Type 2 diabetes risk may be influenced by blood type

According to the research team, including Dr. Guy Fagherazzi of the Center for Research in Epidemiology and Population Health at the Gustave Roussy Institute in France, past studies have investigated the association between blood type and stroke, finding people with blood type AB are at higher risk.

In one study that found such an association, the researchers note there was also a higher number of diabetes cases among individuals with blood type AB. Other studies - although small - have reported similar findings. This led them to investigate the link between blood type and diabetes in a larger cohort.

Dr. Fagherazzi and colleagues analyzed data from 82,104 women who were a part of the French E3N study - a cohort of almost 100,000 female teachers that began in 1990.

From an analysis of health questionnaires the women completed, the team identified 3,553 women who received a diagnosis of type 2 diabetes between 1990 and 2008. Blood samples from the women were collected between 1995 and 1997.

Women with blood type B+ at 35% higher risk of type 2 diabetes. The results of the analysis revealed that women with blood type A were 10% more likely to develop type 2 diabetes than women with blood type O, while women with blood type B were 21% more likely to develop the condition.

Women with blood type AB were found to be at 17% higher risk of type 2 diabetes than those with blood group O, but the researchers say this result was "not statistically significant."

The team then assessed the women's risk of diabetes by their Rhesus factor - the presence of Rhesus antigens in the blood. However, they found there was no difference in type 2 diabetes risk between those who were Rhesus positive (R+) and those who were Rhesus negative (R-).

Next, the team assessed the risk of type 2 diabetes by both women's blood type (A, B, AB or O) and Rhesus factor. Each possible combination was compared with blood group O negative (O-), as this is classed as a universal blood group because it has no A, B or Rhesus antigens present.

The researchers found that women who were blood group B positive (B+) were 35% more likely to develop type 2 diabetes than those with blood group O-. Women with blood group AB+ were at 26% higher risk of type 2 diabetes, those with blood group A- were at 22% higher risk and those with blood group A+ were at 17% increased risk.

The team says their findings for blood groups O-, B- and AB- were not statistically significant.

Commenting on their results, Dr. Fagherazzi says:

"Our findings support a strong relationship between blood group and diabetes risk, with participants with the O blood type having a lower risk of developing type 2 diabetes.

Therefore, the effects of blood groups should be investigated in future clinical and epidemiological studies on diabetes. Further pathophysiological research is also needed to determine why the individuals with blood type O have a lower risk of type 2 diabetes."

However, the team suggests a number of potential factors that might explain their findings. For example, they point out that blood grouping is linked to specific molecules related to type 2 diabetes. Another study has associated blood type with gut bacteria composition, which may be linked to type 2 diabetes.

Study author Dr. Françoise Clavel-Chapelon - also of the Center for Research in Epidemiology and Population Health at the Gustave Roussy Institute - acknowledges the fact that their study population only included women but notes that no biological mechanisms were identified that suggest their findings were sex-dependent.

"Information on the participants was self-reported, but this is unlikely to substantially affect the results," he adds.

Tips to allergy sufferers for easy breathing this holiday season

The many smells and tastes of the holidays that get so many in a festive mood can sicken others, thanks to allergic reactions. But with some seasonal savvy, allergy sufferers can breathe easy this festive time of year.

"The dust from the boxes and on the decorations that have been packed away in dank basements or dusty attics is triggering reactions in my allergy and asthma patients," said Rachna Shah, MD, affiliate faculty member at Loyola Chicago Stritch School of Medicine and allergist at Gottlieb Memorial Hospital.

The holidays are supposed to be some of the happiest times of the year. But popular seasonal items, such as fresh trees, scented air fresheners and live plants make the holidays miserable for many.

Here are Dr. Shah's top five tips for easy breathing this holiday season:

1) Clean The Tree - Artificial or real, a tree can cause allergy problems. "A tree that is moldy increases the spore counts in the home exponentially after just a few days, triggering reactions and illness," says Dr. Shah. "Some have found relief by spraying down the tree with water to remove mold and then limiting the amount of time the tree is indoors to 12 days or less."

The clean fragrance from the live balsam, fir and pine trees is pleasing, but it can aggravate respiratory conditions. "No variety of live tree is less allergenic than any other," says Dr. Shah. "Artificial is the best if you have allergies." The scent of a freshly cut tree as well as elements of its care can wreak havoc on your airways and nasal passages. "The water in the tree holder also grows stagnant and collects mold, which is detrimental to those with allergies," Dr. Shah says. Decorations used to adorn the tree may also be dusty, scented or carry irritants. If you choose an artificial tree, make sure the branches, as well as decorations, are dry and moisture-free. "Artificial trees and holiday decorations can grow mold if they get wet, as they often do in humid basements or attics," she warns.

2) Prepare for Parties - Bring your own treats, especially for kids, at social gatherings where allergenic foods may be plentiful and an only option. "Those with egg, nut or dairy allergies especially can play it safe and enjoy the parties if they know what they are eating and drinking," says Dr. Shah. "Communicating in advance with the host can help avoid illness."

3) Pamper the Pet - Dogs and cats spend more time indoors during the winter months and often bring allergens in with them from their trips outdoors, contaminating the environment for those with sensitive respiratory systems. "Have your dog and cat groomed more often to remove dander and hair," says Shah. HEPA filters also help filter pet hair of all kinds as well.

4) Relax - "Anxiety has been shown to increase asthma symptoms," says Dr. Shah. "Use relaxation methods such as deep breathing, meditation or yoga to maintain control during the holiday hustle-bustle."

5) Never Use Scented Candles or Home Fragrance Oils - The popularity of home fragrance products and scented specialty candles reaches a peak during the holidays - and so do allergies. Unplug the electric scent distributors and take a pass on the potpourri simmering pots. "Far from creating an inviting home, the fragrance aggravates the sinuses and respiratory system so sufferers can't breathe," Dr. Shah said.

6) Avoid Real Poinsettias and Fresh Floral Arrangements - "The moist soil encourages the growth of mold. And if there is mold in your house, you are breathing mold spores," Dr. Shah said. This causes air passageways to swell, which restricts airflow. It can even cause skin rashes.

7) Keep the Humidity in Check - Warm and cool air humidifiers are up and running in many homes now that the cold, dry air is here. "Get a gauge and keep the humidity no higher than 48 to 50 percent," Dr. Shah said. "Too much humidity encourages the growth of mold, which triggers allergic reactions."

8) Store Holiday Decorations in Large Plastic Tubs - Save yourself some sneezes next year by purchasing large resealable plastic tubs to store decorations. Dust them occasionally during the year.

Link between low blood glucose, cardiovascular events revealed

Professors Kamlesh Khunti and Melanie Davies, scientists from the University of Leicester's Diabetes Research Centre, have confirmed an association between hypoglycaemia and an increased risk of cardiovascular events and mortality in insulin-treated patients with diabetes, which could lead to changes in the way some patients' treatment is managed.

As part of an international collaboration with scientists from Imperial College London, the QIMR Berghofer Medical Research Institute and Novo Nordisk A/S -- using data from the UK Clinical Practice Research Datalink database -- Professors Khunti and Davies demonstrated that, following hypoglycaemia, insulin-treated patients with diabetes had an ~60% higher risk of cardiovascular events, and were between 2-2.5 times more likely to die over the same period as patients who did not experience hypoglycaemia.

The research was supported by the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care East Midlands (NIHR CLAHRC EM), and the NIHR Leicester-Loughborough Diet, Lifestyle and Physical Activity Biomedical Research Unit.

Kamlesh Khunti, Professor of Primary Care Diabetes & Vascular Medicine at the University of Leicester, who led the research, said: "This is one of the first studies to report the risk of cardiovascular events and mortality in people with both type 1 and type 2 diabetes. The risks are very significant and we need to identify these patients early with a view to implementing strategies to reduce their risk of hypoglycaemia."

Patients with diabetes are at higher risk of cardiovascular disease due to the formation of atherosclerotic plaques in blood vessels; this is a major cause of early death in these patients. The results of the study show that hypoglycaemia, which occurs when a patient's blood glucose becomes dangerously low, can trigger potentially fatal cardiovascular events.

Melanie Davies, Professor of Diabetes Medicine at the University of Leicester and Honorary Consultant at Leicester's Hospitals, commented: "The data from this important and large piece of research confirms what we already know in people with type 2 diabetes and extends our knowledge in those with type 1 diabetes. It also confirms the significance of hypoglycaemia and the link with an increased risk of cardiovascular events, a risk that persists over a long time period. Going forward we need to focus on management strategies that help patients minimise their risk of having hypoglycaemic events."

The findings of this investigation are a stark reminder of the challenges facing patients with diabetes and could lead to changes in the management of insulin-treated patients, particularly those at high risk of cardiovascular events.

