TOP HOMOEOPATHIC REMEDIES FOR HEART FAILURE

Heart failure (HF) often referred to as chronic heart failure (CHF), occurs when the heart is unable to pump sufficiently to maintain blood flow to meet the body's need.  The terms congestive heart failure (CHF) or congestive cardiac failure(CCF) are often used interchangeably with chronic heart failure. Signs and symptoms commonly include shortness of breath,excessive tiredness, and leg swelling The shortness of breath is usually worse with exercise, while lying down, and may wake the person at night.  A limited ability to exercise is also a common feature.

Common causes of heart failure include coronary artery disease including a previous myocardial infarction (heart attack), high blood pressure, atrial fibrillation, valvular heart disease, excess alcohol use, infection, and cardiomyopathy of an unknown cause. These cause heart failure by changing either the structure or the functioning of the heart There are two main types of heart failure:heart failure due to left ventricular dysfunction and heart failure with normal ejection fraction depending on if the ability of the left ventricle to contract is affected, or the heart's ability to relax The severity of disease is usually graded by the degree of problems with exercise Heart failure is not the same as myocardial infarction (in which part of the heart muscle dies) or cardiac arrest (in which blood flow stops altogether). Other diseases that may have symptoms similar to heart failure include obesity, kidney failure, liver problems, anemia and thyroid disease

HOMOEOPATHIC REMEDIES

In my experience the following homoeopathic  remedies are found to be very effective

Strophanthus Q – It is an excellent diuretic without any side effects . It increases the systole and  diminishes the rapidity. Heart’s action weak , rapid, irregular, due to muscular debility and insufficiency. Cardiac pain and dyspnea . Pulse rapid, alternating with slow, weak , small , irregular . It has no cumulative effects and restores tone to a brittle heart

Digitalis  6— For weak dilated heart without the side effects of allopathic Digoxin. Sudden sensation as if heart stood still. Sensation as if heart would cease beating, if he moves, must hold the breath and keep still. Irregular heart especially with mitral valve disease. Cardiac failure after fevers Cardiac muscular failure when asystole is present.  Heart dilated after sprains. Pulse weak and quickened by least movement

Convallaria  majalis Q – It is an excellent heart remedy in decompensated heart where the heart is overdistended and dilatation had begun and where absence of compensatory hypertrophy and venous stasis had been there .Feeling as if heart beat throughtout the chest. Sensation as if heart ceased beating , then starting very suddenly

Ctrataegus Q- It is a heart tonic and can be given in any stage of heart ailments . It is an excellent antiarrythmic, sedative in irritable patients with cardiac symptoms. Heart weakness  with oppression , stitches, and insomnia. Extreme dyspnea on least exertion. Heart dilated , first sound weak

My Resinous Heart

Being not quite in the forest in my new living space, I'm acutely aware of how much I soak up by returning to the trees. The last two days I've been called into unfamiliar places, but upon entering I remembered my belonging. 

 The air shifts as the sun is filtered by leaves, trunks, and brush. It's cooler, more moist, and the smell is poignant. Perfumed with pine resin and warm summer loam, I breathe deeper in the forest. I feel my gait slow down and my senses sharpen. I being to notice details, like teeth on the leaves, and the shades of green dancing before me. 

 I'm enchanted by the way the sun shines through the needles, as if today is the only day I'll see it shine just so. 

I'm teased by the shapes that could be wood or animal. 

I'm reminded of lineage at the rock walls. 

I love everything about the forest. The smell, the mystery, the trees, bushes and forest floor plants. Everything right down to the dirt, cones, and litter. 

The conifers are two-toned right now, as they don their shiny new tips. These white pine tips are excellent browsing for the wayward herbalist. 

Several of these tips soaked in vinegar provide a delicious source of bioflavanoids. 

I walked a little deeper into the woods, where there seemed to be a deer path just clear enough for me to follow. I could smell water and crushed sweet fern. The Mitchella carpeted this seldom trodden area. 

Even the rocks stir memories. 

Being a smallish human, a large stick is always good to carry. 

The ferns are especially lush back here. Dappling the feet of the trees and inviting in fairy folk.

They cascade down the hillside towards the water. 

Wild blueberries everywhere. 

Shapes only crafted by the trees themselves. 

Tiny new lives are protected. 

New friends introduce themselves.

Lifelong loves rendezvous.  

Far away the outline of the trees is deeply green against the fluffy clouds. 

