1. Do you tend to get every cold and flu that goes around?
2. Do you have sore joints that are made worse by modest exercise?
3. Ever get skin rashes of unknown origin?
4. Are you unusually sensitive to the sun?
5. Do your joints swell up?
6. Do you suffer chronic pain in your hands, wrists, ankles, or feet?
7. Is your grip getting weaker?
8. Are you losing muscle?
9. Do you have chronic sinus infections?
10. Are fungal infections like athlete’s foot a common occurrence?
11. Do you have frequent bladder or urinary tract infections?
12. Do you have chronic intestinal pain or discomfort?
13. Do you have dental problems associated with periodontal disease?
14. Does it feel to you that your leg or back pain is chronic?
15. Do you take anti-inflammatory medications regularly?
16. Do you frequently take prescribed antibiotics to get over an infection?
17. Have you ever been diagnosed with any of the following
a Epstein-Barr virus
b Herpes virus
c Candida albicans
d Lyme disease (Borrelia burgdorferi)
e A waterborne parasite like Entamoeba histolytica or cryptosporidium
f HIV
g Cytomegalovirus
h Clostridium
One of the medical doctors on our research team came into my office at the Functional Medicine Clinical Research Center one morning and slapped a newspaper down on my desk. “What do you think of this?” he asked.
“This” was a front-page photograph of two outstretched hands holding sixteen different pills. The caption below the photo identified the person whose hands were pictured as a thirty-eight-year-old mother of three—we’ll call her Jane—and it labeled her condition as erythromelalgia, a rare autoimmune disease that periodically causes the ankles and feet or hands and arms to swell, turn red, and become hot to the touch. The condition is so painful that people afflicted with the condition often cannot walk or wear shoes. Jane was unable to stand long enough to prepare meals, couldn’t leave the house for any extended period of time, and certainly couldn’t wear shoes. The sixteen different pills in the photograph represented the medication regimen she followed to manage her symptoms. The regimen included some very strong painkillers. But Jane was still disabled.
“We can help this woman,” my colleague announced emphatically. “Let’s see if we can get her into the clinic.”
I hesitated. I knew that our research clinic had had no direct experience with this very uncommon autoimmune disease. What made him think we could do something for Jane? “Because,” he answered, “our approach has had such tremendous success with other autoimmune diseases like rheumatoid arthritis and lupus. I’m confident it will work here.”
By “our approach,” he meant the functional medicine approach of a personalized lifestyle program. As he put it to me that day, “At worst it can do no harm, and it has the chance to help her regain some of her lost quality of life.”
So began our experience with Jane. She acceded to our request to participate in our clinical research trial, part of a larger study being carried out at the time under the auspices of an independent institutional review board. The trial would evaluate the impact on autoimmune disease of a lifestyle program prescribed on an entirely personalized basis. She would not be asked to change her medication or her traditional treatment regimen; rather, the aim was to assess the influence on her quality of life of a functional medicine treatment program consisting of lifestyle measures personalized for her genetic uniqueness and physiological condition.
Of course, everyone has a lifestyle. Functional medicine understands that lifestyle intersects with the individual’s unique genetic legacy to either support good health or contribute to chronic illness—and to influence the outcome of any medical therapy. Prescribing a personalized lifestyle for a patient with a chronic illness will, at the very least, maximize the success of that individual’s traditional medical therapy.
Such a program begins, as it did with Jane, by incorporating the diagnostic findings of the patient’s traditional-medicine practitioners with a comprehensive patient-centered assessment of her diet, habits and behavior, environment and surroundings, family and personal health histories, and genomic profile. We also carried out a variety of specialized tests to evaluate the functional status of Jane’s immune system, endocrine hormonal system, nervous system, and gastrointestinal system.
When the team put all the data together, the findings suggested that some form of foreign exposure was triggering the immune response that underlay Jane’s symptoms. The medical literature had no evidence of an environmental trigger for the specific condition of erythromelalgia, but other autoimmune diseases are often triggered by exposure to foreign chemicals, so the next challenge was to determine the specific environmental exposure that might be triggering the response in Jane.
