Monthly Archives: December 2012


We all know that the key to weight loss is eating less and exercising more. However, dropping to under 1,200 calories without supplementation leads to nutrient deficiencies, which perpetuates the myth that lower calorie diets are dangerous

It is comforting to know that nurses are one of the few groups left who understand the suffering experienced by patients who are overweight and who recognise obesity as a problem worthy of effective action. Weight control is difficult and unfortunately it is much easier to eat calories than it is to exercise them away. A calorie gap of 3,500 calories between the calories eaten and those used is necessary to dispose of a single pound of excess body fat – 3,500 calories represent
a substantial amount of exercise. If the calories actually eaten are more than the calories used by the other activities of the day, the exercise will only reduce the calorie excess and not result in weight loss. It might, however, slow the weight gain. It really is necessary to eat less in order to manage weight.

No easy solution

There is no secret to weight management: the calories eaten have to be considerably less than those being used for a sustained period of time. The continued health of the patient requires them to consume all the essential nutrients necessary for life and health, which becomes increasingly difficult as the amount of food consumed is reduced or treatments actively promote malabsorption.
If we maintain a varied selection of foods, we can feel reasonably confident that we are getting the complete array of essential nutrients. However, while the plants and animals we choose for food each have some of the essential nutrients required by man, none has them all. To get the right amounts for sustained health from unsupplemented foods it is absolutely essential that we eat in excess of 1,200 calories. Eating foods with lower calorie totals cannot provide all the nutrients that we need. The myth that dropping calories below about 1,200 in order to lose weight is unhealthy is true, but not because the calories are low – a fat person has an enormous store of calories available. The problem is that dieters become nutrient deficient.
Providing the missing nutrients, however, permits dropping the calorie intake much further without harm, as long as there are reserves of fuel left in the body. Fuels available for the body are glucose (stored as glycogen) and fat. An obese individual has about 37,000 calories in reserve for each stone of excess weight and therefore has no realistic need to eat more. He just needs to get the essential nutrients. When these come from a nutrient-complete formula food, the results are ideal: complete nourishment and minimal calories. Supplying the essential nutrients in a prepared mixture, such as in an enteral feed, assures that nutrient deficiencies do not occur.

The role of the pharmacist

An expanding network of pharmacists is offering a range of treatments for weight problems. They have the training, the respect of the public, the contact hours and the desire to offer weight management as a professional service. NICE recommends that specialists be used for extended very low calorie diets (VLCDs).1 These pharmacists are trained and experienced specialists in the use of VLCD.
Pharmacies following this route are achieving a great deal and GPs and nurses are becoming much more comfortable directing overweight patients to these highly trained and experienced pharmacists. At the same time the availability of trained pharmacists is becoming more widespread, which is making these experts much more accessible to a wider deserving population.


Weight loss is more than a cosmetic issue. Weight loss can lower blood pressure, normalise blood lipids, practically
eliminate type 2 diabetes, reduce the severity of asthma, bring relief to arthritics, increase the fertility of women, relieve sleep apnoea, provide an opportunity for patients to be considered for elective surgery, decrease the need for antidepressants, make exercise more possible and thus improve cardiovascular health, and vastly improve the quality of life for patients in a prejudiced and intolerant world. Pharmacists are emerging as the weight management specialists, providing lifestyle advice, effective treatments and support, as well as follow-on help for the most difficult aspect of managing weight: the longterm maintenance of weight lost. Your overweight patients will appreciate knowing about it.

PDF version: 4-3-sharing-advice


S.N Kreitzman Ph.D. (Nutritional Biochemistry) R.Nutr. (UK Registered Nutritionist),
S. A. Kreitzman, & V. Beeson Howard Foundation Research Ltd. Cambridge UK

Obesity is a serious problem in modern society, and one that needs to be urgently addressed by healthcare professionals. Unfortunately, widespread obesity management will not be possible until healthcare professionals accept the brutal fact that advising an obese patient to ‘eat less” is as misguided as managing an alcoholic by advising him or her to “drink less.”
In the first instance, advanced obesity management must recognise that there is a difference between people who become .)ese and the rest of the normal weight j,opulation. Not every drinker becomes an alcoholic, and in the same way, only some people become obese. This is not a trivial comparison. Many people can and do control their eating behaviour arid never appear to be in danger of escalation into obesity. For those who do become obese, however, their food behaviour often displays the compulsions and cravings of an addiction. Indeed, it is when food consumption is put into the context of other addictive behaviours that the nature of the roblem
becomes clear.
The link between addiction and obesity is finally now being reflected in the search for drugs to combat obesity, as can be seen
in the 30 July, 2010 report in the Lancet on the use of naltrexone in conjunction with bupropion as a weight loss treatment. It is important to recognise the basic fact that there is a component of addiction in food abuse and ultimately obesity. The most powerful long term treatment for addictions is complete abstinence from the addictive substance. A reformed smoker is someone who does not smoke, and a reformed alcoholic is someone who does not drink Comprehending this simple reality explains why total food replacement formula (very low calorie diets) are extremely effective and conventional low calorie diets are much less effective for seriously overweight patients. To treat any addiction (including obesity) effectively it is necessary to stop the substance of abuse. Very low calorie diets – essentially low fat enteral feeds – are absolutely necessary because they permit a patient to safely stop eating for prolonged periods. No lifestyle or behavioural change can be effective while the patient is caught in the biological quagmire of addiction. The advantage of a Total Food Replacement programme is that nutrition is provided by an engineered
formula that is nutritionally complete,
allowing the dieter to remove the addictive substance (food) from his or her life and remain healthy while the weight is lost. The value of a total food replacement formula programme in the treatment of overweight and obesity should now be obvious. TOTAL food replacementis the only means by which those who are subject to food abuse may avoid the addictive stimulus that perpetuates their weight problem.
The rapid proliferation of type 2 diabetes is currently one of the more serious healthcare problems. Current estimated costs to the NHS for treatment of this problem are a staggering El million per hour. In almost all cases however, a simple treatment exists that costs the NHS nothing, can normalise blood sugars within a few days (even in long standing diabetes) and in most cases actually put type 2 diabetes into remission. This important clinical knowledge is inadequately recognised because of the mantra for evidence based care. It is impossible to design a double blind placebo controlled study of VLCD.
While case studies are often considered to be a lesser level of evidence, the balance of believable evidence must shift, especially when the number of cases being audited becomes virtually the entire treatment population. For the past 25 years GPs and pharmacists have been treating overweight and obese patients with VLCDs and monitoring their progress weekly over the course of their treatment. Those medical details and weekly progress reports have all been recorded over the years, and a number of audits from individual GP
practices and a 25 practice meta-audit have been published.
As the population of GP practices and pharmacies has expanded and computerised patient records have become more available, it has become Training to use VLCD properly requires education
Dieters can safely remove the addictive substance (food) and remain healthy theoretically possible to audit the entire population. A sample from a group of pharmacies in the Republic of Ireland has provided audit data for over 9000 Lipotrim patients. A single pharmacy in Prestwich, Manchester has provided audit data for over 1100 dieting Lipotrim patients. Since these patients are seen weekly and progress recorded by health professionals, the information should be viewed as highly credible and EVIDENCE BASED.
At Prestwich 1148 overweight patients with a median BMI of 33.6 kg/m’ were enrolled into the Lipotrim weight management programme. Of these, 25% were morbidly obese with a BMI >40 kg/ m2. At the time of audit, during which manypatients were still actively dieting, the median BMI had decreased to <30 kg/m2. 94% of the dieters lost more than 5% of their pre-diet weight, 47% lost more than 10% and 21% of the patients lost more than 20%. Importantly, all patients with type 2 diabetes had their medication stopped by their GP.’ The weight losses (comparable in most cases to that achieved by bariatric surgery) are having the same effect on type 2 diabetes as that reported for surgical procedures. The effect is in fact so dramatic, patients are not permitted to start the diet unless the GP has stopped diabetic medication. Blood sugars will normalize within a few days, and with afew weeks weight loss it is unlikely that any further diabetic medication will be required.
Training to use VLCD properly requires education. There are simply too many myths. The training programme for pharmacists running the Lipotrim weight management programme was awarded the SMART Best Educational Training Award For Pharmacists in 2002. Based upon sound physiological principles that most professionals know but are continuously seduced to ignore, there must be a greater recognition of need for VLCD, the only widely available tool for obese patients mired in the addiction aspect of food abuse. •
1. (Data presented at the 2010 National Obesity Forum Conference by Pharmacist Fin McCaul)

PDF version: 2-1NAPC advanced obesity management

Maximum Safe Rate of Weight Loss in Pharmacies

People walking

Published on Thursday, 25 October 2012 14:35
Posted by Vicki Mitchem

Rapid safe weight loss in a pharmacy setting with VLCD programmes monitored by healthcare professionals, are documented by audits using Lipotrim’s unique patient tracker software.

The diet can produce weight loss at sufficient rates to result in sustainable remission of type 2 diabetes and benefit to many weight related co-morbidities.

The Lipotrim weight loss programme, monitored exclusively by healthcare professionals has been in extensive use in the UK for more than 25 years. A rapidly expanding network of over 2000 pharmacies currently offer the VLCD service and the unique Lipotrim Patient Tracker computer software for managing patient records has permitted continuous auditing of results and detailed evaluation of population subsets.

Overweight or obese people requesting the programme are assessed for suitability on the basis of initial BMI and a detailed medical history. Those requiring medical cooperation, such as those with type 2 diabetes or medicated hypertension make suitable arrangements with their GP prior to dieting or are excluded. Those with contraindicated conditions, such as insulin dependant diabetes or pregnancy are excluded from the programme.

Suitable patients follow a strict regime of total food replacement using nutrient complete formulas, essentially very low fat enteral feeds, with adequate water intake and black tea or coffee permitted in addition. Appropriate prescribed medications are continued as well. No other foods, beverages or supplements are permitted.

Dieters are monitored and weights recorded weekly – only 1 week’s supply of formulas can be obtained at each visit and obvious non-compliance is corrected or the dieter is offered alternative weight loss advice.

Records are maintained on the Patient Tracker programme.

The extreme flexibility of the Patient Tracker software, in addition to documenting and visualising each individual patient’s experience, allows for presentation of evidence of the weight loss achievements of cohorts of patients. This has become important for commissioning and the ability of grouping patients from an individual surgery permits documentation to the surgery of the collective progress of their patients,

Results from thousands of patients’ audits document that the percentage of initial weight lost generally averages well over 5% and in most cases over 10%. Successful weight loss is found even in the extremely high BMI patients, who are usually refractory to weight management attempts, causing many people to believe that the only option for these people is expensive and invasive bariatric surgery.

Patients with high BMI, have to deal with many difficult issues and for these people, standard approaches to weight loss have often been ineffective. They fail because they all are attempting to control addictive behaviour while permitting continued use of the substance of abuse. It does not work with alcohol or tobacco. It does not work with drugs and it rarely works with food. For seriously overweight people, the most effective treatment is to totally stop the substance of abuse, which is why a Total Food Replacement programme is so much more effective.

Obtaining the required complement of nutrients from common foods requires many more Calories than is consistent with rapid and substantial weight loss. The advantage of a Total Food Replacement programme is that nutrition is provided by a nutritionally complete formula, allowing the dieter to remove the addictive substances (food) from his or her life while the weight is lost and the medical consequences of the excess weight are relieved..

The value of a total food replacement formula programme in the treatment of overweight and obesity should now be obvious. TOTAL Food Replacement is arguably the only means by which those who are subject to food abuse may avoid the stimulus that perpetuates their weight problem.


S.N Kreitzman Ph.D, R.Nutr. (UK Registered Nutritionist), S. A. Kreitzman, & V. Beeson Howard Foundation Research Ltd. Cambridge UK

Recently the media world has been absolutely saturated with articles carrying headlines
such as “Type 2 Diabetes Can be Cured by Extreme Diet”. This is important news, and it is imperative that the information be clearly understood. Your patients’ health – and perhaps their lives – depends upon your recognition of the value of this information. Unfortunately, the sensationalist language with which the reports have couched the results will unnecessarily discourage many overweight people. Even healthcare providers may ignore the message. Patients will continue to needlessly suffer from the dire consequences of diabetes. It is important to recognise that although the language may be extreme, the diets are not.


First of all, it must be made clear that the results that have received so much publicity recently are not “news”. The only unique aspect of this particular study(1) is the degree to which it has managed to dominate the media, when more than 30 prior years of scientific and medical publications (involving thousands of diabetic patients) have seen diabetes put into remission within a few days on a very low Calorie diet (VLCD). Not a word of these studies appeared in the public media and only those healthcare professionals who kept current with the scientific literature were aware of the findings. Even they, however, were discouraged by the sinister notion of an “extreme diet”.
There is nothing “extreme” about the mod-
ern Very Low Calorie Diet. Before we come back to that, it is also critical to understand that neither the diet used in this report nor a proper VLCD cause the “cure of diabetes” any more than bariatric surgery can cure diabetes. The immediate drop in blood sugar with surgery or VLCDs is due to the sudden unavailability of dietary carbohydrates, which forces the body to utilise the excess sugar it carries in circulation and storage. The crucial fact is that remission of type 2 diabetes is due to weight loss. Excess weight is well known to be a major contributor to the development of diabetes and the loss of the excess weight will usually reverse the process. Ultimately, the carbohydrate provided by the diet formula, supplemented by 3 carbon sugars released from triglycerides as fat becomes mobilised for energy, keeps blood sugar at a normal level and diabetes in remission. What the modern nutrient complete VLCD can do very effectively is ensure weight loss at a maximum safe rate, without the need for the risks of bariatric surgery with the inevitable subsequent nutritional problems caused by nutrient malabsorption.


