Researchers have discovered what appears to be the first animal evidence linking aging and age-related diseases such as cancer, Alzheimer’s and Huntington’s.
They found a class of molecules in the roundworm C. elegans and in humans that can prolong the life of the worm and prevent the accumulation of abnormal proteins that cause a serious disease similar to Huntington’s.
The molecules are known as small heat shock proteins. They prevent the accumulation of abnormal proteins by binding to cellular proteins that are damaged or unfolded, a practice that may be able to stave off both aging and age-related disease.
Many diseases, including Alzheimer’s, Huntington’s, Parkinson’s and prion diseases, are thought to be caused by protein clumping or aggregation--and the list is growing.
The current finding suggests that heat shock proteins may influence many age-related illnesses, and the pharmaceutical industry is already looking for ways to increase the activity of heat shock proteins. If the drugs work, they may be able to protect protein function and even extend life.
In a past study, researchers found that modifying the daf-2 gene in C. elegans doubled the worms’ lifespan. The same pathway has also been found to affect lifespan in fruit flies and mice and is likely to control human lifespan as well.
Another study found that the long-lived, altered daf-2 worms accumulated disabling proteins later in life, which means that they not only live longer but also have a delayed onset of age-related disease.
In the current study, researchers found that the expression of genes for four small heat shock proteins "sharply increased" in the long-lived daf-2 mutant worms, and that two key proteins, DAF-16 and HSF-1, were required for the boost.
Researchers used a technique called scientists RNA interference, or RNAi, to show that the heat shock proteins account for a substantial part of the worms' increased lifespan.
They also found that decreased heat-shock protein gene expression accelerated the onset of Huntington's-like "polyglutamine" protein aggregation.
Researchers concluded that regulating the small heat shock proteins could influence both aging and age-related diseases.
Science Blog May 2003
Neurodegenerative diseases, which range from Huntington's and Alzheimer's diseases to cystic fibrosis and Creutzfeldt-Jakob disease, the human form of mad cow disease, are caused by a variety of mutant genes.
They are characterized by the loss of nerve function and share the common element of misfolded proteins that lead to protein aggregation, or the accumulation of insoluble proteins that can result in toxicity and disease.
As the study above states, it appears that the growth of these accumulations can be suppressed by heat shock proteins.
Heat shock proteins, also known as stress proteins because they are activated when a cell undergoes environmental stress like heat, cold or oxygen deprivation, act like chaperones, making sure that proteins are in the right shape and are in the proper place.
It appears that heat shock proteins may be very useful in combating Alzheimer’s, Huntington’s, Parkinson’s and prion diseases in the future by clearing the abnormal protein accumulations behind the disease.
It also appears that heat shock proteins play a role in stimulating the immune system.
Eating sugar and grains also has an enormous influence on the immune system. If you eat a typical American diet, you will likely obtain a variety of illnesses due to this immune impairment, and I discuss the importance of cutting grains and sugars from the diet in my new book, The No-Grain Diet.
And, let’s not forget one of the primary influences on aging:
High insulin levels.
So, we want to minimize the amount of sugar and grains we consume to keep our insulin levels minimal. Exercise is also profoundly beneficial in this respect as it another potent influence that will lower insulin levels.
In terms of Alzheimer’s disease, I have put together the following list of recommendations to increase your chances of preventing the disease:
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