Sit spots in secret alcoves are my favorite place to accomplish my journaling. 

I heart trees. 

CORONARY ARTERIES HOLD HEART REGENERATING CELLS

Endothelial cells residing in the coronary arteries can function as cardiac stem cells to produce new heart muscle tissue, Vanderbilt University investigators have discovered.

The findings, published recently in Cell Reports, offer insights into how the heart maintains itself and could lead to new strategies for repairing the heart when it fails after a heart attack.

The heart has long been considered to be an organ without regenerative potential, said Antonis Hatzopoulos, Ph.D., associate professor of Medicine and Cell and Developmental Biology.

"People thought that the same heart you had as a young child, you had as an old man or woman as well," he said.

Recent findings, however, have demonstrated that new heart muscle cells are generated at a low rate, suggesting the presence of cardiac stem cells. The source of these cells was unknown.

Hatzopoulos and colleagues postulated that the endothelial cells that line blood vessels might have the potential to generate new heart cells. They knew that endothelial cells give rise to other cell types, including blood cells, during development.

Now, using sophisticated technologies to "track" cells in a mouse model, they have demonstrated that endothelial cells in the coronary arteries generate new cardiac muscle cells in healthy hearts. They found two populations of cardiac stem cells in the coronary arteries -- a quiescent population in the media layer and a proliferative population in the adventitia (outer) layer.

The finding that coronary arteries house a cardiac stem cell "niche" has interesting implications, Hatzopoulos said. Coronary artery disease -- the No. 1 killer in the United States -- would impact this niche.

"Our study suggests that coronary artery disease could lead to heart failure not only by blocking the arteries and causing heart attacks, but also by affecting the way the heart is maintained and regenerated," he said.

The current research follows a previous study in which Hatzopoulos and colleagues demonstrated that after a heart attack, endothelial cells give rise to the fibroblasts that generate scar tissue.

"It looks like the same endothelial system generates myocytes (muscle cells) during homeostasis and then switches to generate scar tissue after a myocardial infarction. After injury, regeneration turns to fibrosis," he said.

Understanding this switch could lead to new strategies for restoring regeneration and producing new heart muscle after a heart attack, during aging or in disease conditions such as diabetes and high blood pressure, he said.

"If we can understand the molecular mechanisms that regulate the fate switch that happens after injury, perhaps we can use some sort of chemical or drug to restore regeneration and make muscle instead of scar," Hatzopoulos said. "We think there is an opportunity here to improve the way we treat people who come into the clinic after myocardial infarction."

EARLY SIGNS OF HEART TROUBLE IN OBESE YOUTH FOUND

A study that used two-dimensional echocardiography to closely examine the hearts of 100 children and teens found physical and functional signs of future heart problems already developing in obese children

In the study, published online today in the Journal of the American College of Cardiology, researchers from the University of Leipzig Heart Center in Leipzig, Germany, performed the echocardiograms on 61 obese children and 40 non-obese children ages 9 to 16. The two-dimensional echocardiogram uses ultrasound to provide cross sectional images of the beating heart as well as an assessment of blood flow through the valves and chambers of the heart. Researchers also conducted extensive blood chemistry analysis.

Researchers observed unique changes in the shape and function in the hearts of the obese children compared to the non-obese children in the study. In addition, obese children had significantly higher blood pressure and higher levels of LDL cholesterol, known as "bad" cholesterol, while HDL cholesterol, "good" cholesterol, was significantly lower. As a group, obese children also had a reduction in diastolic function, enlarged heart chambers signs of increased cardiac workload, and other unfavorable conditions.

"Children are ideal subjects to observe the effect of obesity on the heart," said the study's lead author Norman Mangner, M.D., of the Heart Center Leipzig. "This is because they are likely free of clinically relevant cardiovascular disease adults may suffer from."

Manger said additional studies are needed to determine if these changes are reversible with weight loss, and to determine the predictive value of these early cardiovascular changes.

WOMEN MORE LIKELY TO DEVELOP ANXIETY AND DEPRESSION AFTER HEART ATTACK

Women are more likely to develop anxiety and depression after a heart attack (myocardial infarction; MI) than men, according to research presented at Acute Cardiovascular Care 2014 by Professor Pranas Serpytis from Lithuania.

 Acute Cardiovascular Care is the annual meeting of the Acute Cardiovascular Care Association (ACCA) of the European Society of Cardiology (ESC) and takes place 18-20 October in Geneva, Switzerland.