It is something of a paradox that a dietary programme that actually provides an individual with all essential dietary needs should be considered “extreme”. Although conventional “chatroom wisdom” might place great importance on the Calorie content of the dietary intake, this concern is actually unwarranted. A car’s tank may hold 40 litres of petrol, but there is no point in filling the tank with this amount if the tank is already full. Overweight individuals have an enormous number of Calories in reserve in their fat stores. In essence, their petrol tank is already full. In evolutionary terms, that is what fat is for: to provide Calories, when required, at a rate of 7700 Calories for each kilogramme of stored body fat. The number of dietary 9-1imgCalories needed (Calories entering the body from the outside) is determined by the nutrient content of the food consumed. Without supplements, the nutrient availability in ordinary foods is sufficiently diffuse that it is virtually impossible to construct a nutrient-complete diet that adds up to less than 1200 Calories daily. With a normal food diet, cutting the Calorie intake below 1200 Calories creates inevitable nutrient deficiencies and the dieter becomes ill. A modern nutrient complete VLCD is simply an enteral feed with sufficiently low fat that many of the daily Calories have to be drawn from the fat reserves of the body. That is what is commonly known as a “diet”.
Very Low Calorie Diets have been in worldwide use for more than 30 years with a tremendous safety record. Although they may differ somewhat in their composition (and in the professional competence of those monitoring the programme) they have been repeatedly shown to be very safe. Safety of use is determined entirely by recognition of the concurrent medical conditions at the time of use. For example, the use of a VLCD by a diabetic patient needs the doctor to stop hypoglycaemic medication prior to the patient dieting. If the weight loss reduces blood pressure in a patient using anti-hypertensive drugs, the patient may become overmedicated. If a person diets while they are being assessed for thyroid hormone supplementation, the blood thyroxin levels will be inaccurate and the dose will be wrong. These diets really work and therefore care is needed in selection and monitoring of patients. The provision of a proper maintenance programme (not always available from various VLCD purveyors) makes a great difference in the prevention of recidivism. Long tem outcomes are therefore programme specific.


Don’t let sensationalist language used in media reporting hinder patients benefiting from a valuable mode of treatment. Properly formulated and monittored VLCDs save lives. Appropriate maintenance formulations help reduce recidivism.
There is considerable long -standing scientific literature demonstrating that the rapidity of weight loss confers additional positive health benefits (independent of the actual amount of weight which is lost) when compared with food-based diets or higher energy level formula diets. This applies particularly to non-insulin dependent diabetes mellitus (see, for example Lean et al2),1990; Henry & Gumbiner, 1991; Wing et a1,1991 (4); Hernandez-Bayo et a1,1985(5), Paisey 1998(6) in which metabolic control and lipid profile is markedly improved by the rapid fall in weight using VLCD. Wider recognition of this and much more literature, as well as the current experience of over 2000 pharmacists and GPs using Lipotrim will hopefully put an end to the use of off-putting language which discourages acceptance of an important medical tool.


1. Lim E. L et al Reversal of type 2 diabetes: normalisation ofbeta cell function in association
with decreased pancreas and liver triacylglycerol Diabetologia D0110.1007/s00125-011-2204-7
2. Lean MEJ, Powrie JK, Anderson AS Et Garthwaite PH. Obesity, weight loss and prognosis in type 2 diabetes. Diabetic Med, 7: 228-233, 1990.
3. Henry RR Et Gumbiner B. Benefits and limitations of very low calorie diet therapy in obese
NIDDM. Diabetes Care, 14:802-823, 1991.
4. Wing RR, Marcus MD, Salata R, Epstein LH, Miaskiewicz S Et Blair EH. Effects of a very low calorie diet on long term glycemic control in obese type II diabetic subjects. Arch Int Med,
151: 1334-1340, 1991.
5. Hernandez-Bayo JA, Herranz L et al. Factors related to successful outcome after rapid weight loss in obese patients. Internat J Obes 19 Supp12: 379S, 1995. with NIDDM.
6. Paisey RB, Harvey P, Rice S et al. An intensive weight loss programme in established type 2 diabetes ans controls: effects on weight and atherosclerosis risk factors at 1 year. Diabetic Med 15: 73-79,1998.

PDF version: 9-1-Lipotrim Advertorial gp final


Special report in PDF


Foreword 3 John Hancock, Editor

Diabetes and Obesity
A Modern Problem; an Eternal Obstacle 3
Stephen Kreitzman Ph.D, R.Nutr. Valerie Beeson, Shawm Kreitzman, Howard Foundation Research, Cambridge UK

The Case for VLCDs over Medication Benefits of Rapid Weight Loss Overeating Akin to Alcoholism The Lipotrim Alternative
No Excuse for the Current Level of Type 2 Diabetes
Prevention More Cost Effective than Treatment 10
John Hancock

Prevalence and Impact A Range of Solutions Shortfalls in Care
A Lack of Awareness
Prevention More Cost Effective than Treatment Stronger Together
Reform to Rethink
Make What Works Work Well 12

Not Unseen but not Understood
A Realistic and Achievable Programme Achieving and Maintaining a Healthy Weight An Integrated Approach
Education for Better Outcomes

Lipotrim 14 Camilla Slade, Staff Writer

Too Much and Too Little Less Calories, Less Weight
Reform to Rethink 15
Camilla Slade, Staff Writer

GPs at the Heart of Things NHS Diabetes
Getting it Right Matters Nutrition
Make What Works Work Well 17
John Hancock

Facing the Real Issue
Different Solutions; Same Objective Planned, Agreed and Appropriate
References 18



8-1To fully understand the medical value of nutrient- complete formulated foods as a tool for weight management, there are a few fundamental concepts that need to be explained. These include the protein sparing modified fast; the mechanisms and value of ketogenic diets, minimum safe energy intakes and enteral food formulas. The value of this approach is amply demonstrated by substantial clinical evidence accumulated over a period of nearly 40 years.
Beginning in 1975, a series of reports from the Bistrian and Blackburn medical team demonstrated the value of a very low-energy dietary regime for weight management in a variety of difficult obese patients. This team had the advantage of considerable nutrition expertise and they devised a protein sparing modified fast — essentially a home-concocted Very Low Calorie Dietary formulation that was nutrient complete. Unfortunately the remarkable success (and safety) of this approach was obscured by commercial greed – not by the medical team, but by external commercial exploitation. A commercial product was developed and widely sold that contained virtually no nutrition. it was based upon a hydrolyzed nutritionally incomplete protein (collagen) in cherry syrup. This product was heavily promoted and widely hyped and inevitably, it resulted in a number of deaths.
Quite properly, the Liquid Protein Diets have not been available since the late 1970s. Unfortunately however, a total lack of nutritional understanding led to the assumption that low energy liquid formulations were dangerous as a concept. In fact there are now nearly 40 years of worldwide experience with numerous properly formulated nutritionally complete products which should be evidence enough of safety.
There is an often stated mantra, surprisingly even from nutrition specialists, that there must be some level of calorie intake (in the neighbourhood or 1000 to 1200 calories per day) below which diets become unsafe. Once again, it is simply the superficial understanding of food and nutrition biochemistry that has given this notion some credence. All common foods may be thought of basically as recycled nutrients from the plants and animals we choose to consume. All are complex formulations of the chemicals that make up the composition of those plants and animals. Many of these chemicals are common to all living things and some of them are useful and even necessary for human health. They also contain large numbers of chemicals that are either inert or toxic to other animals, including humans. The key point, however, is that there is no naturally occurring food that contributes all the required nutrients for humans. We therefore require a varied diet to attempt to create a mix that will maximize the chemistry we need and minimise the problematic substances.
The crucial point here is that – given the varying chemistry of the plants and animals we consume — it is virtually impossible to assemble a nutrient-complete daily diet with a total of less than around 1200 calories. When food diets with lower calorie intakes are provided, nutrient deficiencies invariably cause illness. It is very important to note here that it is the nutrient deficiencies — and not the low calorie count — that causes the problems.
When it became clear that nutrient complete enteral feeds could be provided that contained, by design, all the essential nutrients, it demonstrated that the minimum calorie intake was nowhere near the 1200 calorie barrier. In fact, modern formulations have a calorie component determined primarily by the calorie contribution of the essential amino acids and essential fatty acids (and to a lesser extent by the lactose from the necessary milk component, which provides very high quality proteins to the formulations). These limits however are closer to 400 calories per day, not 1200.
The most effective and safe formulations are those that induce ketosis. Ketones are a by-product of the incomplete breakdown of free fatty acids. They are essential for sparing protein utilization and helpful in controlling the hormonal balance between insulin and giucagon, which helps control hunger. Many of the body’s tissues can use free fatty acids as fuel, but critically there are a few (including the brain) that cannot. Unless there are sufficient ketones present, which are water soluble and can pass through the blood brain barrier to provide energy for brain function and survival, the body must de-aminate amino acids from proteins to create glucose. Glucose can not be created from fat. This is why ketones are protein sparing. Virtually all tissues, with the possible exception of liver, can use ketones for energy.
It is clear from the controlled accessibility of very low energy diets through healthcare professionals, that detailed records are available of the successful results of this form of treatment. A large number of these results have been published. Proper nutrition, provided in defined very low calorie formulations, results in maximum safe rates of weight loss and there is considerable evidence to support its value to modern medicine.
S.N Kreitzman Ph.D, R.Nutr. (UK Registered Nutritionist)
V. Beeson Howard Foundation Research Ltd.

PDF version: 8-1-nhsta0002a


Audit Results using the Lipotrim Patient Tracker

by Gareth Evans

The current excitement generated by the press coverage of the Newcastle University study of diabetic patients using weight loss by a very low calorie diet to “cure” diabetes, necessitates a wider recognition of the well established programmes already available. The Lipotrim weight loss programme, monitored exclusively by healthcare professionals has been in extensive use in the UK for more than 25 years. A rapidly expanding network of nearly 2000 pharmacies currently offer the VLCD service and although many have used manual methods to audit their patients’ achievements, the newly provided Patient Tracker computer software for managing patient records has permitted continuous auditing of results and detailed evaluation of population subsets.

For example, in addition to auditing the total experience of patients enrolled in the pharmacist-run service, the results can be examined in many different ways. The cohort can be divided by gender, by age, by initial or final BMI, by amount or percentage of weight loss achieved, or by medical history (hypertension, diabetes, depression, thyroid problems etc.). The programme extends beyond weight loss, as there is a refeeding transition back to ordinary foods and a full maintenance programme, which is proving extremely successful in the pharmacy environment. With this Tracker audit tool, therefore, evidence is also available documenting the long term maintenance outcome after dieting.

As a pharmacist who has been using the Tracker to keep my Lipotrim patients’ records for some time now, I would like to share a current audit of my patients’.

Materials and Methods

Overweight or obese people requesting the programme are assessed for suitability on the basis of initial BMI and a detailed medical history. Those requiring medical cooperation, such as those with type 2 diabetes or medicated hypertension make suitable arrangements with their GP prior to dieting or are excluded. Those with contraindicated conditions, such as insulin dependant diabetes or pregnancy are excluded from the programme.

Suitable candidates follow a strict regime of total food replacement using nutrient complete formulas, essentially very low fat enteral feeds, with adequate fluid intake and only black tea or coffee permitted in addition. Appropriate prescribed medications are continued as well. No other foods, beverages or supplements are permitted.

Dieters are monitored and weights recorded weekly – only 1 week’s supply of formulas can be obtained at each visit and obvious non-compliance is corrected or the dieter is offered alternative weight loss advice.

Records are maintained on the Patient Tracker programme.



Total Population of Dieters completing 3 or more weeks on Total Food Replacement

Mean Start Weight 91 kg – Mean End Weight 81 kg

Total weight lost to date of audit – 3865 kg


Table 1 N= 382 330 Females 52 Males

Mean Start wt 91kg Start BMI 32.7 End BMI 29.0 % wt loss 10.8
Median Start wt 88.2 kg Start BMI 32.0 End BMI 28.4 % wt loss 9.0

The next series of tables demonstrates the value of the Lipotrim service in overweight patients, reducing the likelihood of their progression to obesity, as well as obese, super obese, morbid obese or even super-morbid obese patients.


Table 2 N= 121 BMI 25-30

Mean Start BMI 28.1 End BMI 25.4 % wt loss 9.3
Median Start BMI 28.3 End BMI 25.4 % wt loss 8.0


Table 3 N= 141 BMI 30-35

Mean Start BMI 32.4 End BMI 28.9 % wt loss 10.9
Median Start BMI 32.3 End BMI 29.1 % wt loss 12.0


Table 4 N= 73 BMI 35-40

Mean Start BMI 36.9 End BMI 32.4 % wt loss 12.9
Median Start BMI 36.7 End BMI 32.6 % wt loss 11.0


Table 5 N= 29 BMI 40-45

Mean Start BMI 42.2 End BMI 36.1 % wt loss 14.4
Median Start BMI 42.0 End BMI 36.3 % wt loss 11.0


Table 6 N= 5 BMI 45-50

Mean Start BMI 47.4 End BMI 37.2 % wt loss 21.2
Median Start BMI 47.3 End BMI 36.9 % wt loss 22.0



Other subsets of the patient information that are of interest include:


Table 7: Obese people who exceeded the 5% criterion for medical benefit of weight loss.


Tables 8and 8a: Some dieters choose to interrupt their diet for varied reasons and then return for a subsequent diet period. Their first and second dieting courses can be examined separately.

Table 9: After a period of weight loss, it is necessary to re-introduce carbohydrates in a controlled manner to minimise weight regain due to carbohydrate loading. Minimal weight change is expected despite reintroduction of normal foods. This phase is 1 week long.

Table 10: The Tracker software distinguishes between periods of dieting and maintenance providing evidence of minimal recidivism when patients are properly supported in the pharmacy environment.

