Feeds:
Posts
Comments

Posts Tagged ‘Research’

Researchers have found that the insulin signaling pathways in worms have a direct bearing on their lifespan. This research is particularly interesting because humans and worms share very similar insulin signaling pathways.

Over a decade ago, the first part of this research led to some positive news as researchers found that certain mutations involved in the insulin pathways can greatly extend lifespan in worms.

“In the early 90s, we discovered mutations that could double the normal life span of worms,” Kenyon said. Those mutations effected insulin signals. Specifically, a mutation in a gene known as daf-2 slowed aging and doubled life span. That longer life depended on another “FOXO transcription factor” called DAF-16 and the heat shock factor HSF-1.

Unfortunately, the recent results show that adding sugar to the worm diet has the opposite effect.

By adding just a small amount of glucose to C. elegans usual fare of straight bacteria, they found the worms lose about 20 percent of their usual life span. They trace the effect to insulin signals, which can block other life-extending molecular players.

Here is the technical aspect of the results:

In fact, glucose makes no difference to the life span of worms that lack DAF-16 or HSF-1, they show. Glucose also completely prevents the life-extending benefits that would otherwise come with mutations in the daf-2 gene.Ultimately, worms fed a steady diet containing glucose show a reduction in aquaporin channels that transport glycerol, one of the ingredients in the process by which the body produces its own glucose. “If there is not enough glucose, the body makes it with glycerol,” Kenyon explained. That glycerol has to first get where it needs to go, which it does via the aquaporin channels.

There are a few ways in which the result from studying worms affects us as humans.

A diet with a low glycemic index seems like a safe bet for now. One of the scientists was alarmed enough with the data to make serious changes to her diet:

As an aside, Kenyon says she read up on low-carb diets and changed her eating habits immediately — cutting out essentially all starches and desserts — after making the initial discovery in worms. The discovery was made several years ago, but had not been reported in a peer-reviewed journal until now.

Another area of concern is medicine. Current drugs may be offering treatment which carry as of yet unknown long term side effects. Fortunately, as is the case with anti-depressant medication, science is continually advancing to make our lives better and this research will undoubtedly result in better life saving medicines.

She says the findings may also have implications for drugs now in development for the treatment of diabetes, which are meant to block glucose production by inhibiting glycerol channels. The new findings “raise a flag” that glycerol channels might be doing something else, she says, and that drugs designed to block them might have a downside.

A long term study recently found a connection between consuming two servings of diet soda daily and a significant decline in kidney function. How do different types of artificial sugars factor into these results? Is there any connection between these two studies?

Aging in humans is far more complex than in worms.

“Although we do not fully understand the mechanism by which glucose shortens the life span of C. elegans, the fact that the two mammalian aquaporin glycerol-transporting channels are downregulated by insulin raises the possibility that glucose may have a life-span-shortening effect in humans, and, conversely, that a diet with a low glycemic index may extend human life span,” the researchers write. Kenyon also points to recent studies that have linked particular FOXO variants to longevity in several human populations, making the pathway the first with clear effects on human aging.

Glucose and the insulin signaling pathways are probably just one piece in a complex puzzle explaining the aging process. With every piece of the puzzle that gets illuminated and understood we come one step closer to allowing science an opportunity to stop aging.

Read Full Post »

A surefire way to suck the romance out of any kiss is to envision it as free shipping for germs. Recent research by British scientists sheds light on why that is actually a good thing.

Writing in the journal Medical Hypotheses, researcher Dr Colin Hendrie from the University of Leeds said: ‘Female inoculation with a specific male’s cytomegalovirus is most efficiently achieved through mouth-to-mouth contact and saliva exchange, particularly where the flow of saliva is from the male to the typically shorter female.’

Cytomegalovirus is likely to be only one of many germs which take advantage of kissing as a transfer system and which can confer benefits rather than harm to the recipient.

Cytomegalovirus, which lurks in saliva, normally causes no problems. But it can be extremely dangerous if caught while pregnant and can kill unborn babies or cause birth defects.

These can include problems ranging from deafness to cerebral palsy.

Kissing, over the course of several months and increasing in intensity, transfers small amounts of the virus each time. The result is a built up immunity to the virus, thereby cutting the risk of infection and potential damage to the fetus tremendously. Previous research had hypothesized that kissing was important because it conveyed fitness information about the individual through saliva. Given this new data and given that there are many other methods for determining fitness, kissing is not likely to have evolved as a means of determining fitness from an evolutionary perspective.