Professor Serpytis said: "The World Health Organization predicts that by 2020 depression will be the second leading cause of disability and mortality in the world, surpassed only by ischaemic heart disease. Major depression follows MI in approximately 18% of cases and is an important predictor of disability and poor quality of life in the year post-MI."

He continued: "Patients with depression are nearly 6 times more likely to die within 6 months after an MI than those without depression. The increased risk of death in patients with depression persists up to 18 months after the MI. But despite the fact that post-MI depression is common and burdensome, the condition remains under-recognised and undertreated."

The current study investigated the impact of gender and cardiovascular disease risk factors on the risk of developing depression and anxiety after an MI.

The study included 160 patients admitted with a myocardial infarction to the Vilnius University Hospital Santariskiu Clinics in Vilnius, Lithuania. Patients were interviewed at least 1 month after the MI to collect information on demographic (including sex, age, education, marital status) and clinical characteristics (incidence of diabetes mellitus, previous treatment for hypertension, previous MI), other cardiovascular disease risk factors (smoking, physical activity), and history of mental health issues.

Depression and anxiety were both assessed using the Hospital Anxiety and Depression Scale (HADS): no depression and anxiety (0-7 score), possible depression and anxiety (8-10 score), mild to moderate levels of depression and anxiety symptoms (11+ score).

The researchers found that nearly one quarter of patients in the study were depressed (24.4%) and of those, 28.2% had received treatment with antidepressants (p<0.05). The average HADS score for depression was 6.87 (±4.6) in men and 8.66 (± 3.7) in women (p<0.05). For anxiety the mean score was 7.18 (±4.6) in men and 8.20 (±3.9) in women (p<0.05).

Professor Serpytis said: "We found that women were more likely to develop anxiety and depression after a heart attack than men. More research is needed to discover the possible reasons for this."

The researchers also found an association between anxiety and smoking. In the study, 15.6% patients were current smokers and their mean HADS score for anxiety was 10.16 (±4.9). An additional 77.5% of patients had never smoked and their mean HADS score for anxiety was 7.3 (±4.1), while the 6.9% patients who had quit smoking more than 2 years ago had a mean HADS score for anxiety of 4.55 (±3.7) (p<0.05).

Professor Serpytis said: "Current smokers were more likely to have anxiety after an MI than never smokers or people who had quit smoking more than two years ago. We did not find any association between smoking and depression after an MI."

Physically inactive patients tended to be depressed, with a mean HADS score of 8.96 (+4.1). Overall, 64% of patients with depression said they were not physically active (p<0.05).

Professor Serpytis said: "Women are misrepresented in many clinical studies on MI even though they often have worse outcomes. Our study shows that women are more likely to develop anxiety and depression after MI than men but until now this issue has been largely unnoticed. Clinicians should assess MI patients, particularly women, for anxiety and depression so that timely treatment can be started."

He concluded: "Our study suggests that encouraging patients to quit smoking and increase their physical activity levels should reduce their risks of anxiety and depression after MI. More research is needed on the links between myocardial infarction and mental health problems."

COMMON ANTIBIOTICS LINKED WITH HEART DEATH

The antibiotic clarithromycin -- widely used for treating common bacterial infections -- is associated with an increased risk of heart deaths, finds a study published on thebmj.com today.

The authors say their findings require urgent confirmation, given that many millions of people are prescribed the drug each year. But they stress that the absolute risk is small and that prescribing practice should not be changed until results have been confirmed in an independent study.

Clarithromycin belongs to a group of antibiotics known as macrolides. Macrolide antibiotics prolong the duration of electrical activity of the heart muscle (known as the QT interval) and are therefore thought to increase the risk of potentially fatal heart rhythm problems.

Given this background, the cardiac safety profiles of individual macrolides need to be studied in greater detail to help guide clinical treatment decisions.

So a team of Danish researchers decided to assess the risk of cardiac death associated with clarithromycin and another macrolide called roxithromycin, compared with penicillin V, an antibiotic with no known cardiac risk.

Using national databases, they identified over 5 million treatment courses among Danish adults aged 40-74 years from 1997 to 2011 (160,297 with clarithromycin, 588,988 with roxithromycin and 4,355,309 with penicillin V).

Individuals with serious disease, who may be at high baseline risk of death, were excluded from the analysis.

