Going “Green” with Autophagy as Your Evolutionary Health Care Plan

Look around at the world today and you will see something gone wrong. Increased rates of heart diseases, all types of cancers, fears of pandemic flus and other degenerative conditions becoming more prevalent such as arthritis, auto-immune disorders, and alzheimers.

Is this just part of a wake-up call on an evolutionary level?

Where did We go Wrong?

Today’s environment that we live in (including the foods that we eat) is far from the natural conditions that people lived in long ago. That is not to say we all need to move back into caves and hunt for food, but we should focus on the more important recent (esp the last hundred years) changes that are taking our health in the wrong direction.

Those big changes include:

While I am not going to ever point out just one thing to blame for our sad state of health today, they all play a part. We need to start looking at the damage being done on the body as a whole and how it effects us at the cellular level. Optimizing health at the cellular level is vital.

For example, what is cancer? Essentially it is a bunch of cells gone bad and destructive. If left unchecked it will continue to damage other cells and create more and more “cells gone bad”. Do this in your lung and you have lung cancer, in your brain and you have brain cancer, etc.

So in our modern goal of health awareness and reducing risks of disease, we should be looking to focus our efforts on maintaining health at the cellular level (which means creating less destruction and increasing repair/rebuilding).

The Only Known way to Live Longer/Healthier

Scientists have known for a long time that there is really only one proven way to increase the lifespan of animals in test conditions (as well as improve health in humans). This is what is known as Calorie Restriction (or CR).*

*Editor Update: New CR study results (2012) casts doubt on guaranteed longevity benefits and is discussed in more detail here.

Here is an excerpt from a recent article in the New York Times on the calorie restriction experiment:

A curious aspect of the Calerie project, though, is that it is not meant to study weight loss or if one type of diet is better than another. Instead, Calerie is investigating how (and if) a spartan diet affects the aging process and its associated diseases. To the Calerie researchers, these are quite distinct. The aging process, which researchers sometimes call “primary” or “intrinsic” aging, refers to the damage that ordinarily accumulates in our cells as we grow older, a natural condition that seems to have limited the maximal lifespan of humans to 120 years. Diseases that accompany the aging process — often called “secondary aging” — are those afflictions increasingly prevalent in the elderly, like cancer, diabetes and cardiovascular disease.

There seems little doubt that calorie restriction can have significant effects on secondary aging. A recent spate of papers in some of the world’s leading medical journals demonstrate that in small studies, human subjects following such diets experience astounding drops in cardiovascular risk factors; a forthcoming review on cancer risks in animals with such diets, moreover, suggests a stark correlation — fewer calories mean fewer tumors.

Fontana connected his point to his continuing observations of some Calorie Restriction Society members. “In terms of cardiovascular diseases — the No. 1 cause of death; 4 out of 10 people die of it in the U.S. and Europe — we know that they will not die of cardiovascular death,” Fontana said. His subjects have cholesterol around 160, blood pressure around 100 over 60, high HDL, low triglycerides and very low levels of inflammation. “So these people won’t develop these diseases,” he said. “And I think that’s an important finding. Because every day doctors are publishing hundreds of papers on circulation research and medications that are lowering blood pressure or cholesterol by a small bit. And here we have such a powerful intervention that is basically cleaning out the arteries.”

Calorie Restriction is a natural way in which the body can produce less damage and be more resistant to damage at the cellular level. All this leads to a healthier and longer life. Also it seems that there is another process going on that helps to repair the damage due to aging. This could hold the key to helping not only treat people with diseases, but also help people live longer (by slowing down the destructive aging process).

Cell Death and Recycling

More and more light is being put into how the cells can “recycle” their own damaged parts and create a new and healthy cell in the process. This is what is known as autophagy and could be one of the keys to living longer and healthier!

Here’s a good summary from the University of Florida Health news on UF scientists reveal how dietary restriction cleans cells:

During the aging process, free radicals . – highly reactive byproducts of our cells’ respiration – wreak havoc on our cellular machinery. Mitochondria, the tiny power plants that keep a cell functioning, are especially vulnerable to this type of damage. The effects can be disastrous – if malfunctioning mitochondria aren’t removed, they begin to spew out suicidal proteins that prompt the entire cell to die. Cell death, on a whole-body scale, is what aging is all about.