Table 7 N= 231 BMI > 30 who lost 5% or more of initial weight

Mean Start BMI 35.3 End BMI 30.8 % wt loss 12.7
Median Start BMI 34.5 End BMI 30.1 % wt loss 11.0


Table 8 N= 78 Dieters who had 2 dieting courses First time

Mean Start BMI 32.1 End BMI 29.1 % wt loss 9.0
Median Start BMI 31.2 End BMI 28 % wt loss 7.5

Table 8a N= 78 Dieters who had 2 dieting courses Second time

Mean Start BMI 31.1 End BMI 29.6 % wt loss 4.7
Median Start BMI 29.7 End BMI 28.1 % wt loss 3.5


Table 9 N= 140 Refeeding week

Mean Start BMI 27.5 End BMI 27.4 % wt loss -.2
Median Start BMI 26.6 End BMI 26.6 % wt loss 0


Table 10 N= 249 Maintenance after dieting

Mean Start BMI 28.1 End BMI 28.1 % wt loss 0.1
Median Start BMI 27.2 End BMI 27.0 % wt loss 0


Patients who are medicated for various weight related ailments can often be considered as different categories of patient. Many hypothyroid patients have experienced great difficulty with weight management. Depression and hypertension often have a weight component in the aetiology of the problem.

Table 11: Examines patients on medication for hypertension

Table 12: Examines patients on medication for hypothroidism

Table 13: Examines patients on medication for Depression


Table 11 N= 22 Patients with High Blood Pressure

Mean Start BMI 36.2 End BMI 32.0 % wt loss 11.6
Median Start BMI 37 End BMI 32.2 % wt loss 8.5


Table 12 N= 9 Patients with thyroid hormone replacement

Mean Start BMI 34.5 End BMI 29.4 % wt loss 14.2
Median Start BMI 34.7 End BMI 28.9 % wt loss 10.0

Table 13 N= 13 Patients with Depression

Mean Start BMI 33.2 End BMI 28.2 % wt loss 13.0
Median Start BMI 32.2 End BMI 28.9 % wt loss 11.0



The extreme flexibility of the Patient Tracker software, in addition to documenting and visualising each individual patient’s experience, allows for presentation of evidence of the weight loss achievements of cohorts of patients. This has become important for commissioning and the new ability of grouping patients from an individual surgery permits certification to the surgery of the collective progress of their patients, These results can be of value for CPD as well.

As can be seen from the multiple tables presented as illustration, the percentage of initial weight lost generally averages well over 5% and in most cases over 10%. Even the median values, which documents the half-way values of the ranges, are generally very close to the mean. Successful weight loss is found even in the extremely high BMI patients, who are usually refractory to weight management attempts.

In addition to demonstrating the successful loss of weight by the dieters, regardless of the sub-category for grouping, it is important to note that even though there are some variations in patients’ experiences with re-feeding (Table 9) and follow on maintenance (Table 10), the overall lack of weight regain from the patients post-diet demonstrates the value of the pharmacist and the Lipotrim programme for long term weight control.




Despite the fact that these results reflect the efforts of a single pharmacist in a programme that currently lists nearly 2000 pharmacies throughout the UK and Ireland, it is important to have the tools that can satisfy the need for documentation of achievement in this era of evidence-based treatments. The success of this pharmacy service has considerably enhanced my professional satisfaction as a pharmacist.






S N Kreitzman PhD and V Beeson
(University of Cambridge, Howard Foundation Research, Cambridge, UK)

Objectives: To assess the weight losses and weight maintenance achieved with obese, often medically compromised, patients following a common Lipotrim treatment protocol.
Design: Data collation from voluntary responses by the practices to a general request for weight statistics, in a way that respects patient confidentiality. The sample of practices represents approximately 15% of those following the common protocol at the time of assessment.
Setting: 25 general practices and 2 hospital clinics in the UK.
Subjects: 818 obese patients registered with the practices or under medical referral to the hospital clinics The medical conditions ranged from apparently uncomplicated obesity to severely medically compromised patients, all treated under closely monitored conditions. Initial BMIs ranged from 24.4 to 78.7.
Interventions: Three, phased protocols, for weight loss, transitional refeeding and weight maintenance. Weight loss phase based upon Total Food Replacement under strict medical control – with specific, nutrient complete formula VLCD. Weight maintenance based upon modification of eating behaviour to significant dietary fat restriction. Considerable educational
materials provided throughout programme; approached conceptually as an addiction control problem.
Main outcome measures: Body weight and Body Mass Index at start of programme, at end of weight loss phase and the most recent follow-up available for each patient.
Results: Weight losses totalling in excess of 16,000kg with high levels of compliance and clinically encouraging weight maintenance results.
Conclusions: Obesity can be managed effectively under a variety of practice conditions, even in ‘heart sink’ patients who have repeatedly failed in the past to control their weight, despite the best efforts of the clinical team.

Despite the prevalent academic knowledge of the medical problems associated with obesity (1-13), the frequent failure to achieve weight loss in obese patients has discouraged many practitioners from using weight loss as a primary treatment (2,18). Unless obesity is tackled, however, the scenario of a possible 25% of the population being obese by the year 2005 instead of the Health of the Nation target levels of 6 to 8 percent as in 1990 (14,15), will continue to be a health care frustration.

The impact of effective obesity treatment in general practice, however, is very dramatic. When patients with type II diabetes lose significant weight quickly, glycaemic control is improved better than the same weight loss achieved more slowly, and this appears robust even in patients where some weight is regained (7, 9, 10, 11, 16, 17).

In non insulin dependent diabetes mellitus (NIDDM), hypoglycaemic agents are generally stopped within a week or two (9). An impressive percentage of patients with hypertension have
also been able to reduce dosage or totally eliminate medication, often after only modest weight loss (7,11).

The impact of such major health improvement sin patients with long-standing and progressive disease provides the momentum for practices to continue to devote effort and resources to obesity management (25).
This paper reports a META-AUDIT of weight loss and maintenance results from ongoing obesity management programmes in UK general medical practice sites and hospital clinics following a common treatment protocol.
Total weight lost by 818 patients was 16,211kg (16+ tonnes).

Weight information relating to the obesity control programmes was obtained from 25 UK general practices and 2 hospital clinics. Patients were not identified to the investigators, except by a sequential code number at each site. The information provided from each location included height, initial weight and date, end of weight loss phase (refeed) weight and date, and the last recorded follow-up weight and date. About half of the patients were still in the weight loss phase of the protocol at the time of the audit. This posed analytical dilemma. It was decided to treat the weight of those still dieting at the date of audit as if it were a refeed weight with a maintenance time of zero. Only in the separate maintenance data analysis does the category of
refeed refer purely to those patients who have completed their weight loss phase and resumed conventional food for at least one month.

At each site, patients join the programme solely at the medical discretion of the doctor who is versed in the protocol. In accordance with NHS practice, there is no financial consideration to the practice, from any source. The role of the GP is primarily the medical selection of appropriate patients and the monitoring of prescribed medications, which often have to be reduced or stopped as a result of the weight loss.
Patients are seen weekly, usually by a designated and trained practice nurse. In rare cases, extremely medically fragile patients are dieted and these cases are generally seen regularly by the GP. In general practice, the GP orders the Lipotrim formula foods weekly by positive release using a Special Order. This assures that patients cannot obtain the diet from the chemist without the knowledge and approval of the GP who is properly informed about the Lipotrim programme (26-28).
The Lipotrim is a nutrient complete very low calorie diet (VLCD) formulation. The diet is purchased from a local Pharmacist. This is the patient’s only access to the diet. Control of access is totally under the GP’s authority. Patients are expected to comply with the rigid diet and maintenance protocols. These are explained in detail by written material, video and audio taped sessions. Interactive lecture sessions are provided for patients and staff. Most practices limit the number of patients treated at any one time. Available places are rapidly filled from a waiting list.

The results demonstrate that significant (Table 1) and sustained (Table 2) improvement in the weight of obese patients can be achieved under varied medical practice conditions.

Individual practices were able to achieve a range of mean rates for weight loss in their patients (figure 1). The expected rate of weight loss for full compliance with the programme is an average of 1.46kg per week (1 stone per month). This was achieved.

A subset of 414 patients, who had completed their weight loss phase at the time of audit and were attempting to maintained their weight, were evaluated.

The clinical options for very fat people are limited. Most GPs despair of treating the massively obese. The population in this audit compilation included 215 patients over BMI 40, 30 patients over BMI 50 and 7 patients over BMI 60. Results from these patients are documented in Table 3 A-C respectively. Many of these patients are still in the weight loss phase (see Table 3).

The widespread apathy apparent in the general medical reluctance to deal with the obesity problem stems from a long history of futile efforts. Whether this is related to the ineffective modes of treatment offered, a general lack of understanding by either the patient or health professional, or a combination of both, is not clear. The prevailing view has become ‘diets do not work’ (18, 27). This view needs to be altered to reflect the very real difference between dieting protocols. Some standard weight reduction diets can work for some overweight patients. Applying the same approaches to the obese, however, will frequently result in failure. Obese patients require a more decisive treatment protocol (28). Rates of weight loss achieved per practice were shown in Figure 1.

The premise that weight control is futile is unjustified and clinically insupportable when one considers that obesity itself is a risk factor for many serious clinical conditions (19). A large proportion of normal surgery time is spent dealing with many minor ailments, which are fundamentally weight related and which can escalate into serious disease when the weight problem reaches obesity (Body Mass Index >30) (20). Obesity occurring within a family unit can compromise the well being of that unit. The family ‘ill health’ is particularly problematic when the mother is obese. Depressive states and impaired quality of life (8) can affect a significant part of the patient’s daily routine and impact on the rest of the family members. A multiplicity of problems can be traced to obesity within the family.

Much is said about the need to educate and modify lifestyle (20), but the impact of dietary education is considerably grater when the patient is in a positive state of mind, with improved self esteem resulting from weight loss. Sedentary lifestyles are often a consequence of the excessive weight. With weight loss, most patients become significantly more active. This has been shown to increase the probability of maintenance of the lost weight (21).

For the obese, clinical weight goals may not necessarily be to achieve thinness. A more immediate goal may be to control elevated blood sugar or high blood pressure. It may be to allow
the patient access to certain surgical procedures, for blood lipid control or increased mobility or pain relief in an arthritic patient. Clinical judgement will require consideration of age, lifestyle and medical condition in setting realistic weight targets for an individual patient. The current ‘fashion figure’ is not the appropriate determinant of the weight target in the obese.

Weight regain needs to be put into perspective. The percentage of patients maintaining weight loss after medical obesity treatment far exceeds previous statistics (22). Long term weight maintenance at encouraging levels is now commonly reported for medical VLCD programmes (23,24), particularly when these include behavioural modification. There are no permanent cures for obesity. Despite this, an increasingly large number of patients can manage to maintain control for long periods after weight loss, albeit to varying degrees. A patient, however, who has lost 100kg and has regained 50kg is still 50kg lighter. This is particularly important where the lowered weight has allowed necessary surgery to be performed or improved another condition. The evidence of Wing, previously cited, and others (7, 11, 16, 17), suggests that some health benefits of weight loss (glycaemic control) can outlast the weight loss.

Dropout rates are important, but difficult to document. While the weight losses in this assessment are dramatic, no weight programme is universally successful. It is especially difficult to
assess the proportion of non-starters from the data available. The referral procedures into the programme vary widely from site to site. At some sites, access to the programmes is exclusively based upon the medical requirement for weight loss in an attempt to mitigate a pre-existing clinical condition. These referred patients are sometimes reluctant to comply or are disinterested in weight loss. In others, there is a component of self-referral, although the regulation of admission to the programme still remains entirely under the control of the practice. How many patients are referred to the programmes and decline participation cannot be estimated from the data available.
Also difficult to document accurately are the percentages of patients who attempt the protocol but find the initial days too difficult for their current level of motivation. Some practices
provided data from those patients who failed to attend beyond 1 week, but most did not.

Our analysis, therefore, includes all patients who participated for at least 2 weeks. The data demonstrates that established patients complete the course. Figure 2 depicts the fraction of the 818 patients who stopped dieting within monthly intervals.

In Figure 3, the mean BMI changes for the subset of patients whoceased dieting within those monthly checkpoints are presented. Patients conclude dieting for many and varied reasons, only one of which is non-compliance and failure. These failures are included in the 6 percent (51 patients) of patients who discontinued during the first 4 weeks of treatment. Patients stop when they have achieved clinical goals, as discussed previously. It is evident from this graph that patients, on average, continue their weight loss programmes until they are no longer obese, regardless of their BMI at the start.

National Task Force. Very Low Calorie diets. JAMA 1993, 270, 8, 967974.

West KM. Diet Therapy of Diabetes: An Analysis of Failure. Ann Intern Med 1973, 79, 425434.

Anderson J W, Hamilton C C, Brinkman Kaplan V. Benefits and Risks of an Intensive Very Low Calorie Diet Programme for Severe Obesity. Am J Gastroenterology 1992, 87, 1, 615.

Chiang B N, Perlman L V, Epstein L V. Overweight and Hypertension: A review. Circulation 1969, 39, 403421.

Maxwell M H, Heber D, Waks A U, Tuck M L. The Role of Insulin and Norepinephrine.

Kannel W B, brand N, Skinner J J, Dawber T R, McNamara P M. The Relation of Adiposity to Blood Pressure and Development of Hypertension: The Framingham Study. Ann Int Med 1967, 67, 1, 4859.

Wing R R. Use of very low calorie diets in the treatment of obese persons with non insulin dependent diabetes mellitus. J Am Dietetic Assoc 1995, 95, 5, 569572.

Sarlio Lahteenkorva S, Stunkard A, Rissanen A. Psychosocial Factors and quality of life in obesity. Int J Obesity 1995, 19, 6, S1S5.

Paisey R B, Harvey P, Rice S, Belka I, Bower L, Dunn M, Paisey R M, Frost J, Goldman P, Ash I. Short term results of an open trial of very low calorie diet or intensive conventional diet in type 2 diabetes. Practical Diabetes Internat 1995, 12, 6, 263267.

Kirschner M A, Schneider G, Ertel N H, Gorman J. An Eight Year Experience with a Very Low Calorie Formula Diet for Control of Mahor Obesity. Int J Obesity 1988, 12, 6980.

Wing R R, Greeno C G. Behavioural and psychosocial aspects of obesity and its treatment. Ballier’s Clinical Endocrinology and Metabolism 1994, 8, 3, 689703.

Office of Health Economics. Obesity 1994, 112.