A total of 285 cardiac deaths were observed during ongoing use with the study drugs, 18 of which occurred during use of clarithromycin and 32 during use of roxithromycin.

After adjusting for factors such as age, sex, baseline cardiac risk and use of other medication, ongoing use of clarithromycin was associated with a 76% higher risk of cardiac death compared with use of penicillin V. There was no increased risk of cardiac death with clarithromycin after treatment had ended.

The absolute risk difference was 37 cardiac deaths per 1 million courses with clarithromycin. No increased risk of cardiac death was found with ongoing or past use of roxithromycin.

"Our study expands on the available knowledge of the cardiac safety of macrolides, being the first large scale population based observational study to show significantly increased cardiac risk with clarithromycin and the relative cardiac safety of roxithromycin," write the authors.

The authors emphasise that the absolute increase in risk is small and should have limited, if any, effect on the prescribing practice in individual patients. However, they note, "clarithromycin is one of the more commonly used antibiotics in many countries and many millions of people are prescribed this drug each year; thus, the total number of excess (potentially avoidable) cardiac deaths may not be negligible."

Before these results are used to guide clinical decision making, "confirmation in independent populations is an urgent priority given the widespread use of macrolide antibiotics," they conclude.

MIGRAINE WITH AURA MAY LEAD TO HEART ATTACK BLOOD CLOTS FOR WOMEN

Women who have migraines with aura, which are often visual disturbances such as flashing lights, may be more likely to have problems with their heart and blood vessels, and those on newer contraceptives may be at higher risk for blood clots, according to two studies released today that will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego, March 16 to 23, 2013.

The first study showed that migraine with aura is a strong contributor to the development of major cardiovascular events such as heart attack and stroke. The Women's Health Study involved 27,860 women, 1,435 of whom had migraine with aura. During the 15-year study, there were 1,030 cases of heart attack, stroke or death from a cardiovascular cause. The study examined the relative contribution of various vascular risk factors to these major cardiovascular events.

"After high blood pressure, migraine with aura was the second strongest single contributor to risk of heart attacks and strokes," said study author Tobias Kurth, MD, ScD, of INSERM, the French National Institute of Health and Medical Research in Bordeaux and Brigham and Women's Hospital in Boston. Kurth is also a Fellow of the American Academy of Neurology. "It came ahead of diabetes, current smoking, obesity, and family history of early heart disease."

Kurth cautioned that while people with migraine with aura have an increased risk, it does not mean that everyone with migraine with aura will have a heart attack or stroke. He said people with migraine with aura can reduce their risk in the same ways others can, such as not smoking, keeping blood pressure low and weight down and exercising.

The second study looked at women with migraine who take hormonal contraceptives and the occurrence of blood clots. The study involved women with migraine with and without aura who were taking both newer contraceptives such as the contraceptive patch and ring and older contraceptives. Of the 145,304 women who used the contraceptives, 2,691 had migraine with aura and 3,437 had migraine without aura.

Women with migraine with aura were more likely to have experienced blood clot complications such as deep vein thrombosis with all types of contraceptives than women with migraine without aura. For example, 7.6 percent of women with migraine with aura who used a newer generation combined hormonal contraceptive had deep vein thrombosis compared to 6.3 percent of women with migraine without aura, but the timing of the two events is not clear. The occurrence of blood clot complications was also higher in women with migraine who took contraceptives than women taking the contraceptives who did not have migraine.

"Women who have migraine with aura should be sure to include this information in their medical history and talk to their doctors about the possible higher risks of newer contraceptives, given their condition," said study author Shivang Joshi, MD, MPH, RPh, of Brigham and Women's Falkner Hospital in Boston and a member of the American Academy of Neurology.

Kurth's study was supported by the National Institutes of Health. Joshi's study was supported by the Graham Headache Center Research Fund.

MOST PATIENTS DONT GET COUNSELING ABOUT SEX AFTER HEART ATTACK

Most patients don't receive counseling about resuming sexual activity after having a heart attack, according to new research in the American Heart Association journal Circulation.

Researchers interviewed 3,501 heart attack patients in 127 hospitals and one month later by telephone in August 2008-January 2012 in the United States and Spain. The patients' median age was 48 years and two-thirds were female.

One month after their heart attacks, only 12 percent of women and 19 percent of men reported they received sexual counseling from their healthcare provider -- though most reported they were sexually active within the year before their heart attack.