Dr Hendrie said: ‘Information concerning body tone, smell, reproductive condition, disease state and, of course, personal physical and oral hygiene can all be gained solely from close physical proximity.’

‘The small amount of additional information from kissing is an unlikely pressure for its development.’

People have subconsciously understood for a long time that germs can be transferred via kissing, hence that use of copious amounts of alcohol when strangers kiss. Clearly, it is being used as an antiseptic.

Read Full Post »

Here is a “dog bites man” story from researchers at Columbia University Medical Center and Massachusetts General Hospital.

It is no secret that anabolic steroids have all sorts of nasty side effects.

Anabolic steroids can cause many adverse effects. Most of these side effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension, and harmful changes in cholesterol levels: some steroids cause an increase in LDL cholesterol and a decrease in HDL cholesterol. Anabolic steroids have been shown to alter fasting blood sugar and glucose tolerance tests. Anabolic steroids such as testosterone also increase the risk of cardiovascular disease or coronary artery disease. Acne is fairly common among anabolic steroid users, mostly due to stimulation of the sebaceous glands by increased testosterone levels. Conversion of testosterone to dihydrotestosterone (DHT) can accelerate the rate of premature baldness for males who are genetically predisposed, but testosterone itself can produce baldness in females.

There is a whole bunch more (we left out some of the nastier bits) where that came from. Now we can include damage to kidneys as a side effect of abusing anabolic steroids too. In fact, the damage incurred is worse than what is seen in the kidneys of morbidly obese individuals.

The investigators studied a group of 10 bodybuilders who used steroids for many years and developed protein leakage into the urine and severe reductions in kidney function. Kidney tests revealed that nine of the ten bodybuilders developed a condition called focal segmental glomerulosclerosis, a type of scarring within the kidneys. This disease typically occurs when the kidneys are overworked. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe.

However, some good news also comes from this study:

When the bodybuilders discontinued steroid use their kidney abnormalities improved, with the exception of one individual with advanced kidney disease who developed end-stage kidney failure and required dialysis. Also, one of the bodybuilders started taking steroids again and suffered a relapse of severe kidney dysfunction.

If stopped in time, kidney function can improve enough for daily functioning. Kidneys in particular are so vulnerable to the effects of anabolic steroids because they are affected both directly and indirectly:

The researchers propose that extreme increases in muscle mass require the kidneys to increase their filtration rate, placing harmful levels of stress on these organs. It’s also likely that steroids have direct toxic effects on the kidneys. “Athletes who use anabolic steroids and the doctors caring for them need to be aware of the potentially serious risks to the kidney,” said Dr. Herlitz.

Read Full Post »

Gene therapy has been successfully used to restore vision in patients suffering from a rare genetic disorder. The nature of this disorder means that the therapy is much more successful in children than adults.

Leber’s congenital amaurosis (LCA) causes sight to deteriorate beginning at birth and and resulting in complete blindness before the age of forty.

Children born with one form, LCA2, have defects in a gene called RPE65 that helps the retina’s light-sensing cells make rhodopsin, a pigment needed to absorb light. Without rhodopsin, the photoreceptor cells gradually die.

Gene therapy works by using a modified virus as a delivery system to get specific genes into specific areas. (Take a look at our article Is Chronic Fatigue Syndrome Caused By A Virus? for some background about how viruses work explained in plain English). Researchers first tested the therapy on dogs and found they could partially restore sight by using a virus loaded with the RPE65 gene. Then the researchers conducted a limited study on six young adult humans, which also resulted in sight improvements.

But the Penn researchers knew from their studies in animals that children should improve even more because they have more intact retinal tissue than adults do. Today in an online paper in The Lancet, their team and collaborators in Europe report full study results for three of the adults they treated earlier and nine more patients, including four children ages 8 to 11. The children gained more light sensitivity than the adults did–their light sensitivity increased as much as four orders of magnitude, versus one–and they made far fewer mistakes in an obstacle course.

This is one of those good news/bad news stories.

The bad news:

  • Older individuals with this disorder have lost more tissue, and therefore the therapy can be significantly less effective.
  • This therapy only applies to blindness caused by a specific defective gene, and will not benefit someone suffering from any other type of blindness.

Now, the good news:

  • Gene therapy sounds great in theory but has had few successes in real life applications. The success of this study will serve as boost to continue research into gene therapy.
  • Other vision diseases are caused by genetic defects. In the near future it may be possible to do a simple blood test to determine which defective gene a child has and then apply the appropriate therapy to prevent a loss of vision from occurring in the first place.

