Fasting and Eating for Health (30 page)

One of my patients with asthma, who had tried to fast with another physician in the past, claimed she vomited and became nauseated whenever she fasted.

Therefore, she could not fast for longer than a few days. After fasting her a few days, as predicted, she developed vomiting and nausea. I then looked at her blood and urine and it showed she was dehydrated with hemoconcentration (increased red blood cell concentration) and an increased BUN level. When I asked her if she was drinking at least four glasses of water a day as I had recommended, she said she never likes to drink much when she fasts. She was drinking less than 8 ounces of water a day. As soon as I corrected this by increasing her fluid intake, the problem stopped and she was able to fast without difficulty.

It is to be expected that the glucose level will fall and remain at low levels during the fast, typically between 40 and 65, except in the type II diabetic patient, who may have a near normal or slightly elevated glucose level during the fast. If it is imperative for a person with type I diabetes to fast, glucose levels should be tested regularly and the insulin dose appropriately adjusted to the lowered needs of the fast.

Electrolytes such as potassium, sodium, and chloride are exceedingly stable during a fast. Even though early in the fast the body loses quite a bit of sodium and potassium, this excretion falls as the fast progresses. Generally, the electrolytes remain at low normal levels throughout the rest of the fast. If the potassium level drops to 3.2, the fast should be broken unless the physician supervising the fast chooses to monitor the blood test more frequently to make sure the level does not continue to drop. Obviously, once the level has reached 3.2, one should not wait a week to run the next potassium check if the patient continues the fast. I recommend ending a fast for any person who has a 154

potassium level lower than 3.0.

At any sign of sudden, extreme weakness during a fast, the potassium level should be considered suspect and rechecked. However, gradual loss of energy or the slow development of weakness as the body attempts to conserve energy by decreased activity is normal during the fast and to be expected.

Liver enzymes occasionally increase early in the fast. As the fast continues, they slowly return to normal. I have noted the elevation of liver enzymes more frequently in patients with autoimmune illnesses, connective tissue disorders, and psoriasis; this may represent the contribution that inadequate liver function contributed to their underlying disease state. In the psoriasis patient, for example, and even in fibromyalgia patients, the return to normal liver function during the fast or soon after parallels the improvement in their skin disease or symptoms of muscle pain.

Due to the large demands on the liver for energy metabolism early in the fast, bilirubin levels rise initially and then fall gradually as the liver adapts to the fasting state.12

Cholesterol levels increase considerably in the fast, reflecting a breakdown of atheromatous material. As discussed in Chapter 5, the level of total cholesterol may double over the patient's baseline in an individual with a history of atherosclerotic plaque, whereas the patient without diseased arteries will not show such an increase in cholesterol. Both LDL and HDL levels increase, but I have noted that the sharp rise in cholesterol in cardiac patients is predominantly of the LDL type.

Other researchers have noted minimal increases in cholesterol levels and a more predominant increase in the HDL component. These conflicting findings may represent the increased level of activity encouraged or permitted by other researchers and the fact that juices may have been consumed.13 I interpret the strikingly higher elevation of LDL cholesterol seen in my fasting patients with atherosclerosis as being due to the increased effectiveness of the total fast over

"juice fasting" in breaking down atheromas. I also forbid vigorous exercise, permitting only gentle back-mobility movements, flexibility and joint-mobility exercises, and a little walking.

Many physicians who routinely monitor blood cholesterol levels in their office are not aware that an elevation of cholesterol occurs even when a patient fasts overnight for a blood test and then has it drawn late in the day rather than in the morning. Fasting lipid profiles should be drawn first thing in the morning to prevent this phenomenon from disturbing the results.

Physicians may also be confused and the patient disappointed and discouraged when the individual who started adhering to a strict, extremely low-fat, zero-cholesterol diet has an increase rather than a decrease in his or her cholesterol level. I have noted from monitoring the lipid profiles of many such patients that not only is it possible to observe a temporary rise in triglycerides during this adjustment phase, but also the total cholesterol may 155

occasionally rise significantly. When this occurs, it is observed during the first two to six months after the dietary change; then these lipid levels begin to drop and show notable improvement later on. My patients are often warned not to be discouraged by the early tests, which do not yet represent their significant decreased risk.

