Secrets of Your Cells: Discovering Your Body's Inner Intelligence (9 page)

Another woman told a story that could be a fertile area for research. She had adopted a baby girl about eight months earlier and felt that the baby had not bonded to her. “Could it be because of smell?” she asked. It’s a good question. Is it possible that we could help adoptive moms and babies connect more closely if the adopting mother had a piece of cloth containing the birth mom’s perspiration?

Smell, Self, and Memory

Fundamental to self-identity, both immunity and olfaction function to detect molecules that belong to us and those that don’t.
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And both systems are also linked to memory. Certain kinds of immune cells can actually remember a previous invader and protect us should it attack
again. Through certain smells we remember loved ones, traumatic events, and other experiences that are important to us. My mom, for example, wore Estée Lauder perfume whenever she got dressed up. Smelling or remembering that scent always brings my loving mom—part of my memory and identity—back to me.

Another example of the connection between smell and memory occurs in Alzheimer’s disease; loss of the sense of smell often precedes memory loss and the loss of the sense of self.
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Yet loss of smell does not always signal Alzheimer’s disease. A zinc deficiency also can result in a loss of smell and taste as well as diminished immune function.
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Have you ever taken a zinc lozenge to help heal a sore throat? Zinc is a potent immune activator and may restore a lost sense of smell.

Physical Markers of Self (Biometrics)

In addition to cellular markers, our bodies provide other self-identifying characteristics, including fingerprints, retinal prints, voiceprints, and genetic footprints. All are unique; most do not change with age or health status. (On rare occasions with certain neurological syndromes, fingerprints may change, while retinal patterns can change in people with diabetes.)

An interesting phenomenon occurs in a very small population of women with chronic fatigue syndrome (CFS): they lose their fingerprints!
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Chronic fatigue syndrome is a complicated body-mind illness involving a debilitating fatigue that lasts longer than three months, an exhaustion so profound that people are unable to do the things they used to do. And in this respect, they have indeed lost part of themselves—the people they have been in the world. CFS is often diagnosed as “all in your head,” and there is no clear universal treatment, but we know it represents failure of immune balance, for frequently the individual’s blood reveals a hyperactive immune state. Often a viral infection precedes the onset of the disease, and the immune cells continue to react as if the virus is still present long after it has passed.

The Cellular Sleuths Detailed: The Immune System, Protector of Identity

The protector of cellular identity, the immune system, is one of the most complex networks in the body. Here I offer a brief yet fairly technical overview of the science of how immune cells work. It is truly a miraculous process that continually affirms my sense of the divine nature of the cell.

Our vastly diverse immune network is a combination of interactive cellular communities, magic potions of molecules, and the individual’s daily experience: attitudes, emotions, stresses, and happiness.
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The immune organization is truly a body-mind experience. The primary cells involved are the white blood cells, and the main molecules are called antibodies and cytokines. Add in the workings of the brain, hormones, and lifestyle, and you still have only
part
of the immune network.

The white blood cells, designated as the primary sleuths, sense danger lurking in the microenvironment. There’s actually a whole family of white blood cells involved in this mission: neutrophils, eosinophils, lymphocytes, dendritic cells, and monocytes-macrophages. In the grand scheme of cellular self-protection, once the immune cells recognize a foreign invader as “not self,” they will attack and destroy it. (It is worth mentioning that in more than thirty years of teaching about the immune system, I have repeatedly asked students to come up with a metaphor for this behavior that does not involve warfare. No one has yet—perhaps you will.)

Defensive Posture

There are basically two groups in this family of immune cells: the innate primitive phagocytic scavenger cells and the more sophisticated, educable lymphocytes. Our innate cells (neutrophils and monocytesmacrophages) are responsible for nonspecific, quick-action immune responses. On the other hand, lymphocytes are responsible for the
long-lasting, learned immune responses. The more primitive scavengers, or phagocytes, are the first to detect foreign agents such as the larger microorganisms. These cells “eat” other threatening cells or cellular debris, hence the name phagocyte. They slither around, changing shape to get into the smallest spaces and tissues, detecting any invader that has breached the sanctuary. They can detect bacteria, fungi, and even dust particles in the lung. Phagocytic cells defend us against infection yet never remember what they’ve done.

The second arm of immune defense, the lymphocytes, will come in to complete the job as well as eliminate the more hidden, smaller viruses, and they will remember these intruders’ identities. This more sophisticated acquired immune response depends on lymphocytes, which are educated throughout our lifetime. You will read more about their role further on.

All of these cells are endowed with surface markings that enable them to recognize and respond to “not self.”

An Inflaming Scenario

You’re in the garden trimming a rose bush when a hidden thorn snags your finger. Ouch! A drop or two of blood oozes from the wound, and millions of cells are called to rescue and repair the tiny tear in your skin. The fluid plasma in which the blood cells swim floods the area, washing out and diluting any toxins. The white cells hear the alarm. Neutrophils pick up signals from invading microorganisms, recognize them as “not self,” latch onto them, and gobble them up, killing and digesting them in the process. To nourish these immune cells, red blood cells rush in to bring oxygen and remove waste. Platelets, another kind of tiny blood cell, help wall off the area so that the invader and any accompanying toxins stay put. Within the first twenty-four hours of the thorn’s “attack,” the other scavenger population, the monocytes, come in to finish the job.

Bacteria and fungi are the pathogens most readily eliminated through this process. Once they are gone and the area is cleaned up, chemical signals instruct the cells to build new tissue.