There is a lot of excitement in the air because of the successful results. Take a look here to see a video of one of the patients, Cory Haas, breezing through an obstacle course a mere three months after therapy.

The LCA2 trials are a rare success for the field of gene therapy, which has also cured children with the immune disorder known as bubble boy disease. And they should pave the way for treating more vision disorders. “It’s an incredible launching pad to be able to target other diseases,” says Penn gene therapy researcher Jean Bennett, who led the study.

Showing that the LCA2 gene therapy treatment works best in children is “a big step” for inherited blindness, says geneticist Frans Cremers of Radboud University Nijmegen Medical Center in the Netherlands, who wrote an accompanying commentary in The Lancet. He notes that eight other vision diseases, including retinitis pigmentosa, have now been treated in mice and are ready to be tested in people. The challenge, he says, will be to expand genetic testing of people with blindness so as to find enough eligible patients for clinical trials of these rare disorders.

Read Full Post »

Eva Redei, the David Lawrence Stein Professor of Psychiatry at Northwestern’s Feinberg School has published new research which explains why antidepressants don’t work for so many people.

There are two prevailing theories about the causes of depression. One is that depression can be caused by stressful life events and the second is that depression results from an imbalance in neurotransmitters. However, medications based on those theories are treating effects, not causes.

Most animal models that are used by scientists to test antidepressants are based on the hypothesis that stress causes depression. “They stress the animals and look at their behavior,” she said. “Then they manipulate the animals’ behavior with drugs and say, ‘OK, these are going to be good anti-depressants.’ But they are not treating depression; they are treating stress.”

That is one key reason why current antidepressants aren’t doing a great job, Redei noted. She is now looking at the genes that differ in the depressed rat to narrow down targets for drug development.

She said another reason current antidepressants are often ineffective is that they aim to boost neurotransmitters based on the popular molecular explanation of depression, which is that it’s the result of decreased levels of the neurotransmitters serotonin, norepinephrine and dopamine. But that’s wrong, Redei said.

Redei examined the genes involved in both stress and depression. Of the 254 genes related to stress and the 1275 genes related to depression there is an overlap of only 5 genes.

“This overlap is insignificant, a very small percentage,” Redei said. “This finding is clear evidence that at least in an animal model, chronic stress does not cause the same molecular changes as depression does.”

If current medications are only treating effects then research should be focused on finding and treating the causes.

In the second part of the study, Redei found strong indications that depression actually begins further up in the chain of events in the brain. The biochemical events that ultimately result in depression actually start in the development and functioning of neurons.

“The medications have been focusing on the effect, not the cause,” she said. “That’s why it takes so long for them to work and why they aren’t effective for so many people.”

Her animal model of depression did not show dramatic differences in the levels of genes controlling neurotransmitters functions. “If depression was related to neurotransmitter activity, we would have seen that,” she said.

Unfortunately, although we now know those theories are wrong, we still do not have a theory that is right.

Read Full Post »

Eat, Drink & Be Merry

We recently discussed the apparent contradiction between the facts that America is fatter than ever and people are living longer than ever. BMI is the determining factor in declaring Americans overweight.

However, the theory which says America should be suffering health problems and increased mortality because of increased obesity is quite wrong.

So why are death rates dropping and people living longer? Something must be wrong with the model — it’s pretty hard to quarrel with the data as being inadequate. Certainly the increased incidence of obesity should have produced something by this time (it started 30 years ago).

In case you have been living in a cave or something, there are several serious flaws with the BMI which make it unsuitable for determining health. A new German study by Matthias Lenz of the Faculty of Mathematics, Computer Science, and Natural Sciences of the University of Hamburg and his co-authors present these and other results in the current issue of Deutsches Ärtzeblatt International:

The Süddeutsche Zeitung published an advance notice of the report (http://www.sueddeutsche.de/gesundheit/140/489526/text/), which shows that overweight does not increase death rates, although obesity does increase them by 20%. As people grow older, obesity makes less and less difference.

For coronary heart disease, overweight increases risk by about 20% and obesity increases it by about 50%. On the other hand, a larger BMI is associated with a lower risk of bone and hip fracture.

In relation to cancer, the overall death rate among extremely obese men (BMI above 40) is no higher than among those of normal weight. Men who are overweight even have a 7% lower death rate. No significant association was found in women.

