Type 2 Diabetes Could Be a Cause of Erectile Dysfunction


Type 2 diabetes may be a causal factor in the development of erectile dysfunction (ED), with insulin resistance a likely mediating pathway, results of a large-scale genomic analysis suggest. The data also uncovered a genetic locus linked to ED.

Jonas Bovijn, MD, DPhil, Big Data Institute at the University of Oxford, United Kingdom, and colleagues gathered data on more than 220,000 men across three cohorts, of whom more than 6000 had ED.

The researchers initially showed that a region on chromosome 6 is linked to the development of ED. The location suggested that the condition is associated with dysregulation of the hypothalamus.

Next, they performed a Mendelian randomization analysis, which examined the relationship between gene mutations known to be associated, in this case, with cardiometabolic factors and the outcome of ED.

The research, published online December 20 in the American Journal of Human Genetics, showed that a genetic predisposition to type 2 diabetes increased the risk for ED. The risk was driven primarily by susceptibility to insulin resistance.

Bovijn said in a release: “We know that there is observational evidence linking erectile dysfunction and type 2 diabetes, but until now there has not been definitive evidence to show that predisposition to type 2 diabetes causes erectile dysfunction.”

“Further research is needed to explore the extent to which drugs used in the treatment of type 2 diabetes might be repurposed for the treatment of ED,” the team notes.

Co–senior author Anna Murray, PhD, University of Exeter Medical School, United Kingdom, said in the release that “until now little has been known” about the cause of ED.

Previous studies have suggested there is a genetic basis for ED. The new study goes further by demonstrating that a genetic predisposition to type 2 diabetes is linked to ED, according to Murray.

“That may mean that if people can reduce their risk of diabetes through healthier lifestyles, they may also avoid developing erectile dysfunction,” she said.

Michael Holmes, MD, PhD, of the Nuffield Department of Population Health at the University of Oxford, who was one of the senior authors, agreed.

“Our finding is important, as diabetes is preventable, and indeed one can now achieve ‘remission’ from diabetes with weight loss, as illustrated in recent clinical trials.

“This goes beyond finding a genetic link to erectile dysfunction to a message that is of widespread relevance to the general public, especially considering the burgeoning prevalence of diabetes,” Holmes said.

Large Studies Key

Although the prevalence of ED is known to increase with age, rising to 20% to 40% among men aged 60 to 69 years, the genetic architecture of the condition remains poorly understood. This is at least in part due to a lack of well-powered studies.

The researchers therefore conducted a genome-wide association study (GWAS) using data on 199,362 individuals from the UK Biobank cohort and 16,787 people from the Estonian Genome Center of the University of Tartu (EGCUT) cohort, both of which are population based.

In addition, they included information on 7666 participants in the hospital-recruited Partners HealthCare Biobank (PHB) cohort.

The prevalence of ED, which was determined on the basis of self- or physician-reported ED, the use of oral ED medication, or a history of ED surgical intervention, was 1.53% in the UK Biobank, 7.04% in EGCUT, and 25.35% in PHB.

The researchers believe that the difference in prevalence rates between the cohorts may relate to the older average age for men in PHB, at 65 years, vs 59 years in the UK Biobank and 42 in EGCUT. In addition, the prevalence in the UK Biobank cohort may have been affected by a “healthy volunteer” selection bias and a lack of primary care data.

GWAS on the UK Biobank data indicated that there was a single genome-wide significant locus at 6q16.3 between the MCHR2 and SIM1 genes, with rs57989773 the lead variant.

Pooled meta-analysis of the combined cohorts indicated that rs57989773 was associated with ED at an odds ratio of 1.20 per C-allele (P = 5.71 × 10-14).

Synthesizing previous research on SIM1, which is highly expressed in the hypothalamus, in both human and rodent models, the team found that rs57989773 is associated with syncope, orthostatic hypotension, and urinary incontinence.