Berg F F. Health risks of obesity. Obesity and Health 1993, 10-35.

The Health of the Nation. Department of Health. London HMSO, 1992.

The Health of the Nation. Health Survey for England 1991. Social Survey Division of OPCS. London HMSO, 1993.

Hernandez-Bayo J A, Herranz L, Megia A, Martinez-Olmos M A, Hillman N, Grande C, Pallardo F. Factors related to successful outcome after rapid weight loss in obese patients with NIDDM (Abstract). Int J Obesity 1995, 19, 2, S135.

Hanefeld M, Welk M. Very low calorie diet therapy in obese non-insulin dependent diabetes patients. Int J Obesity 1989, 13, 2, 33-37.

Berg F M. Effectiveness of treatment. Health risks of obesity. Obesity and Health 1993, 85-89.



Marks and Schrijver

Reports on tasks

for scientific cooperation

7.3 – Collection of data on products intended

for use in very-low-calorie diets.

Report September 2002

submitted on behalf of the VLCD European Industry Group to the SCOOP
working group on very-low calorie diets between 1998 and 2001, consolidated


John Marks
Life Fellow, Girton College, Cambridge CB3 0JG


. Manager Corporate Regulatory Affairs for foods for particular
nutritional uses (PARNUTS) – Royal Numico NV








1.1`The prevalence of
excess weight

Excess weight and

Weight increase and

The economic cost of


2.1. The prime

Published monitored

Experience in general
(mainly free sale) use

Putting the spectre of
liquid protein diets to rest

Clinical audits on safety of


Investigation of reputed
deaths with nutrient complete VLCD

Audits on subjects with BMI
under 30

Audits on the prime

Special tests for


evidence of cardiac integrity

Data on side

General side


Bone density

Data on eating

Data on aspects of use and
control in practice

Resting metabolic rate
reduction during and after dieting

Relationship between diet
energy and rate of weight loss


Continuous versus
intermittent use



3.1 Examination of body composition determination methods

3.1.1 Reliability of the analytical methods

Kjeldall method for nitrogen determination

3.1.3 Reliability
of indirect methods of estimating the body protein economy

Variation introduced by different formulae for indirect

3.1.5 Summary of the reliability of composition estimates

Significance of these variations to the Forbes/Prentice graphs

3.2 Re-examination
of old and examination of new data on body composition changes

Re-examination of the Forbes/Prentice graphs

3.2.2 The body
composition studies expressed in terms of BMI status

3.2.3 Body
composition studies expressed in terms of the energy value of the

3.3 The Keys (1950)
Minnesota study – an appraisal

3.4 A
re-appraisal of the Forbes and Prentice graphs

3.5 Further data
relating to body composition study determination

3.6 Summary of the
body composition determinations

3.7 Submission
related to the matter of positive and negative nitrogen balances

3.8 Studies which
provide information on desirable carbohydrate level.

Observations made after the circulation of
the first draft of the report to the working group.



5.1 Medical
precautions for the use of VLCD

5.2 Medical
supervision of individuals apparently healthy apart from excess





When the SCOOP
Task 76.3 was first announced, the VLCD European Industry Group asked to submit
a report which had been prepared by one of us (JM) in March 1998. The SCOOP
Committee, during the first plenary meeting in Maastricht, The Netherlands on
March 15th and 16th 2000 accepted this report. A request
was made by the Committee that those sections of the report which were concerned
with scientific and medical data be updated to early 2000 and submitted as a
discussion paper for the next meeting. Subsequently a series of further papers
was requested by the Committee and submitted in the years 2000 and 2001 by JM
and JS.

The present
document which is referred to in the SCOOP Report to the EU Commission of August
2001 as Marks J and Schrijver J (2001) is the summation of all these reports
from March 2000 to July 2001. It has been edited to try to remove any overlap
resulting from the need, during the various meetings of the Committee to explain
the background to the further reports. In addition the information is not
presented in strict chronological order but in relation to the topics that were

Possible conflicts of

These original
documents were prepared by one or both of us as independent scientists and were
not discussed with the European VLCD Group. However members of that group were
very helpful in finding copies of overseas scientific papers not available in
United Kingdom libraries and in providing background data relating to their own

Neither of us is
currently employed by any of the member companies of the European VLCD Group
though John Marks has, in the past received a fee as Consultant to Cambridge
Nutrition Ltd.. Over the period of the preparation of this report John Marks has
been a Life Fellow of Girton College, Cambridge.

Jaap Schrijver has his
expertise in biochemistry and nutrition. He is employed by Royal Numico NV since
1991. He holds the position of Manager Corporate Regulatory Affairs for foods
for particular nutritional uses (PARNUTS). These foods include VLCD products
although the company has currently not an interest in these products. As a
representative of the Dutch association for PARNUTS foods, he participates in
the regulatory activities of the Association of the Food Industries for PARNUTS
(IDACE). The IDACE secretariat has its office in Paris.



I want to express my particular thanks to Dr Stephen Kreitzman and Valerie
Beeson of Howard Foundation Research Ltd. (Lipotrim), who undertook a substantial
proportion of the original research on which Section III, the ‘Recent Scientific
Studies’ is based. Not only did they make available to us copies of the
published work, but also shared with us much of the basic data so that we could
convince ourselves that their results, which demonstrated substantial
misunderstanding in much published metabolic work, could be thoroughly checked.
On the basis of this, we were not only able to confirm the validity of the
Kreitzman and Beeson studies, but from their bibliographies undertake
cross checks of the errors or omission in the earlier work.

We want to make it quite clear that we found no evidence of deliberate
distortion or deliberate misinterpretation in the early works. Most of
the errors occurred because the biological scientists did not fully understand
the assumptions involved, exactly what their indirect methods of
determination meant or the extraneous factors that influenced their results
and interpretations.




This report presents evidence for VLCDs
collected since the Scientific Committee for Foods Report of 1990.

In 1990 the SCF Report was based largely
on the experience of one (United States) group and ignored not only reports
prepared by European Member States (UK and The Netherlands) but also extensive
studies by European nutrition experts.

In addition to work which was not
reviewed for the 1990 report, there is a large body of new evidence since 1990
(at least 177 published scientific studies on over 26,000 people) and 10 years
of further extensive use in many countries. Most of this new information comes
from conditions of free sale and is well documented.

In earlier reports it was suggested that
studies of the safety of VLCD should be undertaken under conditions of use in
the community. This information is now available from various studies and shows
the considerable levels of safety of the modern nutritionally complete very low
calorie (energy) diets.

During the SCOOP Committee meetings it
was accepted that though the term very low energy diet is scientifically more
accurate, the term very low calorie diet (VLCD) is so widely known and used that
this is the term that should be adopted for the SCOOP Task 76.3 Report. In
consequence we have also adopted this terminology.


This report reviews over
400 published scientific and clinical studies to early 2000, undertaken on
VLCDs, on over 50,000 people. Thus it is likely that VLCDs are the most widely
studied of all weight reducing diets. In addition, it records the main findings
in a series of audit studies undertaken during the routine use of VLCD.

The vast majority of the
studies identify the compositional standards and the length of administration
and this document concentrates on those papers. In almost 20,000 people use was
for more than four weeks, giving good evidence on safety of long-term use.

In addition current formula VLCDs have been used by well
over 25 million people in the international community over a period of over
twenty years.

In addition to
this critical review of the available safety and efficacy data in clinical use,
there have been a substantial number of recent experimental studies which have
shown that some of the earlier research reached erroneous conclusions. This
report reviews this data and highlights some important new scientific
conclusions which have practical implications.

Overall conclusions

A modern nutrient-complete VLCD provides
a highly effective and safe method of weight reduction. The use of VLCD has
benefits on excess weight related disorders which appear to be superior to those
of LCD or food based plans probably on the basis of the more rapid weight

On the basis of monitored clinical
experience coupled with recent body composition studies a scientifically based
standard for composition and labelling can and should be established for

In view of the
undisputed need to help the very large number who need to lose weight, as many
safe methods as possible should be made easily and readily available. This
includes VLCDs, where the safety can be shown to be at least as good as diets in
the >800kcal energy range. VLCDs should therefore be available on free sale
on the same terms as diets of over 800kcals (see Commission Directive

The following more detailed summaries and conclusions were
presented to the SCOOP Working Group:

I Overweight and
obesity are rapidly and substantially increasing problems in all European Union
Member States (Section 1).

Over the past decade the prevalence of excess weight has increased by
some 50%. About 20% of the European middle aged are now obese and a further 30%
or more are overweight (Section 1.1) Excess weightis now accepted as having
reached epidemic proportions

increases steadily from a BMI of about 24 (towards the upper range of normal)
upwards. The problems associated with excess weight include not only serious
diseases, but also psychological and social ills (Section 1.2)

Excess weight is strongly
correlated with increasing mortality, so that at a BMI of 40 there is a greater
threat to life than smoking 20 cigarettes per day (Section

The economic cost of excess
weight is substantial, with direct costs amounting to 1-5% of the health care
costs in most first-world countries (Section 1.4)

The evidence supports the view that all
effective and safe weight control methods should be readily available for
all those who have excess weight.


The experimental studies and clinical experience reviewed here demonstrate that
products with an adequate and specified macronutrient and micronutrient
composition but an energy content below 800kcals per day (VLCD) are at least as
safe as those of higher energy content (LCD)

Special closely monitored clinical
studies in over 50,000 people, many for prolonged periods with laboratory
investigations and electrocardiographic monitoring show no evidence of
pathological changes as a result of the use of VLCD. This confirms the practical
experience of use of VLCD in over 25 million people during more than 20 years.
(Sections 2.1& 2.3)

The studies reviewed here show that
products with an adequate macronutrient and micronutrient composition, but an
energy content in the range 400-800kcals per day (VLCD) are at least as safe as
those of higher energy content LCDs at starting BMI levels down to 25 and
finishing BMI levels in the normal range (20 to 25). (Sections 2.3 &

The submission about safety is based upon
the following data


Summary of the available
published data on diets under 800kcals








Date of publ

Up to


















Energy cont


Up to 450





Over 450







Up to












Up to





45 to











Under 4





4 wks or





re-classified at the request of the Working Group






































NB. The figures do
not total because some papers do not contain full information.

Several papers covering at least 500 subjects have been omitted because the full
paper could not be examined.

full listing of these studies is given as Appendix I and a full bibliography
for them is given as Appendix II.

Despite the fact that no deaths with
liquid protein diets (PLD) have been identified since 1977/1978, it is still
being suggested that experience with these diets have relevance. The information
relating to LPD was re-examined and confirmation given to the Working Group that
these have no relevance to current VLCD. (Section 2.3.1 &2.2)

Clinical studies have demonstrated

i)There are a negligible number of
significant adverse reactions in the studies (over 50,000 dieters) or in routine
use in several millions under free sale use (Section 2.3)

iii) There is no damage to the
heart or other organs (Section 2.)

iv) Various other concerns
expressed in the previous reports on VLCDs (consequences of rate of weight loss,
additional difficulty in weight maintenance and weight cycling) are no greater
than with LCD (Section 2.5 & 2.6)

v) The results with VLCD are as good,
if not better than with the use of other methods of dieting (Section 2.6) In a
group study in which there is good compliance, the rate of weight loss depends
upon the energy level of the diet (Section 2.6).

vi) The only way to achieve
long-term weight maintenance is by a fundamental change in lifestyle. However
the results achieved by such change after weight reduction by VLCD are at least
as good as with those other non-invasive methods (Section 2.7)

vii) Cholelithiasis is not a specific
disorder of VLCD use and different formulations affect the incidence (Section
2.7). There is a requirement for essential fatty acids. If the essential fatty
acids are derived from normal fat (which would require above 7g per day normal
fats) this also provides sufficient fat to avoid cholelithiasis

Modern, nutritionally complete VLCDs are
not only more effective than all other non-invasive methods of weight reduction
but are at least as safe

Section III Many recent studies have been
undertaken which have established a clear understanding of the properties of

1)A thorough examination of body
composition estimation has indicated that there is substantial lack of
reliability and reproducibility in most of the methods that have been used for
weight loss studies. With the exception of neutron activation, which is
expensive and not widely available, all the methods are indirect estimates. This
implies that the estimate is influenced by variation in formulae which are used
for converting the observation to the estimate (Section 3.1).

ii) Apart from technical errors in
the estimation, attention is directed to physiological variations that can
profoundly alter the results. Considerable attention to detail in the study is
necessary (Section 3.1.5)

iii) In consequence it is
inappropriate to compare in the same chart, data derived by different techniques
(Section 3.2.1).

iv) The most widely used reasonably
reliable indirect technique is hydrodensitometry and unless otherwise stated we
have concentrated on data derived by this technique.(Section 3.1.5)

v) Unrecognised analytical variation may
explain the conclusions of Forbes on compositional changes during weight loss
(Section 3.2.1)

vi)..The Keys (1950) Minnesota study has
been quoted as confirming that fat free mass (FFM) loss is greater in
individuals with less fat, who diet by any means. Re-examination of the data
indicates that while this may be true in those at BMI levels less than 20, at
these levels dieting is in any case un-necessary and contraindicated. It is
irrelevant down to the least level (about BMI 25) at which dieting is justified.
(Section 3.3)

vii) The loss of lean body mass
(protein) is inherent to any weight loss, regardless of energy intake, because
weight gained is not 100% fat. There is no proportionately greater lean body
mass loss with VLCD providing over 40g high quality protein per day than with
LCD (Section 3.4 & 3.5)

viii) Re-examination of the old data and
further new observations support the view peoposed by Garrow and others in the
1970s, that at all pre-dieting BMI levels between about 60 and 25, FFM
represents about 25% of the weight loss (range about 20-30% probably depending
on genetic factors). This is true for any energy value diets containing
appropriate macronutrient levels (Section 3.5)

Attention is directed to the
fact that as loss of lean body mass is inherent in any weight loss, there is an
obligatory nitrogen loss during weight loss. Hence excess nitrogen loss is only
relevant if it is greater than the obligatory loss. At daily intake levels of
40-50g protein in the diet, loss in excess of that which is obligatory is
unusual. (Section 3.7)

There is no clinical or
valid experimental evidence which indicates that carbohydrate levels above those
currently available and widely studied, i.e. about 40-45g per day (about 90% of
the available clinical data) have any merits.(Section 3.8)


From examination of the extensive
scientific work available (Appendices II & III), and consideration of the
various national and international regulations and codes of practice, the
compositional conclusions currently in force for VLCD


Range of minima between 40-50g with a
minimum nutritional quality as defined by WHO/FAO (FAO, 1991)


Either no recommendation; or in some
regulations a range of minima for available carbohydrate between


A minimum of 7g neutral fat per day which
would provide not less than 3g linoleic acid and 0.5g linolenic acid with a
linoleic/linolenic acid ratio between 5 and 15


This has been the subject of separate
consideration and these internationally agreed levels should be


The fibre recommendation should allow for
soluble fibres to be used. The minimum should be 10g per day. The available
carbohydrate component of this should be included in the carbohydrate


is a range of minima between 400-450kcal. The energy value per se has no direct relevance and the
minimum should be established based upon the energy provided by the defined
minimum for the macronutrient recommendations.