According to the authors’ analysis, overall mortality is unchanged by overweight, but increased by 20% by obesity, while extreme obesity raises it by up to 200%.

Futurepundit raises a few interesting points:

What I’m expecting: Genetic testing might show us what our relative risks are for a large variety of diseases and this knowledge could push us toward different ideal weights depending on which diseases we have the greater risks for. Also, some people are probably genetically better adapted to carrying more weight.

Note that you have other options for slowing bone decay aside from carrying more weight around. Exercise, better food, and a combination of vitamin D and vitamin K might cut bone fracture risks with age.

Weight studies are problematic because weight can vary due to muscle mass as well (albeit less often). Also, people can lose weight during the early stages of an illness before they even know they are sick. How well did the researchers adjust for these factors?

According to the CDC:

BMI is a fairly reliable indicator of body fatness for most people.

In light of this new study, will the CDC change it stance on using BMI data as a way of reliably gauging the health of Americans?

If the BMI chart is based on an illogical formula concocted over 200 years ago and can only give a general assessment of obesity in a population while failing on an individual level, why is it still in use by the government?

The answer is because government loves to create problems for which it is the solution. Pay close attention to what is happening here because this is a pattern that repeats over and over again.

We would not bet on it because it is not the first time nanny staters in the government have used bogus data to justify their agendas regardless of scientific truth, nor will it be the last. Rather than letting those busybodies get you down, learn how to eat your way to happiness. Being drunk and gassy is one recent formula for living a long life, although can easily be a life of bachelorhood if you are not careful to find the right wine/broccoli balance.

Read Full Post »

A major question rested heavily on the minds of certain people in the scientific community: can you taste carbonation?

One way to answer that question would be to consume a carbonated beverage in an environment which prevents the bubbles from bursting.

Ryba added that the taste of carbonation is quite deceptive. “When people drink soft drinks, they think that they are detecting the bubbles bursting on their tongue,” he said. “But if you drink a carbonated drink in a pressure chamber, which prevents the bubbles from bursting, it turns out the sensation is actually the same. What people taste when they detect the fizz and tingle on their tongue is a combination of the activation of the taste receptor and the somatosensory cells. That’s what gives carbonation its characteristic sensation.”

Perhaps some of you are interested in a little bit of history. What on Earth prompted people to indulge in fizzy beverages? Hint: it predates Coca-Cola.

In 1767, chemist Joseph Priestley stood in his laboratory one day with an idea to help English mariners stay healthy on long ocean voyages. He infused water with carbon dioxide to create an effervescent liquid that mimicked the finest mineral waters consumed at European health spas. Priestley’s man-made tonic, which he urged his benefactors to test aboard His Majesty’s ships, never prevented a scurvy outbreak. But, as the decades passed, his carbonated water became popular in cities and towns for its enjoyable taste and later as the main ingredient of sodas, sparkling wines, and all variety of carbonated drinks.

Other research has been conducted on our sense of taste for sweet, sour, salty, bitter and savory. Jayaram Chandrashekar, Ph.D., David Yarmolinsky Ph.D. and Lars von Buchholtz, Ph.D. teamed up to find the source responsible for detecting the taste of carbonation.

Here is the science of what they found:

Carbonic anhydrase 4, or CA-IV, is one of a family of enzymes that catalyzes the conversion carbon dioxide to carbonic acid, which rapidly ionizes to release a proton (acid ion) and a bicarbonate ion (weak base). By so doing, carbonic anhydrases help to provide cells and tissues with a buffer that helps prevent excessive changes in pH, a measure of acidity.

The scientists found that if they eliminated CA-IV from the sour-sensing cells or inhibited the enzyme’s activity, they severely reduced a mouse’s sense of taste for carbon dioxide. Thus CA-IV activity provides the primary signal detected by the taste system. As CA-IV is expressed on the surface of sour cells, Chandrashekar and co-workers concluded that the enzyme is ideally poised to generate an acid stimulus for detection by these cells when presented with carbon dioxide.

They worked with mice, which have a sense of taste similar to human. The question remains, why do mammals taste carbonation at all?

The scientists are still not sure if carbon dioxide detection itself serves an important role or is just a consequence of the presence of CA-IV on the surface of the sour cells, where it may be located to help maintain the pH balance in taste buds. As Ryba says, “That question remains very much open and is a good one to pursue in the future.”

Thanks to their hard work you can rest assured it is not merely your imagination.

Read Full Post »

Older Posts »