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What Is Nuclear Factor-Kappa Beta?

July 2006

By Julius G. Goepp, MD

For the past seven years, Life Extension has published extensive articles about chronic inflammation and the numerous diseases it causes, such as cancer, atherosclerosis, arthritis, dementia, and more.

In these articles, we showed how aging people over-express a molecule called nuclear factor-kappa beta, which then ignites a lethal inflammatory cascade throughout the body.

An abundance of new scientific studies has validated the multiple pathological effects inflicted by nuclear factor-kappa beta. Fortunately, scientists have discovered methods to safely suppress this insidious chronic inflammation-inducing agent. Aging humans are thus able to protect against a major cause of age-related disease.

In this article, we enlighten Life Extension members about what nuclear factor-kappa beta is and what can be done to suppress it.

Understanding the relationship between nuclear factor-kappa beta (NFkB) and inflammation is critical to maintaining your health and longevity. Over the last several years, scientists have gained new insights into how NFkB functions in the body. As a result, we are on the verge of finding ways to overcome our genetic predisposition toward degenerative conditions such as cancer, heart disease, arthritis, and even asthma.

Simply put, NFkB is a protein that acts as a switch to turn inflammation on and off in the body. Scientists describe NFkB as a “smoke sensor” that detects dangerous threats like free radicals and infectious agents. In response to these threats, NFkB “turns on” the genes that produce inflammation. As we age, NFkB expression in the body increases, provoking widespread chronic inflammation and setting the stage for diseases ranging from atherosclerosis and diabetes to Alzheimer’s. The knowledge of this simple fact should motivate us to counteract NFkB’s deleterious effects and thus guard against many of the diseases commonly associated with aging.

As we have reported over the last several years, inflammation is the key initiating factor in major degenerative diseases. In fact, some scientists estimate that inflammation underlies up to 98% of the diseases afflicting humans, including a vast array of seemingly different conditions such as cancer, heart disease, diabetes, and neurodegenerative disorders.1

NFkB is an instigating factor that unleashes inflammatory responses in chronic disease conditions. For example, NFkB can signal our cells to continue to multiply long past their normal life span, which can promote cancer. Furthermore, NFkB can further spark the smoldering inflammation that damages joint tissues, thereby provoking crippling arthritic conditions. NFkB likewise plays a role in spurring inflammation in the nervous system, which can set the stage for the onset of various neurological disorders. Scientists believe that NFkB-induced inflammation in the airways may play a role in asthma.


In recent years, numerous studies have shed light on the disease-promoting effects of NFkB and the benefits of quieting its activity in the body. For instance, recent studies indicate that NFkB plays a role in the following conditions:

  • Autoimmune joint disease: NFkB plays a crucial role in both rheumatoid arthritis and systemic lupus erythematosus, according to Spanish researchers.2 These two autoimmune conditions are known to produce severe joint pain and deterioration, as well as other symptoms that dramatically impair quality of life. Effective therapies to block NFkB may positively modulate these disease processes.
  • Hepatitis C: Infection with the hepatitis C virus is a growing cause of liver disease and liver cancer, and (unlike hepatitis B) there is no vaccine to protect against this deadly threat. In early 2006, Japanese scientists determined that NFkB plays a key role in the process by which the hepatitis C virus leads to the proliferation of human liver cancer cells.3
  • Inflammatory bowel disease: Crohn’s disease is an inflammatory bowel disease associated with symptoms such as severe abdominal pain, diarrhea, weight loss, and rectal bleeding. Recently, scientists noted that therapies that improve the symptoms and pathological signs of Crohn’s disease may work by decreasing levels of NFkB.4
  • Survival after heart attack: The death of heart muscle due to a blocked coronary artery is known as a heart attack. If the heart cannot adequately repair itself after such an attack, a common result is heart failure, in which the heart muscle cannot pump enough blood to meet the body’s needs. New findings from 2006 suggest that blocking NFkB may support cardiac muscle healing and prevent heart failure following heart attack.5
  • Prostate cancer: Zinc has long been known for its role in supporting healthy prostate function. Research from 2006 suggests that NFkB may provide the link between zinc and protection against prostate cancer. Zinc supplementation suppresses NFkB’s signaling effects, and researchers believe this may help prevent the metastasis of malignant prostate cancer cells.6
  • Diabetes: Insulin resistance in muscle tissues is a key factor in type II diabetes. In a recent investigation, researchers studied the muscle tissue of people with type II diabetes and found signs of increased NFkB activity. Reducing NFkB through exercise training in these individuals led to improvements in blood sugar metabolism.7

