was floored by the drug’s effect.

The Cymbalta prescription was 30 mg daily for the first week, then 60 mg the second week. The Cymbalta was working so beautifully that on the eighth evening, I kept the dose at 30 mg (I was in charge of administration). Next day, my mother had a partial relapse and asked, “Do you think it’s because you didn’t double the dose?” I said, “Yes. Well, tonight you’re getting 60 mg.”

Early next morning while still in bed, my mother boldly said, “I feel SO strong, like I can just swing my legs off the bed and stand right up!” She then began talking about going out for breakfast and doing some shopping to buy ingredients to make bread and meat pies  --  while still in bed. 

Another three weeks on 60 mg worked wonderfully, and then we had to increase to 90 mg. Cymbalta restored my mother’s appetite, wiped out panic attacks, brought back her laughter, resurrected social connections, and motivated her to stick to an exercise plan.

Since taking Cymbalta, my mother has had NO “my whole body hurts” episodes, and the shoulder pain (eventually diagnosed as rotator cuff tears) has significantly diminished  --  or perhaps her perception of it has. And when the shoulder pain does occasionally act up, my mother doesn’t sweat it, whereas pre-Cymbalta, she’d sob away and completely shut down.

About five weeks after starting Cymbalta, my mother’s energy level began plummeting; she felt increasingly drained and excessively sleepy, even though her mood remained normal. We took her to the ER, and a blood test revealed a medical condition, hypothyroidism, that’s known to cause depression. She started treatment the next day. In retrospect, my mother had been showing signs of low thyroid for several months, but we didn’t think much of the subtle symptoms.

Also, about five weeks after beginning Cymbalta, my mother signed with a new medical plan that didn’t cover Cymbalta, and thus had to gradually transition to a comparable dose of Effexor. These two unexpected developments extended my stay with my parents.

Effexor, like Cymbalta, is a seratonin/norepinephrine reuptake inhibitor. The transition from Cymbalta to Effexor was smooth, save for a disabling case of persistent dizziness on the last dose-changing day -- yet despite that, my mother was upbeat.

In summary, my mother is now gradually tapering off Effexor; apparently, the depression is now under control with the treatment for that medical disorder. There are NO problems with the Effexor tapering, and absolutely NO relapse of the depression, which is strong evidence that the depression’s underlying cause was the low thyroid.

(Original publication date: January 2010)

Best Types of Exercise for Depression and Weight Loss

Exercise fights depression and weight loss, and one study after another confirms the strong tie between exercise and alleviation of depression symptoms. I’m a certified personal trainer. A Southern Methodist University study shows that exercise is a potent treatment for depression and anxiety.

Before starting a workout program, the study authors recommend a health assessment to clear the patient for physical activity. The general recommendations for exercise apply to depressed but apparently healthy people. This means 150 minutes weekly of moderate-intensity exercise, or, 75 minutes of vigorous exertion.

But which will work better for depression, and weight loss: 150 minutes of moderate-intensity, or 75 minutes of rigorous exercise a week? Go for the 75 minutes, hands down. Intense exercise causes hormonal changes in the body that trigger weight loss in the form of fat lost, while keeping valuable muscle tissue intact.

Moderate level workouts fail to do this. Intense exercise that elicits the best hormonal response is the kind called high intensity interval training, as well as a kind of exercise called burst training.

A 2002 issue of the Journal of Applied Physiology reports that high intensity training, involving sprints, produced 96 percent more human growth hormone when compared to slower long duration jogging. Growth hormone release creates breakdown of fat, which means weight loss. Other benefits include increased energy, increased libido and improved sleep, and these improvements will go a long way in alleviating symptoms of depression.

People with depression, including depression caused by weight loss struggles, can begin by walking…the anaerobic way, for maximum weight loss. However, include strength training in your regimen. Don’t just do cardio.

Strength training, like cardio (walking, running, cycling) can be done intensely. Intense exercise helps alleviate depression simply because it creates a feeling of accomplishment. You’ll be much more amazed at yourself after doing high intensity interval training as opposed to mere, boring long duration cardio like prolonged boring pedaling on an elliptical machine or endless laps walking around the block.

Another type of exercise that will fight depression and encourage weight loss is the martial arts. Martial arts, by their nature, involve bouts of intense training, or burst-style training. Plus, the sense of accomplishment will be unlike anything you’ve ever experienced; I’ve trained in the martial arts for years, and it just feels so great developing skills in this discipline. And weight loss will be a sure result, and this of course will help relieve your depression, as you become fitter.

Source: Southern Methodist University (2010, April 6). Mental health providers should prescribe exercise more often for depression, anxiety, research suggests. ScienceDaily. Retrieved January 6, 2011, from http://www.sciencedaily.com­ /releases/2010/04/100405122311.htm


What Happens During MRA: Patient Describes Heart Imaging Procedure

You know what an MRA is, but what exactly happens during an MRA – here is my firsthand account.

I recently had an MRA – no, not MRI, but MRA. An MRA is a type of MRI, actually. MRA stands for magnetic resonance angiogram (or angiography). Perhaps your doctor has told you that you should have an MRA. Or maybe you’ve already made the appointment for the magnetic resonance angiogram.