Multiple sclerosis: First evidence of a rogue protein

Scientists have previously known that rogue proteins cause brain damage in other diseases of the brain such as Alzheimer's, Parkinson's and Creutzfeldt-Jakob disease.

In this study, scientists from the University of Surrey, University of Texas Medical Center and PrioCam Laboratories produced unique molecules, called antibodies, to fight against these rogue proteins. They discovered that these antibodies were able to recognise rogue proteins in Creutzfeldt-Jakob disease, as well as additional molecules associated with other neurodegenerative diseases.

The antibodies were then used to investigate whether rogue proteins existed in the brain tissue and spinal fluid of patients with multiple sclerosis. The scientists concluded that multiple sclerosis may be caused by a protein that permanently adopts a rogue state.

"Multiple sclerosis represents a substantial health burden, affecting the quality of life of many people," said Dr Mourad Tayebi from the University of Surrey.
"Our discovery proposes a new and alternative way to conduct research into multiple sclerosis, by, for the first time, identifying a clear link to other neurodegenerative diseases. The results are important in redefining the molecular and cellular make-up of these diseases, and provides an important milestone in the quest for a laboratory test and an effective cure."

Co-Senior author, Dr Monique David from the PrioCam, said, "Our research indicates that rogue proteins share a common structure and may share similar pathogenic mechanisms. This study consistently and reproducibly links the presence of abnormally shaped proteins to multiple sclerosis."

How Testosterone Helps the Heart

As it is commonly reported in the media that steroids can cause your heart to blow a ventricle, kidneys to implode, and your liver to disintegrate. But is this actually true? Well in reality, the more you learn about steroids, the more you come to realize that, like all drugs, there is a difference between their intelligent use and outright abuse. So we will take a look at the effects of testosterone on the heart and see how these common conceptions hold up.

For ages now, we’ve all heard the repeated saying that anabolic steroids are bad for the heart. Some physicians will tell you that testosterone raises your risk of heart disease by lowering your good cholesterol and raising your bad cholesterol. It is also reported that steroids are known to induce an enlargement of the heart or even cardiac hypertrophy.

In reality, the dangers of steroids are overstated and may even be good for the heart.

What are the cardiovascular effects of steroids?

In a recent test, bodybuilders had various aspects of the heart measured such as the carotid intima-media thickness, arterial reactivity, left ventricular dimensions to name a few. These measurements indicate whether bodybuilding, steroid usage, or both affect the shape, function, activity and size of the heart.

The doctors found some obvious and not so obvious results. The bodybuilders who used steroids were physically stronger than those who didn’t and the use of steroids was not found to cause any significant changes or abnormalities of arterial structure or function.

In essence, when both groups of bodybuilders were compared with sedentary controls, any changes in heart function were common to both steroid-using and non-steroid-using bodybuilders. So all said and done, what we learn from this study is that bodybuilding itself can alter, not impair, arterial structure or function and steroids do not appear to impair cardiac function.

TRT heart 2Does MRFIT need a T boost?

The Multiple Risk Factor Intervention Trial (MRFIT) is a study that examined changes in testosterone over a 13 year period in 66 men aged 41 to 61 years. The researchers concluded that changes in total testosterone are related to cardiovascular disease risk factors.

The average testosterone levels at the beginning of the study were 751 ng/dl and decreased by 41 ng/dl. Also, men who smoked or exhibited Type A behavior were found to have even greater decreases in T levels. The change in testosterone was also associated with a decrease in in the good cholesterol and an increase in triglyceride levels.

The conclusion stated that decreases in testosterone levels as observed in men over time are associated with unfavorable heart disease risk.

In a similar study, researchers in Poland examined if testosterone replacement therapy in aging men positively affected heart disease risk factors. It noted that twenty-two men with low T levels received 200 mg of testosterone enanthate every other week for one year. Throughout this treatment, total cholesterol, testosterone, estradiol, LDL and HDL were measured. The researchers concluded that T replacement returned both testosterone and estradiol levels back to normal and normal levels. They also found that T replacement lowered cholesterol and LDL, which is the bad cholesterol without altering HDL, which is the good cholesterol and there was no change in prostate size or function.

This study proved that T replacement doesn’t appear to raise heart disease risk – and it may actually lower your risk. There are many physicians out there today that should be prescribing low dose testosterone to middle age and aging men for muscle tone, both libido and for cardiac reasons.

It’s been long shown and proved that men have a higher risk of heart disease. One of the risk factors implicated is testosterone. The recreational use of testosterone can alter lipoprotein levels and in many cases reports exist that describe bodybuilders who’ve abused steroids and have experienced heart disease or even sudden death. But one can still ask, is the causal association one of truth or just an association? Well, researchers at the University of North Texas recruited twelve competitive bodybuilders for a comprehensive evaluation of the cardiovascular effects of steroids. Six heavyweight steroid-using bodybuilders were compared with six heavyweight drug-free bodybuilders.

And sure enough the heavy steroid users had lower total cholesterol and HDL levels as compared to the drug-free athletes. What was unexpected was that the steroid users also had significantly lower LDL and triglyceride levels as compared to the non-steroid users. In addition, the juicers also had lower Apo-lipoprotein B levels, which is a marker for heart disease risk. Thus, the authors concluded that androgens do not appear to raise the risk of cardiovascular disease. Thus the conclusion of this study is that the negative cardiac side effects of steroids are most likely overstated.

We know that as we age, circulating testosterone levels naturally decrease. For most men, the testosterone decrease goes from high normal to mid to low normal. There is also data that shows that there’s an inverse relationship between T levels and blood pressure as well as abdominal.

Testosterone replacement lowers abdominal obesity and restores testosterone levels back to normal. Positive side effects of restored testosterone is correlated with stronger sex drive, better mood, lower cardiovascular, disease risks, better muscle tone, stronger bones and improved memory. It should also be noted that while conservative use gives a pronounced positive health benefit, higher doses might not necessarily lead to further health benefits.

Positive Effects of anabolic steroids on the Heart

Anabolic steroids will cause your kidneys to implode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon. We read it on the Internet and saw an after school special about it, so it must be true, right?

Actually, the more you learn about anabolic steroids, the more you come to realize that, like all drugs, there’s a difference between their intelligent use and outright abuse. In this article, Doug Kalman takes a look at the effects of Testosterone on the heart. What he found may surprise you.

Over the years we’ve all heard the repeated mantra that anabolic steroids are bad for the heart. Some physicians will tell you that gear raises your risk of heart disease by lowering your good cholesterol (HDL) and raising your bad cholesterol (LDL). In fact, as some docs will tell you, anabolic steroids are known to even induce cardiac hypertrophy (enlargement of the heart). And since you can’t flex your heart in an effort to woo women, who’d want that?

But, as in every story, there’s more than one side. In fact, let it be said, the dangers of anabolic steroids are overstated and, hold onto your seats, may even be good for the heart. Let’s examine some of the scientific studies on the positive effects of Testosterone on the heart.

What are the cardiovascular effects of anabolic steroids?

Cardiologists at the Royal Prince Alfred Hospital in Australia recruited both juicing and non-juicing bodybuilders for a study. Each bodybuilder had various aspects of the heart measured (carotid intima-media thickness, arterial reactivity, left ventricular dimensions, etc.). These measurements indicate whether bodybuilding, steroid usage or both affect the function, size, shape and activity of the heart.

The doctors found some obvious and not so obvious results. Predictably, those bodybuilders who used steroids were physically stronger than those who didn’t. What was surprising was that the use of steroids was not found to cause any significant changes or abnormalities of arterial structure or function.

In essence, when the bodybuilders (both groups) were compared with sedentary controls, any changes in heart function were common to bodybuilders. The take home message from this study is that bodybuilding itself can alter (not impair) arterial structure/function and that steroids do not appear to impair cardiac function.

Does MRFIT need a T boost?

A famous cardiac study was published about 10 years ago. It soon became on ongoing study known as the Multiple Risk Factor Intervention Trial (MRFIT). The present study examined changes in Testosterone over 13 years in 66 men aged 41 to 61 years. The researchers determined if changes in total Testosterone are related to cardiovascular disease risk factors.

The average Testosterone levels at the beginning of the study were 751 ng/dl and decreased by 41 ng/dl. Men who smoked or exhibited Type A behavior were found to have even greater decreases in T levels. The change in Testosterone was also associated with an increase in triglyceride levels and a decrease in the good cholesterol (HDL).

The authors concluded that decreases in Testosterone levels as observed in men over time are associated with unfavorable heart disease risk. (2) Sounds to me like a good reason to get T support/replacement therapy in the middle age years!

