which plays an important role in aging. The solution—termed
“allotropic expression”—involves the use of gene therapy to introduce copies of the 13 unique mitochondrial genes into the nucleus.
4deATh-resisTAn T CeLLs—These include visceral fat cells and senescent cells that have lost the ability to reproduce
and that accumulate in the cartilage in joints. These also include
immune cells that lose their effectiveness over time and don’t
make room for other kinds of immune cells, resulting in immune
system decline in the elderly. The solution is to use distinctive
molecules on the target cells for the injection of a drug to kill
the cells or have the immune system kill the cells.
5Tissue s Tiffening—Caused by extracellular cross links (proteins outside the cells that form chemical attachments),
tissue stiffening, such as hardening of the arteries or the loss of
flexibility in ligaments, can be solved by finding or engineering
enzymes or proteins to break the cross links.
6ex TrACeLLuLAr AggregATes—Amyloids in between cells cause diseases such as Alzheimer’s disease and diabetes. The
solution is a vaccine to stimulate the immune system to purge
the junk outside of cells.
7in TrACeLLuLAr AggregATes—There’s also junk inside cells, which they can’t completely clear. This causes atherosclerosis and is important in several types of neurodegenerative
diseases and in macular degeneration. One solution lies in employing microorganisms, present in soil, that have enzymes
capable of breaking these aggregates down.
This list is complete based upon current knowledge, but it’s
possible that some cause of aging is missing. In addition, some
of the assumptions underlying the proposed solutions may not
be correct. The real issue, however, is the probability of devel-
oping safe and effective therapies for all these conditions.
Writing in a 2005 European Molecular Biology Organiza-
tion (EMBO) report, Huber Warner, associate dean for research
at the University of Minnesota College of Biological Studies,
points out: “Most therapeutic ideas, even the most plausible,
come to nothing—in pre-clinical studies or clinical research, the
proposed interventions are found to be toxic or induce unwel-
come side effects, are mooted by more successful ideas, or, most
control group is either diabetic or pre-diabetic. It will be another decade or so before researchers can determine whether
calorie restriction increases the maximum life span of long-lived primates (which, for rhesus monkeys, is about 40 years).
How long calorie restriction extends human life would be
of academic interest in population mortality, given rising obesity levels. But resveratrol, which is in the skins of grapes and
is thought to be the source of the cardio-protective effects of
wine, appears to mimic the effect of calorie restriction in animal
studies. Resveratrol extends the life span of worms, fruit flies,
and fish. It lowered mortality 30 percent in mice fed a high-fat
diet. A study of low-dose resveratrol in mice reported a striking
overlap of calorie restriction and resveratrol in heart, skeletal
muscle, and brain. It concludes, “Resveratrol, at doses that can
be readily achieved in humans, fulfills the definition of a dietary
compound that mimics some aspects of CR (calorie restriction).”
A Massachusetts-based pharmaceutical company, Sirtris
Pharmaceuticals, is developing drugs based on the effect of
resveratrol and calorie restriction on sirtuins, the enzymes associated with aging. It currently has drugs in clinical trials for
Type 2 diabetes, heart disease, and cancer. To the extent these
drugs are better or safer than existing drugs, they may offset
the expected increase in mortality from rising obesity. In fact,
because several new drugs are being tested for diabetes and
other diseases, it’s probable that some eventually will result in
improved treatments that will offset the higher mortality associated with growing obesity in the general population.
How long
calorie restriction
extends human life
would be of
academic interest
in population
mortality, given
rising obesity
levels.
vik TOR BLazhUk/ iSTOCkPhOTO
engineered negligible senescence
Aging can be thought of in two ways: primary aging, the increasing frailty and susceptibility to age-related diseases, and
secondary aging, the pathology that ends life. While all warm-blooded animals age, primary aging may not be inevitable.
Engineered negligible senescence was used by the author and
gerontological theoretician Aubrey de Grey to describe interventions that will reverse accumulated metabolic damage in
cells, thereby postponing aging indefinitely. The SENS (
Strategies for Engineered Negligible Senescence) website describes
therapy, possible with current or foreseeable biotechnology, that
addresses seven major categories of aging damage:
1CeLL Loss Wi Thou T repLACeMen T—This affects brain and heart cells, among others, and can be fixed by stimulating
cell division (by exercise or injection of growth factors and hormones) or by introducing new ones through cell therapy. Stem
cell research should provide for this.
2nuCLeAr Mu TATions (CAnCer)—This could be cured by a process, referred to as whole-body interdiction of lengthening of telomeres, in which cells would have their telomerase
genes removed, thereby limiting the number of times they could
divide and preventing cancer from growing. Stem cells that need
to divide would be replaced by cells with restored telomeres
every 10 years or so.
3Mi ToChondriAL Mu TATions—Mitochondria are parts of cells that produce energy. The process can damage some DNA,