There are many reasons to have an MRA, and just because your doctor has ordered this procedure, doesn’t mean it will find something wrong with you.

What happens during an MRA?
After filling in the paperwork, you’ll wait.  The technician who did my procedure was the person who came into the waiting room to summon me. I was led to a room and told to slip into two gowns (I don’t remember the reason why two were necessary, but it made sense at the time). I then waited in an area for people waiting to get an IV portal inserted into their arm for the contrast dye.

What happens during an MRA?
The procedure uses contrast dye to make the blood vessels visible. So I waited briefly, then was called into a room where a nurse prepped me for the IV portal. Then I was sent back to the little waiting room.

The technician then summoned me. I had asked for a chance to speak to the cardiologist who’d be present. I was also told I couldn’t wear earplugs (magnetic resonance procedures produce loud noise) because I had to wear headphones to be able to communicate with the technician during the exam. I briefly spoke to the cardiologist, and then was taken to the MRA room.

What happens during an MRA?
I lied on the table. The technician placed some heart monitor leads on my chest. I had been told that during the procedure I’d be having to hold my breath, usually for 20 seconds at a time. The technician placed a thick, weighty rectangular-shaped thing on top of my chest, and did something with the IV portal, though she did not inject the dye.

The dye is injected from another room. I don’t know how this works, but after I had lied on the table, she had rigged something with the IV portal, while I was lying flat with my eyes closed. I was told the test would take an hour, more likely an hour and 15 minutes.

A little hand pump was placed in my other hand and I was told that if I needed to be taken out of the MR tube, to squeeze the pump.

The MRA was of my heart (I’ll get to the reason in a moment), so my head was completely in the tube. Many times I was told (through the headphones by the tech) to “Inhale, exhale, now take a deep breath and hold.” Then she’d say, “Breathe.” This pretty much defined the experience, though there were several points during which she told me to relax for a few minutes while she made adjustments from the other room.

Believe it or not, only the last few minutes of the procedure involved the contrast dye. She alerted me when she was giving it to me (while I was still inside the tube). I had no reaction to it. Next thing I knew, the exam was done.

Why did I have the MRA? I had had a visit with a cardiologist as part of heart disease screening (both parents have heart disease). He detected a Class II heart murmur. The subsequent echocardiogram was normal, so the only thing he could think of that was causing the murmur was pulmonary stenosis (narrowing of pulmonary artery). A magnetic resonance angiogram would detect this.

In my case, the MRA turned out completely normal, and my cardiologist has concluded that the murmur is a “functional flow” type which can develop in athletes (of which I am). It is harmless.

Mitral Regurgitation: Exercise Tolerance Testing & Surgery

Exercise tolerance testing can determine if mitral valve regurgitation requires surgery.

If you have mitral valve regurgitation, you don’t necessarily need surgery. You may have mitral valve regurgitation and not even know it.

Mitral valve regurgitation is actually fairly common, afflicting about 20 percent of people over 55. Though this condition can be fatal, it may also be mild, causing fatigue, shortness of breath, excessive urination, swollen feet or ankles, heart palpitations and even a cough.

Mitral regurgitation involves backward leakage of blood and can lead to abnormal heart rhythms, which can bring on strokes; and can also cause ventricular tachycardia, and this can cause sudden death. So even though mitral regurgitation can be mild enough not to require surgery, it can also be severe enough to kill.

Nevertheless, a simple test using a treadmill can go a long way in revealing a patient’s degree of mitral regurgitation. The exam is called exercise tolerance testing, and can be useful in determining if a patient will need surgery. The report appears in the American Journal of Cardiology (2007), and the research was conducted by New York-Presbyterian Hospital/Weill Cornell Medical Center.

"Mitral regurgitation can be very benign, going unnoticed for many years, or can be severe, impeding the heart's proper function and leading to complications, even death,” explains Dr. Jeffrey S. Borer, a study co-author.

Dr. Borer further explains that exercise tolerance testing is simple and can be done in doctors’ offices, eliminating the need for expensive imaging exams. Exercise tolerance testing can show if a patient’s mitral valve regurgitation is getting worse and if it requires surgery.

If a patient with mitral regurgitation does well on the treadmill, he or she “will likely remain healthy and not have to undergo further testing for a number of years,” says principal investigator Dr. Phyllis G. Supino. Historically, exercise tolerance testing with the treadmill has been used to assess coronary artery disease; it’s commonly known as a “stress test” and involves imaging.

In mitral regurgitation, the valve fails to close properly (completely) when the heart contracts. This restricts blood flow throughout the body. A stethoscope will detect a distinct heart murmur with this condition.

The study followed 38 patients for seven years who had chronic severe mitral regurgitation that was not caused by a previous heart attack. The patients had exercise tolerance testing at the beginning of the study. The exercise tolerance duration was set for 18 minutes maximum.

If a patient was able to sustain exercise for at least 15 minutes, he or she had a five-fold lower yearly risk of acquiring heart failure or other heart problems requiring surgery, when compared to subjects who were not able to sustain exercise for 15 minutes. For a person requiring surgery, there are two treatment options: mitral valve repair, and mitral valve replacement.