In a similar study, researchers in Poland examined if Testosterone replacement therapy in aging men positively effected heart disease risk factors. Twenty-two men with low T levels received 200 mg of Testosterone enanthate every other week for one year. Throughout treatment, Testosterone, estradiol, total cholesterol, HDL and LDL were measured.

The researchers determined that T replacement returned both Testosterone and estradiol levels back to normal and acceptable levels. They also found that T replacement lowered cholesterol and LDL (the bad cholesterol) without altering HDL (the good cholesterol). Furthermore, there was no change in prostate function or size.

The take home message from this study is that T replacement doesn’t appear to raise heart disease risk and it may actually lower your risk. It appears that more physicians should be prescribing low dose Testosterone to middle age and aging men for both libido, muscle tone and for cardiac reasons.

What about younger men?

It’s been long established that men have a higher risk of heart disease. One of the risk factors implicated is Testosterone. Reportedly, the recreational use of Testosterone can alter lipoprotein levels and, in fact, case reports exist describing bodybuilders who’ve abused steroids and have experienced heart disease or even sudden death. But the question remains, is the causal association one of truth or just an association?

To answer this, researchers at the University of North Texas recruited twelve competitive bodybuilders for a comprehensive evaluation of the cardiovascular effects of steroids. Six heavyweight steroid-using bodybuilders were compared with six heavyweight drug-free bodybuilders.

As expected, the heavy steroid users had lower total cholesterol and HDL levels as compared to the drug-free athletes. What was unexpected was that the steroid users also had significantly lower LDL (the bad cholesterol) and triglyceride levels as compared to the non-steroid users. In addition, the juicers also had lower apolipoprotein B levels (a marker for heart disease risk). Thus, the authors concluded that androgens do not appear to raise the risk of cardiovascular disease. The take home message from this study is that the negative cardiac side effects of steroids are most likely overstated.

In a little more progressive study, researchers at the Albert Einstein College of Medicine in the Boogie Down Bronx (the BDB to those in the know) examined Testosterone as a possible therapy for cardiovascular disease. The researchers note that T can be given in oral, injectable, pellet and transdermal delivery forms. It’s noted that injections of Testosterone (100 to 200 mg every two weeks) in men with low levels of T will decrease total cholesterol and LDL while raising the HDL.

In fact, Testosterone therapy has been found to have antianginal effects (reduces chest pain). Low levels of Testosterone are also correlated with high blood pressure, specifically high systolic pressure. The researchers determined that returning T levels back to normal and even high-normal levels have positive cardiovascular effects and should be considered as an adjunctive treatment for maintaining muscle mass when someone has congestive heart failure.

Putting it all together

Strong research demonstrates that the risks of negative cardiovascular effects of steroids are overstated. In fact, a recent paper published in the Canadian Journal of Applied Physiology questioned the whole risk of using steroids. (6) Joey Antonio, Ph.D. and Chris Street MS, CSCS published strong data showing that the risks of steroid use are largely exaggerated, much like scare tactics used by your parents while you were a kid. Of course, it goes unsaid that abuse of anything will lead to unwanted consequences.

We know that as we age, circulating Testosterone levels naturally decrease. For most people the Testosterone decrease goes from high-normal to mid to low normal. Data shows that there’s an inverse relationship between T levels and blood pressure as well as abdominal obesity (that paunch we see on so many middle age males).

Testosterone replacement lowers abdominal obesity and restores Testosterone back to normal levels. Restored Testosterone is correlated with better mood, better muscle tone, stronger sex drive, lower cardiovascular disease risks, stronger bones and better memory. It’s important to note that while conservative use gives a pronounced positive health benefit, higher doses may not necessarily lead to further health benefits.

What to do

If you see your body composition changing (your gut starts looking like your Uncle Lester’s), your strength or muscle tone diminishing despite your hard training and good diet, and your sex drive not matching up to TC’s columns, have your Testosterone levels checked. The acceptable normal range for Testosterone to physicians is 300 mg/dl to 1100 mg/dl. Yes, that’s a pretty wide range.

In the clinic, we see people with the complaints consistent with “andropause” (a term for male menopause) and/or increased cardiovascular risk having Testosterone levels between 300 mg/dl and 550 mg/dl. Bringing it up to the mid to high-normal level is what gives the health and “youthful” benefits. Traditionally 200 mg/dl of supplemental Testosterone given every one to two weeks improves body composition, lowers total cholesterol and LDL, while raising HDL.

It appears that supplemental T is a healthier and safer way to go than many of the drugs used to treat poor lipid profiles. The data presented in this article applies for males over 35, not those who are 18. If you think that you can benefit from Testosterone therapy look for physicians who market themselves as “anti-aging” or “longevity physicians” as well as the more progressive endocrinologists or cardiologists.

Erectile Dysfunction.Tadalafil (Cialis)

Tadalafil (Cialis) is the third oral medicine approved by the U.S. FDA for the treatment of erectile dysfunction. Like sildenafil (Viagra) and vardenafil (Levitra), tadalafil inhibits PDE5 (as described earlier).

How effective is Tadalafil (Cialis)?

The safety and efficacy of Tadalafil in the treatment of erectile dysfunction was evaluated in 22 clinical trials involving more than 4,000 men. Seven of these trials were randomized, prospective, placebo-controlled studies of 12 weeks' duration. Two of these studies (involving 402 men) were conducted in the United States, and the other five studies (involving 1,112 men) were conducted outside the United States. Two of these trials were conducted in special populations with erectile dysfunction; one in men with diabetes mellitus, another in men who developed erectile dysfunction after nerve-sparing prostate cancer surgery.

Effectiveness of Tadalafil in these studies was assessed using a sexual function questionnaire. Study participants also were asked if they were able to achieve vaginal penetration and to maintain erections long enough for successful intercourse.

In all seven trials, Tadalafil was significantly better than placebo in improving men's ability to achieve and maintain erections. Improvements in erectile function was observed in some patients at 30 minutes after taking a dose; and improvements can last for up to 36 hours after taking Cialis when compared to placebo.

How should Tadalafil (Cialis) be administered?

The recommended starting dose of Tadalafil for most patients is 10 mg taken orally approximately one hour before sexual activity. The dose may be adjusted higher to 20 mg or lower to 5 mg depending on efficacy and tolerability. The maximum recommended dosing frequency is once per day, although for many patients Tadalafil can be taken less frequently since the improvement in erectile function may last 36 hours. Tadalafil may be taken with or without food. Tadalafil is also available in 2.5 mg. or 5 mg. dosages for daily use

What are the side effects of Tadalafil (Cialis)?

Tadalafil is generally well tolerated with only mild side effects.

The most common side effects reported include:

• headache
• indigestion 
• back pain 
• muscle aches 
• facial flushing
• nasal congestion.

Back pain and muscle aches occurred in less than 7% of patients and usually occurred 12-24 hours after taking Tadalafil. The back pain and muscle aches associated with Tadalafil were characterized by mild to moderate muscle discomfort in the lower back, buttocks, and thighs, often aggravated by lying down. The back and muscle aches resolved in most patients without treatment within 48 hours. When treatment was necessary, acetaminophen (Tylenol) and nonsteroidal anti-inflammatory drugs (NSAIDs) such as Motrin, Advil, or Aleve were effective. Approximately 0.5% of all the patients using tadalafil discontinued the drug due to back pain or muscle aches.

Reports of abnormal vision were rare; it occurred in less than 0.1% of patients using Tadalafil.

There have been rare reports of priapism (prolonged and painful erections lasting more than six hours) with the use of oral PDE5 inhibitors such as vardenafil, sildenafil, and tadalafil. Men with blood cell diseases such as sickle cell anemia, leukemia, and multiple myeloma have higher than normal risks of developing priapism. Untreated priapism can cause injury to the penile tissue and lead to permanent loss of potency. If there is prolonged erection (longer than four hours), immediate medical assistance should be sought.

Who should not use Tadalafil (Cialis)?

Tadalafil can cause hypotension (abnormally low blood pressure, which can lead to fainting and even shock) when given to patients who are taking nitrates. Patients taking nitrates daily should not take tadalafil. Most commonly used nitrates are medications to relieve angina (chest pain due to insufficient blood supply to heart muscle because of narrowing of the coronary arteries). These include nitroglycerine tablets, patches, ointments, sprays, pastes, and isosorbide dinitrate and isosorbide mononitrate. Other nitrates such as amyl nitrate and butyl nitrate are found in some recreational drugs called "poppers."

Tadalafil should not be used with alpha-blockers, medicines used to treat high blood pressure and benign prostate hypertrophy (BPH) because the combination of Tadalafil and an alpha-blocker may lower the blood pressure greatly and lead to dizziness and fainting.