Moreover, the common risk variant for ED at 6q16.3 is linked to blood pressure and adiposity, as well as male sexual behavior in mice.

The researchers, therefore, suggest that a potential mechanism for the effect of the MCHR2-SIM1 locus on ED could be the hypothalamic dysregulation of SIM1.

The team also performed Mendelian randomization analyses to examine the potential causal role of cardiometabolic traits in ED risk.

Factors included type 2 diabetes, insulin resistance, systolic blood pressure (SBP), low-density lipoprotein (LDL) cholesterol levels, smoking heaviness, alcohol consumption, body mass index, coronary heart disease, and educational attainment.

The analysis revealed that type 2 diabetes was causally implicated in ED, with the risk for ED increased 1.11-fold with each 1-log higher genetic risk for type 2 diabetes (P = 3.5 × 10-4).

Insulin resistance was found to be a likely mediating pathway for the relationship, with an odds ratio for ED of 1.36 per 1 SD genetic increase in insulin resistance (P = .042).

SBP also had a causal effect on ED risk, at an odds ratio of 2.34 per 1 SD increase in SBP (P = .007).

LDL cholesterol was found to have a minor impact on the risk for ED, at an odds ratio of 1.07 per 1 SD increase in levels (P = .113). There was no association between ED and either smoking heaviness or alcohol use.

Source:Medscape.com

Early Menarche, Menopause Tied to Higher CVD Risk


More frequent heart screening for women may be useful

Several reproductive factors contributed to a higher risk of cardiovascular disease among women, including early periods and early menopause, researchers found.

A history of hysterectomy was also linked with increased risk of cardiovascular disease (CVD) and coronary heart disease, reported Sanne AE Peters, PhD, and Mark Woodward, PhD, both of the University of Oxford in England.

However, history of oophorectomy, as well as age at first birth, had either no associations or only minor inverse associations with increased risk for cardiovascular disease, the authors wrote in Heart.

They pointed to “increasing evidence” that in addition to traditional risk factors such as elevated blood pressure, smoking, and obesity, certain reproductive factorsmay be linked with later cardiovascular disease, though the evidence is “mixed and inconsistent.”

This cross-sectional analysis of UK Biobank data comprised 267,440 women and 215,088 men ages 40 to 69 without a history of cardiovascular disease. The authors found that during 7 years of follow-up, there were 9,054 cases of cardiovascular disease, 5,782 cases of coronary heart disease, and 3,489 cases of stroke. Women comprised about a third of cardiovascular disease cases, a little under 30% of coronary heart disease cases, and about 40% of stroke cases.

Examining demographic data for women, the mean age was 56, about half were from a higher socioeconomic bracket in the U.K., and 60% said they never smoked.

Results were mixed for certain reproductive factors and increased risk for cardiovascular disease. The mean age for menarche was 13 years, and women who had their first periods prior to age 12 had a higher risk of cardiovascular disease (adjusted HR 1.10, 95% CI 1.01-1.30) than women who had menarche at a later age. Similar increased risks were seen for coronary heart disease (adjusted HR 1.05, 95% CI 0.93-1.18) and stroke (adjusted HR 1.17, 95% CI 1.03-1.32).

Sixty-one percent of women in the study were postmenopausal, with a mean age at natural menopause of 50 years. But early menopause was also linked with increased risk of cardiovascular disease (adjusted HR 1.33, 95% CI 1.19-1.49), coronary heart disease (adjusted HR 1.29, 95% CI 1.10-1.51), and stroke (adjusted HR 1.42, 95% CI 1.21-1.66).

Likewise, history of hysterectomy was linked with an increased risk of cardiovascular disease (adjusted HR 1.12, 95% CI 1.03-1.22) and coronary heart disease (adjusted HR 1.20, 95% CI 1.07-1.34).