This entire scenario is one you have experienced again and again: it’s called
inflammation.
Next time you get a cut, insect bite, bruise, or burn, watch what happens. The area reddens, swells, heats up, and becomes painful; these are the four classical signs of the inflammatory process—signs that your immune cells are working.

Inflammation is the most basic immune response.
Whether a foreign organism or an irritating dust particle triggers the assault, white blood cells are aroused to handle the situation. Anything that breaches our physical boundaries can damage the self and excite these cells into defensive action.

Unfortunately, this response can get out of balance; scientists are discovering that many diseases are inflammatory in nature.
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For instance, though we have become convinced that high-fat diets lead to coronary artery disease, compelling research indicates that inflammation of the blood vessels is a major underlying factor.
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The tissue-damaging effects of diabetes are also partially attributed to inflammation, as are the long-range dangers of obesity.

To mitigate inflammatory assaults, be physically active and enjoy a diet full of fruits and vegetables: rich sources of molecules called antioxidants that can help lessen the dangers of excessive inflammation. When you learn about and understand cellular behavior, you also learn what you can do to help lessen or prevent the damage of an out-of-control cellular response. Your cells will love you for it!

The Second Call to Arms

The other group of white cells, the lymphocytes, protects us against viruses and continued assaults by other microscopic invaders. The lymphocytes known as T, B, and NK cells provide different collaborative roles in protecting us. Thymus-derived T cells are the regulators:
T helper cells activate the immune response; T suppressors turn it off. The B cell family produces antibody molecules to coat and neutralize antigens—antibody-coated antigens are easier to eliminate. And for the most part, B cells require the support of T cells to carry this out. “Natural killer” NK cells are the earliest defenders against viral infections, killing virus-infected cells directly within hours of attack, even before the rest of the immune collaboration takes place. They also appear to be sensitive indicators of psychological and lifestyle influences on immune health.
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This means their activity is easily measured in the test tube. Feeling lonely? Your NK cells may become sluggish. Meditate or watch a funny movie and you pep up these cells.

While the scavengers are born with skills to immediately recognize and remove microscopic threats, the T and B lymphocytes need time to develop their selective powers before becoming fully armed to eliminate the invader (called acquired, learned, or specific immunity). Another distinction between lymphocytes and scavenger cells is that most lymphocytes can develop memory. As I mentioned earlier, the scavengers (monocytes and neutrophils) simply do their job, remembering nothing afterward. In contrast, memory lymphocytes, made during an infection or immunization, protect against future assaults by the same offending organism. That’s why people who receive the measles vaccine are protected for a lifetime; a population of their lymphocytes can instantly recognize and eradicate any measles virus that might assault them. One of the things that continually amazes me about the immune network is the number of fail-safes and alternate means to eliminate danger that are built into the system. And the cells do not operate in a vacuum: what we do can help or hinder their abilities. We live in a truly collaborative relationship with these cells, a partnership dedicated to keeping us healthy.

The “immune dance” of the acquired or learned immune response is an astonishingly complex choreography that brings together all aspects of body, mind, and molecules. It shows that our cellular universe is a very cooperative and collaborative one protecting our survival. Our
lifestyle, nutrition, and physical activity as well as stress all play a part in this dance; long-term chronic stress can slow down immune responsiveness, while relaxation strategies can improve it.
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Now let’s walk through the steps of this dance.

The Eleven Steps of the Learned Immune Response

1.
 
Recognition of “not self”—an invader.
The scavenger monocytes and dendritic cells begin the dance. Once cells detect the invader, an almost magical performance is choreographed.
2.
 
Dismantling the invader.
Once recognized as a danger, the offending organism is broken into pieces that stimulate immune reactivity. These stimulating pieces are called antigens. The dismantling cells, called antigen-processing cells (APC), include monocytes-macrophages and dendritic cells.
3.
 
Recognition markers point out the invader.
The antigen is moved onto the surface of the antigen-processing cell, like a flag. The cell circulates, looking for a T helper cell that recognizes this offending antigen. T helper cells are endowed with the ability to recognize about a million different antigens, though each specific T cell recognizes only one.
4, 5.
 
Molecular messaging—a feverish response.
Invasion! Once the appropriate T helper cell is found, it receives a chemical signal from the antigen-processing cell to make more copies of itself. These chemical signals are called cytokines and interleukins, which are molecular messages between cells. IL1 (interleukin 1) signals the T helper cell to make more helpers (5) able to recognize the specific antigen. The T helpers choreograph the rest of the dance. In addition to affecting immune cells, IL1 also travels up to the brain, increasing body temperature and making you sleepy, helping you conserve energy to fight the infection. For many invading organisms, an elevated body temperature is
lethal. In fact, fever is another hallmark of a working immune network. Though we often interpret a fever as “something’s wrong,” on the contrary, it is telling us that our immune network is working fine. Studies of people with influenza virus infections who took aspirin to lower their temperature indicate they actually experienced longer-lasting symptoms than did people who took no aspirin. In fact, aspirin lowers a fever by lessening the immune response.
6, 7.
 
T cells look for B cells.
The T helper cell, now carrying the antigen flag of the invader, goes on the prowl to find a B lymphocyte that recognizes the same antigen. The B cell spots it and sends another molecular signal (7) so that more B cells are produced that recognize this specific danger.
8, 9.
 
B cell expansion and antibody production.
As this population of B cells expands, they mature into plasma cells, which manufacture antigen-neutralizing proteins called immunoglobulins or antibodies (9). There are several classes of immunoglobulins: IgG, the most predominant form, is present in the blood, while IgA is primarily in the saliva and gut. IgM is the first form produced, whereas IgE is made in response to parasites and allergens.

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