Does Sugar Shorten Lifespan?

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.

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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.

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Life Begins At 100

There are more people alive today above the age of 100, called centenarians, than ever before. The curious part of this tale is how healthy many of them are relative to their compatriots who did not live as long.

It is becoming clear that people who break through the 90-plus barrier represent a physical elite, markedly different from the elderly who typically die younger than them. Far from gaining a longer burden of disability, their extra years are often healthy ones. They have a remarkable ability to live through, delay or entirely escape a host of diseases that kill off most of their peers. Supercentenarians – people aged 110 or over – are even better examples of ageing gracefully.

Healthy is relative term for someone that old. In fact, very few people who live to be 100 are able to avoid certain chronic conditions entirely. Centenarians are divided into 3 categories regarding their health: delayers, survivors, and escapers.

Not all of the oldest old survive by delaying illness or disability, though – many soldier through it. Jessica Evert of Ohio State University in Columbus examined the medical histories of over 400 centenarians (The Journals of Gerontology Series A, vol 58, p 232). She found that those who achieve extreme longevity tend to fall into three categories. About 40 per cent were “delayers”, who avoided chronic diseases until after the age of 80. This “compression of morbidity”, where chronic illness and disability are squeezed into ever-shorter periods at the end of life, is a recent trend among ageing populations. Another 40 per cent were “survivors”, who suffered from chronic diseases before the age of 80 but lived longer to tell the tale. The final 20 per cent were “escapers”, who hit their century with no sign of the most common chronic diseases, including heart disease, cancer, diabetes, hypertension and stroke. Intriguingly, one-third of male centenarians were in this category, compared with only 15 per cent of women (see “Two paths to 100”).

There is conclusive evidence pointing to genetics as a contributing factor in such extreme longevity. Precisely how much is still being debated. Environmental factors like exercise and diet should not be dismissed even if some centenarian reports smoking 60 cigarettes a day for decades.

Scientists are working hard to uncover whatever genetic secrets are responsible for a long healthy life. Very little has been found to date.

Until recently, the only exception was ApoE, and in particular a variant of this gene known as e4, which bestows carriers with a much higher than average risk of developing Alzheimer’s and heart disease. Across the world, this unfortunate version of ApoE is about half as common in centenarians as in younger adults. Last year, a second promising candidate emerged – a variant of a gene called FOXO3A. At the University of Hawaii, a team led by Bradley Willcox, Craig’s identical twin, found that people who carried two copies of a particular form of the gene were almost three times as likely to make it to 100 than those without the variation, and also tended to start their journey into old age with better health and lower levels of stroke, heart disease and cancer (Proceedings of the National Academy of Sciences, vol 105, p 37). “There are so many false positives in this field that FOXO3A is very exciting,” says Bradley Willcox.

FOXO3A is involved in several signalling pathways that are conserved across animal species. It controls the insulin/IGF-1 pathway, which influences how our bodies process food. It also controls genes that protect cells from highly reactive oxygen radicals – molecules often thought to drive human ageing through the cumulative damage they wreak on DNA. FOXO3A could even protect against cancer by encouraging apoptosis, whereby compromised cells commit suicide. The variant of FOXO3A associated with longevity is much more prevalent in 100-year-olds even than in 95-year-olds, which clearly demonstrates the value of studying the centenarian genome.

As was discussed earlier in regards to Alzheimer’s disease, it is interesting to note that men who survive to be 100 are in better shape than women.

Men, meanwhile, have the double disadvantage of being both more prone to risky behaviours throughout their lives and more likely to succumb to chronic illnesses as they age. This means that men who do make it to their century must depend more on genetic trump cards to see them through.

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The Case Of The Shrinking Brain

It was believed that a significant amount shrinkage was inevitable as a healthy brain aged, as though aging should be the mental equivalent of taking a cold shower. As it turns out, that belief is wrong.

Previous studies of the brain in older people may have inadvertently included individuals going through the early stages of dementia. The results of a long term study were recently revealed in the September issue of Neuropsychology (an APA publication).

After examining behavioral data collected from 1994 to 2005 (with scans taken between 1997 and 1999 depending on when people entered the study), the researchers divided participants into two groups: one group with 35 cognitively healthy people who stayed free of dementia (average starting age 69.1 years), and the other group with 30 people who showed substantial cognitive decline but were still dementia-free (average starting age 69.2 years).

By dividing the people into separate groups the researchers were able to determine that a reduction in brain volume as we age should not be considered the norm. Rather, it is a sign of dementia.

In contrast to the 35 people who stayed healthy, the 30 people who declined cognitively over nine years showed a significant effect for age in the hippocampus and parahippocampal areas, and in the frontal and cingulate cortices. In short, among the people whose cognition got worse, older participants had smaller brain areas than younger participants.

Thus, the seeming age-related atrophy in gray matter more likely reflected pathological changes in the brain that underlie significant cognitive decline than aging itself, the authors wrote. As long as people stay cognitively healthy, the researchers believe that the gray matter of areas supporting cognition might not shrink much at all. “If future longitudinal studies find similar results, our conception of ‘normal’ brain aging may become more optimistic,” said lead author Saartje Burgmans, who is due to receive her PhD later this year.

As we pass certain age milestones, the odds of having dementia get higher. A study published in Neurology (the medical journal of the American Academy of Neurology) noticed something strange in the statistics for individuals above the age of 90. Women are 45% likely to suffer from dementia, whereas for men it is a much lower 28% likelihood.