Again, the team started with environmental toxins known to be associated with autoimmune diseases—mercury, certain drugs, specific pesticides, plasticizers, and petrochemical by-products—but came up empty. They finally found a clue in one of the food sensitivity tests administered during the examination phase—namely, an adverse immune reaction to gluten, the common protein in wheat. This seemed slightly odd because Jane showed none of the classic digestive symptoms of gluten sensitivity; that did not necessarily mean, however, that the gluten connection was out of the question. As we saw in Chapter 4, gluten is a family of interrelated proteins found in grains. Each member of the gluten family has its own personality, slightly different from that of the others. So intolerance to different members of the gluten family of proteins can vary from person to person. The team therefore decided that further evaluation was warranted.
More testing confirmed the original finding: Jane’s immune system “saw” gluten as a foreigner. That her response was unusual was precisely the point: when Jane’s unique immune system confronted what it saw as a foreign protein in her digestive system, it was uniquely activated to respond in its own way, sending a message to the whole body that a foreigner was on board: get ready to do battle.
Yet the team knew that the presence of the foreigner was only part of the answer. It typically takes multiple environmental factors working together to tip a physiological process off balance, so it was essential to explore other factors that might be contributing to Jane’s immune imbalance. As we learned in the previous chapter, even small contributors can accumulate into a total load effect that can push the immune system past a certain threshold—the straw that breaks the camel’s back—and result in the appearance of an illness. Indeed, the team found that in addition to Jane’s unique genetic susceptibility to gluten in her diet, a high intake of other inflammation-stimulating foods—foods containing saturated fats, sugars, and trans fats—an estrogen imbalance, and altered intestinal function all contributed to the aggravation of her erythromelalgia.
The personalized lifestyle medicine program developed for Jane thus focused on diet, eliminating gluten entirely, and recommending specific foods and supplements to rebalance her gastrointestinal function and to boost her estrogen metabolism. The next four months were amazing. Jane’s pain and swelling started to subside. Her rheumatologist was able slowly to decrease her multiple medications, eliminating them one by one. Jane had told us she had three wishes for herself—to stand at the kitchen counter long enough to prepare meals for her children, to walk the length of the local shopping mall, and to be able to go outside in the spring and tend her garden. The first two of those wishes came true in those first four months of her personalized lifestyle program. Her kids actually bought her a pair of running shoes and walked with her through the mall.
After six months, Jane was taken off virtually all her medication and was reasonably symptom-free. She learned that if she strayed off her program, she could feel the symptoms returning. It was great feedback—sufficient to encourage her continued adherence to her program.
One year after her first visit to the center, Jane returned to present her doctor and nutritionist with a photograph of herself at the end of the hiking trail atop the 4,167-foot Mount Si, near Seattle, Washington. In the photograph, she brandished a sign above her head that thanked both doctor and nutritionist for what she called “the miracle” of her return to health.
If it was a miracle for Jane, it rested on a scientific conclusion derived from our understanding of how the body’s physiological process of defense works. The fact remains that because of the immune system’s interconnections with the body’s other core processes and with the external environment, an imbalance in that system very nearly brought Jane’s life to a standstill, adversely affecting her from head to toe. Yet if she is an example of what such an imbalance can do to a life, she also shows us how substantive changes in diet plus a prescribed regimen of supplements can bring the body’s process of defense back into balance and cure a disabling chronic illness.
A SIMPLE MATTER OF DEFENSE
True, understanding the immune system is a little like trying to understand particle physics or cosmology: the more you ask about the system, the more it demonstrates its complexity. But science has come a long way in learning how our defense process is influenced by the interactions between our genes and our environment, and that knowledge drives functional medicine’s revolutionary approach to the often disabling chronic illnesses that arise from immune system imbalance.
The prevailing view of autoimmune diseases like rheumatoid arthritis, systemic lupus erythematosus (SLE), and multiple sclerosis continues to be that they are inherited genetic conditions that impel the immune system to attack the body. In such a view, some people are simply born with an immune system that sees the rest of the body as a foreigner against which the immune system must mount a defense. What we learned in the genomic revolution, however, doesn’t support this characterization.
For one thing, linking specific genes to the entire family of more than eighty different autoimmune diseases just doesn’t compute. In fact, we now suspect that the genetics of any specific autoimmune disease can explain only some 30 percent of its origin. The other 70 percent, of course, is in the connection between an individual’s genes and his or her environment, diet, and lifestyle.
