by Harold J. Kristal, D.D.S.
with James M. Haig, N.C.
Our work with Metabolic Typing puts us in a unique position
to observe relationships between particular disease conditions
and the different Metabolic Types. A Metabolic Type can be
understood as the characteristic way in which an individual
produces and processes energy. By addressing the individual at
this fundamental level, we are able to match up their metabolism
with an appropriate diet that will help to protect the body
from the development of the common degenerative diseases. This approach
is in line with, and a contemporary restatement of, the
traditional naturopathic orientation to healthcare, where the
individual as a whole is addressed, rather than just their
specific disease condition. The survey that is presented below
shows a direct correlation between diabetes and cancer and
specific Metabolic Types in our own patient population. It
reinforces the concept that different dietary approaches are needed for
individuals to regain or maintain optimal health, and provides
important pointers as to how to use dietary intervention to
prevent such diseases from occurring in the first place. Before
we look at the details and implications of our patient survey,
we will first set the stage with a general overview of the
principles underlying Metabolic Typing. Metabolic Typing: An Overview
In 1987, I was introduced to a little known nutritional
protocol that addresses the individual at the foundational
metabolic level, rather than directly addressing any particular
disease condition. The basic thesis of this Oxidative system
approach to metabolic balancing is that imbalances which sooner
or later manifest as outright diseases originate when our blood pH
deviates too far from the ideal of 7.46. It was George Watson, Ph.D.,
a full professor at the University of Southern California and
author of the classic book Nutrition and Your Mind: The Psychochemical Response,
who first introduced this theory to the world. Watson’s typing
methodology, later refined by Rudolf Wiley, Ph.D., was based on
the functioning of the Oxidative system, the complex of
processes that generate energy at an intracellular level. Within
this system, individuals are typed according to the speed at
which they convert nutrients into energy, in the form of ATP
(adenosine triphosphate). The creation of optimal energy through
optimal blood pH is the path I have followed from 1987 to this
day.with James M. Haig, N.C.
In 1996, nutritionist William Wolcott introduced me to another metabolic balancing protocol, based on the autonomic nervous system (ANS). This Autonomic system, rooted in the early research of Francis M. Pottenger, M.D., and further developed by William Donald Kelley, D.D.S., relies on a different metabolic pathway than the Oxidative system. It looks to the relative dominance of the two divisions of the ANS (sympathetic and parasympathetic) as the primary barometers of metabolic balance. The main contribution of Wolcott himself, who had worked for many years directly with Dr. Kelley, was the realization that either one or the other of these two dominance systems — as Wolcott termed the Oxidative and Autonomic systems — is the primary factor controlling each individual’s metabolism. This syncretistic approach, incorporating both dominance systems, is what we now refer to as Metabolic Typing (see Figure I).
Figure I | ||
Metabolic Dominance Systems | ||
Oxidative System | Autonomic System | |
Slow Oxidizer (alkaline) | Sympathetic (acid) | |
Fast Oxidizer (acid) | Parasympathetic (alkaline) |
Thus, what we refer to as the Group I diet — lower in protein and fat, and higher in complex carbohydrates — is shared by the overly alkaline Slow Oxidizer and the overly acidic Sympathetic. Because the same foods have opposite pH effects in members of the two dominance systems, the Group I foods acidify the overly alkaline Slow Oxidizer while alkalizing the overly acid Sympathetic, thereby helping to move both types towards a balance point, albeit from opposite directions. Similarly, the Group II diet — higher in protein and fat, and lower in complex carbohydrates — helps to alkalize the overly acidic Fast Oxidizer and acidify the overly alkaline Parasympathetic. Thus, from a Metabolic Typing perspective, the pH effect of any given food is not fixed, as is usually assumed, but is determined to a large extent by the particular metabolism (or, more accurately, by which dominance system controls the metabolism) of the individual consuming it (see Figure II).
Figure II | ||
Group I and Group II Diets | ||
Group I | Group II | |
Slow Oxidizer (alkaline) | Fast Oxidizer (acid) | |
Sympathetic (acid) | Parasympathetic (alkaline) | |
Lower in protein and fat | Higher in protein and fat | |
Higher in complex carbs | Lower in complex carbs | |
Group I foods acidify the overly acidic Fast Oxidizer, but acidify alkalize the overly acid Sympathetic | Group II foods alkalize the overly alkaline Slow Oxidizer, but the overly alkaline Parasympathetic | |
This brief introduction to the principles of Metabolic Typing is intended to provide a context for the results of a patient survey that we recently conducted at our Metabolic Nutrition clinic in San Rafael, California. I began working with the Oxidative system of Metabolic Typing in 1987, and since then have typed over 6,000 individuals. In 1996 I switched to the integrated form of Metabolic Typing (incorporating the Autonomic system along with the Oxidative), and have worked to refine our methodology over the ensuing years. The data in the survey I will be discussing are drawn from approximately 1,450 patients typed since the year 2000. At this point, I feel that our typing protocol has approximately a 90% accuracy rate.
