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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2495396/pdf/postmedj00315-0056.pdf

Postgraduate Medical Journal (March 1973) 49, 203-209. Case Report

Features of a successful therapeutic fast of 382 days' duration

W. K. STEWART M.D., F.R.C.P.E., M.R.C.P. Lond. LAURA W. FLEMING B.Sc. University Department of Medicine, Dundee DD1 4HN, Scotland

Summary A 27-year-old male patient fasted under supervision for 382 days and has subsequently maintained his normal weight. Blood glucose concentrations around 30 mg/100 ml were recorded consistently during the last 8 months, although the patient was ambulant and attending as an out-patient. Responses to glucose and tolbutamide tolerance tests remained normal [tolbutamines, Orinase, is a first generation, ~1960, potassium channel blocker, used for type-2 diabetes, a sulfonylurea.[1]]  The hyperglycaemic response to glucagon was reduced and latterly absent, but promptly returned to normal during carbohydrate refeeding. After an initial decrease was corrected, plasma potassium levels remained normal without supplementation. A temporary period of hypercalcaemia occurred towards the end of the fast. Decreased plasma magnesium concentrations were a consistent feature from the first month onwards. After 100 days of fasting there was a marked and persistent increase in the excretion of urinary cations and inorganic phosphate, which until then had been minimal. These increases may be due to dissolution of excessive soft tissue and skeletal mass. Prolonged fasting in this patient had no ill-effects.

Introduction Current opinion on fasting therapy for the obese is perhaps best summarized by the view that fasting for relatively short periods is beneficial, whereas longer term fasting (i.e. longer than 40 days) has an element of risk attached (Lawlor & Wells, 1971). It is generally agreed that the long-term outlook for the achievement and maintenance of ideal body weight is poor (MacCuish, Munro & Duncan, 1968; Lawlor & Wells 1971) unless a weight close to the ideal is achieved during the supervised phase (Munro et al., 1970), a process which in the majority of cases would involve a prolonged rather than a short-term fast. Several years ago a grossly obese young man presented himself for treatment. Initially there was no intention of making his fast a protracted one, but Requests for reprints: Dr W. K. Stewart, Department of Medicine, University, Dundee DD1 4HN, Scotland. since he adapted so well and was eager to reach his 'ideal' weight, his fast was continued into what is presently the longest recorded fast (Guinness Book of Records, 1971). This report describes some of the features which emerged during the 382 days of his fast. Methods Patient treatment Patient A.B. aged 27 years, weighed on admission 456 lb (207 kg). During the 382 days of his fast, vitamin supplements were given daily as 'Multivite' (BDH), vitamin C and yeast for the first 10 months and as 'Paladac' (Parke Davis), for the last 3 months. Non-caloric fluids were allowed ad libitum. From Day 93 to Day 162 only, he was given potassium supplements (two effervescent potassium tablets BPC supplying 13 mEq daily) and from Day 345 to Day 355 only he was given sodium supplements (2 5 g sodium chloride daily). No other drug treatment was given. Initially, the patient was treated in hospital but for the greater part of the time he was allowed home, attending regularly as an out-patient for check-up. Twenty-four hour urine collections were made periodically throughout the fast. His mean urinary creatinine excretion was 1541 mg/24 hr, with a 25% variation, which indicates reasonable collections. No faecal collections were made, but evacuation was in fact infrequent, there being 37-48 days between stools latterly. Venous blood specimens were obtained approximately once a fortnight and tests of carbohydrate metabolism (intravenous glucose tolerance, tolbutamide and glucagon tests) (Marks & Rose, 1965; Oakley, Pyke & Taylor, 1968) were undertaken on nine occasions during the fast. All three tests were carried out consecutively on the same day, following a standard procedure whereby the tolbutamide was given 1 hr after the glucose infusion, when blood glucose concentrations had returned to normal, and the glucagon was given 11 hr after the tolbutamide.