"Even with life-threatening illness, people value their sexual function and believe it is appropriate for healthcare providers to raise the issue of resuming sexual activity," said Stacy Tessler Lindau, M.D., M.A.P.P., study lead author, associate professor of obstetrics and gynecology and geriatric medicine and director of the Program in Integrative Sexual Medicine at the University of Chicago Medical Center.

In rare instances when healthcare providers counseled about sexual activity, they often recommended restrictions more conservative than medical guidelines. For example, those patients given restrictions more most often told to limit sex (35 percent), take a more passive role (26 percent), and/or keep their heart rate down (23 percent).

"Healthcare providers should let their patients know that for most it is OK to resume physical activity, including sexual activity, and to return to work," Lindau said. "They can tell their patients to stop the activity and notify them if they experience chest pain, shortness of breath or other concerning symptoms. If the healthcare provider doesn't raise the issues, I encourage patients to ask outright: 'Is it OK for me to resume sexual activity? When? Is there anything I should look out for?'"

In the United States and worldwide, heart disease is the leading cause of death. About 720,000 people have a heart attack in the United States each year and about 20 percent are 18-55 years old.

In 2013, the American Heart Association published a scientific statement about counseling patients with cardiovascular disease about sexual activity. The statement concluded that sexual counseling should be tailored to the individual needs and concerns of cardiovascular patients and their partners/spouses.

"When the topic of sexual function is left out of counseling, patients perceive that it's not relevant to their medical condition, or that they are alone in the problems they have resuming normal sexual activity," Lindau said.

ACID REFLUX DRUG MAY CAUSE HEART DISEASE

Drugs that help millions of people cope with acid reflux may also cause cardiovascular disease, report scientists from Houston Methodist Hospital and two other institutions in an upcoming issue of Circulation(now online). It is the first time researchers have shown how proton pump inhibitors, or PPIs, might cause cardiovascular problems

In human tissue and mouse models, the researchers found PPIs caused the constriction of blood vessels. If taken regularly, PPIs could lead to a variety of cardiovascular problems over time, including hypertension and a weakened heart. In the paper, the scientists call for a broad, large-scale study to determine whether PPIs are dangerous.

"The surprising effect that PPIs may impair vascular health needs further investigation," said John Cooke, M.D., Ph.D., the study's principal investigator. "Our work is consistent with previous reports that PPIs may increase the risk of a second heart attack in people that have been hospitalized with an acute coronary syndrome. Patients taking PPIs may wish to speak to their doctors about switching to another drug to protect their stomachs, if they are at risk for a heart attack."

Commonly used proton pump inhibitors in the United States are lansoprazole and omeprazole, and these drugs are purchasable over the counter as brands or generics. The FDA estimates about 1 in 14 Americans has used them. In 2009, PPIs were the third-most taken type of drug in the U.S., accounting for $13 billion in sales. PPIs are used to treat a wide range of disorders, including gastroesophageal reflux disease, or GERD, infection by the ulcer-causing Helicobacter pylori, Zollinger-Ellison syndrome, and Barrett's esophagus.

Recent studies of proton pump inhibitors use by people who've already experienced severe cardiovascular events have raised concern about the anti-reflux drugs, at least for this subgroup of patients, said Cooke, chair of the Department of Cardiovascular Sciences and director of the Center for Cardiovascular Regeneration at Houston Methodist DeBakey Heart & Vascular Center.

PPIs are initially inert. After oral consumption, they are activated by specialized cells in the stomach. Once active, the molecules suppress the movement of protons into the intestine, which reduces the amount of acid present there and in the stomach.

In mouse models and cultures of human endothelial cells, Cooke and lead author Yohannes Ghebramariam, Ph.D., found that PPIs suppressed the enzyme DDAH, dimethylarginine dimethylaminohydrolase. That caused an increase in the blood levels of ADMA (asymmetric dimethylarginine), an important chemical messenger. They found ADMA in turn suppressed the production of another chemical messenger, nitric oxide, or NO, proven by 1998 Nobel Prize winners Furchgott, Ignarro, and Murad to impact cardiovascular function. Quantitative studies in mouse models showed animals fed PPIs were more likely than controls to have tense vascular tissue.

"We found that PPIs interfere with the ability of blood vessels to relax," said Ghebremariam, a Houston Methodist molecular biologist. "PPIs have this adverse effect by reducing the ability of human blood vessels to generate nitric oxide. Nitric oxide generated by the lining of the vessel is known to relax, and to protect, arteries and veins."