Diabetes, Cancer and Excess Weight Survey
Sometime in 1997 I started to notice a pattern emerging among our patient population: most of those with Type II diabetes were the Group II Metabolic Types (Fast Oxidizers or Parasympathetics) while most of those with cancer were Group I Metabolic Types (Slow Oxidizers or Sympathetics). After informally saying for several years that each of these figures was around 80%, I decided to instruct my staff to analyze our recent patient files and determine the exact numbers. We also tallied the percentages of individuals coming to our clinic with weight problems. The results (which are shown below, in Figure III) more or less confirmed my original suspicions.
Figure III | |||
Diabetes, Cancer and Excess Weight Survey Based on an analysis of approximately 1,450 patient files |
|||
Diet Groups and Metabolic Types | Diabetes (Type II) | Cancer | Overweight |
Group I | |||
Slow Oxidizers | 16% | 35% | 15% |
Sympathetics | 12% | 43% | 25% |
Group I Totals | 28% | 78% | 40% |
Group II | |||
Fast Oxidizers | 50% | 19% | 47% |
Parasympathetics | 22% | 3% | 13% |
Group II Totals | 72% | 22% | 60% |
My estimate of 80% of diabetics being Group II Metabolic Types was not too far off. The survey shows that the actual number is 72%. Of these, the majority (50%) are Fast Oxidizers. At first glance this may seem counterintuitive, because Fast Oxidizers, by definition, metabolize carbohydrates rapidly (leading to their relatively acid blood pH). Fast Oxidizers typically have an aggressive insulin response, which efficiently “unlocks” the insulin receptors on the cell membrane to allow glucose to be taken inside the cell to be oxidized for energy. However, if you combine an accelerated metabolism of carbohydrates with the excessive long-term intake of refined carbohydrates that typifies the standard American diet, you have the perfect set-up for insulin resistance. Large amounts of insulin produced over an extended period of time will lead to a “blunting”, or reduction of the sensitivity of the insulin receptors, increasingly reducing their efficiency, a process analogous to the way in which we can learn to “tune out” an annoying sustained sound. As we now know, based largely on the groundbreaking work of Professor Gerald Reaven, insulin resistance is the primary predisposing factor for Type II diabetes.
The Group II diet, which is recommended to the Group II Metabolic Types (Fast Oxidizers and Parasympathetics), is a higher protein and fat, and lower carbohydrate diet. However, for diabetics we have created an even lower carbohydrate version of this diet, which we refer to as the Diabetic Protocol (this is described in some detail in our book, The Nutrition Solution: A Guide to Your Metabolic Type, and explored in our monthly seminars for health professionals). For the 28% of our diabetic clients who are Group I Metabolic Types (Slow Oxidizers and Sympathetics), we diverge from our usual Group I diet plan (which is a higher carbohydrate diet), and recommend that they also adopt the Diabetic Protocol. The reason for this is simply that blood sugars that are radically outside of the normal range must be stabilized before we can even consider putting an individual on the higher carbohydrate Group I diet plan.
My estimate of our cancer patients was almost completely accurate, with 78% falling into the Group I category. What did surprise me was that more of these were Sympathetics (43%) than were Slow Oxidizers (35%). There is a widespread assumption in the alternative health community that cancer is associated with excess “acidity”, though rarely are the parameters of this supposed acidity defined. At the tissue level, cancer cells do indeed typically produce excess lactic acid, which might be expected to result in a compensatory alkalinity in the pH of the blood. The 35% of cancer cases in our survey who are Slow Oxidizers do indeed have alkaline blood, but the larger number of Sympathetics (43%) has acid blood. (Note that, for our purposes, we are using the terms acid and alkaline relative to the perceived ideal venous blood pH of 7.46; all blood is mildly alkaline in the absolute sense). Whether acid or alkaline, both of the Group I Metabolic Types require a diet lower in protein and fat and higher in complex carbohydrates. This diet helps to acidify the overly alkaline Slow Oxidizers, but alkalize the overly acidic Sympathetics (this is because, as we have already seen, foods affect members of the Oxidative and Autonomic systems in opposite ways). This dietary approach is generally in sync with the prevailing nutritional consensus for cancer patients.
The results from our weight survey indicate that excess weight is a significant problem for both groups, but especially for the Group II Metabolic Types (60%). This has important ramifications for the ongoing discussion within the nutritional community about what kind of diet is most effective for weight loss. For the last thirty or more years, the prevailing nutritional wisdom — repeated endlessly by the media and mainstream medicine alike — has been that a low fat diet is the best way to control weight. This paralleled a widespread advocacy in alternative health circles for a vegetarian or semi-vegetarian diet. The egregious consequences of this oversimplified approach, especially in the mainstream arena, are seen in the alarming increase in the numbers of overweight and obese adults and (even more alarmingly) children. While various individuals have always questioned this low fat dogma (most notably Robert Atkins, M.D.), it was only this last summer that it reached the level of a national debate following the publication of Gary Taubes’ provocatively titled article What if It’s All Been a Big Fat Lie? in the New York Times (Sunday July 7th). This, in turn, was an elaboration of an earlier article published in Science (for a more in-depth examination of Taubes’ articles, please refer to www.bloodph.com; click on the Newsletter link, then select September 2002).