For another thing, the idea that you’re born with a weak or strong constitution and are just stuck with the consequences is genetic determinism all over again. Even without the advances in knowledge in the wake of the genomic revolution, this is pretty obviously not the case. You don’t have to be a physician or medical researcher to notice that chronic sinus and intestinal infections can continually alter immune system function. Exposure to drugs, chemicals, and toxic minerals can alter the immune system function. Stress and the hormones that are released during stress can alter immune system function. Activity patterns, exercise, obesity can all alter immune system function. Exposure to sun and other forms of radiation can alter immune system function. And obviously diet and specific nutrients—or their lack—can alter immune system function.
You get my point. Our physiological defense process is in constant communication with how we live, what we eat, and our environment. These factors are continually talking to our immune system, which continually determines whether it is hearing from friend or foe, and which then talks back based on that determination. What we used to think of as immune-related or autoimmune diseases are really functional disorders arising from an altered immune response. And again, what dictates the response is the unique genetic makeup of the individual at its moment of exposure to very specific events or characteristics of the environment.
Remember the celiac disease discussed in Chapter 4? It’s a condition in which damage to the small intestine prevents nutrients from being absorbed, and it is associated with a range of digestive symptoms as well as dementia. Celiac is routinely described as an autoimmune disease occurring in genetically predisposed individuals, and it is triggered by gluten, the protein found in wheat, barley, rye, and therefore in many kinds of foods—soups, salads, sauces, cereals, cookies, crackers, and more.
But the relationship between the autoimmune condition and the genetic predisposition works with a certain subtlety, as I’ve learned from one of the preeminent researchers of the disease, Dr. Alessio Fasano, a pediatric gastroenterologist and director of the Center for Celiac Research at Massachusetts General Hospital and Harvard Medical School. Yes, says Dr. Fasano, there are genes that increase susceptibility to celiac, but the individuals carrying those genes in their book of life will not experience the disease unless and until they consume gluten. When they do, the protein, which is well tolerated by most people, can become a toxin; the toxin can trigger a defensive reaction by the immune system, and that reaction produces collateral damage around the body. It’s a classic example of the old adage that one man’s meat is another man’s poison, although in this case it’s bread, not meat, that carries the poison—literally.
In the same way, there are autoimmune disorders that result from exposure to specific medications or chemicals in the environment. You probably know someone who cannot tolerate penicillin; you may have a friend who can’t go to the theater with you if the show uses a fog machine to create a smoke effect. Each of them has some susceptibility gene that can get defensive in the face of the trigger, and the defense manifests itself as a burning sensation on the skin and a swollen throat if the trigger is penicillin, or as wheezing and teary eyes as the fake fog spreads from the orchestra right up to the balcony.
So the takeaway message vis-à-vis autoimmune diseases is that, with a very, very few exceptions, they are not hardwired in the genes and are thus not inevitable for the person carrying the susceptibility genes. There are indeed important environmental, dietary, and lifestyle triggers that can alter the function of the immune system so that it reacts—even overreacts—and initiates injury to the body itself. But if we alter the environment, diet, and lifestyle behaviors that influence the expression of the genes regulating our immune system processes, we can end, reverse, and avoid the injury.
WHERE IT IS AND HOW IT WORKS
Take a look at the body’s defense system, shown here in Figure 4.
As we learned back in Chapter 4, more than half of the body’s immune system clusters around the gastrointestinal tract; that is its area of highest concentration. But it also resides in the lymph glands that are distributed throughout the body and are particularly apparent in the armpits, groin, breast, tonsils, and neck. The reason you can say you know you’re sick when you have swollen glands in your neck is that the swelling is a result of a spurt of increased activity in the immune system. That spurt indicates that the body is responding to some sort of foreign invasion—or is manifesting a chronic condition.
White cells are the workforce of the immune system, which is divided into two functional units. One unit, the cell-mediated immunity department, is populated by T cells and serves as the immune system’s infantry, which is to say that the T cells engage in hand-to-hand combat with foreign invaders. The other unit is the humoral department—the word comes from the old reference to bodily “humors,” or fluids; this is the immune system’s air force. It launches the antibodies that are the system’s Patriot missiles. Secreted by specialized cells called B cells within the immune system, the antibodies seek and destroy incoming foreign substances.
It is important to understand that T cells and B cells really do perform two different functions. Our tolerance for things that we may be exposed to across the span of our lives is controlled to a great extent by our B cells, whereas the T cells control our immediate response to a foreigner. Because B cells neutralize toxins by secreting antibodies against them, they have a lot to do with allergic disorders. T cell function, by contrast, defends against viruses, bacteria, and transformed cancer cells.