The researchers found PPIs led to an approximately 25 percent increase in ADMA in mouse and tissue cultures, and reduced the ability of mouse blood vessels to relax by over 30 percent on average.

Also contributing to this report were Paea LePendu, Ph.D., Jerry Lee, Daniel Erlanson, Ph.D., and Nigam H. Shah, Ph.D. (Stanford University) and Anna Slaviero, Ph.D., and James Leiper, Ph.D. (Imperial College London). Work was funded with grants from the National Institutes of Health, the American Heart Association, the Stanford SPARK program, and the Stanford Translational Research and Applied Medicine (TRAM) program.

Circulation is published by the American Heart Association.

The Methodist Hospital recently changed its name to Houston Methodist Hospital.

Can Neuropathy Lead To Heart Failure

Today's post from healthline.com (see link below) may have you grabbing the phone to make a doctor's appointment straight away, so let's start with the disclaimer that the condition described in this article is very rare indeed! Not only that but heart failure due to neuropathy is only possible if you have autonomic neuropathy (you know, the sort that affects your involuntary functions, breathing, circulation, digestion, sexual function etc etc). The article (like so many) implies that this is only relevant for diabetes patients, which of course is not true (diabetes is the most common cause of neuropathy but there are 100 others!). Nevertheless, it does sound alarming and even logical that the nerve damage that affects so many bodily functions can also affect heart performance. If you have been diagnosed with autonomic neuropathy and are experiencing several of the symptoms associated with that form of neuropathy, you really need to make sure your doctor is aware of far reaching consequences and is taking the necessary steps to test for early warning signs. In this respect, you may need to take the discussion to him or her and not wait for the doctor to think of it. You may even need to be referred to a neurologist to check everything out but it's your body - if you're worried, you need to do something about it.

Ask D'Mine: When Neuropathy Can Kill
 
Written by Wil Dubois | Published on 09 May 2015

The prospect of diabetes complications can be scary indeed. In this week’s edition of our weekly diabetes advice column Ask D’Mine, our columnist Wil Dubois (himself a longtime type 1 who also works as a diabetes educator) offers some thoughts on killer neuropathy, following a troubling news report from overseas.

As our own Mike Hoskins read the news, he started worrying about what it could mean for his own life, so he’s reaching out to Wil himself today for some straight-up 411 on this topic.

Mike H, type 1 of DiabetesMine, writes:

Wil, I read an an article in a British newspaper recently, about a 41-year-old woman with type 1 who died one night while sleeping. She had been diagnosed a quarter-century ago, and was living with autonomic neuropathy. Her husband is quoted as saying she didn’t experience a heart attack or low blood sugar, which is what immediately came to my mind. Instead, a pathology report apparently confirmed that her autonomic neuropathy had “traveled to her chest and stopped her heart from beating in the night.”

WHAT?! I’ve been living with type 1 for many years now and am partially hypo unaware, so the thought of a severe hypo at night killing me is a big fear of mine. But I’ve never heard of this before! Yes, I’ve also lived with neuropathy in my feet and toes for about 10 years now... and I do realize there is more than one type of neuropathy. Still, should I be worried that this could happen to me??

Wil@Ask D’Mine replies: Advanced warning: This will be a downer of a column, filled with pain, despair, and death. We’re going to talk about an extreme complication of diabetes that’s rarely discussed, but may be frightingly more common than any of us wants to accept.

First, can neuropathy stop a beating heart? Yes. I’m sorry to say that it can. But to understand the mechanics behind the grim reaper’s scythe, you need to know a little more about how the heart beats and about the two flavors of neuropathy.

Oh God, where to start? I guess with the blue candle, which of course is a symbol in our D-community of lost loved ones. My condolences to British soccer player Stephen Reeves, the man who lost his T1 wife Louise (pictured) -- and on their wedding anniversary no less! As we say in this part of the world: Siento mucho, which translates to “I am so very sorry.”

Now on to neuropathy. Mike mentioned living with it in his feet and toes. We tend to use “neuropathy” almost like slang, but in most cases its proper name is diabetic peripheral neuropathy (DPN) because it’s the result of damage to the peripheral nerves. It’s caused by the corrosive effects of elevated blood sugars over time, and the best guess is that between 60 and 70% of all D-folks have some degree of peripheral neuropathy. In some people it causes a loss of sensation, and in others is causes phantom pain that ranges from hardly noticeable, to mildly annoying, to absolutely horrific.