The 60% of our overweight clients who are the Group II Metabolic Types require a diet higher in protein and fat, and lower in carbohydrates. This explains why the Atkins diet, which in many respects is a more extreme version of our Group II diet, can be so effective for many people. Fast Oxidizers and Parasympathetics require a higher percentage of proteins and fats than carbohydrates to maintain their proper weight, as well to optimize their health in general. For the Fast Oxidizers, these Group II foods slow down the overly rapid rate at which they would otherwise metabolize carbohydrates, and also help to short-circuit the process of insulin resistance. For the Parasympathetics, these same foods help to stimulate the under-active sympathetic branch of the ANS, helping them to achieve metabolic balance in their primary dominance system. Of course, a certain percentage of these overweight Group II types are diabetic, in which case we defer to the Diabetic Protocol.
But the Atkins-type approach is not effective, nor desirable, for everyone. The remaining 40% do indeed require a lower protein and fat, higher complex carbohydrate diet. For the Slow Oxidizers, too much protein and fat would tend to further slow down their already sluggish metabolisms, whereas complex carbohydrates add fuel to the fires of oxidation. For the Sympathetics, whose metabolisms tend to be already in overdrive, too many proteins and fats would tend to be overly stimulating, whereas complex carbohydrates help to activate the under-active parasympathetic branch of the ANS, thereby helping them to achieve metabolic balance. It is important to stress that it is complex, not simple (refined) carbohydrates that we are recommending to the Group I Metabolic Types. While the glycemic index suggests that there is not much difference in glycemic value between the simple and complex versions of certain carbohydrates (e.g. between white and brown rice), the reality is that the higher fiber content of the complex carbohydrates does indeed produce a slower oxidation rate. (The glycemic index measures the glycemic peak value derived from a given food over a defined period of time, but without regard for how long it takes within that time period to reach that level).
Once again, we can see from these examples how the “one-size-fits-all” approach to diet simply is not adequate. The advocates of either high carbohydrate or low carbohydrate diets are about half right and half wrong, though our survey suggests that the low carbohydrate advocates have a statistical edge! It should be pointed out that the survey presented here is from a particular patient population in a particular geographic area, with its own specific demographics. Whether these percentages would hold true in a larger population group, or in other geographical/demographic areas remains to be seen, though informal feedback from colleagues in other areas suggest that they would.
It should also be said that, just a we need to be leery of genetic determinism (the simplistic assertion that genes cause disease), we also need to be leery of what we could call “metabolic determinism”. While our survey results show a statistical tendency for diabetes and cancer to be more prevalent among the Group II and Group I Metabolic Types respectively, we should be very careful not to assume that individuals within these groups will necessarily succumb to these diseases. Plenty of healthy people can be found in both of these groups. Jeffrey Bland went to great lengths in his book Genetic Nutritioneering to point out that genes do not, in and of themselves, cause disease; rather, disease results from a complex interplay of environmental and lifestyle factors that alter the expression of the genes in the direction of a specific disease system (i.e. the genotype is modified to express the phenotype of the disease). Similarly, diabetes and cancer are not “caused” by belonging to a certain Metabolic Type, but by a complex of factors. However, it can safely be assumed that individuals who fall into one or the other of our metabolic groupings (Groups I and II) do indeed have a greater tendency to develop these diseases, a tendency that can be significantly reduced by modifying the diet according to the recommendations for the relevant Metabolic Type. While a tendency does not imply a predictable result, clearly it makes sense to do whatever one reasonably can to avoid such a result. Metabolic Typing can be seen as a powerful preventative tool that points individuals towards a way of eating that will help to minimize the possibility of the development of these degenerative disease conditions while maximizing the possibility of a long and healthy life.
References
Bland, Jeffrey S., Ph.D. Genetic Nutrioneering. Keats, 1999
Reaven, Gerald M., M.D. Pathophsiology of Insulin Resistance in Human Disease. Physiological Reviews 75(3):473-485, 1995
Pottenger, Francis M., M.D. Symptoms of Visceral Disease. Mosby, 1944
Taubes, Gary. The Soft Science of Dietary Fats. Science, March 30, 2001
——— What if It’s All Been a Big Fat Lie? New York Times Magazine, July 7, 2002
Watson, George, Ph.D. Nutrition and Your Mind: The Psychochemical Response. Harper and Row, 1972
Wiley, Rudolf A., Ph.D. BioBalance. Essential Science Publishing, 1998
Wolcott, William. The Metabolic Typing Diet. Doubleday, 2000
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