[1] Expanded the total market by bringing under medical care diabetics who were formerly not treated

Estimations:  Plasma and urinary electrolytes, phosphate, uric acid and creatinine were measured by routine methods (available on request). Blood glucose was estimated by glucose oxidase. Magnesium in both plasma and urine was measured by atomic absorption spectrophotometry (Fleming & Stewart, 1966).

Results:  Body weight loss:  During the 382 days of the fast, the patient's weight decreased from 456 to 180 lb. Five years after undertaking the fast, Mr A.B.'s weight remains around 196 lb.

Blood glucose levels;  Blood glucose concentrations decreased systematically (Fig. 1) and remained around 30 mg/100 ml from the fourth month onwards. Values below 20 mg/ 100 ml were occasionally seen towards the end of the fast. [This explains his sometimes eating small amounts towards the end of the fast.  Despite the hypoglycaemia the patient remained symptom-free, felt well and walked about normally. Tests of glucose tolerance showed unimpaired capacity for glucose uptake (Table 1). Apart from Day 7, the glucose assimilation coefficient remained between 10 and 1 6 (low normal) throughout the fast… the 10 min increment in blood glucose remained between 62 and 75 mg/ 100 ml until refeeding, when it became greater than 100 mg/100 ml. Responses to the intravenous tolbutamide test also remained normal until Day 355, brief episode of fainting immediately after the intravenous injection. Responses to intravenous glucagon were reduced from the early days of the fast onwards and by Day 269 and subsequently, there was no responsive increment in blood glucose at all. A normal increase was seen by Day 7 of the refeeding period, at which time the only sustenance had been entirely carbohydrate in nature (1000 kcal daily as modified liquid glucose BPC, 'Hycal'-Beechams).

Plasma Concentrations:  Over the first 4 months there was a systematic decrease in plasma potassium concentrations but the small daily supplement of 13 mEq potassium, which was then given, increased the potassium level.  After a further 10 weeks, no more potassium was given, and plasma potassium remained normal.  . For 6 months towards the end of the fast there was a limited period of hypercalcaemia (10-8-11 6 mEq/l) but this remitted spontaneously during the final month. [Reflects bone loss through remodeling and the loss of excess bone as weight was reduced.]  As expected, plasma urea decreased during the first 2 weeks of fasting and thereafter remained steady between 15 and 20 mg/100 ml. Plasma uric acid, which was high at 12-6 mg/100 ml prior to the fast (possibly reflecting pre-admission attempts at fasting), remained generally at this level throughout with one or two brief increases to 17 mg/100 ml which were not sustained  [Possible reflecting muscle loss.  I think a protein shake should have been given.]  Symptomatic gout did not occur.  Plasma magnesium concentrations (Fig. 2) decreased over the first few weeks and thereafter stabilized between 1-2 and 1-4 mEq/l.  Erythrocyte magnesium concentration remained unchanged and normal. 

Urinary electrolyte excretion (Fig. 3):  The excretion of sodium, potassium, calcium and inorganic phosphate decreased to low levels throughout the first 100 days, but thereafter the excretion of all four urinary constituents, as well as of magnesium, began to increase. During the subsequent 200 days sodium excretion, previously between 2 and 20 mEq daily, reached over 80 mEq/24 hr, potassium excretion increased to 30-40 mEq daily and calcium excretion increased from 10-30 mg/24 hr to 250- 280 mg/24 hr. Magnesium excretion (which was not measured during the first 100 days) reached 10 mEq/ 24 hr between Days 200-300. Phosphate excretion, which had decreased to under 200 mg/24 hr, also increased to around 800 mg/24 hr, even exceeding 1000 mg/24 hr on occasion. Peak excretions of all these constituents were seen around Day 300, after which there was a marginal decrease, but excretion remained high. There was no indication in the characteristics of the weight-loss response, which was steady and sustained, or in the persistently low blood glucose or urea levels, which would have suggested that he had been surreptitiously eating.