Eighty-five percent of women had been pregnant, and 44% of women had two children, while 42% of men had fathered two children. Compared with women and men without children, there was a significantly higher risk of coronary heart disease in women (adjusted HR 1.21, 95% CI 1.05-1.40). But because these risks were similar among men (adjusted HR 1.13, 95% CI 1.04-1.23), the authors concluded that “this is unlikely to be due to a biological cause.”

The authors suggested that, “More frequent cardiovascular screening would seem to be sensible among women who are early in their reproductive cycle, or who have a history of adverse reproductive events or a hysterectomy, as this might help to delay or prevent their onset of CVD.”

Fluoride Linked to Coronary Heart Disease


Dental fluorosis is a condition caused by too much fluoride, and it’s on the rise in the United States, despite the US government knowing about it for some time now. Though it can happen to anyone, the condition (which ruins teeth) affects more children than adults, primarily because children’s teeth are still developing and more susceptible to fluorosis.

But did you know that dental fluorosis is also a biomarker for coronary heart disease?

Fluoride Linked to Coronary Heart Disease

When Will the Fluoride Poisoning Stop?

Per the Centers for Disease Control (CDC) in 2010: “Prevalence of dental fluorosis was higher among younger persons and ranged from 41% among adolescents aged 12-15 to 9% among adults aged 40-49.” That rate of 41% in adolescents aged 12-15 increased from 22.6% back in 1986-87 (almost double).

The U.S. Department of Health and Human Services planned in 2010 to lower the amount of fluoride allowed in water, though so far there has been no change to the amounts of fluoride added.

Today, the CDC still promotes fluoridation to water as well fluoride dental products.

Fluoride and Heart Disease

In 2013, a study in Ireland was prompted over concern with that fluorosis might be linked with cardiovascular disease. Cardiovascular disease is the most common cause of death in Ireland.

The study found that the concern was indeed justified: “Dental Fluorosis is a biomarker for coronary heart disease (CHD). Professor Takamori’s research team observed that children with dental fluorosis have a higher incidence of heart damage and an increase in abnormal heart rhythm than those without fluorosis.”

In lieu of the evidence, will the government of Ireland stop their policy of mandatory fluoridation of the population of Ireland?

And regarding the US?

Dental Fluorosis in the United States

Well, in summary:

In 2010, the US government knew people were ingesting dangerous levels of fluoride, knowing causing florosis in 40% of children (among other things) and now potentially contributing to the increasing incidence of cardiovascular disease in the United States. Regulators said the amount of fluoride in drinking water should be lowered. However…

  • 2011: There was no change to fluoride levels allowed in drinking water
  • 2012: There was no change to fluoride levels allowed in drinking water
  • 2013: There was no change to fluoride levels allowed in drinking water
  • 2014: We are still waiting…

Meanwhile, US dentists still promote the use of fluoride treatments, fluoride toothpaste, and fluoride mouthwash, despite the evidence that it is linked to heart disease, and other illnesses.

A daily walk ‘can add seven years to your life’


A daily walk 'can add seven years to your life'
Exercise brings benefits at whatever age the person starts.
Just 25 minutes of brisk walking a day can add up to seven years to your life, according to health experts.

Researchers have found that moderate exercise could halve the risk of dying from a heart attack for someone in their fifties or sixties.

Coronary heart disease is the UK’s single biggest killer, causing one death every seven seconds, and exercise has long been seen as a way to reduce the risks by cutting obesity and diabetes.

A new study presented at the European Society of Cardiology (ESC) Congress suggested that regular exercise can increase life span.

A group of 69 healthy non-smokers, aged between 30 and 60, who did not take regular exercise were tested as part of the study at Saarland University in Germany.

Blood tests taken during six months of regular aerobic exercise, high-intensity interval training and strength training showed that an anti-ageing process had been triggered and helped repair old DNA.

“This suggests that when people exercise regularly, they may be able to retard the process of ageing,” said Sanjay Sharma, professor of inherited cardiac diseases in sports cardiology at St George’s University Hospitals NHS Foundation Trust in London.