In the case of mitral valve replacement, a mechanical valve may be used, or a pig or cow tissue valve may be used. You may cringe at the idea of having pig or cow tissue inside your body if you have mitral regurgitation requiring surgery, but you should hope you get pig or cow tissue, because a tissue valve replacement requires only temporary blood thinner use; whereas people with mechanical valve replacements must be on a blood thinner for the rest of their life.


Leg Blood Clot Detection After Surgery Made Easier with CTV

Blood clots in legs following surgery can be detected with CT venography.

Surgery can cause blood clots in legs that may travel to the lungs (pulmonary embolism) and kill the patient. A huge risk factor for blood clots forming in the legs is surgery, which is why patients wear compression stockings and are on anticoagulant drugs after surgery.

But these measures don’t 100 percent guarantee against blood clot formation in the legs after an operation. When a blood clot in the leg breaks free, it can travel “upstream” and lodge in the lungs, killing a person instantly, though in 90 percent of cases, the patient survives.

But don’t let this 90 percent figure reassure you, because pulmonary embolisms strike 600,000 Americans every year! One-tenth of that is 60,000: 60,000 deaths every year in the U.S. from pulmonary embolism.

A chest CAT scan can detect a pulmonary embolism. However, it would be a lot better if scanning-technology could spot a blood clot in the legs – before it dislodges and travels to the lungs. And indeed, we have that technology: CT venography.

"That's the major advantage of doing CT venography, because it allows us the chance to see the clot in the legs before it breaks off and goes to the lungs," says Jeffrey Kline, Director of Emergency Medicine Research at Carolinas Medical Center in Charlotte, N.C.

As practical and simple this technology is, only one-fifth of hospitals – that have CT venography equipment – actually perform this test on patients after surgery to detect blood clots in the legs, says Dr. Kline. This is very puzzling to me, because if a hospital has this technology, why not use it on all post-surgical patients? And why don’t all hospitals have this technology in the first place? Why wait till a blood clot breaks free from the leg and takes up real estate in the lungs, causing instant death?

A pulmonary embolus can kill a person after a deep vein thrombosis forms in his lower extremity while on a long airplane flight, where a CT venography isn’t available. But for people already in hospitals, at risk for thromboembolic disease as a result of surgery, the CT venography should be a standard post-operative procedure!

CT pulmonary angiography (CTPA) can detect blood clots in the lungs – “can,” that is; DVTs in smaller arteries can be missed! However, CT venography can give physicians a clearer picture of what’s going on in the patient.

This was a study conducted at New York Presbyterian Hospital involving over 1,500 patients. The conclusion? When CTPA and CTV are combined, the detection rate of DVT (blood clots) was increased by 20 percent. The CT venography would immediately follow the CTPA, thereby eliminating the need for additional contrast dye, and the CTV takes only three minutes.


Source: http://www.sciencedaily.com/videos/2005/0609-scanning_for_leg_clots.htm

Why High Blood Pressure Damages Heart and Kidneys

High blood pressure is a ruthless condition that causes disaster throughout the body, especially to the heart, but the kidneys also suffer as well. Just because you can’t “feel” high blood pressure (also known as hypertension), doesn’t mean that it’s not that serious. 

And just because it doesn’t require too many brains to take your blood pressure at your kitchen table with a handheld gadget that you can purchase at Walmart, doesn’t mean that hypertension is something to sneeze at. High blood pressure kills.

I consulted with Dr. Michael Fiocco, Chief of Open Heart Surgery at Union Memorial Hospital, one of the nation's top 50 heart hospitals. He explains, “Hypertension contributes to coronary artery disease by stressing the arterial lining.  This leads to atherosclerosis.”

Atherosclerosis is buildup of dangerous plaque in the arteries. When the coronary arteries become at least 70 percent blocked with this plaque, this is considered severe heart disease. A small percentage of severe heart disease cases are actually missed by stress tests such as a treadmill stress test.

Dr. Fiocco continues, “Also, the stress on the left ventricle (main pumping chamber) causes the ventricle to thicken or hypertrophy.”  Hypertrophy means increase in size. “This hypertrophy leads to more demand for oxygen by the muscle and also decreases the heart’s ability to relax.  Therefore, hypertension leads to not only coronary artery disease, but dysfunction of the left ventricle, and ultimately heart failure.”

Quite frankly, there is no excuse for high blood pressure, since this condition can easily be detected, right in your own home with a portable tool that’s easy to use, and the condition can also be treated.

Dr. Fiocco continues, “Hypertension will also injure the very small arteries known as arterioles.  These are very difficult to see on an angiogram since they are so small, but atherosclerosis in these vessels, referred to as small vessel disease, can lead to significant dysfunction and angina.  This is similar to how hypertension injures the kidneys, by injuring small vessels, and there is no bypass or stenting that can be done to fix this once it occurs.  It can be avoided as long as hypertension is avoided.  The damage is not reversible, but certainly can be halted by controlling the blood pressure.”

To help permanently lower your blood pressure, restrict processed foods. This will automatically shave off a lot of sodium in the diet. Eat 8-10 servings a day of any combination of whole fruits and raw vegetables. Juice some of the produce to make consumption easier. Consider that a 7-8 ounce glass of juiced fruit/vegetables counts as one serving. Add unsalted nuts and seeds to your diet, and exercise!

Can Heavy Lifting, Squatting, Deadlifting Cause Aneurysm?