Discussion:  Body weight loss and length of fast;  The amount of weight lost and the rate of loss were not strikingly different from that of an earlier patient (Stewart, Fleming & Robertson, 1966) who reduced his weight from 432 to 235 lb during 350 days of intermittent starvation.  The amount of weight lost by Mr A.B. was 276 lb, with an average rate of loss of 0-72 lb/day, comparing favourably with the rates of weight loss in other long-term fasts (> 200 days) which have ranged from 0-41 lb/day (Thomson, Runcie & Miller, 1966) to 0 67 lb/day (Runcie & Thomson, 1970). The nearest comparable fasts are one of 256 days (Collison, 1967, 1971), those of 249 and 236 days (Thomson et al., 1966) and two of 210 days (Garnett et al., 1969; Runcie & Thomson, 1970).

There have been reports of five fatalities coinciding with the treatment of obesity by total starvation (Cubberley, Polster & Schulman, 1965; Spencer, 1968; Garnett et al., 1969; Runcie & Thomson, 1970). One was attributed to lactic acidosis during the refeeding period following a 3 week fast (Cubberley et al., 1965). Two were considered to be due to ventricular failure, occurring during the fast, at 3 and 8 weeks respectively in patients who had shown evidence of heart failure before beginning the fast (Spencer, 1968). One patient (Runcie & Thomson, 1970) died on the thirteenth day of his fast from small bowel obstruction. Only one of the five 'fasting' deaths has been associated with a fast of more than 200 days' duration. It occurred during the refeeding period after a fast of 210 days in an apparently well young woman (Garnett et al., 1969). Following this particular report doubt has been cast on the safety of the treatment of obesity by total fasting (Garnett et al., 1969; Rooth & Carlstrom, 1970). However, the allopurinol[1] which had been given may have had unfavourable effects on nucleotide metabolism (Stewart & Fleming, 1969).

Blood glucose changes:  Decreased (Jackson et al., 1968; Runcie & Thomson, 1970), increased (Schless & Duncan, 1966) and normal (Anderson, Herman & Newcomer, 1969) glucose tolerance have all been described as occurring during fasting. The categorization of obese patients into 'diabetic' and 'non-diabetic' groups, even although none was overtly diabetic prior to fasting, is according to some a prerequisite in the evaluation of glucose tolerance during fasting, with the 'non-diabetic' showing decreased tolerance and the 'diabetic' showing unaltered or improved tolerance (Schless & Duncan, 1966; Jackson et al., 1968).  When assessed by the rate of decrease in glucose concentrations following intravenous glucose administration as recommended, our 'non-diabetic' patient showed no systematic change in glucose tolerance throughout the fast or afterwards. It would appear that there is considerable individual variation, both in the level of blood glucose maintained during prolonged fasting and in the response to a glucose load. However, it is obvious that even patients such as ours, who do become markedly hypoglycaemic, can tolerate their fasts as well as those who maintain more normal sugar levels.

Plasma electrolyte changes Progressive hypokalaemia was not a feature in our patient following the cessation of potassium supplementation. Two of twenty-five patients have developed hypokalaemia, despite potassium supplements (Munro et al., 1970). It may be that the release of potassium from cellular tissue during fasting of the obese can be sufficient in some cases to maintain plasma levels despite continued urinary loss. The temporary period of hypercalcaemia is difficult to explain. It was unassociated with any other evidence of parathyroid hyperactivity and coincided with a slight increase in plasma phosphate concentration, within the normal range.  The coincidence between the hypercalcaemia and the occurrence of markedly increased excretion of both calcium and phosphate is impressive. It may be that the hypercalcaemia was associated with resorption of some bone salt which was no longer required in the skeleton to support the former excess weight. Hypercalcaemia, to our knowledge, has not been remarked in any of the other long-term therapeutic fasts.