Fortunately, younger cells are adept at reducing, recycling and rebuilding. In this process, damaged mitochondria are quickly swallowed up and degraded. The broken down pieces are then recycled and used to build new mitochondria. However, older cells are less adept at this process, so damaged mitochondria tend to accumulate and contribute to aging.

“Cell survival is dependent upon the ability of the cell to reduce and recycle by a mechanism called autophagy,” said William Dunn Jr., Ph.D., a professor of anatomy and cell biology in UF’s College of Medicine and senior author of the study,

and more from this really good article in Scientific American on How Cells Clean House:

Mitochondria, for instance, are the organelles primarily responsible for generating energy within a cell, and they can send signals to other parts of the cell that initiate apoptosis, or cellular suicide.

Cells induce apoptosis for a variety of reasons, all more or less for the greater good of the organism. For example, the body continually generates more cells than it needs, and they must be eliminated. An aging cell that has ceased functioning efficiently may kill itself to make room for younger, more robust cells. A cell that switches from normal growth to cancerous proliferation can also be induced to commit suicide, making apoptosis one of the most important built-in barriers against cancer. Apoptosis depends on a complex series of cellular events, rigorously orchestrated by numerous protein signals, and so the death of the cell by apoptosis is considered to be a programmed event.

But a faulty mitochondrion can wreak havoc if it sets off apoptosis at the wrong time. Among the by-products of a functioning mitochondrion are reactive oxygen species (ROS)—oxygen ions and other oxygen-based molecular fragments. Working with such volatile chemicals often causes mitochondria to leak some of their contents, including the signaling proteins that initiate apoptosis. In other words, a minor flaw in a small part of the cell can lead, inadvertently, to the death of the entire cell. The accidental cellular demise of a few skin cells might not be a big deal, but such a loss of memory neurons in the brain would definitely spell trouble.

The escape of such large amounts of ROS poses a cancer threat, because ROS that reach the nucleus may induce malignant changes in genes. Once again, autophagy can come to the rescue, removing the dysfunctional mitochondria from the cell. Eileen White of Rutgers University believes that autophagy also mitigates genome damage in cancer cells, thereby helping to prevent new tumors from forming.

Most people take it for granted that many diseases become more frequent with age, including cancer and the degeneration of neurons. The reason, in part, may be a decline in the efficiency of auto­phagy. According to Ana Maria Cuervo of the Albert Einstein College of Medicine, the current thinking is that cellular systems, including autophagy, undergo a steady loss of function with age.

Recall that a restricted food supply—incipient starvation—speeds up autophagy.

The programmed cell death/self-suicide of a cell, otherwise known as apoptosis, is a good thing in some cases. While you don’t want all your cells to die off, you definitely don’t want the cancerous cells gone bad sticking around and creating more damage. It could be summed up that a defective apoptosis system is a big reason for the progression of cancerous cells in a body. If left unchecked, the cancerous cells spread and create more. A functioning apoptosis system would call for the cancerous cells to commit suicide and stop the progression.

So it seems that autophagy through various pathways can not only help stop new progression of cancerous cells, but may also help improve apotosis signaling through healthy mitochondria. Add this to a continual process of healthy cell repair and “going green” (recycling) at the cell level may be the real fountain of youth.

Understanding Aging to Reduce Diseases

Researchers are now currently looking for a pharmaceutical treatment to increase autophagy in healthy cells and apoptosis in cancerous ones (although more is not always better and with every treatment seems to come more negative side effects). By looking at the real source of the problem (aging), evolutionary solutions can be seen in helping people with diseases associated with it.

from this recent article in the Boston Globe on Age-old woes, New Tactic.

The drugs in Sirtris’s pipeline are aimed at treating two diseases associated with aging: type 2 diabetes and cancer. The drugs target sirtuins, the enzymes identified by Gaurente and others as regulating cell metabolism.