Does that nasty headache from heavy weight lifting mean you might have an aneurysm?

Sometimes heavy weight lifting (squats, deadlift, etc.) can cause a headache, and make you think this is an aneurysm. I’m a certified personal trainer, and I do know for certain that a headache, while doing heavy lifts, can be brought on by dehydration, even though you may not feel thirsty.

To help rule out dehydration as the cause of a bad headache that occurs during or after deadlifting, squatting or some other heavy weight lifting routine, drink plenty of water prior to working out; a tall glass worth. 

Fifteen minutes into your routine (including any warming up), guzzle some more water. Every 15 minutes drink water; not a tiny sip, but guzzle it at the fountain. Also make sure that you’ve been adequately nourished throughout the day with nutritious food.

If you nevertheless develop a headache during your weight lifting, or shortly after, this may be due to an increase in the venous pressure of the brain, according to Teresa Caulin-Glaser, MD, Executive Director at McConnell Heart Health Center/Riverside Methodist Hospital in Columbus, Ohio, and Clinical Associate Professor in the Department of Internal Medicine/Division of Cardiology at Ohio State University.

Dr. Glaser also mentions what is known as a primary thunderclap headache, which may be caused by heavy weight lifting (and we all know how heavy and wicked a good set of deadlifts or barbell squatting can be).

The primary thunderclap headache is related to the vasoconstriction of the blood vessels that feed the brain.

If you’ve been worrying about an aneurysm being triggered by your weight lifting, or if you’re troubled by headaches following your workouts, even though you’ve been drinking plenty of water, speak to your physician just to play safe. You might also want to consider hiring a personal trainer for a few heavy deadlifting and squatting sessions to make sure that you’re positioning your body correctly, and breathing correctly during these heavy lifts.

Dr. Caulin-Glaser says to cease working out if you experience a sudden-onset bad headache.

An aneurysm (leaking variety) may present with only one symptom: sudden, severe headache. A ruptured aneurysm typically presents with a most horrible headache plus other symptoms like blurred vision, nausea, vomiting and confusion.

Source: http://www.mayoclinic.com/health/brain-aneurysm/DS00582/DSECTION=symptoms

How a Cardiologist Can Miss Severe Heart Disease in Women

A cardiologist provides insight into how a specialist can examine a woman with severe heart disease and then tell her she’s in great shape.

Cardiologists do indeed miss severe heart disease in women (men as well, but more prevalently, women). One reason is because despite all the mounting media attention given to women’s heart disease, many doctors take the symptoms more seriously in men, and also, symptoms of heart disease in women oftentimes differ from those in men.
 
I consulted with Dr. Suzanne Steinbaum, Director, Women and Heart Disease, Heart and Vascular Institute, Lenox Hill Hospital, NY.
 
Dr. Steinbaum explains, “Communication between doctor and patient is critical.  We have all heard many stories of young women who were dismissed by their doctors as being healthy, only to find out later that they had heart disease.  It is important, from the patient's perspective to discuss all the symptoms, and address all concerns.  Discussing family history is crucial in giving your doctor a true understanding of your own risk.”
 
Dr. Steinbaum adds, “Heart disease is invisible until is presents itself, so even if you are thin and fit, you can still be at risk.” 
 
Diet is a big player in coronary artery disease. No matter how hard you train in the gym, you cannot out-train bad nutrition. You may look great and be able to knock off pushups and run 5Ks, but a processed-food diet and mental stress can cause plaque to build up inside your coronary arteries.
 
“Baseline EKG's, echocardiograms and blood tests don't always predict who is going to have a heart attack, and even simple stress tests without imaging studies may be misleading,” says Dr. Steinbaum. “Communicating symptoms and changes in activity levels might be the first clues that there are cardiac problems.”
 
Unfortunately, though some women are aware of recently-new symptoms, they don’t connect them to possible severe heart disease. My mother experienced shortness of breath for months and attributed this to narcotic painkillers, which CAN cause labored breathing. 
 
Then one morning she upchucked, after suffering shortness of breath, and still, did not make a connection. My father even questioned her on what she ate the day before! Severe coronary plaque buildup was the last thing on their minds at this point. However, the vomiting tipped me off and I took her to the ER where she was diagnosed with reflux disease and released! 
 
Two days later I took her back for chest pains. She was admitted, and the next day I was told by three doctors that a massive heart attack was imminent due to blockages of at least 97 percent in five coronary arteries. 
 
Ten months prior, my mother’s cardiologist (not one of the three) told her, “You’re the last person I’d ever think would have a heart attack.” Ten months later she had emergent quintuple bypass surgery.
 
Dr. Steinbaum says, “Sometimes your sixth sense tells you something
is significantly wrong.  As a patient, you must empower yourself.” 
 
One way a woman can do that is to undergo a calcium score test which is pretty accurate for determining the likeliness of heart disease, and near-future attack, which kills about 267,000 U.S. women every year – over six times the rate of breast cancer death.
 
Source: http://www.womensheart.org/content/HeartDisease/heart_disease_facts.asp

Heart Disease: Make Lifestyle More Important than Genes

When it comes to heart disease, you can make lifestyle more important than genes; you need to know HOW to make lifestyle trump genes for heart health!