Plasma magnesium changes:  Decreased plasma magnesium concentrations have not previously been reported during prolonged fasting. On the contrary normal plasma magnesium concentrations, despite magnesium 'depletion' in muscle tissue, have been described (Drenick et al., 1969) during short-term fasting (1-3 months). The only other relevant report is a remark (Runcie & Thomson, 1970) that one patient who fasted 71 days had a normal plasma magnesium level of 2-2 mEq/l at the time when she developed latent tetany. [Tetany or tetany seizure is a medical sign consisting of the involuntary contraction of muscles,  Can be cxaused by low levels of calcium, carbon dioxide, magnesium, excess potassium.] 

Urinary excretion patterns:  A breakdown in the renal control of electrolyte excretion has been reported to occur in some patients after 40 or 100 days during prolonged fasting (Runcie & Thomson, 1970). The increased urinary excretion of not only sodium and potassium but also calcium, magnesium and phosphate, noted in our patient, may be of similar origin. The concurrent development of these losses represents a definite change in the pattern of renal excretion after about 100 days of fasting. A similar increase in the urinary excretion pattern of sodium, potassium, calcium, phosphate and magnesium was noted during protracted intermittent starvation in a previous patient (Stewart et al., 1966). It is conceivable that some specific deficiency, perhaps of potassium or magnesium, may have brought about this 'nephropathy' but its real nature is at present conjectural. The concentrations of plasma monovalent cations as well as phosphate, appeared to be essentially stable. Once the long-term fasting levels were established, plasma magnesium, glucose and urea levels also remained stable. Apart from the plasma calcium and bicarbonate concentrations, there were no other alterations in plasma constituents coincidental with the change in urinary excretion. The overall stability of the plasma constituents studied therefore contrasts vividly with the concurrently developing increase in the urinary losses of both monovalent and divalent cations, together with inorganic phosphate which occurred after about 100 days of fasting.  Such symptom-free developments are possibly more compatible with the release of surplus structural or other tissue components than with disadvantageous decompensatory loss of electrolytes from the extracellular fluid occurring as a result of some kind of nephropathy. It has been shown (Naeye, 1969) that hyperplasia and hypertrophy, not only of adipose tissue, but also of heart, kidneys, pancreas, liver and spleen occurs in obese subjects. It is suggested that the increased excretions described may have originated in dissolution of this soft tissue and associated skeletal excess. Accordingly, the electrolyte losses described are not regarded as representing a necessarily disadvantageous development during fasting.

Conclusions: 

Short-term fasts, although demonstrating to the obese patient his ability to lose weight, have a poor long-term outlook with respect to subsequent weight gain (MacCuish et al., 1968). We have found, like Munro and colleagues (1970), that prolonged supervised therapeutic starvation of the obese patient can be a safe therapy, which is also effective if the ideal weight is reached. There is, however, likely to be occasionally a risk in some individuals, attributable to failures in different aspects of the adaptative response to fasting. Until the characteristics of these variations in response are identified, and shown to be capable of detection in their prodromal stages, extended starvation therapy must be used cautiously. In our view, unless unusual hypokalaemia is seen, potassium supplements are not mandatory. Xanthine oxidase inhibitors (or uricosuric agents) are not always necessary and could even be potentially harmful (British Medical Journal, 1971) perhaps particularly in the long-term fasting situation.  In most obese patients, there exists a weight loss 'barrier' representing a balance between the desire to lose weight on the one hand and the desire to eat on the other. When the first desire continues to overcome the second, the prolongation of therapeutic fasting should not be ruled out. The various biochemical features which developed in our patient are not considered to be expressions of a failure in adaptation. Starvation therapy can be completely successful, as in the present instance.



[1] Allopurinol, sold under the brand name Zyloprim among others, is a medication used to decrease high blood uric acid levels.[1] It is specifically used to prevent gout, prevent specific types of kidney stones, and for the high uric acid levels that can occur with chemotherapy. Allopurinol was approved for medical use in the United States in 1966. The most serious adverse effect is a hypersensitivity syndrome consisting of fever, skin rash, eosinophiliahepatitis, and worsened renal function.[17] Allopurinol is one of the drugs commonly known to cause Stevens–Johnson syndrome and toxic epidermal necrolysis, two life-threatening dermatological conditions.[17

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