Armed with these functional units, the system practices what is called immune surveillance, continually patrolling the body looking for enemies to combat. Think of your immune system as a readiness patrol on the lookout at all times for any foreign invaders or attackers. The patrol has no eyes to see with, but it does have an extraordinarily sensitive sense of touch. Transported by the bloodstream and lymph system around the body, the white blood cells move in and out of tissues and organs. As they do so, they constantly come in contact with other occupants of those tissues and organs. If one of those occupants seems like a foreigner—be it a bacteria, a virus, a transformed human cell, or a foreign chemical or protein—the white blood cells undergo a personality change. They morph from peaceful travelers minding their own business into vigilant warriors ready to do battle.
Once upon a time, it was thought that such constant vigilance and reaction happened only in states of illness. It is now recognized, however, that a low level of immune activity goes on pretty routinely against damaged cells or molecules; this is a good thing, because it keeps those damaged cells or molecules from accumulating in the body and thereby possibly creating disease. It is only when this search-and-destroy function is overly active that we start to see healthy tissues suffering from bystander injury.
But of course, that is always the issue with the defense process (or any physiological process): too much is as bad as too little. The human immune system is a double-edged sword. If it is insufficiently active, we get sick; if it is overly active, we may suffer collateral damage. It must find the resting place that keeps it in balance, that keeps it self-regulating. How do you regulate a double-edged sword? By having the ability to turn it both ways.
Our genes, of course, are the regulators, and that is exactly what they are able to do—modulate the immune system selectively from one edge to the other. The genes assigned to immune system response are on chromosome 6. This chromosome has approximately 2,000 genes out of the total 25,000 in the human code of life; 140 of the 2,000 genes on chromosome 6 constitute what is termed the major histocompatibility complex, the MHC. The MHC genes control the way the white blood cells interact with the various foreign substances or invaders. As they receive, transcribe, and translate the messages they receive from events and factors in the external environment, the MHC genes shift from one sword edge to another. It’s not unlike turning the analog dials on a sound system—volume up if the genes sense foreign invaders and need the immune system to be more active, volume down if they sense friends and need to tell the immune system to be less active. They keep turning the dial, shifting the sword, adjusting the system’s level of activity in order to find just the right resting place, the immune system’s point of perfect balance.
We human beings with reason and willpower have the ability to change, eliminate, or add environmental factors and events sending messages to our gene regulators so that they can turn down a defense process that may be running too hot or turn it up if it has cooled down too far.
And here’s something that I find absolutely fascinating and very, very pertinent. Located on the same chromosome 6 are the genes for such autoimmune diseases as rheumatoid arthritis, SLE, celiac disease, ankylosing spondylitis—the “bamboo spine” that typically afflicts young men—and the autoimmune disease known as Hashimoto’s thyroiditis, a condition with alternating bouts of hypothyroidism and hyperthyroidism and with symptoms that can affect the entire body. Is it a coincidence that the genes for these diseases are colocalized with the genes that control the function of the immune defense system that triggers these diseases—and that have turned the dial so that one edge of the sword has gone wildly hyperactive? I think not. And neither do many other experts in the fields of autoimmunity and genetics.
The colocation of these genes tells me that in most cases, we are not born with an autoimmune disease. Rather, we are born with genes that sense factors and events in our environment, lifestyle, and diet as either friend or foe and then respond accordingly. If the response is extreme, we call it an immune disease. If the genes that control the immune response sense the exposure as less threatening, then we have intermittent chronic symptoms. Either way, the focus needs to be on the gene-environment intersection.
I can’t claim to be the sole or original progenitor of this thinking. When I was working at the Linus Pauling Institute of Science and Medicine in 1982, Pauling recounted an exchange he had had in 1940 with Nobel laureate Karl Landsteiner. Their exchange concerned the function of the immune system and the formation of antibody proteins, the things B cells create to give us long-term immunity. Conceding that he was neither a biologist nor an immunologist, Pauling told Landsteiner that he nevertheless believed that the way immune antibodies work must have something to do with their structure. That night, after the exchange between the two men, Pauling went home and read Dr. Landsteiner’s book on the immune system; the next day he sent Landsteiner a sketch of how antibodies might be formed and how they might work as immune agents capable of developing tolerance in us toward substances to which we have never previously been exposed. Pauling’s sketch became the classic model from which researchers were eventually able to elucidate the immune defense process in which the antibody binds to a toxin it has perceived, the antigen, forming a complex that initiates the immune response.