“We may never avoid be-coming completely old, but we may delay the time we become old. We may look younger when we’re 70 and may live into our nineties.

“Exercise buys you three to seven additional years of life. It is an antidepressant, it improves cognitive function and there is now evidence that it may retard the onset of dementia.”

The advice from experts is that everyone should do at least 20 minutes of walking or jogging a day, given the sedentary lifestyles and changes in diet that have contributed to high death rates from heart disease. Exercise can also improve brain functioning.

Exercise brings benefits at whatever age the person starts. People who start exercising at the age of 70 are less likely to go on to develop a condition that leads to irregular or racing heart rates in 10 per cent of people aged over 80.

“The study brings a bit more understanding of why physical activity has that effect,” said Christi Deaton, Florence Nightingale Foundation Professor of Clinical Nursing Research at Cambridge Institute of Public Health.

“It helps us understand the process of cellular ageing, as that’s what drives our organ system and body ageing, and the effects physical activity can have on the cellular level.

“The more active you are, and it doesn’t matter when you start, the more benefit you are going to have.”

Heart attacks are mainly triggered by coronary heart disease, which kills around 73,000 people in the UK every year and is the leading cause of death in both sexes. Heart disease generally affects more men than women, although from the age of 50 the chances of developing the condition are similar for both.

According to a separate study, hundreds of young people die every year from “electrical faults” in their otherwise healthy hearts triggered by intense sporting activity.

Sudden cardiac death (SCD) is a rare occurrence that affects one in 50,000 athletes, although most who die are men, researchers found. In the 35 year history of the London Marathon, only one woman has died compared to 13 men.

The study’s authors, from St George’s University Hospital in London, found that a large proportion of cases of SCD in sport occurred in people with anatomically normal hearts, but with inherited faults in the heart’s electrical system that causes them to miss beats and trigger death.

Low plasma testosterone associated with CVD risk factors


Key cardiovascular disease risk factors were associated with low plasma testosterone in men, but after adjustment, there was no association with mean carotid intima-media thickness, incident cardiac thickness or mortality, according to recent findings.

Adrian Dobs, MD, of the division of endocrinology, diabetes and metabolism at Johns Hopkins University School of Medicine, and colleagues evaluated 1,558 men (mean age, 63.1 years) not taking androgen therapy and without coronary heart disease, stroke or heart failure to determine the relationship between plasma testosterone and mean carotid intima-media thickness. The relationship with incident CVD, cardiac mortality and all-cause mortality was also examined.

Adrian Dobs

Adrian Dobs

The median plasma total testosterone was 377.6 ng/dL. No significant association was found between testosterone levels, age, race, LDL cholesterol or use of lipid-lowering medications.

Significantly higher BMI, greater waist circumference, higher prevalence of diabetes and hypertension and lower HDL cholesterol were found among participants with lower testosterone (all P for trend <.001).

Mean carotid intima-media thickness was 0.9 mm. No association was found cross-sectionally between testosterone quartiles with carotid intima-media thickness after adjustment for CV risk factors (P for trend=.56). Similarly, no association was found between incident coronary heart disease or incident cardiac heart failure and quartile testosterone after multivariable adjustment.

Overall, there were 347 deaths and 29 attributed to cardiac causes; however, there was no association between all-cause mortality or cardiac mortality and quartile testosterone after multivariable adjustment.

“Low serum testosterone in men did not predict the later development of heart disease,” Dobs told Endocrine Today.“However, it was highly associated with cardiac risk factors. Thus, low testosterone should be viewed, not as causative of later cardiac problems, but rather as a marker to suggest that aggressive treatment of classical risk factors need to be addressed.” – by Amber Cox

How Twitter Can Predict Heart Disease: Negative Tweets Associated With Stress, Higher Risk Of Disease


Twitter data compared to CDC data
The authors compared CDC data on heart disease risk with their own estimates based on Twitter language. 