Tadalafil is not recommended for men with the following conditions:

• unstable angina (chest pain due to coronary artery disease that occurs at rest or with minimal physical exertion),
• low blood pressure (a resting systolic blood pressure less than 90mm Hg),
• uncontrolled high blood pressure (greater than 170/110 mm Hg),
• recent stroke or heart attack (within six months),
• uncontrolled, potentially life-threatening abnormal heart rhythms,
• severe liver disease,
• severe heart failure or disease of the heart valves, for example, aortic stenosis,
• retinitis pigmentosa.

Therefore, men with these conditions should not use Tadalafil without having these conditions evaluated and stabilized first. For example, men with uncontrolled high blood pressure should have their blood pressure controlled; and men with potentially life-threatening abnormal heart rhythms should have these rhythms controlled.

When there is angina or heart failure, the doctor may need to determine whether the heart has enough reserve to safely carry out the work necessary for sexual activity by performing cardiac treadmill stress testing.

What precautions should be taken when using Tadalafil?

In most healthy men, some of the drug will remain in the body for more than two days after a single dose of Tadalafil. Metabolism (clearing of the drug from the body) of tadalafil can be slowed by liver disease, kidney disease, and concurrent use of certain medications (such as erythromycin, ketoconazole, and protease inhibitors). Slowed breakdown allows Tadalafil to stay in the body longer and potentially increase the risk for side effects. Therefore, the dose and frequency of tadalafil has to be lowered in the following examples:

Men with severe liver disease should not take Tadalafil. Men with mild to moderate liver disease should not exceed Tadalafil dose of 10 mg once daily.

Body weight heavily influenced by gut microbes: Genes shape body weight by affecting gut microbes

Our genetic makeup influences whether we are fat or thin by shaping which types of microbes thrive in our body, according to a new study. Scientists identified a specific, little known bacterial family that is highly heritable and more common in individuals with low body weight. This microbe also protected against weight gain when transplanted into mice. The results could pave the way for personalized probiotic therapies that are optimized to reduce the risk of obesity-related diseases based on an individual's genetic make-up.

By studying pairs of twins at King's Department of Twin Research, researchers identified a specific, little known bacterial family that is highly heritable and more common in individuals with low body weight. This microbe also protected against weight gain when transplanted into mice.

The results could pave the way for personalised probiotic therapies that are optimised to reduce the risk of obesity-related diseases based on an individual's genetic make-up.

Previous research has linked both genetic variation and the composition of gut microbes to metabolic disease and obesity. Despite these shared effects, the relationship between human genetic variation and the diversity of gut microbes was presumed to be negligible.

In the study, funded by National Institutes of Health (NIH), researchers sequenced the genes of microbes found in more than 1,000 fecal samples from 416 pairs of twins. The abundances of specific types of microbes were found to be more similar in identical twins, who share 100 per cent of their genes, than in non-identical twins, who share on average only half of the genes that vary between people. These findings demonstrate that genes influence the composition of gut microbes.

The type of bacteria whose abundance was most heavily influenced by host genetics was a recently identified family called 'Christensenellaceae'. Members of this health-promoting bacterial family were more abundant in individuals with a low body weight than in obese individuals. Moreover, mice that were treated with this microbe gained less weight than untreated mice, suggesting that increasing the amounts of this microbe may help to prevent or reduce obesity.

Professor Tim Spector, Head of the Department of Twin Research and Genetic Epidemiology at King's College London, said: 'Our findings show that specific groups of microbes living in our gut could be protective against obesity -- and that their abundance is influenced by our genes. The human microbiome represents an exciting new target for dietary changes and treatments aimed at combating obesity.

'Twins have been incredibly valuable in uncovering these links -- but we now want to promote the use of microbiome testing more widely in the UK through the British Gut Project. This is a crowd-sourcing experiment that allows anyone with an interest in their diet and health to have their personal microbes tested genetically using a simple postal kit and a small donation via our website (www.britishgut.org). We want thousands to join up so we can continue to make major discoveries about the links between our gut and our health.'

Ruth Ley, Associate Professor at Cornell University in the United States, said: 'Up until now, variation in the abundances of gut microbes has been explained by diet, the environment, lifestyle, and health. This is the first study to firmly establish that certain types of gut microbes are heritable -- that their variation across a population is in part due to host genotype variation, not just environmental influences. These results will also help us find new predictors of disease and aid prevention.'

How to Train Through Injuries

Don't assume that medical practitioners will tell you everything you need to do to recover. Recovery is your responsibility. Spend your downtime focusing on the basics and dialing in movement patterns. All recovery is aerobic in nature. Do aerobic conditioning to speed recovery. Move every day, even the injured area if possible. Work around specific injuries. Upper body injuries are the easiest to train around. Taking a month off from squats and deadlifts isn't a bad idea. If you concentrate on posterior chain and core work, you'll hit new PR's when you resume squatting and deadlifting. Lower body injuries can be difficult to work around, but with a few good strategies you can continue to train and retain most of your strength.

The most important element of training through any injury is mindset. You have two options:

Wallow in self pity and allow yourself to regress while you slowly recover to your new, lower baseline. See the injury as an opportunity and challenge to correct weaknesses and recover as quickly as possible. I suggest number two. Your mindset will dictate how successful your recovery is.

Recovery is Your Responsibility
Don't assume that the medical practitioners you're working with will be instructing you on everything you can do to recover as quickly as possible. This isn't a knock on doctors or physical therapists. Most of them spend an extremely limited amount of time with patients and can hardly get them to do the minimum amount of rehab.

In fact, studies have shown that most people are so apathetic that they won't even take life-saving drugs more than 50% of the time, let alone do anything that involves more than stuffing a pill in their mouth.

Having a successful and speedy recovery is your responsibility, no one else's.

How Injuries Affect Training
Your immune system is intricately tied into your body's response to exercise. When you lift a heavy weight or smoke a conditioning workout, cellular damage occurs. This causes a cascade of other responses that end with you becoming bigger, faster, or stronger. This dynamic interaction means that your body's response to the same stimulus is constantly changing.

Any injury that causes a large systemic immune response will disrupt your body's response to training and ability to tolerate stress. You need to modify your training to account for how stressed your immune system is throughout the recovery process. Exercise beyond your body's ability to recover is a "pathogenic" stressor and slows recovery instead of stimulating it.

Basics of Recovery
ouch
Work on your weaknesses
Training what you suck at, well, sucks. But take this as an opportunity to improve. If you're like 99% of lifters, you need better aerobic capacity, movement, and breathing. In addition to that, you'd likely benefit from spending some time focusing on the basics and dialing in movement patterns again.

If you don't know what you suck at, just ask yourself what you dread training the most. Better yet, ask a training partner or friend who isn't afraid to hurt your feelings about what your weaknesses are.

Figure out weaknesses and attack them. Common weaknesses include:

• Conditioning
• Movement
• Breathing
• Exercise Technique
• Don't ignore conditioning

All recovery is aerobic in nature. Blood flowing around an injured site as well as throughout the body promotes exchange of waste and the rebuilding of cells and speeds recovery.

Aerobic conditioning also develops the fat oxidation capacity of your liver, which allows it to clear out immune system waste products more quickly. In addition, aerobic conditioning allows for greater parasympathetic tone, which promotes rest and recovery.

I can hear the excuses now. "I'm trying to gain muscle." "I don't want to get weak." These bullshit excuses are the plaintive cries of mediocrity. Unless you're an elite-level power lifter, Olympic lifter, or bodybuilder, you have no excuse to be deconditioned.

Let's clarify what I mean by "elite" because that's a term that gets bandied about almost as ridiculously as "warrior" lately. Nobody who deadlifts twice their own bodyweight is strong. A double bodyweight deadlift just means that you aren't weak. At my gym the strength standard for endurance athletes is a double bodyweight deadlift.

Similarly, no one who weighs 200 pounds is too heavy to have a decent aerobic capacity. I work with multiple athletes that weigh 200-220 pounds who regularly place well in endurance events (triathlons, marathons). You have no excuse. Get to work.

So, do your aerobic conditioning. Work up to 2-3 times per week for 60-90 minutes. Circuits of various low threshold movements can be a substitute for steady state aerobic work.

Movement is nutrition
Whenever you injure a soft tissue (muscle, ligament, tendon), movement is your best friend. As long as you use common sense and stay within the range of motion and loads your medical practitioners outline, you'll be doing your body a favor. Movement stimulates increased blood flow around the injured site, thus feeding nutrients and getting rid of waste byproducts.

Movement is also a stress (a positive one when you listen to your body) and it stimulates scar tissue formation. This is important because scar tissue develops in specific formations to handle the stress that it's placed under.

If you don't stress the injured site during recovery, you won't develop scar tissue that can handle the movements and types of stress that it'll be under when you're healthy and return to full speed. Known movements, performed at a low intensity for reasonable volume, speed up recovery.