Much of the discussion at the Harvard lifespan conference centered on sirtuin modulators, which appear to provide the same benefits as calorie restriction (CR) – a practice enthusiasts believe will extend their life spans. Their faith is based on the results of studies with yeast, flies, and primates.

Resveratrol, found most abundantly in red wine and Japanese knotweed, is the best-known sirtuin modulator. Many scientists speculate that the resveratrol in red wine is behind the “French paradox,’’ the low incidence of heart disease in the French despite their love for fatty foods.

Message is Simple: Eat Less (and Eat Real Foods)

While researchers are trying to come up with patented pharmaceutical versions to enhance autophagy (and they will probably not be cheap either), we already have those systems built in if we send the right signals to help increase their function. Namely through a “restricted food supply”, like the “feast-famine” environments that our bodies were designed to survive.

While CR is certainly not the most realistic nor enjoyable solution for many, there is still many of the same benefits found with Intermittent Fasting (or IF). The benefits of IF is you can also maintain lean bodyweight (muscle) while burning fat and still enjoy eating. Plus, it is the cheapest way I know of that you can reduce your risks for degenerative diseases!

So while health care costs are going through the roof and medical treatments are too expensive for many to afford, maybe it is time we all start to realize the evolutionary plan for the body to help heal itself. It costs nothing more than just personal awareness into how you eat effects your own health. Eat less and eat more “real foods” is the best advice I think we all need to take to heart (and tell others to do as well). The bonus is if you eat mainly real foods anyways, that it is hard to actually overeat in the first place!

More related quotes and articles on Autophagy


Aging denotes a postmaturational deterioration of cells and organisms with the passage of time, an increased vulnerability to challenges and prevalence of age-associated diseases, and a decreased ability to survive. Causes of this deterioration may be found in an enhanced production of reactive oxygen species (ROS) and oxidative damage and incomplete “housekeeping.” Caloric restriction is the most robust anti-aging intervention known so far. Similar beneficial effects on median and maximum life span were obtained by feeding animals a 40%-reduced diet or by every-other-day ad libitum feeding. In both instances, animals are forced to spend a great part of their time in a state of fasting and activated autophagy. …. Several pieces of evidence show that autophagy is involved in aging and is an essential part of the anti-aging mechanism of caloric restriction.

from role of autophagy in aging

As a consequence of the induction of autophagy during short periods of fasting, animals experience diurnal rhythms of autophagy in concert with their circadian cycle.

from Diurnal rhythms of autophagy

Overview of the importance of autophagy and diseases (which still shows there is much we don’t know as well)

Precise regulation of autophagy is necessary to maintain metabolic equilibrium, immune homeostasis, delineate cell fate and influence host cell responses to cytosolic pathogens. A growing number of studies have implicated that inactivation of autophagy-selective responses contributes to inflammatory disorders, neurodegeneration and cancer, but the precise steps at which disease-associated autophagy-related (ATG) genes affect autophagy pathways is unknown at present

and how some viruses actually attack (and inhibit) autophagy/apoptosis

Viral subversion and inhibition of host cell autophagy has been documented for several viruses. In this issue of Cell Host & Microbe,Gannagé et al. (2009) show that the influenza virus M2 integral membrane protein blocks autophagosome maturation, significantly affecting host cell apoptosis.

and Intermittent fasting alleviates neuropathic disease

Charcot-Marie-Tooth type 1A (CMT1A) neuropathies linked to the misexpression of peripheral myelin protein 22 (PMP22) are progressive demyelinating disorders of the peripheral nervous system. In this study we asked whether dietary restriction by intermittent fasting (IF) could alleviate the neuropathic phenotype in the Trembler J (TrJ) mouse model of CMT1A. Our results show that neuropathic mice kept on a five month long IF regimen had improved locomotor performance compared to ad libitum (AL) fed littermates. The functional benefits of this dietary intervention are associated with an increased expression of myelin proteins combined with a thicker myelin sheath, less redundant basal lamina, and a reduction in aberrant Schwann cell proliferation. These morphological improvements are accompanied by a decrease in PMP22 protein aggregates, and enhanced expression of cytosolic chaperones and constituents of the autophagy-lysosomal pathway.

Get Your Free Course Today!