Fifty-one years after sketching that model, Dr. Pauling remained convinced that understanding the origin of immune-related diseases was rooted in how the structure of the immune system altered its function when exposed to different environmental factors or events. Now that it has been reported that the third leading cause of premature death in the United States is the burden of autoimmune diseases, it may be time to consider that the eighty different autoimmune diseases may be more similar in origin than we thought, and that the differences derive from a mismatch between an individual’s genes and his or her environment.
For most of us, however, the question is a bit more mundane and far simpler: How do we address whatever may be disturbing our core defense process? How do we help the immune system find its resting balance and stay there?
YOUR DEFENSE PROCESS: MODULATING THE IMMUNE SYSTEM FUNCTION
We have long known that a number of specific nutrients play important roles in supporting immune system balance. A deficiency in any of these nutrients can adversely influence the functions of T cells and B cells in the immune system—each in a specific way:
Zinc
Omega-3 fatty acids derived from fish
Vitamin A
B vitamins—especially folic acid
Iron
Copper
Amino acids L-lysine and L-arginine
Vitamins C and E
In addition to these nutrients, a number of plants and plant foods have been recognized as containing active substances that can keep the immune system’s thermostat working well. Among these are:
Blueberries
Cranberries
Garlic
Pomegranate
Echinacea purpurea and Andrographis paniculata
Let me give you just a few examples of how specific nutrients can influence gene expression to modulate the defense process and keep it in balance. Let me start with one of the most powerful nutrients of all, ascorbic acid or vitamin C.
To begin with, I must confess to some bias on this topic thanks to my association with Dr. Pauling, whose 1970 book, Vitamin C and the Common Cold, was an immediate—and continuing—best seller. Simply put, it advanced the idea that vitamin C was needed daily at levels significantly greater than those recommended by the Food and Nutrition Board, the influential food-advisory arm of the Institute of Medicine. The book also argued that in cases of viral infections or illness, the need for vitamin C intake was even higher.
Pauling had refined his thinking on the subject through discussions with Dr. Irwin Stone, the biochemist and chemical engineer credited as the first person to advocate the use of vitamin C as a preservative in food processing. Stone had argued that millions of years ago, when humans lost the ability to make vitamin C in the liver, as most animals do, they began to become increasingly vulnerable to infection and toxins. As the American diet grew more and more top-heavy with animal products and reduced the intake of plant foods, that vulnerability accelerated and expanded. The result? Stone proclaimed the vitamin C intake of most humans in this country simply insufficient for optimal immune function.
How much is sufficient? Dr. Pauling liked to compare humans with goats. The latter, about the same size as humans, produce their own vitamin C, as we humans do not. The vitamin is produced in the goat’s liver to the tune of approximately 1,000 milligrams per day per goat under normal circumstances. Under the stress of illness, however, a goat can make as much as 10,000 milligrams per day to meet its increased needs for the nutrient. Dr. Mark Levine, a leading endocrinology researcher, has been exploring the question of recommended daily doses of vitamins for decades.* His research group has found that humans can increase the levels of vitamin C in the blood through daily oral intake up to a point of saturation—in most healthy people, after an intake not exceeding 1,000 milligrams. If the person is ill, however, the turnover of vitamin C is increased, and a bigger oral dose may be required to keep the blood level saturated.
Yet what is the recommended daily allowance that the Food and Nutrition Board suggests? As I write this, the RDA for the average adult nineteen years old or older is 90 milligrams a day for a man and 75 milligrams a day for a woman—more for a pregnant woman, even more for a nursing mother, and much more for a smoker. That’s quite different from the recommendation suggested by Nobel laureate Pauling for optimal immune function and by endocrinology expert Levine to saturate the blood.
The reason for the difference is simple: the RDAs are intended for that elusive average human we’ve met before; they’re based on preventing nutrient deficiency and hedged about with a margin of safety.