Within the context of your specific limitations, move every day, even the injured area if possible.

Breathing matters

Breathing stimulates the lymphatic system, digestion, blood flow (oxygenation of tissues), immune system, and helps "clean" the organs. All of this stimulates faster recovery.

Opioid intake (pain killers), pain, and anxiety due to injury or surgery all have significant effects on your autonomic nervous system, which disrupts breathing patterns. If not addressed, this disruption can compromise recovery due to suboptimal acid-base balance in the body and the cascade of ensuing negative effects.

Most of the immune cells in your body are created by the bone marrow in the heads of the ribs. Proper breathing stimulates blood and lymph flow around the ribs, supporting optimal immune cell production. Non-optimal breathing also affects cognitive function. This impairs your ability to make good decisions and changes your perception of everything.

Learn how to breathe properly and practice every day.

Working Around Specific Injuries
Here are some basics for working around injuries. Apply these within the context of your specific situation. Be smart and do what works for you. These strategies are suggestions, not instructions. Don't do something just because it's listed here.

Shoulder, Hand, Wrist, and Elbow Injuries
Upper body injuries are the easiest to train around. You still have your lower body, core and one unaffected arm to train.

Train the other arm. Just because one of your arms is injured doesn't mean the other one can't be trained.

Try:

• Single Arm Dumbbell Rows
• Single Arm Dumbbell Bench Presses
• Single Arm Dumbbell or Kettlebell Overhead Presses
• Single Arm Pulldowns

Give your spine a break. Taking a month or two off from squats and deadlifts isn't necessarily a bad idea. I did that following my most recent shoulder surgery and after a few months of hip lifts, belt squats, and lots of posterior chain and core work, I returned to squatting and deadlift. I was hitting PR's a few months later because I fixed my weaknesses. My back also thanked me. Spine deload exercises include:

Rear-Foot Elevated Split Squat (weight in one hand + weighted vest)
Lunge Variations (weight in one hand + weighted vest)
Hip Thrust

Incorporating dynamic work is a great way to overload the lower body without having a lot of weight on the spine. Examples of dynamic exercises:

• Box Jumps
• Hurdle Jumps
• Depth Jumps
• Split Squat Jumps
• Squat Jumps
• Knee, Ankle, and Foot Injuries

Lower body injuries can be difficult to work around, but with a few good strategies you can continue to train and retain most of your strength throughout your recovery period.

Train the Upper body. This may seem obvious, but most people think any injury means no training. You can still train the upper body with very few modifications and a good training partner.

Train the uninjured leg. Some options:

• Single Leg Squats
• Single Leg Hip Lifts
• Single Leg Deadlifts

Core Training. A lot of core training involves the lower extremity and without one leg, finding core exercises to do can be difficult. Some of my favorite core exercises for clients with a lower body injury:

• Dead Bugs
• Leg Lowering Exercises
• Straight Leg Sit Ups
• Hanging Unilateral Leg Raises

Lower Back, Hip, and Abdomen Injuries
Injuries around the middle of the body are the hardest to train around. However, that doesn't mean that you can't continue to train.

Train the Upper Body
When I have clients with lower back and abdominal injuries we start with a lot of low intensity upper-body work that doesn't stress the injured area. This usually means simple exercises such as floor presses and chest supported rows. Experiment with supported variations that require less core involvement until you find something that works for you.

Replace intensity with volume and density. It's unlikely you can lift heavy while recovering from this type of injury, so instead focus on doing a lot of high quality, low intensity work in short periods of time. The formula outlined below stimulates blood flow and parasympathetic (rest and recovery) activation.

Movement Work – Light-Weight Lunges, Squats, Deadlifts
Breathing exercises between sets
Here's an example of a circuit combining these different principles:

Kettlebell Romanian Deadlifts (very light with slow lowering phase)
Dumbbell One-Arm Bench Presses
Half-Kneeling Cable Rows (hold at top for 3 seconds)
Deep Breathing Squats
Four sets of 5 reps of all exercises. No rest between exercises; the breathing exercise is the rest between sets.

Stages of Recovery
Initial
The initial recovery period will range in length from weeks to months depending on the severity of the injury. During this time your body is in a constant state of systemic inflammation and recovery. The goal during this period should be to feed the recovery process and correct weaknesses without doing too much and inhibiting recovery.

Use the following guidelines to craft a training plan:

Perform aerobic activities at least 2-3 days per week.
Do some type of movement (squats, hip hinges, rows, presses) every day, but keep the intensity and volume fairly low.
Perform breathing exercises daily.
Focus on correcting weaknesses.
Eat a clean diet. Gut health contributes to sleep quality, immune response, and your overall internal health.
Perform soft tissue work daily over the entire body including around the injured site.
Sleep a lot.
Move throughout the day. My favorites are going on five minute walks or performing short sets of 20-25 air squats, light kettlebell swings, push-ups, and pull-ups every one or two hours (or whatever movements I can do).
Avoid heavy lifting, anaerobic conditioning, or crushing yourself in any other way during a training session.
Middle
The middle stage of recovery begins when you're off all pain meds and are able to start more aggressive physical therapy or training without feeling awful for several days. The systemic hormone response from these days should actually speed the recovery process. Aerobic and other low intensity work should be performed on all "off" days.

Use the following guidelines for the middle part of your recovery:

Alternate between moderately difficult and easy training days.
Easy training days should consist of movement and aerobic work.
Hard training days should follow the set/rep/intensity/rest scheme outlined below because it stimulates a large GH and testosterone response but won't crush your nervous system:

Perform variations of the big lifts: squats, deadlifts, presses, rows, pull-ups.
Do full body workouts, 3-5 main exercises, 3-5 sets per exercise, sets of 5-10 reps.
Perform supersets of 2-4 exercises allowing full recovery between sets.
Use moderate intensity. Leave at least 2-3 reps in the tank and focus on perfect technique.
Light sprints (10-15 seconds) can be performed 1-2 times per week. These are not "all out" days but more like 80-90% effort.
You shouldn't accumulate fatigue over the course of the week. You should feel close to 100% before you perform another strength session.
Back to Normal
dip
The final 10-20% of recovery is always the most frustrating. Working with skilled practitioners can help restore movement and function much faster than if you decide to go at it alone. Key tactics of the final stage of recovery:

Slowly return to full intensity workouts.
Focus on restoring proper mechanics and movement up and down the chain from the site of the injury.
Listen to your body and have training partners critique form or record form on all big lifts to ensure proper movement.
Have a long-term mindset. One training session or season is meaningless in the context of a lifetime. Don't take unnecessary risks in the name of short-term satisfaction.
Now, these are just recommendations and are far from comprehensive. Develop a relationship with the team of people you're working with and make a plan that works for you. It's your body and it's your responsibility to make the best of the situation. Be creative, listen to your body, and most importantly, buy in to the fact that you're in control of how you recover from an injury.

Combating hair loss

In the study, 416 men with male pattern hair loss ages 21 to 45 years old, were randomized to receive dutasteride 0.05, 0.1, 0.5 or 2.5 mg, Finasteride 5 mg, or placebo daily for 24 weeks. The results of the study showed that dutasteride increased hair counts in a dose-dependent fashion and dutasteride 2.5 mg was superior to finasteride 5mg at 12 and 24 weeks.

Although testosterone is the major circulating androgen, to be maximally active in scalp hair follicles it must first be converted to dihydrotestosterone (DHT) by the enzyme 5α-reductase. The importance of DHT as a causative factor in male pattern hair loss is shown by the absence of this MPHL in men with a congenital deficiency of the type 2 5α-reductase enzyme. A type 1 5α-reductase, which also metabolizes testosterone to DHT, differs in its location and amount in different tissues. In the skin, type 1 5α-reductase is the principal isoenzyme in sebaceous and sweat glands. There is no recognized genetic deficiency of type 1 5α-reductase in humans to assess its role in male pattern hair loss.

Dutasteride (Avodart) inhibits both type 1 and type 2 5α-reductase and is approved at the 0.5-mg dose for treatment of symptomatic benign prostatic hyperplasia (BPH). It is about 3 times as potent as finasteride at inhibiting type 2 5α-reductase and more than 100 times as potent at inhibiting the type 1 5α-reductase enzyme.
Dutasteride caused scalp and serum dihydrotestosterone levels to decrease and testosterone levels to increase in a dose-dependent fashion. Whereas 5-mg finasteride decreases serum DHT by about 70%, dutasteride can decrease serum DHT by more than 90%.

Results

In this phase II, dose-ranging study, 2.5-mg dutasteride was superior to 5-mg finasteride in improving scalp hair growth in men between ages 21 and 45 years with male pattern hair loss as judged by target area hair counts, expert panel assessment, and investigator assessment at 12 and 24 weeks.