Having re-examined the clinical and experimental evidence which we have
submitted to the Working Group, we see no scientific reason for changing any of
the above views about the compositional standards which we submitted in March

IV There is substantial medical and
scientific justification for modern nutrient complete formula diets with an
energy value less than 800kcals per day :

i) It is
widely accepted by scientists that formula diets are more effective than normal
food based diets for compliance in weight reduction (Section 4)

ii) There is no perfect single
weight reducing method and a variety of safe diets is desirable to suit
differing desires and prejudices. VLCD can have a significant effect on
motivation and compliance in some people. (Section 4)

iii) There is recent convincing
evidence that the rapidity of weight loss confers additional positive health
benefits independent of the weight loss in, for example, non-insulin dependent
diabetes mellitus and hypertension (Section 4)

Modern nutrient-complete formula VLCD
have an important place in weight reduction

V The precautions for VLCD use
should be those which apply to any method for losing weight

i). The report endorses physiological
and medical contraindications and precautions that have already been extensively
published, but emphasises that these apply to all forms of effective weight
reduction and not just to VLCD (Section 4.1).

ii).As with any weight loss diet, medical
supervision is only necessary if there are medical complications (Section

iii).Those with defined medical conditions,
those dieting for prolonged periods and those receiving prescription drugs
should seek medical advice and/or supervision – following the same advice as
those using LCD.

iv) .Continuous use of VLCD to the desired
weight is preferable to intermittent dieting for both physiological and
psychological reasons, and has no disadvantages (Section 4.3)

This report

The need for any product claiming weight
loss to demonstrate safety and efficacy.

Minimum compositional standards for all
diets, including those in official reports, and in the media.

Advice that those dieting for more than
three weeks by any method should seek medical advice.


prevalence of excess weight

The increase in the incidence of obesity
is so great in most developed countries that it can be regarded as a pandemic.
Over the past decade obesity has almost doubled in many countries and the
average adult is currently adding an estimated one gram per day to its weight.
Since overweight (BM1 25 – 30) and obesity (BMI >30) are factors in both
mortality and morbidity, there is a real need not only to prevent any further
increase in the problem but also to reduce the weight of those who are already

There is no dispute that the ideal
approach to weight problems is to avoid them by a judicious change in the
lifestyle of the population. This involves an increase in physical activity and
a reduction in food intake, particularly foods high in fats. Such social change
has so far proved impossible to achieve. However, even if it can be achieved in
future, it will still be necessary to reduce the weight of the substantial
proportion of the population which is currently overweight or obese.

1.2 Excess weight
and morbidity

Numerous studies have shown that women
are far more likely than men to become overweight and that there is a higher
incidence of obesity in the lower social classes (both men and women) in most
industrially developed countries. Since the early 1980s there has been a
considerable increase in the prevalence of overweight and obesity in most
western countries. Thus, for example, Gregory et al. (1990); White et al. (1993)
and Cox (1993) all demonstrated that in the United Kingdom, the proportion of
those who were overweight rose by some 50% for women and 30% for men over the
decade of the 1980s. One of the recent British surveys (Central Statistical
Office, 1996), showed that the average weight for both men and women had risen
still further, such that the average BMI for each sex now lies in the overweight
range (average BMI men 26.0; women 25.8). Over the 15 year period from 1980 to
1995 the prevalence of obesity almost doubled (from 8% to 15% – Wilding, 1997).
At present, in the UK, 62% of adult women are either overweight or obese. And
the proportion is forecast to further increase (estimate 25% women and 20% men
obese early in the next millennium).

Nor is this confined to the UK. Recent
studies (e.g. Seidell, 1991; WHO, 1997) have found similar increases in many
countries. Thus in Europe some 15-20% of the middle-aged are obese (more in
Eastern Europe, less in Scandinavia).

1.3 Weight
increase and mortality

Excess weight is associated with a high
level of morbidity, embracing a wide range of disorders which both produce ill
health in the community and are a great burden on national health costs. These
include cardiovascular problems, diabetes, liver disorders and gall bladder
disease, some cancers, excess risk during surgery and a higher incidence of
accidents (Table 1.1). Added to this, increased weight increases the morbidity
in various chronic disorders (such as arthritis) and produces several serious
social and psychological problems.

Table 1.1 The increase in morbidity and mortality
associated with obesity (>30% overweight) in various medical










heart disease





wound infection


Based on Anderson T (1990). The range of
figures takes account of age

and gender and expresses the risk as a
percentage of that of normal-weight

people with these

It has been traditional to regard a BMI
between 25 and about 30 as a mild and largely cosmetic problem of negligible
health concern. This has been highlighted by the use of two different terms –
“overweight” and “morbid obesity” for
different excess weight ranges, though where the dividing line is placed differs
from one authority to another. The studies quoted above demonstrate that there
is a continuum of deteriorating health from about BMI 24. It must be concluded
that the arbitrary division into a morbid condition of obesity and a benign
condition of overweight is not only scientifically unjustified, but is a
dis-incentive to drawing attention to the need to consider any excess weight as
requiring action.

Thus all the information supports the
view that all effective and safe weight control methods should be readily
available for all those who are overweight

increase and mortality

Over several years there have been many
studies which have examined the relationship between either the body mass index
or other indications of obesity and mortality. Among recent studies are those of
Garrow (1992), Pi-Sunyer (1993), Andres et al. (1993) and Manson et al. (1995).
Each has shown that as the weight increases so does the mortality. Garrow (1992)
has expressed it very vividly –“for example, a woman of height 1,58m would be in
the desirable range of weight for her height if she weighed 63kg. If she weighs
100kg [BMI 40] … the mortality ratio is about 250% of that at [her desired
weight]…so this degree of obesity is a greater threat to health than smoking 20
cigarettes a day.” (Figure 1)

However, while the relationship between
major weight increase and mortality is clear, the picture is a complicated one
if looked at in detail, because obesity is also associated with other disorders
which give rise to a reduced life expectancy. Other factors can also change
these related disorders and in consequence the relationship to weight is not
linear throughout the whole obese group. However, “the overall increase in
mortality is approximately 15% for every 10% that the person is above the normal
weight” (Marks, 1997). Reduction in weight produces a significant reduction in
the mortality risk. There is therefore every justification for those who are
overweight to attempt to reduce towards the normal level.

Figure 1.1
The relative risk of premature death compares with the level of
obesity/overweight (BMI). Based on Garrow (1981)

The relationship of weight and mortality
is also strongly correlated with the distribution of fat. Obesity with the main
increase of fat around the waist carries the highest risk, both for all cause
mortality and for that associated with cardiovascular diseases. Recent studies
(Cox & Whichelow, 1996; Ashwell et al., 1996) suggests that the ratio of
waist circumference/height is a very good predictor of mortality and that this
ratio is also a good predictor of reduction in risk when the weight is reduced.
There is evidence that it is more reliable than the BMI in this

Recent studies (Iribarren et al.,1995;
Byers, 1995; Manson et al., 1995) have demonstrated that overweight per se (i.e.
any increase in weight beyond the normal) carries an increased risk and that it
is greater when the overweight is associated with other disorders.

Several of these studies have produced a
clear picture of an increase of serious and life shortening diseases from a BMI
of about 22 upwards. Typical charts for cardiovascular disease and cancer from
the paper by Manson et al. (1995) are shown in Figures 1.2a and 1.2b. A study in
a Finnish population (Rissanen, 1990) showed a highly significant (p =
<0.0001) linear rise in the weight range BMI 20 – 32.5 for coronary heart
disease and musculo-skeletal diseases, while in the United Kingdom Shaper et al.
(1997) reported that the risk of cardiovascular disease associated deaths, heart
attacks and diabetes all increased progressively from a BMI index of <20,
even after age, smoking, social class, alcohol consumption and physical activity
had all been adjusted for. Similar results have been reported by Manson et al.
(1987); Linsted et al. (1991); Lee et al. (1993) inter alia.

Indeed it is now apparent that the ideal
weight from the point of view of low mortality is about BMI 20 to 21. This
implies that it is not enough to concentrate on the treatment of the obese, but
that the management of those who are overweight, particularly when young, also
require attention quite apart from the fact that there is a steady progression
from overweight in youth to obesity in middle age

Figure 1.2 a) and b) Relative risk of death from
cardiovascular disease (a) and cancer (b) according to Body Mass Index amongst
women who never smoked (from Manson et
all, 1995)

Chi for trend =



Chi for trend =



1.5The economic cost of obesity

Although studies in Northern Europe,
particularly Finland (Rissanen et al., 1990) had identified that there were
major direct economic costs associated with obesity, the first of the papers
which attempted to quantify the costs, emanated from the United States (Colditz,
1992). He considered the direct and indirect health costs involved based upon
1986 cost levels. He reached a figure of some $39.3 billion representing some
5.5% of the total health care costs in the United States (Table 1.2). His
figures only represented health care costs. The true economic costs would add
considerable sums to the overall cost to the community.

Table 1.2Estimated costs of five major disorders
associated with obesity

Total $ 39.3 billion

diabetes mellitus










USA figures – 1986 (Colditz et al,

Subsequently, these economic costs have
been studied in Europe, the United States, Australia and New Zealand (Wolf &
Colditz, 1994; Segal et al., 1994; Seidell,1995; Levy et al., 1995; Seidell,
1997). The direct costs, i.e. those costs which are related to the diagnosis and
treatment of both obesity and diseases related to obesity amount to between 1 –
5% of the total national health expenditure in these countries. Seidell (1997)
specifically draws attention to the fact that these only represent the costs of
true obesity and to these should really be added those attributable to
overweight, which with the greater number of patients likely to be involved
would probably amount to at least the same level as those for obesity. To these
must be added indirect costs to society (sick pay, pensions etc); loss of
productivity from sick leave and early mortality; personal costs which arise
from higher insurance premiums, job discrimination, adaptations to cope with
disability etc. Thus the total costs, which have not yet been quantified, are
very large – placing a major strain on the economy of even the most industrially
developed country. These costs are likely to rise even more if safe and
effective diets are not made readily available.


2.1 The Prime

The literature on the management of
obesity in general and the use of VLCD in particular abounds in ex cathedra
statements unsupported by scientific data. To compound the misinformation
available in the literature, these ex-cathedra statements are then further
quoted as though they represented prime data, not only in other papers and
reviews, but also in national and international expert committee

The best way to
break this vicious circle is to examine and report the actual findings in true
prime data publications i.e. those that define the actual individual studies
with enough information to assess their significance. An attempt has been made
to identify and list for this discussion paper as much prime data as possible
for nutritionally complete formula diets with an energy value below 800

This policy of
stressing the prime data also accords with the summary of the SCOOP 76.3 task
“Collection of data on products intended for use in very low calorie diets (EU
document C(2000)498)

It is accepted
that there are accidental “sins of omission and commission” within this
discussion paper, particularly caused by changes in formulations over the years,
but it is submitted that these do not significantly affect the

The data

Published monitored studies

Special closely monitored studies in over
50,000 people who have received many different formulae all giving a daily
intake under 800 kcals. A substantial proportion of these represent
administration for prolonged periods and/or laboratory investigations and
electrocardiographic monitoring. A summary of this data is given in Table

Table 2.1. Summary of the available published data on diets
under 800kcals








Date of publ

Up to


















Energy cont


Up to 450





Over 450







Up to












Up to





45 to











Under 4





4 wks or





NB. The figures in Table 1 do not always total
because some papers either do not contain full information or the information
indicates that a range of intakes used covers more than one category. Several
papers have been omitted either because the full paper could not be examined or
inadequate information is given on the content of the diet which was used. This
is particularly true of several recent papers which just use the designation
‘very-low-calorie diet’, without describing even the calorie content. There are
now several papers using a formula diet which provides 800kcal per day- So far
as possible these have also been omitted This has not been easy, because the
trade name of the diet is similar to that of an earlier version of lower energy
value and some papers do not clarify which formula has been used

A full listing of these studies is given
as Appendix I A full bibliography of them is given as Appendix II. This
bibliography also gives a list of additional papers examined over the period
1987 to 2000 during the preparation of the various versions of reports and
discussion papers on VLCD that have been prepared for different

Experience in general (mainly free sale) use

In addition to these published studies,
there has been extensive free sale use of modern very low calorie diets of
different formulations in many countries over a number of years.

This “free sale, predominantly not
medically supervised” use now covers substantially over 25 million people world
wide. It is submitted that the topic of dieting is so newsworthy in the general
media, that though this does not represent hard data on safety, such a level of
use with virtually no reported morbidity provides valid evidence that free sale
is entirely appropriate given adequate

Despite extensive enquiry
concerning the regular media as well as the scientific literature, we have not
been able to find one single death which can validly be attributed to the use of
VLCD within this medically compromised group in the past 22 years, despite
extensive studies and free sale use by many millions of the population.