It isn’t that RDAs are wrong. It’s that the Food and Nutrition Board is answering a different question. They’re recommending an amount humans need to prevent such nutritional-deficiency diseases as scurvy, beriberi, pellagra, and rickets. For one thing, those are short-latency disorders; that is, it doesn’t take that long between the stimulation that sets a disease in motion and the appearance of symptoms. Yet, as Dr. Robert Heaney, one of the nation’s foremost nutrition researchers, has pointed out, making a short-term vitamin deficiency disease the marker for establishing daily nutrient intake makes no sense when we know that our most pressing chronic health problems stem from inadequate nutrient intake that dates back years.* For example, although these illnesses remain latent for a long time before becoming evident, we can trace osteoporosis to insufficient vitamin D and calcium, and we know that certain cancers are due to insufficient folic acid intake. Wouldn’t greater daily intake make more sense for these long-latency disorders? Shouldn’t they be factored into the equation for recommended daily allowance?
There’s an even better strategy for determining nutrient intake, and that is a strategy based on the concept of biochemical individuality. My experience over forty years in the field is that vitamin C has a greater impact on immune system function than any other single nutrient. I take 2,000 milligrams per day unless I am sick, in which case I take more.
I well remember a particular lecture about vitamin-deficiency diseases that I attended back when I was a university student in the early 1960s. The lecturer was Casimir Funk, the great Polish biochemist who both “discovered” vitamins, isolating thiamine (vitamin B1) from rice polish in 1912, and named them “vital amines”—vitamins—life-giving chemical compounds in the amine family. Dr. Funk ended the lecture with a stirring peroration about how much there was still to be discovered about the role of vitamins in promoting health. That was in 1963. Now here we are in the twenty-first century, and scientists are learning more every day about how nutrients can influence gene expression and cellular function so that they can be biologically based alternatives to drugs. It’s exciting.
Some of this work is taking place at the Jean Mayer Human Nutrition Research Center on Aging at Tufts University outside Boston. One of the extraordinary researchers there is Dr. Simin Meydani. Dr. Meydani is both a nutritionist and a veterinary doctor, as well as the founder of the nutritional immunology laboratory at Tufts. The focus of her pioneering research has been to understand the role of nutrition in the function of the immune system—particularly among the aging. Specifically, her group has delved into the importance of nutritional support in improving the resistance of the elderly to infectious diseases—particularly upper respiratory infections (URIs), which can be a serious medical problem in seniors. Dr. Meydani’s group has demonstrated that such nutrients as vitamin E—and a particular form of vitamin E called tocotrienols—as well as omega-3 fatty acids, epigallocatechin gallate (EGCG) from green tea, vitamin D, and mushrooms all play important roles in supporting the immune system’s defense against viruses that cause URIs.
I expect that some of these nutrients may be new to you. Tocotrienols, for example, are relatives of vitamin E that are found in high levels in palm oil—and can be obtained as supplements as well. A study of women who took 400 milligrams of tocotrienols daily, following an immunization for tetanus, showed an increased B cell antibody response. Similar results were achieved among older individuals who took tocotrienols along with the other natural forms of vitamin E.
Vitamin D is a nutrient we’ve known about for a long time, but its story turns out to be far more complex than just preventing rickets, the bone disease that remains a childhood disease in some of the world’s poorest countries. In fact, it is now well recognized that vitamin D is not truly a vitamin at all, but rather a pro-hormone. That means it is a kind of precursor of a hormone, with little hormonal effect of its own until it is converted into the hormonal form of vitamin D and amplifies its effect. The conversion takes place through metabolic transformation in the liver and kidney by none other than our old friends from Chapter 5, some members of the CYP450 family of enzymes. The hormonal form of vitamin D that results from the conversion has been identified as a central player in regulating the immune system because of its ability to control the expression of the genes that regulate the system.
As with vitamin C, the RDA for vitamin D—600 international units (IU)—seems low for supporting improved immune function. The medical diagnosis of vitamin D status—that is, figuring out how much you have—happens in a blood test for another hormonal precursor, this one called 25-hydroxyvitamin D3. According to the National Institutes of Health, this value should be greater than 30 nanomoles per liter for proper—that is, healthy—vitamin D status.*
Yet a great many people who consume 600 IU of vitamin D per day are nevertheless below this 30 nmol/L level. At the Functional Medicine Clinical Research Center, the suggested norm was 2,000 IU per day—with a caution. Sometimes, excessive vitamin D intake can lead to elevated calcium levels in the blood, a condition that has been associated with heart disease. So it is important not to jump to the conclusion that if a little bit is good, a lot more is better.