Dutasteride 2.5mg vs. 0.5mg

The 2.5-mg dutasteride dose was consistently superior to 0.5-mg dutasteride in promoting scalp hair growth. The 2.5-mg dose was also better than the 0.5-mg dose at suppressing scalp DHT (79% vs. 51%), whereas it was only marginally better at suppressing serum DHT (96% vs. 92%). This difference in the dose-response of serum and scalp DHT to inhibition with dutasteride is likely to be due to the greater contribution of type 1 5α-reductase to scalp DHT concentrations.
Finasteride 5mg vs. Dutasteride 0.1mg

5 mg finasteride suppressed scalp DHT to a similar degree as 0.1 mg dutasteride group (41% and 32%, respectively). Many of the clinical effects (hair count changes, global panel assessment, and investigator assessment) were also similar in these two groups, supporting the similarity in scalp suppression between 5-mg finasteride and 0.1-mg dutasteride.

Adverse Effects

Both Dutasteride and Finasteride were well tolerated in this phase II study, and no new safety concerns have arisen in any of the phase II and phase III studies of Dutasteride given at doses up to 5 mg daily (the 5-mg dose was used in a phase II study for BPH).

There were no significant differences in side effects, serious adverse events, or withdrawals due to adverse events among any of the treatment groups, including placebo. In total, 11 subjects withdrew because of adverse events: 3 were in the placebo group (irritable bowel syndrome and impotency), 7 in the Dutasteride 0.1 mg group (decreased libido, malaise and fatigue, mood disorders, skin disorders, injuries caused by trauma, and gastrointestinal- and neurology-related complaints) and 1 in the Dutasteride 0.5 mg group (gastrointestinal discomfort and pain).

Decreased libido was noted in:

2 subjects in the placebo group
2 subjects in each of the 0.05-mg and 0.1-mg Dutasteride groups
1 subject in the 0.5-mg Dutasteride group
9 subjects in the 2.5 mg Dutasteride group
3 subjects in the Finasteride group

Of the 9 subjects with decreased libido in the 2.5-mg Dutasteride group:

4 resolved while receiving therapy
1 resolved within 3 weeks
1 resolved within 8 weeks of stopping drug therapy
1 subject, decreased libido continued after therapy had been stopped and was presumed by the subject to be unrelated to the trial or drug therapy

Concerning possible sexual adverse events, there was no evidence in the present study that either Dutasteride or Finasteride was associated with impotence. However, 9 men in the 2.5-mg dutasteride group complained of decreased libido, compared with 1 man in the 0.5-mg dutasteride group and 3 men in the Finasteride group. As with previous studies with finasteride, this adverse event was characterized as either mild or moderate in severity and often resolved with continuation of the medication. In the 4-year follow-up of the phase III trials in BPH, dutasteride (0.5 mg) was well tolerated and the incidence of the most common sexual adverse events was low and tended to decrease over time. The only subject to develop gynecomastia was in the placebo group.

Duration of Effects

The serum half-life of Finasteride is 6 to 8 hours. Dutasteride has a serum half-life of approximately 4 weeks, and this long half-life was evident in the persistent suppression of DHT with the 0.5-mg and 2.5-mg doses after Dutasteride treatment was stopped. Because of this long half-life, men being treated with Dutasteride should not donate blood until at least 6 months past their last dose to prevent administration to a pregnant female transfusion recipient.

Who should avoid using Clenbuterol?

Performance enhancing drugs such as Clenbuterol should be used sensibly and collecting as much qualified information as possible is the key to optimizing and reaping complete benefits of Clenbuterol, which is also known as Clen.

Clenbuterol is not to be used by those having a sensitivity to the medication or any of its substances or those experiencing hyperthyroidism, tachycardia, tachyarrhythmia, heart or thyroid diseases, high blood pressure, coronary artery disease, congestive heart failure, prostatic hypertrophy, hyperthyroidism, urinary retention, glaucoma, ischemic heart disease, myocardial infarction (acute period), and hypertrophic obstructive cardiomyopathy. Long-term use of this medication can decrease stamina stages to a considerable level. The medication is also not suggested for expecting and breast feeding females and kids. People with diabetic issues should seek healthcare guidance before starting use of this steroid.

Moreover, Clenbuterol should not be taken by those who are using cardiac glycosides, beta-blockers, sugar lowering drugs, insulin, CNS stimulants, MAO inhibitors, and sympathomimetic agents. It should not be taken by those already administered with or using terbutaline, oxytocin, propanolol and other beta-blockers, digoxin, dinoprost (Lutalyse, Prostamate), monoamine oxidase inhibitors, or inhaled anesthetics.  Under no situation, Clenbuterol should be used or taken through recycled or distributed needles as such a practice increases the chances of injection site pain and sexually-transmitted diseases such as HIV and AIDS. Most of these adverse reactions are extremely rare and most subside by themselves in over seven to ten days.

Deca-Durabolin Weakens Tendons and Collagen

Is it just a coincidence that bodybuilders are more likely to suffer injuries because of heavy training, or does the use of anabolic steroids have any impact on tendon/collagen strength? The research is very preliminary, as only a few studies have examined the effects of anabolic steroids on tendon and collagen strength. It was shown that anabolic steroids alter the biomechanical properties of tendons and reduce tendon flexibility.

Some interesting theories have been suggested as why heavy anabolic steroid use can cause tendon injury, which is based around cortisol production and anabolic steroids. Researches have demonstrated that anabolic steroids combined with tension overload reduced MMP2 activity (MMP2 is a gene responsible for collagen production) and increased serum values of cortisol. During cortisol treatment, the serum levels of genes responsible for collagen production decrease, suggesting that cortisol suppresses the synthesis of collagen production. The reduction in genes for collagen and tendons have been speculated as to why anabolic steroids makes bodybuilders susceptible to injuries. New research links the use of high doses of anabolic steroids to tendon and collagen dysfunction, which may make a bodybuilder think twice about training heavily while using anabolics.

Researchers examined how heavy use of the anabolic steroid Deca-Durabolin affected collagen strength in rats. The rats were separated into two groups: natural training and training with heavy anabolic steroid use. The dose the researchers administered to the rats was considered supra-physiological – Deca-Durabolin (nandrolone decanoate) 5mg/kg of bodyweight.

The rats were cleverly forced to perform resistance exercise, but you can’t just tell a rat to start benching – so the researchers attached weights to the rats’ backs. They dropped the rats into a tank of water and the rats immediately jumped out of the water as soon as they were dunked. Every week, the researchers gradually made the weight on the rats’ backs heavier and heavier until at the end of seven weeks the weight was 80 percent of their bodyweight. The researchers dropped the rats in the tank so that they performed this for 4 sets x 10 repetitions of “jumps” with 30-second rest periods. After that, they rats were sacrificed and the rats’ tendons and collagen were examined for gene expression.

There were some very interesting findings after seven weeks of training with anabolic steroids, compared with the natty (natural) group of rats. The natty group did not have any biochemical changes in the rat tendon/collagen properties, while the anabolic steroid group had major changes. The Deca-Durabolin group had reduced biochemical properties of genes involving tendon and collagen strength.

It is interesting to note that anabolic steroids administration reduced the accumulation of IGF-1 mRNA levels in some tendon regions, compared to the non-treated, trained group. This decrease of IGF-1 mRNA levels induced by AAS administration may be related to the observed decreases collagen expression when considering the possible connection between IGF-1 and collagen synthesis. The anabolic steroids treatment also decreased the MMP-2 mRNA expression (this gene encodes an enzyme for collagen).

The above study is similar to another recently published study, which showed that nandrolone impaired the healing of rotator cuffs of rabbits. In the latter study, male rabbits underwent an incision in the rotator cuff and were divided into groups with anabolic steroids (nandrolone decanoate, 10mg/kg) and natural recovery. Groups that did not receive anabolic steroids showed better healing and more tendon strength compared to groups that received anabolic steroids. Microscopic examination of specimens from the groups with anabolic steroid use showed focal fibroblastic reaction and inflammation, suggesting an impaired healing response.

The key point is that many of these studies were using supraphysiological dosages of steroids that could be like the typical Olympia stack – but the new research suggests that a high-volume approach to training with less weight may be a better approach to use for a bodybuilder than a high-intensity, heavy weight program that puts more stress on the tendons and makes them more susceptible to injury.

Memories have lasting emotional impact on Alzheimer’s patients

Alzheimer’s disease is marked by an inability to recall certain memories, but new research shows that patients diagnosed with the condition can still remember how those memories made them feel.

In a study researchers showed 17 Alzheimer’s patients and 17 healthy patients clips from happy and sad movies.

During the films, all of the study participants expressed signs of sorrow, like crying, and happiness, like laughter. Five minutes later, the individuals with Alzheimer’s couldn’t remember the movies, but they still experienced prolonged feelings of happiness and sadness.