Which is more likely to cause heart disease: lifestyle or genes? The latest study says that genes seem to be more important than lifestyle, in the risk for developing heart disease.
This study, from the Center for Primary Health Care Research in Sweden, didn’t include information as to why people in some primitive cultures (e.g., tons of exercise, no processed foods) have virtually no heart disease, and why some countries have markedly low rates of heart disease (like Japan).

The rate of heart disease increases when peoples from these lands then take up residence in the Western World. Thus, we can’t conclude that genes make these cultures resistant to heart disease.

The CPHCR study followed over 80,000 adopted men and women (all born in 1932 or after) and compared them to their adoptive and biological parents. They developed heart disease between 1973 and 2008.

Is heart disease determined more by genes or by lifestyle?
In the adopted subjects who had at least one birth parent with heart disease, the risk of the illness was 40-60 percent greater than that of a control group. And, there was no elevated risk of heart disease in subjects whose adoptive parents had the condition.

"The results of our studies suggest that the risk of coronary heart disease is not transferred via an unhealthy lifestyle in the family, but rather via the genes," states Kristina Sundquist, lead study author. "But that does not mean that one's lifestyle is not a factor in one's own risk of developing coronary heart disease."

Heart disease: lifestyle vs. genes
I’m a certified personal trainer whose mother underwent quintuple bypass surgery for dangerously blocked arteries. My father has never had symptoms of heart disease, but his coronary calcium score is nearly 1,200!

Two of my brothers had their calcium scores taken; one has heart disease (according to the score), and the other’s score was zero. My own calcium score, very recently taken, is zero. Over the years, have there been lifestyle differences between all five of us that can explain why two of the offspring of people with severe heart disease have a calcium score of zero? YES!

My mother did not exercise. That alone is a potent risk factor for heart disease. Her diet was the standard American diet: Though she was never a big eater, her diet was mostly that of processed foods – the same processed junk that most everyone else in the U.S. eats. According to an article in the American Journal of Cardiology (online), heart disease is a food borne illness.

My father’s diet is even worse in that he eats a lot of bakery and other white-flour-based foods like pancakes. He also has a big appetite for things like bratwurst, candy, gravy, butter and sugary jams. So why hasn’t he needed any bypass surgery, even though he’s four years older than my mother? Maybe this is where genes come in.

But genes or not, a calcium score of 1,200 is frightening. My father has been exercising for about 30 years, but it’s always been pretty much the “go through the motions” caliber of exercise. Despite using machine weights all these years, he never developed a physique that looked like he worked out; he’s always had a “reverse V taper,” no visible muscle in the arms, and no sign of muscle development in the legs.

He has never been one to jog or power walk, and only much later in life did he take up pedaling a stationary bike. So just because someone “works out,” doesn’t mean that the intensity is sufficient enough to produce significant fitness and health benefits. Nevertheless, not pushing through a workout and instead staying in a nice comfort zone is far better than doing absolutely NO strength training, like my mother.

My brother with the heart disease was never much into exercise, though once he learned of his calcium score, he took up exercise. He says he has changed his diet to help halt the progression of coronary plaque. However, every single time he visits or I visit him, I witness him eating no healthier than the average American.

My zero-calcium brother has been exercising vigorously for years and years (weights, and more recently, “Insanity” and martial arts), has been taking supplements all along, and claims to be very conscious about nutrition, though again, whenever I see him, I don’t see much evidence of this.

I have always worked out like a warrior, take a lot of supplements daily, and have practically eliminated trans fats; won’t touch processed meats; eat very little red meat; hardly touch processed foods.

As you can see, lifestyle appears to be a pretty strong factor in whether or not someone in my family has heart disease. So though this particular study points to genes being more important than heart disease, statistics (e.g., very little heart disease in Okinawa) don’t lie.

Sources:

UN Chronicle: The Atlas of Heart Disease & Stroke

Stroke Risk Doubles Within Hour of Having One Drink

Have that drink and your risk of stroke doubles for the next hour, says a 2010 report in Stroke: Journal of the American Heart Association.

It doesn’t matter what type of alcohol, either, when it comes to doubling stroke risk; it could be beer, wine or hard liquor. A stroke is when a blood clot, which may arise in the heart or anywhere in the body, travels to the brain and lodges, cutting off oxygen supply.

The study, called the Stroke Onset Study, involved an interview with 390 patients who had suffered an ischemic stroke (in this case, the blood clot forms in a vessel leading to, or located in, the brain). Interviews occurred three days following the strokes, and covered various aspects of the patients’ lives.

However, patients were interviewed only if they were lucid enough to understand the questions and had retained reasonably clear speech. Fourteen of the people had had liquor within 60 minutes of their stroke.

The researchers concluded, based on all the interview responses, that the risk of stroke was 2.3 times greater in the first 60 minutes; 1.6 times greater in the second hour; and 30 percent lower than baseline after 24 hours. The study adjusted for other potential triggers for stroke, such as having a caffeinated drink.

"The evidence on heavy drinking is consistent: Both in the long and short term it raises stroke risk," says Murray A. Mittleman, M.D., Dr.P.H., senior author of the study and director of the Cardiovascular Epidemiology Research Unit at Beth Israel Deaconess Medical Center in the Harvard Medical School in Boston.