Reports of Death During Improperly Supervised Fasts
It is very important not to fast patients beyond their capacity. One cannot simply rely on how much body fat a person has to decide how long to fast that person. Even obese individuals can develop signs of starvation while still overweight if their muscle reserves fall to dangerously low levels while their fat reserves are still adequate. This would occur only when the fast was excessively prolonged, and has been reported in such patients who have fasted for many months. Cardiac failure could occur in patients who no longer have skeletal muscle reserve and who continue to fast. For this reason, I do not ever recommend a fast of more than 50 days even for obese individuals who feel well and look as though they could fast safely for months.

An obese patient died after seven months of fasting,14 which, rather than illustrating the dangers, illustrates the safety of a prolonged fast. It is hard to imagine that anyone could recommend to a person, no matter how obese, to fast this length of time. After the protein-sparing phase of the fast begins, the body still requires a small quantity of muscle reserves to maintain an adequate level of glucose and other nutrients. If severely obese individuals fast long enough, they may still be overweight, but because their body habitat was mostly fat, not muscle, they could exhaust their muscle reserves while still maintaining an illusion of having sufficient nutrient reserves in their tissues to continue fasting. This gives the false impression that it is safe for them to continue to fast for a very long period of time, when actually, after fasting this long, their muscle reserves are depleted.

The medical literature contains a few studies in which obese patients died during a fast, apparently from ventricular arrhythmias. If we look in detail at these cases, we can clearly see that the individuals were fasted improperly, using multiple drugs during the fast, and had heart failure or renal disease prior to the fast.15,16 For example, in a study reported by Spencer, ventricular arrhythmias occurred in two patients, one weighing 330 pounds who fasted 56

days, and the other weighing 233 pounds who fasted 21 days. These patients drank unrestricted amounts of coffee, tea, and fruit juice during the fast and were given digoxin, diuretics, and anticoagulants. These were not total fasts, and might be more appropriately called a coffee and fruit juice feast.

Regardless, one should never fast a patient on diuretics and heparin, both of which are dangerous during a fast. It is also an added risk to drink coffee while fasting. Cardiac stimulants such as caffeine, and theophylline should be avoided.

Offering Patients a Choice

Fasting should be viewed as a natural physiologic process to which the body 156

eagerly adapts itself. For many disease states fasting provides an appropriate condition for the body to recuperate under its own intelligent direction. The innate wisdom of the human body is a remarkable thing and vividly appreciated as the body sets itself to healing under the conditions of the fasting state.

Fasting for health under competent supervision can be a pleasant and rewarding experience that sets a patient on a new road of superior health. By employing this therapy in their practice, primary care physicians can now offer patients an alternative to drugs and the surgeon's knife, and gain fulfillment from seeing remarkable improvement in the health of their patients. For other physicians the knowledge of this nutritional approach is imperative so that, when appropriate, they can make referrals to a colleague who specializes in this therapeutic modality.

Rather than starting patients on drugs for chronic diseases, now physicians can offer suitable patients a chance to recover their health through natural diet and fasting. If dietary considerations, including the aggressive nutritional approach described in this book, are not offered and discussed with patients initially, their doctors are selling them short. These physicians are not disclosing all the pertinent information that patients need to make informed decisions about their health condition.

Whether the patient has a cardiac condition, hypertension, autoimmune disease, fibroids, or asthma, he or she must be informed that fasting and natural plant-based diets are a viable alternative to conventional therapy, and an effective one. The time may come when not offering this substantially more effective nutritional approach will be considered malpractice.

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1. Fukudo S, Suzuki J, Nomura T, Iwahashi S, Muranaka M, Taguchi F.

Effects of fasting therapy on liver function disorders.
Japanese Journal of
Psychosomatic Medicine-1988;28(6)
:515-523.