Researchers say the findings are significant because they could impact how caregivers treat Alzheimer’s patients.

“Frequent visits and social interactions, exercise, music, dance, jokes, and serving patients their favorite foods are all simple things that can have a lasting emotional impact on a patient’s quality of life and subjective well-being,” Edmarie Guzmán-Vélez, lead author and a doctoral student in clinical psychology, said in a news release.

Experts predict that Alzheimer’s will impact nearly 16 million Americans by 2050 and cost an estimated $1.2 trillion.

Lifting Weights Reduces Lymphedema Symptoms Following Breast Cancer Surgery

Breast cancer survivors who lift weights are less likely than their non-weightlifting peers to experience worsening symptoms of lymphedema, the arm- and hand-swelling condition that plagues many women following surgery for their disease, according to new University of Pennsylvania School of Medicine research.

The findings challenge the advice commonly given to lymphedema sufferers, who may worry that weight training or even carrying children or bags of groceries will exacerbate their symptoms. "Our study challenges the historical medical recommendations for women who get lymphedema after breast cancer, and is another example of well-meaning medical advice turning out to be misguided," says lead author Kathryn Schmitz, PhD, MPH, an associate professor of Epidemiology and Biostatistics and a member of Penn's Abramson Cancer Center. "For instance, we used to tell those who had back pain to rest, but we know now that in many cases, inactivity can actually make a bad back worse. Too many women have missed out on the health and fitness benefits that weight lifting provides, including building bone density. Our study shows that breast cancer survivors can safely participate in slowly progressive weight lifting and gain those benefits without any increase in their lymphedema symptoms. In fact, this type of exercise may actually help them feel better."

In the largest study to date to examine the impact of weight training on this sometimes debilitating, incurable condition, Schmitz's team enrolled 141 breast cancer survivors with a current diagnosis of lymphedema. Half were assigned to a weight-lifting group that participated in small- group, twice-weekly, 90-minute exercise classes for 13 weeks. During that time, with guidance from trained fitness instructors in community fitness centers in Pennsylvania, New Jersey and Delaware, the women worked up to greater resistance and more sets of weightlifting exercise. For the next 39 weeks, the women continued twice-weekly unsupervised exercise, with trainers calling to check in on women who missed more than one session per week. The women wore a custom-fitted compression garment on their affected arm during their workouts, and each week were asked about changes in symptoms. Their arms were measured monthly to ensure any changes were noted as soon as they occurred. The 70 control group participants, meanwhile, were asked not to change their exercise level during study participation.

During the course of the study, women in the weightlifting group experienced fewer exacerbations of their condition, and a reduction in symptoms compared to the women who did not lift weights. There were 19 women in the control group who experienced lymphedema exacerbations that required treatment from a physical therapist, compared to 9 in the treatment group. The proportion of women who experienced an increase of five percent or more in their limb swelling was similar in both groups -- 11 percent of the weight-lifting group and 12 percent in the control group. The researchers theorize that a controlled weightlifting program may have protective benefits, by boosting strength in affected limbs enough to ward off injuries from everyday activities that can aggravate lymphedema symptoms.

"Our study shows that participating in a safe, structured weight-lifting routine can help women with lymphedema take control of their symptoms and reap the many rewards that resistance training has on their overall health as they begin life as a cancer survivor," Schmitz says. "We did the intervention in community fitness centers deliberately, in the hope that positive results seen in our study would continue to be available to breast cancer survivors long beyond the end of the research study."

It is recommended that women start with a slowly progressive program, supervised by a certified fitness professional, in order to learn how to do these types of exercises properly. Women with lymphedema should also wear a well-fitting compression garment during all exercise sessions. The new research was conducted in partnership with YMCAs in Philadelphia, Montgomery and Delaware Counties in Pennsylvania and in Burlington County in New Jersey, as well as Sisters-In-Shape Fitness in Philadelphia. Staff at the Edison-Metuchen YMCA in New Jersey have also been trained to deliver this intervention.

The research was supported by grants from the National Cancer Institute and the National Center for Research Resources.

Testosterone Muscle Hypertrophy. IGF-1 and Testosterone

Hormones, such as human growth hormone (GH) and testosterone, have been shown to play a role in muscle hypertrophy and strength gains. Men suffering from GH or testosterone deficiency have increased fat mass, reduced muscle mass, and reduced muscle force production. The anabolic effects of testosterone on muscle mass are dose- and concentration-dependent. An earlier study demonstrated that supraphysiological doses of testosterone can induce increases in muscle size and strength in younger men without exercise. Testosterone-induced increase in muscle mass is associated with a dose-dependent increase in cross-sectional areas of both type I and type II muscle fibers. However, the mechanisms by which testosterone increases muscle mass are not well understood.

The prevalent dogma for the past 50 years has been that testosterone increases muscle mass by stimulating fractional muscle protein synthesis. Testosterone administration primes skeletal muscle for growth by increasing net protein synthesis, even in the fasted state. The logical extrapolation of a continued increase in net protein synthesis is that it results in increased lean body mass and strength. Additionally, testosterone stimulates many other pathways besides just increasing protein synthesis rates, to stimulate muscle hypertrophy.

Testosterone administration also results in increases in GH secretion, androgen receptor number, satellite cell activity, and increased IGF-1 expression in skeletal muscle. It has also been demonstrated that the increase in muscle anabolism is associated with an increase in the expression of intramuscular mRNA IGF-1. High-intensity resistance exercise has been shown to increase anabolic hormones, but there is confusion as to how important the acute increases in anabolic hormones are.

There has been recent debate as to how effective the acute increases in testosterone concentrations are for increasing muscle mass. A couple of studies have suggested that acute increases in testosterone are not necessary for increases in muscle growth; this has led to confusion as to how to train.

Researchers at the Exercise Metabolism Group at McMaster University reported that muscle hypertrophy took place without acute increases in anabolic hormone concentrations.10 Ten healthy, young male subjects performed unilateral resistance training for eight weeks (three days per week). Unilateral resistance exercise is where you train only one arm or in this case, leg (as opposed to both arms or legs), while the other arm or leg is used as a ‘control’ or untrained muscle. Exercises used in the study were knee extensions and leg presses, performed at 80-90 percent of the subject’s single-repetition maximum (1-RM). Blood samples were collected before, immediately after, 30, 60, 90, and 120 minutes post-exercise.

Total testosterone, free testosterone, GH, and insulin-like growth factor-1, along with other hormones, were analyzed for the first training bout and following the last training bout. Thigh muscle cross-sectional area (CSA) and muscle fiber CSA by biopsy (vastus lateralis) were also measured pre- and post-training. No acute changes in GH, testosterone, or IGF-1 concentrations were observed in the 90 minutes following exercise, and there was no influence of training on the anabolic hormones measured. GH did show a moderate increase 30 minutes post-exercise, but returned to baseline values by 90 minutes. Training-induced increases were observed in type IIb and IIa muscle fiber CSA. No changes were observed in fiber CSA in the untrained leg. Whole-muscle CSA increased by in the trained leg and remained unchanged in the untrained leg.

In conclusion, unilateral training induced local muscle hypertrophy in the exercised limb only, which occurred in the absence of testosterone, GH, or IGF-1 circulating levels. So I guess acute increases in anabolic hormones are a waste of time… well, not so fast. A new study was published which really emphasizes the importance of acute anabolic hormones during resistance exercise.

Bill Kraemer, one of the pioneers in GH research, told the American College of Sports Medicine, “GH and testosterone responses to acute resistance exercise are essential and more importantly, the anabolic hormone response that occurs with resistance exercise is like a symphony and GH and testosterone are an important part of that symphony along with IGF-1, MGF, and other anabolic hormones.”

High-intensity exercise has long been shown to increase testosterone and GH levels, but researchers recently published something in the Journal of Steroid Biochemistry and Molecular Biology that emphasizes the need for high-intensity exercise and backs up what Dr. Kramer has been saying for years.

Those who say that acute increases in testosterone are not necessary are missing an important point: acute increases in resistance exercise-induced elevations in circulating T potentiate gains in muscle strength followinglong-term training. Researchers wanted to know if acute increases in exercise-induced testosterone had any effect on the androgen receptor, which has been shown to influence muscle hypertrophy.

Researchers designed this really cool study to investigate the situation:

• Group A: Young male subjects performed heavy leg extensions only, and immediately had a thigh muscle biopsy.
• Group B: Young men performed high-intensity heavy resistance exercise with both upper- and lower-body work. They performed bench presses, bent rows, and overhead presses. Afterward, the group performed heavy leg extensions followed by a muscle biopsy from the thigh. The researchers had the subjects perform an upper-body exercise with lower-body exercise to elicit a large increase in anabolic hormones.