So how can having a drink raise risk of stroke over the following hour? Blood pressure goes up after having a drink, and blood platelets get stickier, and stickier platelets increase the odds of clot formation.

Interestingly, regular consumption of small amounts of liquor is actually associated with improvement in blood fats and more pliable blood vessels. This may cut the risk of blood clots overall. This in no way, says Dr. Mittleman, means that nondrinkers should start drinking. Nor does this mean that drinkers of small amounts of alcohol (one drink daily) should quit. There isn’t enough data to draw a definitive conclusion regarding alcohol consumption.

A controlled study is needed that involves people randomly assigned to drink, while others don’t. Further, the findings of the Stroke Onset Study don’t apply to people with severe stroke. It’s important to remember that high consumption of alcohol is linked to a number of problems, including liver damage, high blood pressure, breast cancer, obesity and car accidents. If all of this sounds confusing, then simply don’t drink. To date, there is no evidence that abstinence is harmful to one’s health.

Source: http://www.sciencedaily.com/releases/2010/07/100715162910.htm

Stroke and tPA Treatment: MRI Shows Time Window of Stroke

MRI has amazing accuracy at determining time of stroke; crucial knowledge for tPA treatment

Stroke is often successfully treated with tPA, but only if tPA is given within a tight time window from the onset of symptoms: four and a half hours (the window is often named at three hours as well). However, MRI studies show that MRI is a promising tool for determining onset time of stroke.

If tPA is given outside the time window of stroke onset, bleeding in the brain can result. The reports of the MRI study appear in the Dec. 2010 Radiology. TPA stands for tissue plasminogen activator, a clot-busting drug that restores blood flow in the brain.

Stroke strikes about 795,000 Americans every year (including recurring incidents). You need to ask yourself: What am I doing differently than nearly 800,000 fellow Americans that will go a long way in preventing a stroke?

The American Stroke Association says that this condition is the third leading cause of U.S. deaths. About one-fourth of stroke victims cannot receive tPA because time of onset is not known, says Catherine Oppenheim, MD, PhD, lead researcher.

The study involved reviewing data of patients treated between May 2006 and October 2008. Time of symptom onset was definitive; all 130 patients had an MRI within 12 hours of symptom onset. With the MRI data alone, radiologists predicted which patients had onset symptoms for longer than three hours  --  with more than 90 percent accuracy of prediction.

Dr. Oppenheim explains, "When the time of stroke onset is unknown, MRI could help identify patients who are highly likely to be within the three-hour time window when tPA is proven effective and approved for use."

She adds that the use of MRI could revolutionize the way stroke is approached in emergency rooms. "With the use of MRI, all stroke patients could be managed urgently, not just those patients with a known onset of symptoms." These study results are extremely promising, yet more research is needed.

In the meantime, what are you doing to prevent stroke? Here are the risk factors, according to Mayoclinic.com: family history of stroke, TIA or heart attack; over age 55; high blood pressure; high cholesterol; smoking; diabetes; body mass index of at least 25; lack of exercise; cardiovascular disease; birth control/hormone therapies that use estrogen; heavy drinking; being black; and use of cocaine, meth and other such drugs. Having multiple risk factors greatly amplifies the risk.


How Long After Stroke Will Medical Treatment Work?

How long after suffering a stroke will treatment still be effective?

After a stroke, there is a critical time period during which treatment is effective, or most effective. This is why it’s so important to know (when possible, of course) the time of onset of stroke symptoms. Historically, in order for treatment for stroke to work, treatment (intravenous) must start within four and a half hours of the stroke, a very crucial time window of treatment efficacy by the clot busting drug tPA (tissue plasminogen activator).

Only 10 percent of stroke patients have this benefit. But now, brain research being done at Lund University suggests that the length of time after a stroke, for treatment to work, may be up to two days. A substance has been discovered, that stimulates the brain’s self-healing functions following stroke, by the Laboratory for Experimental Brain Research in Lund, along with American researchers.

Key to this process is that these patients can regain some of their lost function during the first six months after the event. The scientists, led by Professor Tadeusz Wieloch, discovered a way to activate a protein that’s in the brain, called sigma-1 receptor. The protein plays a key role in the brain’s ability to recover during that critical time period following stroke.

Rats were induced with stroke. One group was placed in a cage with extra stimulation like ladders; the other group was placed in a bland cage.

Professor Wieloch explains, "After performing a genetic analysis of the rats that stayed in the normal cage and those that were in an enriched cage, we found that many genes were activated by the enriched environment. One of these genes coded for the protein sigma-1 receptor. We then injected the rats with a specific substance that activated the sigma-1 receptor and found that the rats regained their function more quickly than the untreated animals."

The full report is in the journal Brain (2011). The brain has a natural response to an enriched environment. The objective, then, is to re-create and stimulate this natural response of repair. A pharmaceutical company in Japan is now engaged in a clinical trial involving humans.

Stroke strikes 800,000 Americans every year. What are you doing differently than these 800,000 fellow Americans to prevent this catastrophe? Risk factors are many: family history, age 55-plus, high blood pressure, high cholesterol, diabetes, smoking, secondhand smoke, being overweight, not exercising, heart disease, atrial fibrillation, birth control pills, heavy or binge drinking and illegal drug use.