DPN impacts us by hitting at how the brain communicates with our bodies through the so-called voluntary movements we make. If I reach out to take a drink of my cup of coffee, I’ve just used my voluntary nerves. I chose to make a movement and my brain sends messages, via assorted nerves, to the muscles in my arm, hand, and fingers to pick up the cup and move it to my mouth. It doesn’t take any particular degree of concentration to do this, but it does require conscious choice. It’s this voluntary system that’s damaged by peripheral neuropathy.

But that's not the only type of neuropathy, and the other type impacts all the things my brain controls in my body that I don't necessarily think about -- my lungs breathing, my stomach digesting, my sweat glads regulating temperature, and yes, my heart beating. That's run by what's called the autonomic nervous system, and that's what is impacted by Diabetic Autonomic Neuropathy -- or DAN as many in the medical profession call it.

DAN most commonly shows up as urinary or digestive issues, the inability to maintain body temperature, eye trouble, exercise intolerance, and crazy drops in blood pressure causing fainting spells. Oh yes, and “resting tachycardia,” when the heart rate explodes while doing nothing.

There’s more, too. Experts now speculate that “brittle” diabetes is caused by DAN, and even hypo unawareness may also be caused by DAN. Oh, grrrreat…

Hi, Dan, nice to meet you, you son of a bitch.

Can this get any worse?

Yes. A subset of DAN is known as CAN, or Cardiovascular Autonomic Neuropathy. This appears to be what got our D-sister in England. The nerves that ran her heart were damaged by her diabetes, ultimately leading to her heart simply not getting the message to keep beating. So it stopped.

Apparently, CAN is linked to a myriad of types of heart failure, with charmingly technical names like cardiac arrest, cardiac dysrhythmia, sudden cardiac death, painless silent ischemia, and the plain and simple “unexpected death.” Top cardiology experts are duking it out as to whether autonomic neuropathy is “causative” or merely a “contributing factor” but I’m not sure that really matters to us if it’s the bullet or the gun.

How common is this heart-stopper? That’s hard to say, and it depends on what group of PWDs you’re looking at, and what degree of automatic neuropathy you are testing for. In the best-case scenario, some established diabetes researchers think it affects only 2.5% of us. On the other hand, 90% of long-term type 1s on transplant lists have it. One large-scale study using heart-rate variability testing put the incidence at 25.3% of us T1s and 34.3% of our T2 cousins.

How serious is it? Well, don’t shoot the messenger, but if you have DAN, your risk of death is double that of D-folks who don’t have it. If you have CAN, your death risk is five times greater.

The onset of autonomic neuropathy and its deadlier subset are usually described as “slow and insidious,” and typically show up in the sixth decade of life. But not always, as another blue candle case study shows of one of our sisters who was only 26 years old when she succumbed to this complication.

So what is anyone doing about this? Well, interestingly, the American Diabetes Association recommends screening for DAN on diagnosis and annually thereafter for type 2s. For T1s, it suggests screening annually once you are five years post-diagnosis. These are the same intervals as for dilated eye exams, and for the same reason. Nerve damage takes some time to happen. With type 2s, the sugars have usually been elevated for a number of years prior to diagnosis, whereas type 1 comes on like a hurricane and at diagnosis the sugar hasn’t been out of whack long enough to have caused nerve damage.

Five years of diabetes is all it takes to cause damage.

Can it be treated? Not so much. It’s one of those treat-by-prevention kinds of complications, and the main thing is to do is to do your damnedest to control your blood sugar. That will help you avoid it, or keep it from getting worse if you already have it.

So what’s the take-away message from this depressing sermon? Should you be worried about this, Mike? Nah. I don’t think so.

First off, you could be the healthiest man in the world and a piece of Soviet-era space junk could fall out of the sky and squish you flat. Death comes to us all at some point. I think we should all do the best we can to keep as healthy as we can, but beyond that I think that worrying about the details is wasted energy.

To me, nothing changes with the new attention on autonomic neuropathy. As a person with diabetes I’ve known all along -- as should you -- that "heart stuff” will have a starring role on my death certificate. That’s the nature of diabetes. Now maybe there will be a new label for the same scythe of the grim reaper. Call it whatever type of heat failure you will, caused by neuropathy or something else, but in the end, does it really matter which?