This can be contrasted with the extensive
literature which accumulated rapidly and dramatically in the late 1970s and
early 1980s during the brief period when “liquid protein diets” (which bear no
relationship to current nutrient complete diets) were available. Although these
tragic deaths associated with the use of liquid protein diets covered a period
of only about 12 months in 1977, with no further problems after they were
withdrawn from the market, they remain to this day a ‘spectre at the feast’. On
several occasions matters relating to them have been raised by the Working Group
and it is clearly important to put this spectre to rest.

2.2 Putting the
spectre of liquid protein diets to rest.

Doubt has been cast from time to time on
whether the daths in 1977 were indeed solely attributable to the use of liquid
protein diets or whether some of these subjects had been provided with slimming
diets of higher nutritional status. Accordingly at the request of the Working
Group, an examination was made of all the available evidence relating to these
liquid protein deaths in 1977 (Isner et al, 1979; the full report (dated 1979)
of the bureau of Foods, Food and Drug Administration committee meetings
(Contract FDA 223-75-2090), records of evidence submitted to the committee by
the Center for Disease Control, 1979; Food and Drug Administration, 1977,
Schucker & Gunn 1978, Sours et al, 1981; Federal Register, 1980; Federal
Register, 1982; van Itallie, 1984) Additional to this we have examined the three
papers which describe some of the original papers (Michiel et al, 1978; Singh et
al, 1978; Brown et al, 1978): the papers which describe other deaths during
therapeutic starvation for obesity (Cubberly et al, 1965; Kahan 1968; Spencer,
1968; Garnett, 1969) as well as the pioneer studies on PSMF in which there were
no recorded deaths. We have also examined the various AACE Positions
Statements on Obesity up to the 1998 revision in which, from time to time
comments appear on this problem. From this wealth of data and conjecture the
following information emerges:

Survival time was
related to the BMI.

Despite the fact that
there were over 200 commercial LPD in use in the 1976/1977 period in the USA
which were used by a very substantial number of dieters in the BMI range 25-30
there were no deaths in this group.

All the deaths occurred
in those over BMI 30.

There were more than 50
deaths attributed to LPD but only 17 of these were investigated. It is
acknowledged that the other deaths may have had a different pathology – the
situation of these is unknown.

Among the investigated
deaths the survival time is directly related to the BMI in the above 30

The fact that those in
the 25-30 BMI range did not die is probably due to the relatively short use in
those at the lower weight, but it can not be held that “fat is

In the above BMI 30
group it must be remembered that the total body protein before dieting was also
substantially above the normal. If one of the problems with the LPD was a
shortage of one or more essential amino acids, it follows that those with the
highest protein (hence amino acid) reserves would survive longest.

It is not true that
‘high quality VLCD’ were being used as a significant protein source.

No modern type VLCD
were available commercially in the USA until 1980.

Some PSMF type
non-commercial formulae of variable content were under study but the studies
which used these higher quality protein did not lead to any deaths, though it is
clear that the number of patients studies for over 2 months was so few that
deaths would not have been predicted on the basis of the estimate of the risk of
mortality from LPD (estimate some 1/700).

The dietary information
within the quoted LPD reports was, by its nature all hearsay from relatives and
friends and virtually none of it could be verified by independent

There are several
references to the fact that “most consumed daily calorie intakes provided by 85
to 200ml… of hydrolysed collagen or gelatin estimated to supply approximately
300Kcal”. One of the original papers indicated that one patient took just 15ml
per day over the whole period.

The amino acid analyses
indicate that many of the tested products were virtually free of many of the
essential amino acids.

Three women “added high
quality protein to their” liquid protein diet. The amount is never stated but
examination of their rate of weight loss compared with the remaining patients
showed that the increase in calories must have been small. The conclusion of the
USA committee was that the exact cause could not be determined (inadequate
essential amino acids; ? electrolyte disturbances), that some supplementation
with casein may have undertaken by a few people, but this does not amount to
“use of high quality VLCD”.

There was only one man involved. The level of his use of the protein source (not a VLCD) other than LPD
is far from clear. One report suggests that he merely supplemented – “all had
used a LPMF diet as their sole source of calories for some months”, another says
“he used a protein product that was reportedly of high quality”. It is of
interest that this is the only autopsy that records “possible early

Starvation had
previously been shown to produce deaths of the type seen with LPD.

Deaths were not only
the result of self-medication without medical control

No less than 12 of the
17 patients whose deaths were examined were being treated by medical
practitioners. It is frequently suggested – inaccurately that all were

A substantial
proportion were alleged to have had regular electrocardiograms while they were
receiving the LPD.

The deaths could not be
attributed to protein losses in the heart being greater than those in other
organs due to a more rapid protein turnover in that organ

The “weight of the
hearts….was decreased in proportion to the documented decrease in body

There was no evidence
of increased loss of heart muscle protein as a result of the different heart
muscle turnover rate.

Removing liquid protein
diets from the USA market solved the problem

From the 1980 FDA
report and a further FDA report in 1982 it is clear that there were NO further
deaths attributable to weight reduction once the liquid protein diets were no
longer used despite the substantial free sale of a substantial number of
properly formulated VLCD most at that stage with an energy content in the range
300 to 400 kcal per day.

2.3 Clinical audits of
safety of VLCD

2.3.1 Specific audits

from time to time it is suggested in official reports that “there has been a
lack of vigilance in gathering such information”. There is no evidence
whatsoever to support this contention. Indeed quite apart from vigilance by the
various companies monitoring adverse reactions reported in the medical and lay
media, there have been several extensive audits undertaken during use in the
community under health professional care. These include:

An audit of 500 obese women
sequentially joining a modular (12 week) obesity management programme
(formulation: protein 43g; carbohydrate 38/45g) in the United Kingdom, of whom
85% completed 1 month and 50% completed 3 months or more. No serious untoward
events have been encountered during the ten years that the programme has been

Also in the United Kingdom,
a GP-based programme has been active since 1990. The data on the first four
years has been mislaid but it did not contain any significant adverse reactions.
Since 1993, some 31,000 patients have been treated and monitored by their own
practitioners following this programme (formulation for women: protein 43 g;
carbohydrate 38/45g: formulation for men: protein 57g; carbohydrate 33/60g). The
average duration of treatment was 16 weeks and the vast majority have been
followed for at least one year post diet. Many of the practices have submitted
audit results from these clinics to their respective health authorities. Twenty
five such audits were assembled in a paper presented at the Medical Research
Society in the UK and at the European Obesity meeting in Barcelona (Beeson
1994). Full medical records show that there have been no serious adverse effects
over the whole 10 years.

While these
audits cover the generality of the adverse effects during the use of VLCD there
is a possibility that they only represent studies in which the starting BMI was
well above the 30 level. Moreover it might represent those who did not reach the
lower level, which it has been suggested is particularly susceptible to adverse

As a result it
was decided to examine those papers in more detail in which it had been shown
that there was a significant component of subjects in which the starting BMI was
below 30.

2.3.2 Investigations of reputed deaths with nutrient complete

Two papers by Wadden (JAMA:
January & June 1990) have been quoted frequently as information relating to
safety aspects of the use of VLCD, particularly at BMI levels between 25 and 30.
The following comments are relevant:

In the USA in the early
1980s a rumour, based upon an FDA Talk Paper, circulated that some six deaths
might have occurred using the Cambridge Plan International Diet. Emil
Corwin for the U.S. Food and Drug Administration on February 21st
1996 issued the following statement “no deaths have ever been attributed
to the use of the Cambridge Plan International Diet”… “during the last five
years, as many as 7 million persons have used Cambridge’s programs and products”
(Newsday, February 22 1986, page 2)

In 1989, Connolly, a general
practitioner in Ireland reported a sudden death which he alleged was the result
of the use of a VLCD. The heart muscle was examined by a British Home
Office pathologist who reported that there was no evidence of the pathology
associated with “liquid protein diets” and that there was no evidence that this
was a death that should be attributed to the use of VLCD

In 1993 Muller &
Grossklaus reported “Autopsy studies performed on 16 persons whose death was
considered to be related to the use of VLEDs showed that the weight of heart
decreased in proportion to the decrease in body weight” This report was taken to
represent recent deaths in Germany. In fact the reference he gives
is to Isner et al (1979) and this refers to the “liquid protein

In various places in the
Wadden articles there is a statement about reduced safety at lower BMI levels.
The references are always the same – i.e. the work of Forbes and the repetition
of the Forbes views by others. I can not find any other evidence for the statements about
safety. The accuracy of the Forbes work is examined elsewhere in this discussion
paper (Section III)

In this respect, we would
draw attention to the recent paper by Professor Sir Colin Berry entitled
“Bellmanism: the distortion of reason” (Berry, 2000). The views expressed here
are very apposite and particularly on the “imperfect understanding and use of
science, in particular in the evaluation of data. Studies which have been
discredited are cited repeatedly… in relation to the precautionary

2.3.3 Audits of subjects with BMI under 30

In some of the papers it is possible to
establish what proportion of the data represented experience at a BMI
under 30.

In order to make the necessary
calculations it would be necessary to have adequate information to determine
that not only is there good compliance on average within the cohort, but that
the compliance is equally good across the weight range.

It is abundantly clear from the text in
many of the clinical papers that a proportion of those studied have lost such
substantial amounts (or proportions of their starting weight) that they have not
only moved into the BMI <30 range (if they were not there at the start), but
have achieved the normal BMI range. This is obvious if it is appreciated that
the compliant VLCD dieter, loses on average between 1 and 2kg/week. For a woman
of average current height, one BMI unit is equivalent to some 2.64kg. The
published clinical papers indicate that on average over 80% of the dieters are
women. For the men one BMI unit weight equivalent is more but the rate of weight
loss is greater.

Thus with the average weight loss per
week with the majority of the current commercial VLCD, there is a BMI change at
the rate of between about one BMI unit each 2 weeks. For those who start at BMI
30, a BMI about 25 (i.e. down to the normal weight level) will be achieved in
about 8-10 weeks, at least three-quarters of which will be below BMI 30. At
start BMI 35 the average time to normality will be about 18 weeks, with about
half that period below BMI 30.

There are 3 papers which provide
enough information tobe able to calculate, with reasonable accuracy, the proportion of the VLCD
dieting period which represents a BMI level below 30. The basis of the
calculation is such that even for these three studies it is clear that it does
not represent hard data. Nevertheless much of the data cross checks and is
sufficiently representative to be useful, bearing in mind that there are no
serious side effects in the whole series. The information covers several
previously published smaller cohorts, but the three papers concerned are those
of Kirschner et al (1988); Kanders et al (1989) and Bode (1999).

These cover observations using VLCD at
300, 420 and 770kcal per day, though it is not possible to establish with
certainty the exact proportion at each intake because the formulation changed
over time. One merit of all these studies is that they represent data for
observations of at least 12 weeks VLCD dieting a long enough period for any
major adverse effect to occur.

The information from these studies is
summarised in Table 2.2.

Table 2.2 Data on the three papers from which
information on the safety of VLCD at lower BMI levels can be gauged.



data (BMI)


weeks BMI < 30






BMI lost



et al ’88 – men









– women









et al ’89 – men
















– men




















* excluding those not
completing dieting phase

The important points to note

For those with a BMI above
35, dieting for at least 12 weeks is necessary before the BMI falls below

In a major proportion of the
USA literature, with a very high initial BMI level and a short period of VLCD
use there is relatively little data at BMI levels <30

On the other hand, in
Europe, VLCD have been used at lower starting BMI levels and, in consequence
there is greater evidence of safety in the range 25 to 30.

On the basis of
this evidence a reasonable proportion of the VLCD dieting for these studies was
at BMI < 30. Since these represented experience in a substantial number of
dieters for a period of at least 12 weeks, there is substantial evidence of use
of VLCD in the BMI range (i.e. 25 to 30) for which further information was

Taking each of
these papers (Kirschner et al 1988; Kanders et al 1989; and Bode 1999)in

Kirschner summarises
his experience thus: “Complications of obesity i.e. hypertension, type II
diabetes mellitus and hyperlipidemias were remarkably improved after weight
loss. Complications of the VLCD including cardiac abnormalities, were

The relevant
portion of the paper reads:

Complications. A list of side-effects
and complications is presented in Table 4.

4. Complications observed in patients on supplemented fast.



Foot drop



Late hair

Cardiac arrhythmias

Supraventricular tachycardia


The most common problems noted were early
postural lightheadedness and tiredness, The most common late complaint was that
of mild transient hair loss, occurring in approximately 10 percent of the
population. Other complications included eight cases of acute gout, two cases of
foot drop, (thought to be due to sciatic nerve compression from leg crossing
during or after weight loss), and four cases of acute psychosis occurring in
women and generally thought to be a form of sexual panic.

view of the great concern regarding cardiac arrhythmias in patients on VLCDs we
carefully screened for such occurrences. Over the 8-year period, we documented
only one patient who developed a supraventricular tachycardia clearly related to
hypoglycemia ans corrected with intravenous glucose supplementation. Two
patients required hospitalisation for the development of palpitations associated
with multifocal PVCs. To date, we have had no unexplained deaths in contrast to
the experience with liquid protein diets.

Non-complications. In view of the genuine
concern as to the overall safety of VLCDs there were several important
non-complications to record, including: (1) coronary pypass surgery without
complications in eight patients; (2) major breast surgery without complications
in 12 patients; (3) pregnancies occurring while patients were on VLCD (without
subsequent complications) in six women in whom the diet was subsequently

To put this paper in context it should be
appreciated that this represented something in excess of 40,000 weeks dieting
experience in 4026 patients at 420kcal/day with some 10% in the BMI range
<30. The quoted paragraphs followed several that detailed the beneficial
effects of VLCD on medical problems in this same patient cohort.

The equivalent paper by
Kanders et al (1989) gives a substantial amount of information about beneficial
effects. The phrasing of the report suggests that side effects were not a
problem but there is no specific reference to side effects throughout the whole
paper. It is abundantly clear from the nature of the paper, that, had side
effects been a problem, they would have been recorded.