Sources:

http://www.mayoclinic.com/health/stroke/DS00150/DSECTION=risk-factors

9/18/14

Are Poor People More Likely to Have Strokes?

Is it true that poor people are more likely to suffer a severe stroke? Yes, says a recent study. The stroke in question here, as it relates to poor people, is that of the ischemic kind: blocked blood vessels; this occurs in the brain, of course.

The research showing that poor people have more severe strokes of this type comes from the University of Cincinnati (UC). The study showed an association between severity of stroke at presentation, and increasing poverty in the area where the patient resided, and this link was independent of other known risk factors that are associated with the outcome of stroke.

The study looked at over 1,900 cases of stroke (ischemic). Average patient age was 71. The poorest communities were associated with a substantially elevated initial stroke severity – by 1.6 points, based on a severity scale, when compared to the wealthiest category, say the researchers.

The study authors used census tract data for their estimations of socioeconomic status. After other variables were adjusted, the results of this analysis were still significant.

"The magnitude of change in stroke severity for the poorest patients was similar to the effect of having a history of coronary artery disease or high blood pressure," says Dawn Kleindorfer, MD, an associate professor in the department of neurology, and member of the UC Neuroscience Institute.

This study shows the association between higher risk of severe ischemic stroke among poor people. It does not explain why, though, poor people have these more severe strokes. But the researchers offer up some theories: Access to medical care comes to mind, for starters. Cultural factors are also named as a possible contributor, along with compliance to taking medications, and undiagnosed disease.

From a certified personal trainer’s perspective, I’d venture to say that poor people in needy communities have less access to recreational centers and health clubs, which translates to less exercise among poor communities. Lack of structured exercise is a risk factor for stroke, as well as type 2 diabetes and high blood pressure, which also increase the risk. Overweight is more common among poor people, and a body mass index in the overweight range is a risk factor for stroke.

Being poor, however, doesn’t mean that you’re more likely to have a stroke, if you take measures to prevent this catastrophe from happening in the first place. A poor person without medical insurance can still do a lot to help prevent stroke by exercising (no fancy gym necessary; jumping, squatting, lunging and pushups inside the home will do); not smoking; and restricting junk foods.


When the Mediterranean Diet Won’t Prevent Heart Disease

Why heart disease can happen to those who “eat healthy.”
My mother had emergent quintuple bypass surgery and mitral valve replacement, and thus saw a steady stream of doctors and nurses following the procedure. And a number of times, she commented, “I don’t understand how this heart disease could have happened to me. I’ve been on the Mediterranean diet.”

The heart disease consisted of five major arterial feeds in the heart being so blocked (the report said “subtotal occlusion”), that a heart attack was imminent. The catheter angiogram alarmed the cardiologist and he immediately contacted a cardiothoracic surgeon, who dropped what he was doing and headed straight for the hospital.

He wasted no time rounding up his team and getting my mother prepped for quintuple bypass surgery – within two hours of viewing the angiogram. And those words echoed post-operatively: “How could I get heart disease? I’ve been on the Mediterranean diet.”

I kept hearing her say Mediterranean diet. I kept my mouth shut because my mother was in no emotional state to hear that she had absolutely not been  --  I repeat  --  not been, on the Mediterranean diet! In fact, she had never been close to it.

But in her mind, she had been eating according to the Mediterranean diet for years, and thus, in her mind, the Mediterranean diet failed to protect against heart disease. Heart disease kills more Americans than any other malady.

Here is what really had been going on: My mother was never on the Mediterranean diet. She had been on SAD: Standard American Diet. The reason she believed she’d been on the Mediterranean diet was because when it was time to use oil, she used olive oil. When it was time to season food, she used garlic. She ate vegetables  --  from a can. She had a small salad every night with dinner. She ate yogurt.

This, to her, meant the Mediterranean diet. But just what is the Mediterranean diet? I’m a certified personal trainer with extensive knowledge of nutrition and various kinds of eating plans. The Mediterranean diet in large part prohibits processed foods, except for bread, pasta and dairy products.

This means that for the Mediterranean diet, the following kinds of foods are pretty much out: frozen dinners, frozen turkey sausage patties, luncheon meats, pastries/donuts/pie, canned soups, canned gravies, bottled salad dressings, crackers, pretzels, potato chips, ready-made mashed potatoes in tubs, frozen French fries, Dairy Queen ice cream, whipped cream and chocolate syrup.

My mother would regularly eat these items! You can’t get more processed than frozen dinners and luncheon meats! Bottled salad dressings are also highly processed, not to mention Dairy Queen ice cream! Ugh.

The Mediterranean diet means red meat just once or twice a month. My mother consumed ground beef several times a week, and whenever she went out to eat, ordered a hamburger. She often drank ginger ale. But she believed she was on the Mediterranean diet because she added olive oil to her white rice, and sometimes ate berries as an evening snack.

My mother’s food pyramid in no way resembled the food pyramid of the Mediterranean diet. My mother ate the same food that everyone else eats: highly processed, sodium-drenched foods with trans fats, including “hidden” trans fats, saturated fats, preservatives and artificial flavorings and colorings.