Disclaimer: As mentioned way up above, this is not a medical advice column. We are PWDs freely and openly sharing the wisdom of our collected experiences — our been-there-done-that knowledge from the trenches. But we are not MDs, RNs, NPs, PAs, CDEs, or partridges in pear trees. Bottom line: we are only a small part of your total prescription. You still need the professional advice, treatment, and care of a licensed medical professional.

http://www.healthline.com/diabetesmine/ask-dmine-other-neuropathy-can-be-killer-complication#1

CAN WE RESTART THE HEART

In a way, trying to repair age-related heart damage and trying to fight cancer are opposite problems. Your heart cells' ability to regenerate themselves and proliferate into new, young cells degrades as you get older. They simply lose their proficiency at cell division. Cancer cells, on the other hand, are too good at proliferating. They don't know when to stop, and the overgrowth results in tumors.

This is all very simplified, of course, but it's the basic model described by Mark Sussman, chief research scientist at the San Diego State University Heart Institute, who was recently selected by the American Heart Association's Basic Cardiovascular Science division to receive this year's Distinguished Achievement Award.

The heart in particular seems to be resistant to developing cancerous cells.

"When's the last time you heard of anyone having heart cancer? It's almost unheard of," said Sussman.

That's not surprising from an evolutionary standpoint. If heart cells make a grave transcription error during cell division and your ticker ticks its last tock, there's no fixing the problem. So it makes sense that heart cells are incredibly careful when it comes to proliferating.

But it's this very meticulousness that makes heart disease such an intractable problem, Sussman explained. Over time, the cells burn themselves out. Their ability to repair themselves and generate fresh replacements gets progressively worse. By the time you reach old age and start experiencing symptoms of age-related heart disease, your cardiac cells are running on fumes and aren't able to properly divide into new cells.

"There's a razor's edge balancing cellular aging and cancer risk," he said.

What if you could use biotechnology to walk that razor's edge? To use the proliferative and survival properties of cancer-prone cells to rejuvenate cardiac progenitor cells -- a rare type of stem cell that replicates indefinitely into new heart cells--and get them dividing again, without forming tumors?

That's the aim of one arm of Sussman's research at SDSU. Sussman and his colleagues published a paper in the May 29 issue of the Journal of Biological Chemistry exploring the results of taking an enzyme, Pim, known to be associated with growth and survival of certain types of cancer cells, and causing it to be overexpressed in cardiac progenitor cells in mice.

In healthy cells, Pim helps facilitate chromosome splitting, a key part of the cellular division process.

The gene that encodes the production of this enzyme, PIM1, is what's known as a proto-oncogene. That means that by itself, the gene doesn't cause cancer. But when it teams up with another gene, Myc, tumors are likely to form.

Fortunately, the Pim/Myc combination isn't an issue in heart progenitor cells, meaning you could tweak those cells to overexpress the PIM1 gene without raising the risk of cancer.

That's exactly what Sussman's team did. They modified mouse heart progenitor cells to overexpress PIM1 in specific locations within the cell, targeting specific locations with more of the critical Pim enzyme in hopes that it would protect against aging-related heart disease.

And it worked. Compared to controls, the mice with overexpressed PIM1 lived longer and showed stronger cell proliferation. But interestingly, the way it worked was different depending on where in the cell the gene was overexpressed.

If the researchers caused PIM1 to be overexpressed in the progenitor cell's nucleus, they saw increased proliferation into new cells. If they overexpressed the gene in a different region of the cell, the mitochondria, they found that the enzyme inhibited the cell's natural self-destruct signals, causing them to live longer.

One technique enhanced cell division, the other warded off cell death. In humans, depending on a person's individual circumstance, either or both of these effects might help restore their cardiac cells to a younger, healthier state.

Sussman and his colleagues have replicated the results with human tissue obtained from people whose hearts have failed and who are living on a ventricular assist device that pumps their blood for them. The research team is currently trying to obtain funding to do human clinical trials wherein they obtain a patient's own cardiac progenitor cells, modify them to overexpress PIM1, then put them back into the patient's heart in hopes of rejuvenating the tissue and spurring the heart to repair itself.

"We're trying to dial back the clock to when their cells had more regenerative potential," Sussman said. "By understanding how and where Pim affects these cells, we can create specialized Pim molecules that get you all the benefits of youthfulness without the risk of cancer."

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