Organizations such as the Institute for Aging Research (IAR), a multidisciplinary project of the Albert Einstein College of Medicine, have extensively studied people who have exceptionally long and healthy lifespans. Obviously, if we could find some common factor in diet or exercise habits—something that everybody could do to increase their health spans—it would be important information.
While there are some things we can do personally that correlate to longer lives, the truth is that the most important factor comes from the genetic lottery. This is why the IAR’s work includes the identification of longevity genes associated with the so-called superagers, people whose lifespans are about 100 years.
Unlike a great deal of biological research, this is not “pure research.” Scientists studying longevity genes have a very definite goal in mind: to find ways to deliver the benefits of the superagers to the entire population.
I’m aware, by the way, that there is an anti-life-extension movement that opposes all such research. This attitude seems to be related to an environmentalist tendency to favor anything that reduces resource consumption and carbon dioxide production. Since dying seems to accomplish those goals, the apparent thinking is that efforts to live longer lives contradict them and are therefore bad for the Earth. It’s not true, however.
In fact, superagers use far fewer medical resources than the general population. They do so simply by avoiding major illnesses. Though long-lived individuals do exhale more than the general population, the world’s primary resource shortage at the moment is the money to pay for the rising healthcare costs associated with a population that’s growing increasingly older. If we don’t solve this crisis, we’ll face economic problems that could reduce total wealth significantly, at which point the West’s proclivity to invest in environmental spending will collapse. If you want to see environmental awfulness, just go to some Third World country where all resources go to basic survival.
Most people have very erroneous ideas about the root cause of rising healthcare costs, so allow me to restate the central dynamic behind our increasingly strained healthcare and social networks. Because healthcare costs rise exponentially with age for most people, older populations have much higher healthcare costs. Even if all treatment costs remain stable, a population that is older will have higher medical bills than a younger population. As birthrates fall and lifespans continue to increase, therefore, our healthcare costs will grow—unless we find ways to reduce the diseases of aging.
This is a serious and exponentially worsening problem because many governments, including the US’s, are already broke. Actually, it’s worse than that. In the United States, the federal government is borrowing more than a quarter of every dollar spent. This means we’re pushing our bills to the next generation. This is an untenable and unfair situation which has led even to talk of limiting end-of-life medical care as a means of reducing total healthcare costs (Logan’s Run, light version).
Superagers, however, offer another solution. They suffer far fewer of the expensive age-related diseases that are breaking budgets globally. When they do die, they tend to do it quickly and cheaply. This may sound morbid, but it’s not. My own grandmother was a superager; she was remarkably healthy until the very end, at which time she seemed to get all of the diseases that she had been spared during her first hundred years. There were no expensive efforts to sustain her, because there was nothing that could be done… and she went peacefully and painlessly.
In all likelihood, her superager status was conferred by an allele of the cholesteryl ester transfer protein (CETP) gene. This is critically important, because longevity genes are protein machines. We can make those proteins and potentially deliver their benefits to everybody.
CETP and Longevity Genes
I don’t think any other longevity gene has been studied as much as CETP, and for good reason. While it’s true that genes function as networks, the presence of one variant or allele of the CETP yields an extremely high probability of living a very long and healthy life. People with this characteristic are much more likely to avoid cancers, heart disease, Alzheimer’s, and other major diseases.
In the case of the CETP variant we’re discussing, this gene’s protein affects the size of cholesterol in the bloodstream. For reasons that are not well understood, this effects everything from brain to heart function and contributes to extended health spans.
Obviously, this is a desirable outcome from a policy as well as personal perspective. Scientists, therefore, have attempted to produce drugs that would reproduce the superager cholesterol profile. Thus far, efforts such as Roche’s Dalcetrapib and Pfizer’s torcetrapib have failed. This is very new science, and the quest for a drug that would turn everybody into a superager is only now beginning to heat up. However, a drug may not be the best approach to replicating the benefit of the superager CETP allele.
Drugs, after all, have some pretty substantial problems. One is simply that they have to be taken regularly and can be expensive and difficult to fine-tune. Additionally, a biologically active compound may disrupt the complex checks and balances of our natural systems. One example of this kind of disruption is human growth hormone (HGH). While increasing HGH can have some desirable effects, the side effects may be outweigh the benefits. This is because the introduction of exogenous growth hormone throws the fine balance of other hormones out of balance and may lead to serious problems.
When growth hormone is increased using a DNA vaccine that increases growth hormone releasing hormone (GHRH), however, the entire hormonal regulatory axis adjusts. As a result, we see dramatic benefits that include rejuvenation, disease reduction, and increased lifespans in multiple animal species. This approach may not be practical when applied to cholesterol, however.
So let’s think about lipids and the CETP superagers. What we know about people with this genetic characteristic is that their blood—specifically the cholesterol-controlling mechanisms—simply works better than it does in the majority of older people. I find it fascinating to ponder that the blood in our veins may hold the ultimate solution to all kinds of problems, including cancers, heart attacks, and dementia. Researchers are only now beginning to seriously investigate ways to restore older blood to its youthful functionality. GDF11 research is one very promising field.
Stimulating BAT Cells to Fight Obesity
Another area with great promise is brown adipose tissue (BAT). Until recently, it was believed that BAT cells were a feature found only in young humans and other animals. Scientists have been interested in BAT primarily because brown fat cells naturally regulate body weight. When you were young and ate too much, you may remember feeling hot and even perspiring for a period. That’s because BAT was activating to burn those excess calories and clear excessive blood sugar.
BAT is also activated by being cold, which is why we are now seeing businesses that purport to help people lose weight by putting them in super-cold environments temporarily. I don’t yet know, by the way, if this strategy works. We do know that transplants of BAT from young to older animals does lead to weight loss. It has also been shown to reduce or eliminate type 2 diabetes.
This anti-diabetes effect isn’t due only to lower rates of obesity, however. One of the most important discoveries of the last few years is that BAT functions as an organ, generating a number of extremely important compounds, such as adiponectin and betatrophin, as needed. These compounds assist in optimal control of cholesterol function and blood sugars. The fact that we tend to lose our youthful abilities in these critical areas as we age is extremely meaningful.
Honestly, I think the weight loss benefits are sufficient reason to want this biotechnology accelerated immediately. Personally, I’d love to lose the last 10 pounds of belly fat that’s seemingly impervious to exercise and my ability to reduce my caloric intake. Obesity, however, is a leading cause of all kinds of serious diseases, including cancer, heart disease, and dementia. Remember, these are the same diseases that the CETP superagers are resistant to. There’s a distinct possibility that we could see many of the benefits of the genetically lucky transferred to the general population, thus reducing total healthcare budgets to manageable levels.
Moreover, you don’t have to be obese to suffer from the diseases associated with bad cholesterol function and diabetes. Rice-eating cultures, for example, suffer terrible rates of diabetes, apparently because of rice’s high glycemic index, which indicates its ability to send blood sugar levels skyrocketing.
Scientists are working on drugs right now that would replicate the CETP variant that bestows superager characteristics. A more promising area of research is finding some way to prompt the growth and activation of BAT. The simplest solution, however, may be to implant rejuvenated BAT behind the scapula or inside the clavicle where it is naturally concentrated. This technology has the added benefit of being possible now thanks to breakthroughs in induced pluripotent stem cell technology.
I lack confidence in the US regulatory system to accelerate this science, but Japan—which desperately needs a solution to its diabetes problem—has only recently deregulated stem cell medicine significantly. If investors have the vision to take advantage of this opportunity, we may see the first real step toward a world of superagers and radically reduced healthcare costs.
Editor, Transformational Technology Alert
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