Research has shown that dementia prevalence for both men and women increases from age 65 to 85. The frequency of dementia increases with age from less than 2 percent for the 65-69-year-olds, to 5 percent for the 75-79-year-olds and to more than 20 percent for the 85-89-year-olds.

The UC Irvine study, conducted in Laguna Woods, Calif., is among the few to look at dementia in people over age 90. It found that the likelihood of having dementia doubled every five years in women after reaching 90, but not in men. The results also showed that women with a higher education appeared to be as much as 45 percent less likely to have dementia compared to women with less education.

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New Study Reveals More Genes Associated With Alzheimer’s Disease

Two teams conducting parallel studies each found 2 genetic variants associated with Alzheimer’s disease, one of which was common to both studies. Philippe Amouyel’s team identified variants within CLU and CR1, while Julie Williams and her team also identified CLU and added PICALM to the mix. Combined, these 3 variants represent about 20% of the genetic risk relating to getting the disease.

In other words,

“If we were able to remove the detrimental effects of these genes through treatments, we could reduce the proportion of people developing Alzheimer’s by 20%,” Williams, of Cardiff University in Wales, told a press conference. “In the UK alone this would prevent just under 100,000 people developing the disease. So the significance of these results in truly meaningful.”

Alzheimer’s disease is the stuff of nightmares:

Although the course of Alzheimer’s disease is unique for every individual, there are many common symptoms. The earliest observable symptoms are often mistakenly thought to be ‘age-related’ concerns, or manifestations of stress. In the early stages, the most commonly recognised symptom is memory loss, such as difficulty in remembering recently learned facts. When a doctor or physician has been notified, and AD is suspected, the diagnosis is usually confirmed with behavioural assessments and cognitive tests, often followed by a brain scan if available. As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis.

The genomes of over 19,000 patients were analyzed, making the results statistically valid.

One of the new variants is in a gene active at synapses, the junctions between brain cells, and the two others help damp down inflammation in the brain. Inflammation is a known feature of Alzheimer’s, but it is often regarded as a consequence of the disease. Dr. Williams said that the detection of the new variants, which undercut the brain’s efforts to restrain inflammation, suggested inflammation might play a primary role.

Neil Hunt, chief executive of the Alzheimer’s Society agrees that these results can be referred to as a breakthrough and is calling for more research funding.

It is not very often that scientists are prepared to stick their necks out and refer to research results as a “breakthrough”. This is one of those very rare occasions when it is a word that really does fit the bill. The importance of the discovery of three new genes with an association with Alzheimer’s disease in such a short space of time is significant.

Even before this latest development, clinical research was underway investigating different avenues for a cure.

As of 2008 there were more than 400 clinical trials under way to understand and treat Alzheimer’s disease. Over 100 of these studies were in the last phase before commercialization (phase three trials).

Many different investigation approaches coexist. Amyloid beta is a common target, existing many trials which aim to reduce it with different agents such as bapineuzumab, an antibody in phase III for patients in the mild to moderate stage, semagacestat, a γ-secretase inhibitor, MPC-7869, and acc-001, a vaccine to amyloid beta in phase II to be used in the mild stage. However, in a recent study an experimental vaccine was found to have cleared patients of amyloid plaques but did not have any significant effect on their dementia, casting doubt on the utility of such approaches.^[2]

Other approaches are neuroprotective agents, like AL-108 (phase II completed); or metal-protein interaction attenuation, as is the case of PBT2 (phase II completed). Finally, there are also many basic investigations trying to increase the knowledge on the origin and mechanisms of the disease that in the future may help to find new treatments.

Faster, please.

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Use It Or Lose It

Putting your brain to use through years of formal education can serve as a protector against the effects of Alzheimer’s disease. The remarkable effect discovered was not that years of education lower the odds of getting the disease. Instead, researchers discovered that those individuals with more formal education were not showing clinical symptoms of brain deficits compared to other people with Alzheimer’s and without the educational background.

These phenomena are often ascribed to the theoretical concept of cognitive reserve. A high level of cognitive reserve results in a strong individual resilience against symptoms of brain damage; cognitive reserve can therefore be seen as protective against brain damage.

The amount of brain tissue lost was assessed through MRI (Magnetic Resonance Imaging) scans. Somehow, those with the benefit of a formal education showed an equal amount of brain volume lost, yet they were able to function normally.

Human brains are flexible organs, and it’s never too late to give them a workout. Although this study, published in the current issue of the Journal of Alzheimer’s Disease (“Education attenuates the effect of medial temporal lobe atrophy on cognitive function in Alzheimer’s disease: The MIRAGE Study,” Journal of Alzheimer’s Disease, August 2009), used formal education as a convenient guideline, you can get similar benefits by exercising your brain regularly with mentally challenging activities.

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Girl Who Does Not Age, Brooke Greenberg, Baffles Doctors

Brooke Greenberg is the size of an infant, with the mental capacity of a toddler.

She turned 16 in January.

This is an unusual case, to say the least. Doctors and scientists are working hard to try and figure out what’s happening to Brook and what mechanisms underlie it.

Brooke hasn’t aged in the conventional sense. Dr. Richard Walker of the University of South Florida College of Medicine, in Tampa, says Brooke’s body is not developing as a coordinated unit, but as independent parts that are out of sync. She has never been diagnosed with any known genetic syndrome or chromosomal abnormality that would help explain why.

Go check it out for all the interesting details, including a video.

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