2. Chiba T. Fasting therapy for psychosomatic disorders.
Kango Gijutsu
(Japan) 1985 ;31(9) : 1248-9.

3. Bock D, Kohle K, Weimann G, Thomas W, Mente F, Schmidt T, Jaeger M.

Prospective studies of the relationship between psychological and social symptoms with the long-term success of hospital fasting therapy.

Verhandlungen Der Deutschen Gesellschaft F ur Innere Medizin
(Germany) 1978;84:1565-7.

4. Yamamoto H. An electro encephalographic study of fasting therapy with special reference to electro encephalographic power spectral changes.

Japanese Journal of Psychosomatic Medicine
1980;20(4):325-335.

5. Yamamoto H, Suzuki J, Yamauchi Y. Psychophysiological study on fasting therapy. Symposium on Strategies in Psychosomatic Practice and Research at the 12th European Conference on Psychosomatic Research, Bodo, Norway, July 1987.
Psychotherapy and Psychosomatics
1979;32(1-4):229-240.

6. Yashiro N. Clinico-psychological and pathophysiological studies on fasting therapy.
Sapporo Medical Journal
(Japan) 1986;55(2):125-136.

7. Suzuki J, Yamauchi Y, Yamamoto H, Komuro U. Fasting therapy for psychosomatic disorders in Japan.
Psychotherapy and Psychosomatics
(Switzerland) 1979;31(1-4):307-314.

8. Suzuki M, Kamijo K. The hypothalamic pituitary adrenal function in malnutrition: A comparison between psychosomatic diseases treated with fasting therapy and anorexia nervosa.
Folia Endocrinolica Japan
1979;55

(6):739-760.

1. Berke' J, de Waard F. Mortality pattern and life expectancy of Seventh-Day Adventists in the Netherlands.
International Journal of Epidemiology
1983;12:455-459.

2. Snowdon DA. Animal product consumption and mortality because of all causes combined, coronary heart disease, stroke, diabetes, and cancer in Seventh-Day Adventists.
American Journal of Clinical Nutrition
1988;48: 739-48.

3. Campbell TC. A study on diet, nutrition and disease in the People's Republic of China. Division of Nutritional Sciences, Cornell University, Ithaca, New York, 1989; pp. 1-9.

4. Saxton JA. Nutrition and growth and their influence on longevity in rats.

Biological Symposium
1943;11:177.

5. Staszewski J. Age at menarche and breast cancer.
Journal of the National
Cancer Institute
1971;47:935.

158

6. Masoro EJ, Shimokawa I, Yu BP. Retardation of the aging process in rats by food restriction.
Annals of the New York Academy of Science
1990;337-52.

7. Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL. Effects of intermittent feeding upon growth, activity and lifespan in rats allowed voluntary exercise.
Experimental Aging Research
1983;9:1477-94.

8. Marston R. Nutrient content of the national food supply.
National Food
Review,
U.S.D.A. Dec. 1978, pp. 28-33.

9. Berenson GS,
et al.
Atherosclerosis of the aorta and coronary arteries and cardiovascular risk factors in persons aged 6 to 30 years and studied at necropsy (The Bogalusa Heart Study).
American Journal of Cardiology
1992;70:851-858.

10. Carroll KK. Experimental evidence of dietary factors and hormone-dependent cancers.
Cancer Research
1975;37:3374-83.

11. Berg J. Can nutrition explain the pattern of international epidemiology of hormone-dependent cancer?
Cancer Research
1975;35:3345.

12. Barone J, Hebert JR, Reddy MM. Dietary fat and natural-killer-cell activity.

American Journal of Clinical Nutrition
1989;50:861-67.

13. Kozlovsky AS,
et al.
Effects of diets high in simple sugars on urinary chromium losses.
Metabolism
1986;35:515.

14. Williams RD, Mason HL, Powers MH, Wilder RM. Induced thiamine deficiency, in man: Relation of depletion of thiamine to development of biochemical defect and of polyneuropathy.
Archives of Internal Medicine
1943;71:38-53.

15. Lonsdale D, Shamberger RJ. Red cell transketolase as an indicator of nutritional deficiency.
American Journal of Clinical Nutrition
1980;33:205-211.