Over the years, researchers have gathered several risk factors for heart disease ranging from not making a lot of money, to smoking, to stress. Now, a new study shows just how the use of Twitter can help dictate what populations are at risk of coronary heart disease: by identifying which users are tweeting about negative emotions like anger, stress, or fatigue.

The study, led by Johannes Eichstaedt at the University of Pennsylvania (in collaboration with others) and published in the journal Psychological Science, found that a county’s tweets about negative emotions were associated with a higher risk of heart disease for that community, while tweets that were more positive were associated with a lower risk. In a way, Twitter could become a tool for researchers who are trying to understand the psychological health of a community — something that was difficult to measure in the past.

Psychological Signs Of Heart Disease

The researchers studied public tweets from 2009-2010, scattered across 1,300 countries. Language considered negative — such as the word “hate” or swear words — were associated with heart disease mortality, while more positive messages involving words like “friends” or “wonderful” were linked to a lower risk of heart disease mortality. It wasn’t necessarily the people writing negative tweets who were dying of heart disease, however: rather, the tweets were indicative of a higher rate in certain communities.

“The relationship between language and mortality is particularly surprising,” H. Andrew Schwartz, an author of the study, said, “since the people tweeting angry words and topics are in general not the ones dying of heart disease. But that means if many of your neighbors are angry, you are more likely to die of heart disease.”

Along with risk factors like high blood pressure, high cholesterol, diabetes, smoking, obesity, and physical inactivity, other heart disease risk factors are psychological — like stress and depression, which can have an impact on a person’s physical health, desire to exercise, and eat well.

“Psychological states have long been thought to have an effect on coronary heart disease,” Margaret Kern, assistant professor at the University of Melbourne and an author of the study, said in the press release. “For example, hostility and depression have been linked with heart disease at the individual level through biological effects. But negative emotions can also trigger behavioral and social responses; you are also more likely to drink, eat poorly and be isolated from other people which can indirectly lead to heart disease.”

The trick, then, was to examine how negativity in people’s lives — as well as daily experiences of depression or drinking, for example — manifested itself on Twitter.

Twitter As A Tool For Epidemiology

The World Well-Being Project at UPenn is attempting to use Twitter and other social media outlets to better study psychology across large groups, mostly through the use of online language. One study completed by these researchers, published in 2013, examined Facebook status updates from 75,000 people. These status updates allowed the researchers to make surprisingly accurate estimates about each individual’s gender, age, and even personality. This is one of the reasons why Eichstaedt and his team wanted to harness Twitter’s vast sea of language and daily experiences as a way to better understand psychological undercurrents within communities.

“Getting this data through surveys is expensive and time consuming, but, more important, you’re limited by the questions included on the survey,” Eichstaedt, a grad student in the School of Arts & Science’s Department of Psychology at UPenn, said in the press release. “You’ll never get the psychological richness that comes with the infinite variables of what language people choose to use.”

Of course, Twitter’s 140 characters has its limitations; but as social media develops and expands, scientists may learn new ways to harness it for psychological and medical research.

Battle Of The Booze: Is Fine Wine Over Good Beer Really A Healthy Choice?


Beer vs. wine infographic
In battle of the booze, is fine wine or beer better for your health? 

In life, we are told there are two kinds of people: wine drinkers and beer drinkers. America’s thirst for these two popular alcoholic drinks brings back the age-old debate of beer versus wine. The common belief is a glass of fine wine is healthy, but is it healthier than a foamy, cold glass of beer?

Sip (or guzzle down) these facts about wine and beer to decide which one offers the most life-extending benefits.

Fine Wine: Is It Really So Divine?

Health experts have long lauded wine for its numerous health benefits, specifically its antioxidants, which reduce risk for coronary heart disease. About 200 years ago, an Irish doctor noted chest pain (angina) was far less common in France than in Ireland, according to the Harvard School of Public Health. He attributed this stark distinction to “the French habits and mode of living.” Although the French diet includes plenty of butter and cheese, the country has one of the lowest rates of heart disease in the world, and the French’s high consumption of red wine may be why.