The same situation is true
of the report by Bode (1999). He describes reasons for the subjects stopping the
use of the VLCD but these are primarily social. There are no significant medical

We have also obtained access
to the detailed information relating to Lipotrim
Ò a monitored VLCD programme (Kreitzman
& Beeson, 1996). This provides an indication of the VLCD dieting pattern in
the practical commercial area and moreover gives some indication of the post
diet period, though not over a prolonged period.

This study by Kreitzman & Beeson
(1996) was undertaken with trained independent medical observers. Again, no VLCD
related adversa effects were reported.

An audit of 746 case records was made.
This covers an overall period of total food replacement (TFR) by VLCD of 13,446
weeks; a total weight loss in the group of 15,657Kg representing an
average weight loss for each dieter of 20.99kg at an average of 1.2kg per

Of the 746 dieters 140 started below BMI
30. The average BMI before dieting was 28.54 and that at the end of the TFR
period 24.06 (12.16kg) achieved on average in 78.84 days (11.2 weeks) at an
average of 1.08kg per week. All these spent their whole TFR at BMI <30
representing 1,568 weeks TRF. As a matter of interest the average follow up for
this group after re-feeding was 35 weeks and at that stage 79% had maintained
all their lost weight with the average regain under 0.9BMI unit.

The remaining 606 dieters started at
average BMI 34.6. They lost 23.03kg weight on average at an average of
1.18kg/week (total weight loss in this group 13,955kg). Their average number of
days on TFR was 137.10 days (19.6 weeks), achieving an average BMI at the end of
the TFR period of 26.08. Their total TFR period was 11,878 weeks of which 5,465
was under BMI 30.

This means that in this whole group, out
of 13,446 weeks VLCD use, no less than 7,033 weeks (something over 50%)
represented experience at BMI <30. In no dieter at any stage was there any
serious or worrying side effect.

2.3.4 Audits on the
prime data

It was also considered important to
examine the prime data in more detail to determine whether the information
provided covered the broad range of the energy and carbohydrate levels (rather
than just high carbohydrate levels providing energy levels close to

The results of this further analysis are
shown in Tables 2.3 a and b

Table 2.3 A further split of the original data into
Table a) <400kcal, 400-600kcal, 600-800kcal and b) carbohydrate levels
30-40g, 40-45g, 45-50g and >50g..

Kilocalorie content

Number of Studies

Number of subjects
















Carbohydrate content

Number of studies

Number of subjects





















It should be
noted that these figures differ slightly from those in Table 1 – some categories
were not represented and for some a more detailed analysis was not

the further analysis demonstrates not only that a major proportion of the data
was derived from VLCD with an energy value less than 600kcals, but that over 90%
of the subjects were receiving a daily carbohydrate level below 50g.

2.4 Special tests for


Several of the published clinical studies
have investigated laboratory parameters of organ change (eg cardiac,
haemopoietic, hepatic, renal) on a regular basis. Many more have
undertaken spot laboratory checks. These have demonstrated evidence of
improved health due to the weight loss but no adverse effects from the use of
these diets.

Electrocardiographic evidence of cardiac integrity

It was suggested in some of the earlier
reports that even if there appeared to be no overall excessive loss of protein
during the use of VLCD, there might be specific extra and dangerous protein loss
from the heart or other vital organs. However, as mentioned previously, clinical
observations and laboratory investigations over a period in excess of 20 years,
on more than 50,000 subjects using a very wide range of products of different
composition with an energy content under 800kcal, have not demonstrated that any
such problem exists. Nor is there any theoretical reason why damage to specific
organs should occur.

Specifically there is extensive
electrocardiographic evidence of cardiac integrity.

Obesity itself can produce cardiac
changes (Hinkle et al 1969; Eisenstein et al, 1982; Frank et al, 1986; Carella
et al 1996; Quaade et al 1996),). Indeed it has been calculated that an
obese cohort subjected to surgery has 40 times the risk of sudden death compared
to a normal weight cohort (Drenick & Fisler, 1988). Because the use of
the seriously nutritionally deficient liquid protein diets in the early 1970s
(which bear no relationship to the
modern VLCD) led to fatal cardiomyopathies (FDA 1979; Sours et al 1981; Isner
Sours et al 1981; Van Itallie et al 1984, random electrocardiographic recordings
and regular Holter monitoring have been an important feature of studies on the
modern very low energy diets in order to confirm that they do not have similar
adverse effects.

The 12 formal studies (summarised in
Table 2.4) all confirm that well formulated very low calorie

Table 2.4 Studies which examined the
electrocardiograph by Holter monitoring at intervals during the use of




Fisler et al



Amatruda et al



Phinney et al



Ms Lean Baird



Drenick et al



Lockwood et al



Amatruda et al



Kirscher et al


Various details of
monitoring unclear

Weigle et al


95 days

Moyer et al






Doherry et al



diets produce no evidence of adverse
effects on cardiac function. Additionally Linet (1983) ans Singer (1981) found
no abnormality in food based diets (with added vitamins and minerals) at energy
levels below 600Kcals/day.

Indeed calculations demonstrate that the
incidence of sudden death in those being treated with VLCD well below the level
which would be predicted from their age and weight

Examination of
the “liquid protein diet” data on the 17 deaths that were studied (FDA 1979;
Sours et al 1981; Van Itallie et aI 1984) show that the shortest period to any
cardiac abnormality was several weeks. As Meuller and GrosskIaus wrote ( 1993)

“Electrocardiographic changes do not
become evident before 4-6 weeks of hypocaloric dieting” and “In subjects on
VLEDs electrocardiograms are usually negative up to 4-6 weeks” and “a well
supplemented VLED has fewer adverse effects on the electrical activity ofthe
heart” (In fact examination of the original data suggests that the figure is
more like 8 weeks than 4-6 weeks)

Hence the 12 ECG
studies quoted here are not as valuable as they would appear at first sight
because most cover the period before electrocardiographic changes wouId be
expected. It must however be stressed that since 1978 there is no confirmed
evidence of electrocardiographic changes at any stage.

This raises the whole question of the
suggestion made by some authorities that regular routine electrocardiographic
examination should be undertaken (even as frequently as weekly) on all those
using VLCD. This suggestion has no validity-.-.

The data indicates that the
only reliable method for determining changes is by Holter continuous monitoring
which is clearly impracticable. Thus in a study by Lantigua et al (1980) 3 out
of the 6 subjects deliberately subjected to a hydrolysed collagen diet with
added tryptophan showed cardiac conduction abnormalities, of which none were
detected by 12-1ead ECG, only by continuous Holter monitoring.

In six of the 17 who died in
the liquid protein tragedy, normal ECGs had been found while they were taking
the liquid protein diet.

There is no agreement about
the predictive relevance of any electrocardiographic features that might be

One recent
widely publicised study (Greenway et al 1994) purports to demonstrate changes
(particularly in the Q-T segment) related to the energy rather than the protein
content but the changes reported are those seen commonly in untreated obese
people and have no significance relative to the safety of VLCD (Quaade, 1996).
Moreover Hinkle et al ( 1969) pointed out that ” disturbance of heart rhythm and
conduction occur in apparently healthy people with high frequency” while in the
study by Carella et al ( 1996) between 41% and 53% (depending upon the method of
determination) of obese people showed a prolongation of the Q-T interval before
any dietary intervention.

It has also been
postulated that since the protein turnover of myocardial proteins differs from
that in skeletal muscle, this may produce a failure of protein conserving
mechanisms in the heart and greater risks to that organ. Mueller &
Grossklaus (1993) have pointed out that there is no failure of
protein-conserving mechanisms in the heart for ” the weight of the heart
decreased in proportion to the decrease in body weight” and “Myocardial
wasting…is not necessarily associated with reduced functional capacity” and “A
24-week of semi-starvation resulted in a weight loss of 15-20kg…but not
circulatory insufficiency or heart failure” and “These data suggest a normal
myocardial fiber performance in response to semi-starvation”. These views
expressed by Mueller & Grossklaus are in accord with the earlier
observations of Smith (1928) and Amad et al (1965) that the weight loss in the
heart during starvation is proportional to that lost in the rest of the body

The relationship between heart weight and
body weight also applied to those who died in the 1977 liquid protein diet
tragedy (Sours et al 1981, Isner, Sours et al 1981 and Van Itallie et al 1984)
while none of these 17 dieters showed untoward evidence of heart muscle

2.5 Data
on side effects

2.5.1 General side effects

A relatively
small proportion of those taking VLCD experience side effects. The risk of side
effects is greater if the dieter does not follow the directions given on the
diet pack or by any adviser (particularly of strict compliance to the diet and
to drink substantial quantities of water while taking the VLCD). The vast
majority of these side effects are minor and easily corrected. They occur at two
distinct phases – either within the first few days of starting the diet or after
several weeks of VLCD use. The main early side effects are shown in Table

Table 2.5 Early side-effects, possible mechanisms
and appropriate actions

The minor and non-dangerous nature of
these side effects is clear. Perhaps the only one which might require some
further attention is gout, but throughout the whole period during which one of
us (JM) was advising VLCD to dieters during the early trials, He did not
encounter a single episode of gout. We have also discussed this with others with
extensive VLCD experience who confirm that in practice they have never seen a
case of VLCD generated gout.

It is clear that
the major cause of the early side effects is that the advice about the need for
strict diet compliance and a high fluid intake during the use of VLCD have not
being followed.

A list of the main later side effects is
given in Table 2.6 All these side effects may be found with any successful
weight loss process, including surgery. Reassurance is normally all that is

Table 2.6 The main side effects encountered after
prolonged use of VLCD.

2.5.2 Cholelithiasis

For well over 50
years it has been known that there is an increased incidence of cholelithiasis,
particularly cholesterol stones, with obesity (Gross, 1929) and this has been
confirmed by many recent epidemiological studies- These demonstrate that the
incidence of gall bladder disease in the morbidly obese varies from 28% to as
high as 45%, while over 80% show histological abnormalities in the gall bladder
(Williams et aI., 1977; AmaraI & Thompson, 1985; Maclure et al, 1989;
Bennion & Grundy, 1975; Bennion & Grundy, 1978; Tudevant et al, 1973;
Kucio et al, 1988. Everhart, 1993; Sichieri et al, 1991; Thijs et al, 1992; inter alia)

It is also
known that changes in food intake in the normal or obese, by whatever means
(total parenteral nutrition (Roslyn et al. 1983; Messing et al 1983), isocaloric
cholesterol lowering diets, traditional weight reducing diets (Everhart 1993),
jejuno-ileal bypass, gastroplasty (Shiffman et al 1993), VLCD) resuIt in an
increase of cholelithiasis. Moreover other factors, which have no relationship
to weight loss can also cause an increase in gallstone formation in the obese
These include multiple parity (Grodstein et al, 1994, though this is disputed by
Maclure et al 1989), high energy intake (Maclure et al, 1989), cigarette smoking
(Grodstein et al 1994), and current and long-term use of oral contraceptives
(Grodstein et al,1994)- In contra-distinction to these a moderate alcohol intake
as opposed to abstinence is reputed to reduce the gallstone incidence in the
risk population (Maclure et al 1989; Grodstein et al 1994).

Thus there are
many confounding factors which may play a role in any studies of the effects of
diet on the genesis of gallstones. The picture has been further confused by the
fact that many of the recent studies compare modem ultrasound measurements
during VLCD dieting or surgical intervention with previous studies based
entirely on clinical examination incidence. The extent of the difference between
the symptomatic and ultrasonographic incidence is clear from the Shiffman et al,
(1993) study. Following bariatric surgery in 230 patients, he found an incidence
of gaIlstones of 37% by ultrasonography aIthough only 10% showed any

It has been suggested, particularly in
the 1980s and the first half of the 1990s that a rapid loss of weight, such as
that produced by the use of VLCD or following jejuno-ileal bypass and
gastroplasty leads to a higher incidence of gallstones than that which results
from a slower loss of weight (e.g. that which results from a 1200kcal diet). A
careful examination of recent studies of the reputed lithogenic effect of VLCD
shows no clear evidence that this method of weight reduction leads to any
greater incidence of gallstones than other methods which produce the same
overall weight loss (Sturdevant et al, 1973; Mok et al, 1979; Schlierfet al,
1981; Wattchow et al, 1983; Messing et al, 1983; Roslyn et al, 1983; Anderson et
al., 1984; Amaral & Thompson, 1985; Bolondi et al., 1985; Broomfield et al
1988; Jacob et al., 1989; Janowitz et aI., 1989; Liddle et aI., 1989. Yang et
aI, 1990; Marks et al., 1991; Little & Avramovic, 1991; Shiffman,1991; Hoy
et al., 1991; Mazzella et al., 1991; Shiffman et al., 1992; Karnrath et al.,
1992; Heshka et al; 1992; Yang et al, 1992; Dammbach et al, 1993; Everhart,
1993; De Filippo et al., 1993; Festi et al 1993; Spirt et aI 1995; Gebhard et al

Examination of
the literature shows that, with very rare exceptions, claims of increased
incidence of cholelithiasis with rapid weight loss are American. The European
literature is devoid of such reports and conversations with those European
experts who have used VLCD extensively confirm that gallstone formation has not
been a problem. Perhaps even more importantly, in those papers in which the
details of the weight loss programme are recorded, the majority stem from two
commercial weight loss products widely used in the USA but not in

If instead of
just taking the total energy intake, one examines the energy sources involved,
the picture becomes more clear (Table 2.7). Unfortunately no formal study has
been undertaken with the equivalent of the typical European diets (under
600kcals with about 7g fat per day) although there is substantial evidence from
adverse effect incidence in large scale studies in Europe- One of the best
studies is that of Festi et aI, 1998. They compared two VLCD with very similar
energy content but 9glday difference in the fat content. The number of patients
in each group was small, but there was a significant difference (p= <0.01) in
the incidence of new gallstones.

Table 2.7 Relationship of fat intake per day to
percentage of cholelithiasis.

