Home / Juvenon Health Journal / It’s Not Your Fault! Evolution is Too Slow 02/04


Juvenon Health Journal volume 3 number 2 february 2004

It's Not Your Fault!  Evolution is  Too Slow

By Benjamin V. Treadwell, Ph.D.

Modern culture values bodies that are slim, muscular and “healthy.” Yet two-thirds of American adults are overweight. What’s wrong with our bodies, you might ask.

My favorite answer to this question is that most likely there is nothing at all wrong with your body. It’s probably doing at a cellular level what it trained to do for thousands of years. Slow-moving evolution simply hasn’t kept up with the times.

Understanding how the body evolved to process fat provides both motivation and insights to help wage the ongoing struggle against those unwanted extra pounds. The leading actor in this drama is fat cells, or adipocytes. These are specialized cells designed to take up and store excess fuel after its conversion to fat. In the evolution of mammals, including humans, adipocytes are a remnant structure with only a fraction of their former glory.

In primitive animals, many of the activities carried out by the body’s specialized organs including the liver, blood-producing tissues, and the immune system, were performed in one primitive structure, known as the fat body. (Even today, the primitive fruit fly, Drosophilia, retains this structure.) When a pathogen attacked a primitive creature, the fat body turned on mechanisms that metabolize nutrients to produce energy to fight the attack through activation of its primitive immune system. Over the millennia, as evolution proceeded, specialized organs emerged to assume most of the multiple roles of the fat body.

An excess of any food type - whether protein, fat or carbohydrates - is converted to either glycogen or fat for storage.

Mammals have bone marrow to aid in production of red blood cells. White blood cell production involves the spleen, thymus and lymphatic system. The liver is involved in detoxification. Although the ancestor fat body ceded these functions to other organs, its descendents, the adipocytes, to the detriment of modern-day humans, continue to harbor some of the genetic blueprint reflecting their origin. That appears to be especially true for those genes normally associated with our immune system.

An excess of any food type — whether protein, fat or carbohydrates — is converted to either glycogen or fat for storage. When the glycogen stores are filled to capacity, carbohydrates and protein are converted to fat and stored in the adipocytes.

When engorged with fat particles, it appears that adipose tissue becomes a haven for inflammatory cells. This tissue also contains blood vessels, as well as a sizable quantity of immune cells or macrophages. The remnant immune system, once important for coordinating defense from pathogens, is put into a state of confusion by the overload of nutrients (fat).

0302_donutObesity occurs when adipose tissue increases in mass as a consequence of fat storage. This sends signals to the cells comprising the vasculature. These cells produce and secrete inflammatory cytokines (TNF alpha) and substances that attract inflammatory cells (macrophages) to the adipose tissue. These inflammatory substances trigger responses by surrounding tissues and initiate events that ultimately lead to the disease state. The diseases associated with this condition, obesity, are well documented. They include the pre-diabetic state (insulin resistance), type 2 diabetes, and atherosclerosis (hardening of the arteries).

To summarize; primitive creatures used the precursor to the modern day fat cell, the fat body, to serve multiple roles. Mammals, including humans, came into existence as a consequence of gradual replacement of the fat body with more specialized organs. Metabolic processes could now be run more efficiently due to the compartmentalization of numerous metabolic activities formerly contained in the fat body…. but there is a glitch!

With time, the obesity-promoted increase in inflammation, and its subsequent effects on insulin resistance and disease, become systemic. Other tissues, such as muscle and liver, are affected.

The adipocytes of early man probably did not pose a health problem as food was scarce, and the physical activity required to survive was high, thus limiting the possibility of filling these cells to capacity. Unfortunately, the agricultural, industrial and cultural revolutions have created conditions that could lead to man’s demise. Evolution hasn’t caught up. Ironically it was this cell, the adipocyte, that made higher forms of life possible. Now, without necessary life-style adjustments, it threatens to defeat us (both humans and our obese pets).

How does an over-filled fat cell threaten our lives?

The percent of fat tissue present in our bodies is positively correlated with the production of inflammatory substances (cytokines) by the high number of macrophages recruited by the adipose tissue. Apparently, once the fat cell reaches a certain size due to fat content, it is activated to produce factors that attract inflammatory cells. It is this increase in inflammatory cells, macrophages, that triggers events in tissues culminating in insulin resistance, type 2 diabetes and probably atherosclerosis (hardening of the arteries).

With time, the obesity-promoted increase in inflammation, and its subsequent effects on insulin resistance and disease, become systemic. Other tissues, such as muscle and liver, are affected. This systemic effect is at least partially due to the increased release from the adipocyte of fat constituents, or fatty acids. These in turn have been shown to increase resistance to insulin signaling in muscle tissue. (Type 2 Diabetes: A Preventable Epidemic).

One final bit of scientific insight helps to motivate me to watch my weight. Obesity is the product of large, filled-to-capacity, adipocytes. It is directly proportional to the mass of adipose tissue (fat) present in the body. Adipocyte volume is correlated with the disease state. Thus the take-home message is to strive to keep the volume of the adipocyte to a minimum. This in turn will help prevent the accumulation of destructive cytokine-producing macrophages in adipose tissue.

How can we keep the adipose tissue to a minimum? You have heard this before, but it bears repeating. The answer to this question is: proper diet and exercise. Eat a balanced, nutritious diet. Avoid junk food and calorie-dense food. Remember, although a package may claim no fat, those wonderful tasting packaged sweets are rapidly converted to fat and stored in the adipocyte.

0302_beachAs for exercise, perhaps you slipped up and overindulged on sweets, but don’t be overwhelmed with guilt or grief. Your adipocytes are just doing what their ancient heritage directed. Instead, get out and burn it off with the physical activity you enjoy most. Most importantly, never give up on yourself or, for that matter, on your friends.


Research Update

The correlation between obesity and disease – especially insulin resistance,type 2 diabetes and atherosclerosis – has long been noted. Today, prevention of these diseases through proper diet and exercise is the most common recommendation. However, development of drug treatments to slow or stop the development of these diseases is an ongoing goal of medical research. Pharmacological intervention requires precise understanding of the mechanisms that cause an excess of fat cells to lead to disease. Researchers at a leading biotechnology company have recently published compelling support for their hypothesis that “obesity-related insulin resistance is, at least in part, a chronic inflammatory disease initiated in adipose tissue.” For more information, read the journal article here.(Large File: 4.3MB) (RequiresAdobe Reader.)

This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.

Ask Ben
Dr. Treadwell answers your questions about Juvenon™ Cellular Health Supplement

QUESTION: I have been reading a lot of ads regarding human growth hormone (HGH) supplementation. To me it looks like Juvenon and HGH say they do basically the same thing. How would you compare the two?
L.S., via email<

ANSWER: The Juvenon formula is not a hormone. It acts directly on the energy-producing machinery, the mitochondria, of all cells throughout the body. The result is a more energy-efficient cell that expresses itself with more mental and physical energy.

HGH affects cells indirectly by stimulating the synthesis of other hormones and cellular factors. It can stimulate protein synthesis, insulin release, and numerous biochemical pathways that may or may not be of benefit to your health. Some studies have demonstrated increased muscle mass in people taking this supplement. Taking HGH involves significant risk. For example, stimulating protein synthesis and muscle growth may be of benefit to those suffering from certain disorders, such as excessive muscle loss. However, there is evidence that HGH in excessive amounts could activate quiescent tumors, causing cancerous growth. More research is needed. At this time I think it is wise to take HGH only under a physician’s supervision.

Benjamin V. Treadwell, Ph.D., is a former Harvard Medical School associate professor and member of Juvenon’s Scientific Advisory Board.

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