Tuesday, 20 August 2013
The research is profound because it contradicts much of the generally accepted theories of what causes arterial hardening, and the concept may also relate to many other diseases could the associated stem cells be pinpointed.
Song Li, a bio engineering professor at UC Berkeley and a researcher at the Berkeley Stem Cell Center, and his team have uncovered is a dormant stem cell in blood vessel walls, that seems to sit inactive for most of a person's lifetime, before coming to life and causing less functional cells to begin to grow. Li says these new types of cells that start growing in later life, are the root cause of arterial hardening and clogging that are associated with deadly strokes and heart attacks. Originally, it was thought that the smooth muscle cells in the arteries lining become scarred over time, and this leads to the narrow and brittle arteries that play a major part in causing cardiovascular disease. Multipurpose vascular stem cells are growing cells that look much like the smooth muscle cells, but don't function correctly. The cells were not found previously, because there are so few of them, that they were hard to isolate.
Li continues:
"We call them sleeping beauty or sleeping evil cells, because they don't do anything when they're dormant. The stem cells stay quiescent for decades before they start to grow and they make the blood vessels harden."
It almost sounds like something from Blade Runner, where the replicate humans have been deliberately designed to deteriorate and die at a much faster rate than the natural ones. What purpose would it serve the body under standard evolutionary terms to have cells activating later in life that effectively lead to its demise? With the arteries poorly formed, with wrong cell types, the blood flow becomes slowed and can then stopped completely. This causes strokes or heart attacks, depending on the location of the blockage. Strokes and heart attacks are one of the leading causes of death in the United States.
Creating drugs or other genetic treatments to shut down these stem cells or even deactivate them while a person is still young has the potential in the future to prevent arteriole hardening, reverse the damage already done, and even make this type of cardiovascular disease a thing of the past. Perhaps the futuristic Woody Allen movie "Sleeper" where people smoke tobacco and eat a high fat diet because it's healthier is not so far fetched after all.
Li backs up his theory by pointing out that the current ideas, of smooth muscle cells in the artery walls, "differentiating", or basically reverting back to an earlier stage of development and causing the scaring and degeneration seen in hardened arteries, actually had no fundamental proven mechanism to back it.
It is worth noting, of course, that the research is ground breaking and will need to be repeated and confirmed by other research teams, and Li did most of his work on mouse rather than human tissue. Nonetheless, it is an impressive work and one that will soon give drug companies a target to begin preventing growth of these negative "death" cells.
Interestingly, the stem cells that form arteries are also capable of becoming nerve, cartilage, bone and fat cells, suggesting why arteries become brittle or even filled with fat deposits. Li says that trying to attack the problem with diets and lower cholesterol is just attacking the symptoms, much like trying to stop a runny nose when you have a cold.
The research is certainly eye opening, and when we think back 100 years to some of the more outlandish scientific theories that have long since been discarded, it doesn't require much stretch of the imagination to realize that there must still be theories taken to be practically a fact, that are at best misleading or at worse plain wrong. In the spirit of a true scientist, Li has reminded us that we have so much more to understand about our existence. Thats all....
Image Credits: trialx.com
Sunday, 22 July 2012
Yes this truth has unveiled in the 72th American Diabetes Association. Scientists have stated that sexual dysfunction plays a key role for heart diseases in people having type 1 diabetes.
Sara Turek, MPH, and colleagues examined the association of sexual dysfunction with clinical markers of vascular disease in 301 men from the on-going 50-Year Medallist Study who have had type 1 diabetes for more than 50 years. Turek is a coordinator for the study, which is being conducted at the Joslin Diabetes Centre in Boston.
In prior analyses, only about half of the Medallist population has been shown to develop diabetic nephropathy, retinopathy, and neuropathy, which are complications that occur in nearly all type 1 diabetic patients in the general population by about 30 years after their initial diagnosis. The rate of cardiovascular disease in Medallists, however, is similar to that reported in age-matched patients with type 2 diabetes.
Research has also demonstrated that participants in the Medallist Study have usually maintained good long-term glycaemic control.
One issue that had not been addressed in the Medallist cohort was sexual dysfunction. "We have noticed that while sexual dysfunction is a common complaint among male Medallists that significantly impairs their quality of life, there is a paucity of data on sexual dysfunction in men with long-duration type 1 diabetes," Turek commented.
Overall, 210 male Medallists, or 69.8%, had sexual dysfunction as determined by an affirmative response to the question: "Have you ever had sexual problems?"
Males reporting a positive response had a haemoglobin (Hb)A1c of 7.1± 0.9% versus 6.8 ±0.8% in the no-dysfunction cohort (P=0.02). Body mass index (BMI) was 26.1 ±3.8 kg/m2 and. 25.8 ±3.6 kg/m2 (P=0.03) in the two groups, respectively, total cholesterol was 159.3 ±32.1 and 150.1 ±30.6 mg/dL(P=0.02), and high-density lipoprotein (HDL) was 55.1 ±16.2 and 62.1 ±17.8 mg/dL (P<0.01).
In addition, a history of cigarette smoking was associated with prevalence of sexual dysfunction (51.7% versus 39.3% in the sexual dysfunction and non-sexual dysfunction groups, respectively, P=0.05).
The researchers also examined clinical inflammatory markers that are commonly associated with cardiovascular risk and disease including C-reactive protein (CRP), interleukin (IL-6), and plasminogen activator inhibitor type 1 (PAI-1). Only IL-6 was significantly associated with patient reports of sexual dysfunction (P=0.03), and the association was independent of BMI, age, and glycemic control.
The findings suggest that sexual dysfunction follows the pattern of macrovascular complications seen in the Medalist group, Turek said. Also, the association with Il-6 may provide a pathway linking sexual dysfunction and macrovascular complications in this cohort.
Sara Turek said:
"The clinical message is that sexual dysfunction might be a more overt sign of cardiovascular issues or future cardiovascular issues than other clinical markers of cardiovascular disease symptoms such as hypertension, high cholesterol, andatherosclerosis. So if a patient presents with a complaint of sexual dysfunction, the physician may want to screen for cardiovascular problems since erectile dysfunctionmay be a predictor of increased cardiometabolic risk in aging men."
Stephanie Hastings, BA, also a coordinator for the Medalist Study, emphasized that while the determination of erectile dysfunction based on a single question is a limitation to the study, she is confident that the measure provided an accurate assessment of the presence of erectile dysfunction in this group. "Sure, it's subjective and open to interpretation but we spend a lot of time with our patients, and we find that they are very willing to share whatever information we request in order to help us in our research. We plan to follow up with a lengthier questionnaire, which we expect the majority of the participants to complete openly and honestly," she said.