The identification of NFkB as a critical “switch” that “turns on” inflammation has profound implications for both preventing and treating some of today’s deadliest diseases. Clearly, NFkB is something we need to control if our goal is to lead a long and healthy life.

Fortunately, ongoing research continues to uncover a wealth of natural remedies that suppress NFkB’s activity in the body. These remedies provide the foundation for safe, effective nutritional strategies to quell NFkB and disease-provoking inflammation, thus providing a formidable defense against a vast array of deadly diseases and against aging itself.

Interacting with DNA: How NFkB Works

Present in the interior portion (cytoplasm) of every cell, NFkB is normally bound to inhibitory proteins that keep it in an inactive state. When cells are exposed to infectious invaders or stressors such as free radicals or environmental toxins (like cigarette smoke), NFkB is activated. NFkB then travels to the cells’ command center, known as the nucleus, where it binds with DNA to turn certain genes on or off. By interacting with more than 400 different genes, NFkB can thus activate the body’s blueprints for inflammation.1 These gene products are used to coordinate further inflammatory and immune responses in the body.

NFkB and Cancer Development

One of NFkB’s most lethal functions is inducing cancer in our bodies. Scientists are finding that, in addition to its central role in producing inflammation, NFkB plays an equally prominent and related role in the development of cancer.


Initiation: Cells become cancerous when their DNA is damaged by any of a host of factors, including various forms of radiation, oxidative stress, and specific toxins. Such DNA damage occurs over 3 million times per cell per day. Fortunately, because of cellular repair mechanisms, few of these mutations go on to produce cancer. Cells that survive with enough unrepaired DNA to potentially become cancerous are said to have become initiated.

Promotion: Even initiated cells rarely go on to become cancerous, because cells in most tissues have lost the ability to replicate themselves. The process of programmed cell death, or apoptosis, prevents potentially cancerous cells from passing damaged DNA along to future generations of cells. Unfortunately, under certain circumstances, cells regain the ability to replicate. Such “immortalized” cells are said to have undergone promotion, the second stage in cancer development.

Progression: Even at this late stage, our bodies’ defenses normally maintain control even over collections of initiated cells that have undergone promotion. The immune system constantly patrols the body looking for potentially cancerous cells. When it finds them, it destroys these trouble-making cells and mounts an offensive against similar cells found in other body areas. Cancerous tissue that has overcome these defenses is said to be in the final stage of cancer development, known as progression.

Since NFkB plays a role in all three stages of cancer development, understanding its actions as well as strategies to control its activity is crucial to both the prevention and adjuvant treatment of various cancers.

NFkB acts in each of the main phases of cancer development, which are known as initiation, promotion, and progression. NFkB “switches on” genes that allow cells to become initiated, and once initiated, to have their growth promoted, and once promoted, to progress and invade healthy tissue.8 Successful cancers evade powerful repair and control mechanisms at each of the three distinct stages of cancer development.8 Since NFkB is involved in each of the three stages, it is critically important that we understand NFkB’s actions in our bodies and what we can do to better control them.

The NFkB system has emerged as the central actor in the link between inflammation and cancer. NFkB affects both malignant and non-malignant tumor cells. In malignant cells, it turns on genes that create resistance to apoptotic cell death and DNA damage, in effect promoting cancer development by rendering cells capable of reproducing, even when they are exposed to pharmaceutical anti-cancer agents. In non-malignant tumor cells, NFkB turns on genes that produce factors to stimulate blood vessel formation, in support of rapid tumor enlargement and progression. Finally, byproducts produced by NFkB stimulation can also damage DNA, thereby contributing to the very earliest stages of tumor initiation.8