While both groups had a muscle biopsy taken from the thigh after heavy leg extensions, the only difference was that one group did some upper-body work, which enhanced testosterone production.

The group that performed high-intensity, upper-body exercise and lower-body exercises had larger increases in testosterone than the group that only performed a lower-body exercise (i.e., leg extensions), but here is the really cool part. The group that performed bench presses, bent rows, and shoulder presses had a larger increase in androgen receptor function in their legs! I am not advocating a whole-body workout, but what the study shows is that the greater the increases in testosterone, the greater the increases in androgen receptors… even in different body parts (i.e., legs).

So now you have a study showing that you can increase androgen receptors to a larger extent by the acute increases in testosterone.12 This means you could possibly see some growth in your arms, chest, and back by sticking to exercises that generate large increases in testosterone.

I remember reading an article where a bodybuilder swore that doing heavy squats increased his arm size. Based on the current study, this all makes sense. In the study, the acute increases in testosterone were enhanced in the legs by doing high-intensity, upper-body exercise.

Anavar (Oxandrolone)

Anavar is the original brand name of the drug Oxandrolone and it’s one of the most misunderstood of all anabolic steroids. It’s both “underrated” and “over-rated” in many ways.

Anavar is regarded as a mild oral anabolic steroid that has a variety of uses. For someone who’s never taken anabolic steroids before it’s a good “entry” drug in that it doesn’t have a lot of harsh side effects. Of course, that’s only if dosages stay within reason. Therein lies the paradox. With Anavar, what makes it safe, makes it not very effective. And once it becomes effective, it’s not so safe.

Anavar (chemical name oxandrolone) in its pharmaceutical form comes in a 2.5 mg tablet. And it’s that recommended low dose that’s why Anavar is considered so “mild.” In therapeutic dosages, even children can use it. But for bodybuilding purposes the standard dosing would be all but useless. As with any oral, a dosing that is between 25-50 mgs a day is necessary. (Some advanced bodybuilders use up to 100 mgs a day). So in the case of prescription strength Oxandrolone, even if you took 10 tablets a day of the daily dosage, it would still in on the low side.

Anavar was originally developed to treat severe weight loss and has was prescribed for muscle wasting diseases, including AIDS. It was found that dosages of 5-10 mgs a day gave good results. But the prevention of muscle wasting and muscle building are two very different things.

Of course, as with ANY oral anabolic steroid once you go too far beyond 50 mgs or so, that’s when the potential problems begin. However, Anavar is thought of as less toxic to the liver than most other orals. Unfortunately, that belief is complete myth. Once again, the studies on the low toxicity of Anavar were done with the recommended dosages for medicinal purposes. Naturally, at 2.5 – 5 mgs a day one can expect no impact on the liver at all. This skewed evaluation falls under the category known as “bro-ology science.” In other words, someone does some reading, learns a little scientific knowledge, upon which he draws an seemingly reasonable yet erroneous conclusion, which in turn is then parroted endlessly from one so-called “expert” to another and on to a legion of followers. And on and on it goes. Before long, it’s considered common knowledge. Don’t be fooled. Anavar is 17 alpha alkylated , which in simple terms means that it is formulated to prevent breakdown in the liver. This makes for a greater effect but puts a tremendous strain on the liver. THAT is the main problem with orals, NOT the toxicity of the substance itself . And that is why Anavar  in effective dosages should be regarded as hepatotoxic as most other oral steroids.

Dosage and duration are prime factors that always need to be kept in mind. And remember that the dosage of one steroid is not the only issue. It’s the TOTAL amount of all the steroids being used that counts. So when taking more than one oral the total amount of mgs must be considered. This makes it imperative to use supplemental substances to protect the liver when using Anavar.

As for the reasons Anavar is under appreciated, there are many. Anavar can be stacked with any other steroid and can provide a welcome addition to any cycle. If you’re a newcomer to steroids and decide to use Anavar by itself, you can put on some solid muscle…just don’t expect overnight gains. Anavar increases anabolism tremendously, which essentially means it allows the muscles to absorb more protein. So the muscle building process is intensified but keep in mind, it still takes some time to grow muscle . People often confuse actual muscle growth with a steroid taking time to kick in, when in fact it begins working immediately, it’s just that muscle growth takes time to show. You probably won’t notice much at all until the third or fourth week. This is where Anavar is too often underestimated. Since the effect is strictly of an anabolic nature, the muscle grown on Anavar is usually very solid and long lasting. It’s fair to expect up to five pounds of pure muscle from using 25 mgs a day for a month. That may not seem like a lot. When using steroids, people expect to see those numbers on the scale go up (even if it’s temporary or from water weight). That won’t happen with Var which is why many consider it weak. But imagine five pounds of meat spread out throughout your body. That’s a good amount of lean mass.

It would be tempting to spread a cycle of Anavar out to 8, 10 or 12 weeks but no oral should be taken for that amount of time if you value your health. Young athletes often don’t think in terms of long range consequences but take it as truth – new livers are very hard to find! . A simple rule to remember is, the more you take, the more result and the more potential for problems. You have to take the bad with the good. The key is making the most of the cycle so that you can avoid as much of the bad and get as much of the good

Anavar is not considered a good drug for “bulking” for the fact that it doesn’t cause water retention, nor does it increase blood volume. (Something dianabol does to a great degree). Therefore, there is no significant weight gain. But Anavar does increase strength dramatically, due in part to the increase in creatine production and utilization which increases contractile strength, so it can be a great asset to a bulking program where lifting heavier weights is paramount to gaining size. Don’t surprised if your bench goes up 20% within a few weeks. That’s how powerful it truly is.

Anavar is often compared to Winstrol since both produce very “dry” gains, but the two drugs are nothing at all alike. Winstrol is a derivative of DHT , therefore it’s most androgenic and has masculating sides effects. (Hair loss, increased body hair, tougher skin, etc). Anavar has almost no androgenic properties. This is another advantage in that Anavar doesn’t cause a hard shut down of the HPTA. Though like all steroids, its structure is based off of the testosterone molecule, there’s bound to be some suppression, but it will be minimal with Anavar. So if you want to give your cycle some “kick” without stressing the HPTA, or if you’re a first or second timer and want to take something that won’t be that hard to recover from, Var is an excellent choice.

Because Anavar doesn’t cause much water retention high blood pressure shouldn’t be a problem. Because of its mild androgenic nature, it does not “aromatize.” Aromatization is when the body gets flooded with too much androgen and converts some of it into estrogen. That causes bloating, acne, and a possible loss of libido. Due to its low androgenic profile, Anavar is a favorite among women. They can gain muscle without the fear of masculizing side effects such as excess body hair. Excess estrogen is not a problem with Anavar and that too appeals to women going for a leaner more defined look. 5-10 mgs a day are as far as a gal may want to push it though. Too much more than that and the risk/benefit starts to tilt in an unfavorable direction.

Anavar is also unique in that it’s believed to assist in burning bodyfat, especially in the abdominal area. There’s some debate about this. All steroids build muscle and since you need to train and have your diet in check for best results there’s a tendency to look leaner. But with Anavar, the muscles do appear to be sharper and more cut. And there have been studies that have shown Anavar to reduce visceral fat in the stomach area with just moderate exercise. And the subjects kept the fat off after discontinuing usage as long as they continued to exercise and not increase caloric consumption. Very impressive.

This all sounds pretty good, right? Well, there’s more. Anavar is great for improving endurance and focus. Boxers and martial artists love it because they can increase power, speed and force without adding on a lot of weight.

Recovery for Anavar is pretty easy too. (Again, depending on how much and what else is stacked with it). With reasonable dosages it won’t shut down the HPTA and with just the use of some post cycle supplements you can recover fully pretty quickly.

There are a few more down sides though. One is cost. Anavar is among the most expensive oral steroids. And another drawback is the subtle results. At 50 mgs a day, Anavar is not going to produce as drastic a change to your physique as 50 mgs of Dianabol. For this reason it’s usually stacked with a stronger drug such as testosterone. The question then becomes, why use a mild drug if you’re just going to supplement it with a stronger one? That’s up to you and your goals.

Anavar is both strong and mild, harsh and safe, powerful. It has its place. It’s a smart choice for someone looking to “test the waters” of steroid use, or for someone looking for strength without a lot of weight gain or for competitive bodybuilders looking to finish off a cycle with a non bloating drug that will aid in fat loss. Or it can just be used to give some extra “oomph” to your cycle with minimal suppression. You need to decide if that sounds like something that works within your game plan.

Used correctly, Anavar is a potent contribution to even the most advanced cycles. Just keep in mind, it isn’t a free ride. It’s a lot more powerful than people realize – in both good ways and bad.