Fine Wine: Heart And Brain Healthy

A study published in the journal Lancet found there was a strong and negative association between ischemic heart disease deaths and alcohol consumption. The findings revealed there is a positive but inconsistent association with cardiac mortality and saturated and monounsaturated fat intake. The correlation seen between less cardiac deaths and alcohol was attributed to wine consumption.

Resveratrol, an antioxidant found in wine, along with the antioxidant compound quercetin, have been shown to benefit the brain. A 2013 study published in the journal Bio Medical Central Medicine found drinking wine could lower the risk for depression. Since resveratrol and quercetin can suppress high levels of C-reactive protein (CRP) — associated with the likelihood of displaying depressive symptoms — it can actually lessen psychological distress associated with depression.

Fine Wine: Which Wine Has The Most Antioxidants?

Wine’s cardioprotective effect has been linked to the antioxidants present in the skin and seeds of red grapes. These antioxidants, such as flavonoids, may help prevent heart disease by increasing levels of good cholesterol, known as high-density lipoprotein (HDL), and protecting against artery damage, says the Mayo Clinic. Researchers at the University of California, Davis, found Cabernet Sauvignon, Petit Syrah and Pinot Noir, are among the wines with the highest concentrations of flavonoids. White wine was found to have significantly smaller amounts than its red counterparts. A rule of thumb is the dryer the red wine, the better it is for a flavonoid boost.

Good Beer: Is It Better?

The majority of medical literature suggests drinking a glass of red wine is drinking to your health, but can a pint of beer do just the same? Similar to its popular counterpart, beer contains antioxidants and important B vitamins, like niacin and folic acid. A single 12-ounce bottle of beer provides up to 12.5 percent of the recommended requirement of vitamin B6, which is known to help cells and be heart healthy, according to eatright.org, part of the Academy of Nutrition and Dietetics.

Good Beer: Bone And Kidney Healthy

Guzzling a pint or two of beer in a matter of seconds may not only turn you into “beercules,” but it can also give you strong bones. Silicon, which is commonly found in whole grains, cereals, and some vegetables, is known to improve bone matrix quality. A 2013 studypublished in the International Journal of Endocrinology noted silicone supplementation in animals and humans has been shown to increase bone mineral density and improve bone strength. However, while drinking moderate amounts of alcohol (wine as well as beer) is related to greater bone density in men and women over 60, they also found bone mineral density was significantly lower in men who drank more than two servings of liquor per day.

Drinking beer can give you good bone health and reduce the risk of developing painful kidney stones by 41 percent. A 2013 study published in the Clinical Journal of the American Society of Nephrology found beer’s anti-kidney stone properties could possibly be due to beer’s high water content and diuretic effect. Soda and punch was found to increase the risk of developing kidney stones as predicted by the researchers.

Beer vs. Wine: Which Is Healthier?

Wine and beer both provide life-extending benefits, respectively, but neither is healthier than the other. It’s not the beverage of choice but rather the frequency of drinking that may matter when reaping alcohol’s benefits. A 2010 study published in the journal Alcoholism: Clinical and Experimental Research found during a 20-year period, those who didn’t drink alcohol suffered from the highest mortality rates at 59 percent, moderate alcohol drinkers who consumed little or no wine at 50 percent rate, and moderate drinkers who consumed mostly wine had a 32 percent mortality rate. Although this study may confirm wine’s health powers, the researchers delved a bit deeper and found that is not the case.

The UT team found wine offered no greater health benefit than beer or liquor after adjusting for lifestyle factors. The truth is any type of alcohol can offer life-extending benefits. Regular, moderate drinking can increase your longevity and improve your overall health in various ways.

So whether you’re a wine or beer drinker, you’ll still reap the benefits of alcohol. Cheers!

Check out CompareCamp.com’s beer vs. wine infographic below for interesting facts and figures about these two alcoholic drinks.

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