Our institute research team has participated in clinical research on vitamin D with Dr. Michael Holick, one of the world’s leaders in vitamin D.* Holick did his doctoral work at the University of Wisconsin under Dr. Hector DeLuca, who discovered vitamin D in 1968, and the two men collaborated in creating the diagnosis for vitamin D status using 25-hydroxyvitamin D3 in 1973. In Dr. Holick’s view, we have reached a point with vitamin D similar to the situation with vitamin C. That is, as a consequence of people spending so much time indoors, not to mention the use of sun-blocking skin creams that decrease the production of vitamin D in the skin, we’re no longer getting optimal levels of vitamin D.
According to Holick, there is a substantial difference between the level of vitamin D needed to prevent rickets and the level of vitamin D desirable to promote optimal immune function; the latter goes much higher than the standard guidelines. Holick also points out that the explosion of genetic information now available makes it clear that there are considerable genetic differences among individuals in the way they manufacture and metabolize vitamin D in their bodies—which also means there are considerable differences among individuals in how much vitamin D they need. From my own experience, I would suggest that a person with a known imbalance in his or her defense process should start with a daily supplement of 1,000 IU of vitamin D3. This book’s self-assessments for whether or not you might have such an imbalance can be a signal to supplement your defense process, and of course, a health-care provider trained in functional medicine can perform the blood test that DeLuca and Holick devised and interpret it to evaluate your particular need for vitamin D.
Let me give you one final example of a nutritional product that can strengthen your immune system’s ability to self-regulate for balance: the mushroom. Right down the road from our Functional Medicine Clinical Research Center in Gig Harbor, Washington, is a world-class mycologist named Paul Stamets. His particular expertise in the field of medicinal mushrooms is without parallel, and he is a passionate advocate of the benefits of mushrooms in supporting the immune system’s defensive function.*
What mushrooms bring to the battle is a class of unique substances called mucopolysaccharides, which have a specific affinity for sending messages to the T and B cells, which then activate the genes responsible for their function. The National Institutes of Health, to take just one example, has funded clinical studies on the adjunctive effect of specific types of mushrooms in cancer patients and in patients with HIV. For good reason: studies have shown that regular consumption of the common white button mushroom, Agaricus bisporus, is associated with reduced incidence of breast cancer. And Dr. Meydani’s group at Tufts found that the mucopolysaccharides of white button mushroom concentrate activated natural killer activities as part of cell-mediated T cell action.
“A GOOD DEFENSE IS THE BEST OFFENSE”
So we come full circle back to Jane. Her success was a matter not of luck but of asking the right questions about how her genes were responding to her environment in such a way as to make her body present with the disease erythromelalgia. She worked hard carrying out her personalized functional medicine program; compliance was key in helping her win her battle with her immune system and once again make it her friend.
Now there are diseases for which genetic alteration of immune system function is so profound that it is the cause of the disease. They are literally inborn immune diseases; among them are agammaglobulinemia, in which the body does not generate mature B cells; Chediak-Higashi syndrome, afflicting its victims with neuropathy, albinism, and frequent and sometimes fatal infections; congenital IgA deficiency, presenting with a total lack of immunoglobulins; and Wiskott Aldrich syndrome, characterized by skin eruptions and eczema. As a family of congenital immune diseases, however, these represent but a minuscule fraction of the total number of diseases or conditions associated with immune imbalances. For the vast majority of chronic immune problems, the cause is the impact of environmental messages on genetic expression.
The functional medicine approach to these immune system imbalances focuses on that intersection between genes and environment. Its aim is to modulate the factors of the latter to influence the former so as to return the immune system to its resting place and restore its balance. One reason it can do so is that cells, tissues, and organs—everything within the physiological network—are in constant communication.
CHAPTER 6 TAKEAWAY
1. The immune system controls the defense against both infectious and inflammatory diseases.
2. Various environmental chemicals, some constituents of food such as gluten, certain types of intestinal bacteria, and a number of pharmaceuticals can cause chronic inflammatory diseases.
3. Specific nutrients—for example, vitamins C and D—have been shown to have a strengthening effect on immune defense system function when the nutrients are consumed at levels higher than the recommended dietary allowance.
4. Phytochemicals in certain plant foods and botanical medicines have been shown to reduce chronic inflammatory conditions.
5. A program that integrates changes in lifestyle and diet along with specific nutrient supplementation can be effective in restoring proper immune defense processes.