The Mediterranean diet is natural-based, heavily restricting processed foods, and bans trans fats and other synthetic chemicals. This isn’t to say that an adherent to the Mediterranean diet will spoil everything with a once-a-week cheat meal.

But my mother had several cheat meals and snacks a day – thereby disqualifying her eating habits from being protective against heart disease. My mother would have eggs every morning for breakfast, yet eggs are in the second-highest level of the Mediterranean diet food pyramid! And she only periodically ate nuts, seeds and legumes!

I have since enlightened my mother about why her way of eating, all these years, has been anything but the Mediterranean diet. No eating plan that’s based on processed foods has been associated with reduced risk of heart disease or any disease for that matter. The only time the Mediterranean diet fails to protect against heart disease is when a person only thinks she or he is on this plan, but in reality, eats the same junky processed foods as the next person.

Two Supplements May Reverse Plaque in Coronary Arteries

Two supplements may actually reverse buildup of plaque in coronary arteries. This news comes from

The Los Angeles Biomedical Research Institute. There is controversy over whether or not natural supplements can reverse coronary plaque buildup (a disease called atherosclerosis), which is strongly correlated to heart attack risk.

So the researchers studied a group of people who, when compared to the general population, have a two- to four-fold greater risk of heart attack. This group was firefighters, and for the study, they took daily supplements of coenzyme Q10 (coQ10) and aged garlic extract (AGE).

Another group of firefighters did not take these supplements, so that a comparison could be made. An important feature of this study was that these two supplements were investigated in combination.

Nobody in the study was on statins. At the beginning of the study, all subjects had their calcium score taken (a numerical value of measurable plaque buildup). The supplement group took 120 mg and 1,200 mg a day of coQ10 and AGE, respectively. The control group took a sugar pill, but nobody knew which group they were in, and neither did the researchers.

The calcium scores of both groups, at the beginning, did not differ that much. At the end of one year (during which the supplement group took their daily doses), another calcium score test was given. The supplement group had about half the rate of coronary arterial plaque progression as did the placebo group, and this includes an adjustment for typical risk factors for plaque buildup.

So why did the researchers choose the AGE-coQ10 duo? Many studies have already demonstrated garlic’s effectiveness at slowing plaque progression. However, garlic may deplete the body’s natural levels of coQ10. This potent antioxidant needs to be replenished, and hence, the duo.

The researchers stress that the earlier in the game that you take supplements to fight coronary plaque buildup, the better the result. This means that the supplements are most effective during early atherosclerosis, as opposed to advanced.

“For at-risk populations, taking this very cost-effective, easy step may slow down the progress or even prevent many serious complications of atherosclerotic heart disease further down the line,” says Vahid Nabavi Larijani, M.D., research fellow at LABRI, and the study’s co-investigator. Because garlic is a blood thinner, people at moderate risk for coronary artery disease should consult with their physician should they decide to take this herb; it can negatively interact with pharmaceutical blood thinners.


Telomere Length May Predict Coronary Artery Disease

Coronary artery disease and telomere length seem to be associated.

Yet one more possible predictor of coronary artery disease may be the length of telomeres. You know how shoelaces have plastic caps on their tips? Think of telomeres as being the plastic “caps” on the tips of chromosomes in cells, to keep these genetic strands tidy and neat.

Research from the Maddras Diabetes Research Foundation in India reveals some interesting information about telomeres and coronary artery disease. People with diabetes and prediabetes are at increased risk of coronary artery disease. Telomeres in these individuals are much shorter than in the non-diabetic/prediabetic population.

It is believed that an early test can predict disease of the coronary arteries. The research also shows that telomere length shortens between the stage of being prediabetic, and having diabetes. Type 2 diabetes, not type 1, was the focus in this study. It is not definitively clear why, in this population, the length is shorter.

Shortened telomeres are associated with other phenomena as well, and scientists still do not fully understand the mechanism behind telomeres. However, it is believed that somehow, some way, they are connected to the aging process. Older people have shorter telomeres. Younger people have longer ones.

Every time a cell divides, telomere length shortens. When the length reaches a critical point of shortness, the cell ceases to divide any further, and aging begins. In other words, the cessation of cell division is tied to telomere length. Think about this, because what is the opposite of cessation of cell division? Cancer!

Cancer is cell division out of control. The telomeres in continuously replicating cancer cells do not get shorter! Could the cure for cancer be found in the enzyme telomerase, which preserves telomere length?

Though telomerase is present in normal cells, the amount is so marginal that normal cells eventually stop dividing and begin aging and eventually die. But in cancer cells, telomerase is full-on active! In fact, the enzyme is 10-20 times more active in cancer cells than in normal cells.

So why can’t researchers figure out a way to shut off the telomerase in cancer cells, thereby killing cancer cells? Scientists are fervently trying to figure out how to do this.

In the meantime, telomere length holds promising information as far as predicting coronary artery disease. Coronary artery disease is closely tied to lifestyle habits. To significantly reduce risk of coronary artery disease, do both strength training with weights, and cardio workouts, on a regular basis; limit processed foods and sugar; quit smoking or don’t start; lose excess fat; manage stress; and eat plenty of fiber.

Sources:

http://www4.utsouthwestern.edu/cellbio/shay-wright/intro/facts/sw_facts.html