Probably due to
the number of confounding factors, the relationship between the fat intake and
the gallstone incidence is not quite uniform, but there is a very strong
indication that it is the level of fat in the diet rather than the calorie level
per se, which is of prime importance. The mechanism involved would appear to be
the extent of biliary wall motility and regular gall bladder emptying (Kucio et
al, 1988; Marks et al, 1991; Mazzella et al, 1991; Festi et al 1992; Shiffman et
al 1995; Marks et al 1996)-

The available
data, particularly the fact that cholelithiasis is virtually unknown as a
complication with the widespread use of European commercial VLCD, suggests that
a daily intake of about 7g fat is necessary to ensure that gallbladder
contraction is normal. This fits in well with the observation that United States
diet programmes are associated with a higher incidence of gallstones than
European. It also explains why, when one United States commercial formula was
changed, with the addition of extra fat per day, the incidence of reports of
gallstone problems recorded in the American literature almost ceased.

It is clear from
all the evidence that any effective weight reduction leads to an increase in
cholelithiasis during the weight loss. Subsequently the risk is less.
Formulation differences and advice on fluid intake appear to be important.
Whether high protein levels encourage cholelithiasis (by reducing gall bladder
contractions) is not clear. However higher fat levels do discourage gallstones
(by increasing regular gallbladder contractions). As already noted, the
recommended fat level in VLCD (to provide essential fatty acids) of about 7g per
day is advantageous from the point of view of reducing the incidence of

2.5.3 Bone density

During the past few years it has
been suggested that the use of VLCD for weight reduction might lead to calcium
deprivation similar to that reputed to occur during the use of a high fibre
weight reducing diet (Avenell et al, 1994)

In consequence,
several studies have been undertaken to determine the factors causing loss of
bone density in post-menopausal women and whether prolonged use of VLCD (up to
15 weeks of continuous use) would lead to a similar loss of bone mass to that
reputed to be seen with high fibre diets.

For example Van
Loan et al (1998), using dual energy X-ray absorptiometry studied fourteen women
during a 15 week diet period, over which period they lost weight at an average
of 1 kg per week- They found no loss of bone mineraI caIcium in spite of the
marked loss in weight although there was a small loss of bone density. This was
equivalent to the findings of Compston et al ( 1992) during an 8 week study with

From other
recent studies (Pritchard et al, 1996; Brot et al, 1997, Ensrud et al, 1997,
Willing et al, 1997) it is clear that, as could be logically expected, there is
a direct relationship between bone density and body weight. It is largely the
strains on the bones that determines their density. Whether weight is lost
intentionally (by whatever means) or unintentionally, the bone density is
reduced roughly in proportion to the loss of weight..

2.5.4 Data on eating

It has also been suggested that VLCD may
be abused leading to eating disorders such as anorexia and bulimia. There is not
one iota of evidence for this. These disorders are entirely psychological in
origin. By the very nature of these disorders, which are concerned with false
body image, it would be anticipated that there would be an association with
various forms of dieting. However because there is an association, this in no
way implies that dieting is causative.

Even if they were not psychological,
those patients who are involved try to avoid VLCD because they are too energy
dense- They choose less energy dense methods of reducing their weight since the
volume of the alternative low energy dense diets reduces the patient’s hunger
with less energy intake.

2.6 Data
on aspects of use and control in practice

2.6.1 VLCD and the resting metabolic rate reduction during and
after dieting

Several recent
studies (Apfelbaum, 1993. Van Gaal et al., 1992; Coxon et al., 1992;

Kreitzman, Johnson & Ryde,
1992; Rattan et al., 1989) have demonstrated that the initial 15% reduction in
resting metabolic rate is a physiological response to reduced food intake within
the first few days of dieting and is not related directly to the actual energy
intake or to the amount of weight loss. The subsequent long term reduction in
the resting metabolic rate depends on the extent of the weight loss irrespective
of the method and energy levels by which it is achieved (Figure 2.1) (James et
al, 1978; Rattan et al., 1989. Van Gaal et al, 1992; Wadden et al., 1992; Coxon
et al., 1992; Wadden et al., 1990; Kreitzman, Coxon et al., 1992; Kreitzman,
Johnson & Ryde, 1993).

Figure 2.1. The effect of excess body weight on
resting metabolic rate (RMR). Based upon James et al (1978)

It is now clear that the formulae
developed by Schofield et aI. (1985) linking the resting metabolic rate to the
weight are correct and that the views of the Wadden group, heavily quoted in the
1990 SCF Report that the fall in metabolic rate depended upon the rate at which
the weight was lost during dieting were at error

2.6.2 The relationship
between energy deficit and rate of weight loss.

The study by
Kreitzman et al. (1993) demonstrated that the total daily energy expenditure is
not influenced during dieting, whatever the energy intake. The weight loss
showed a high correlation with the total energy expenditure (r = 0.82). In
consequence, in those studies where special attention was directed to ensuring
compliance, the rate of weight loss per week, which depends on the energy
deficit shows good correlation with the energy intake, after the first week of
dieting, during which glycogen and the attendant fluid loss complicate the
picture (Table 2.8)

Table 2.8 Average weight loss per week with
various weight loss procedures

loss procedure

loss/week women




& Summerbell, 1995

diet daily


Heshka et
al, 1996; Wadden, 1993; Topubro & Astrup,

diet daily



300-500kcal diet


et al, 1996 Tyttig & Rossner, 1995 Hoie & Bruesgaard, 1995, Rude
et al, 1993; Wadden, 1993; Toubro & Astrup,

These figures represent averages over at
least an eight week period. Similar conclusions were drawn by Jensen &
Quaade (1996) using somewhat different criteria- It must be noted that, though
the correlation is good for groups of dieters, examination of the individual
weight loss does not always show such a good correlation even when compliance
appears to be good. There are various possible explanations for this (Marks
& Howard,1997).

As would be anticipated from what has
been said about the resting metabolic rate being dependent on the body
mass and not on the rate of its change during dieting, clinical experience and
experimental studies show conclusively that there is no greater difficulty
maintaining the target rate after rapid than after slow weight loss. The
question of weight maintenance is dealt with later.

2.6.3 Weight

Weight cycling
(yo-yo dieting) does not lead to increased fat stores, reduced metabolic rate,
and less effective weight loss with each cycle as was previously suggested. In
several excellent studies (Forbes, 1987; Steen et al., 1988, Prentice et al.,
1992; van Dale & Saris, 1989; Kamrath et al, 1992; Wadden et al., 1992;
Beeson et al., 1989; Bene et al., 1991; Blackburn et al., 1989; Brownell, 1989.
Chen & Cunnane, 1993; Goldberg et al., 1990; Jebb et al., 1991; Kamrath et
al., 1990; Kaplan et al., 1992, van der Kooy et al 1993) it has been shown that
weight cycling does not have an adverse effect on body composition. Hence the
metabolic rate and rate of weight loss of the various cycles are

Earlier studies
in Sweden and the USA (Lissner et al, 1988 a&b; Lissner et al. 1989)
suggested that weight cycling increases coronary disease and hypertension risk,
but this was not confirmed in more recent studies undertaken by the group who
made the original observation (Lissner et al. 1990, 1991; Brownell & Rodin,
1994). It is important to appreciate that Castelli, one of those involved in the
Framingham Heart Study, subsequently affirmed that there is no evidence of any
undesirable physical sequelae from weight cycling. This has been confirmed by
further more recent studies (Willett et al 1995, Wing et al 1995, Itoh et al
1996, Field et al 1999). Nor could Bartlett et al. (1996) find any untoward
psychosocial sequelae.

There had also
been some papers which suggested that weight cycling produced unstable body
weights which in turn lead to a greater mortality risk. More recent studies have
confirmed that there is no relationship between weight cycling and risk of
premature mortality and that the previous observations resulted from a
confounding effect of weight loss due to disease (Williamson 1996, French et al

But even if such an adverse effect exists,
weight cycling is found with all forms of dieting and no causative relationship
between VLCD and the reputed increased risk has been established. Hence it has
no relevance to the current considerations though it has been regarded in the
past as a problem alleged to be related to VLCD.

2.6.4 Continuous versus intermittent use

Some reports state that when a
considerable weight loss is necessary, this should be done in a series of three,
four or six week periods separated by one week or more when the diet is
supplemented by ‘normal’ food of a higher calorie level.

There is no
scientific reason for this procedure, indeed from the point of view of
experience it is highly undesirable and de-motivating. The main effect of the
higher calorie periods is to increase weight by the accumulation of glycogen and
water which serves no useful purpose. Indeed, some studies can be interpreted as
demonstrating that intermittent dieting in this fashion may lead to increased
protein losses. However this is far from proven. Those who accept the appetite
dulling effect of ketosis ( and there are doubts about this effect) stress the
discomfort of the intermittent method. As a result of either or both the weight
increase and/or the effect on appetite, there is a greater risk of an
unsuccessful outcome as a result of people dropping out. Moreover, practical
experience of substantial weight losses by continuous VLCD use over many months
has shown no undesirable effects.

2.7 Long-term

Very low energy diets per se cannot
achieve long-term weight control any more than can any weight loss method. The
only way to achieve long-term weight control is by a fundamental change in
lifestyle (eg regular exercise, smaller meals, lower fat content).

From the
earliest studies of, for example, Stunkard & McLaren-Hume (1959) it has been
clear that, in practice, the vast majority of those who lose weight by whatever
means (reduced food intake, formula diets, exercise, behaviour modification,
drugs etc) are back to about their pre-dieting weight within 1-5 years. In
general terms it appears that bariatric surgery, though it has mortality and
morbidity in excess of medical management may have better long-term results on
weight control. However a recent paper (KIein et aI 2000) stresses that when a
successful cohort of surgical and medical weight losers are compared, the
differences may not be all that great in psychosocial terms.

The obesity
literature now abounds with reports of attempts to effect long-term maintenance
of reduced weight and to define the factors that can predict the chances of
success in the individual (e.g. de Pue et al 1995, Pasman, Saris &
Westerteerp-Plantenga 1999; Karkeila et al, 1999 each looking at different
aspects)- There have been some recent studies of the effect of a lipase
inhibitor (Orlistat e,g, Rossner et al 2000) which appear promising, but there
are so many examples of early enthusiasm and later disappointment in this field,
that it appears wise to exclude these observations for the present. Moreover
there are some unpleasant side effects associated with the use of Orlistat and
this may preclude the long-term use of this preparation.

The current
views on the principles which lead to the best long-term results appear to

It is vital to manage excess
weight as a progressive chronic disorder The longer and more intense is the
support and counselling the better is the result

Long-term support and
counselling by a trained non-professional can be just as or even more effective
than professional care (e.g. Wing & Jeffery, 1999). What matters is
willingness of the advisor to provide long-term adequate firm support with
empathy. Time and patience are essentiaI.

If the reason for the
overeating can be established and alternative strategies established this
appears to help

Reduced fat intake, appetite
reduction (including appetite suppressants e.g Apfelbaum et al 1999) are common
strategies, but perhaps of greater importance is the encouragement of adequate
regular aerobic exercise.

Self-help groups appear to
be of value for some people (Andersen & Grimsmo 1999)

There is no single technique
which works with everybody and tailoring a selection of procedures to the
individual is to be encouraged.

During the 1980s
there was quite a large literature, particularly in the USA and among those who
favoured behaviour modification, suggesting that the use of VLCD reduced the
potential for long-term maintenance and this view was represented strongly in
the 1990 SCF Report. However more recent studies show that the results of
education towards more exercise and smaller more appropriate food intake can be
achieved during and after VLCD use at least as well as with other

Very low caIorie diets have been reported
to be a valuable component of long-term weight reduction and control regimes
(Dietz & Greenberg, 1985; Palgi et al., 1985; Wadden et aI., 1986; Kirschner
et aI., 1988; Sikand et al., 1988; Hovell et al, 1988;

Wadden et al., 1988; Miura et al., 1989.
Cox et aI_, 1989. Wadden et al., 1989; Niemi et al., 1990; Anderson &
Brinkman, 1990. Atkinson, 1990; Donnelly et al., 1991;

Brownell, 1991; Cox et aI_, 1991;
Anderson et al., 1991; Brownell & Wadden, 1991;

Wing et al., 1991; Wadden et al_, 1992;
Anderson et al., 1992; Atkinson et aI., 1992; Blair, 1993 inter alia). Indeed
several studies over the past five years suggest that the long-term results may
be superior when a VLCD is used as one feature of the process which leads to a
lifestyle change (Quaade & Jensen 1995, Wadden & Frey 1997, Andersen et
al 1999, Apfelbaum et al 1999), though this is far from proven. One interesting
feature is that a substantial number of trials in the last few years of the
twentieth century used VLCD as their diet component without referring to it as a
VLCD. This suggests that VLCD are becoming accepted as equivalent in safety to
any formula diet but as more effective. Even more interesting is the fact that
some of the behaviour modification groups who wrote most vehemently against VLCD
in the 1980s are now using and advising VLCD as the diet component of their
overall management.

When the
revision of the original 1998 report to the SCOOP Working Group was first
started, the aim was to try to determine by an analysis of the literature
whether the long-term results using VLCD are at least as good as those with
other energy reduced foods. F or the present this has been abandoned
because the level of variation in the length and intensity of the support and
counselling, the food advice, the form and intensity of the exercise inter alia is so substantial. Added to this
there is considerable variation in the drop-out rate and how the drop-out
information is handled in the analysis presented in the original

However as a
result of a request from the working group we have examined further the question
of a comparison of the long-term results with VLCD compared with the results
that can be achieved in the long-term using other methods and other diets. This
examination confirmed our previous view that it is impossible to find in the
literature valid information on
which a reasonable appraisal can be based that would withstand even minimal
critical analysis.

We would
specifically draw attention to the following table showing a selection of the
various factors identified in the literature as influencing the long term
efficacy viz:

As to:


Pre-treatment data

in different units: kg, kg excess, BMI, %excess,

Mean of
group (?SE), median, range,

definition of normal weight is not given

Educational and work

reason for excess weight


How deal
with dropouts – sometimes not even mentioned

How long;
? goal set; ?what form of diet: ?food, formula, ? calories, ?macronutrient
levels (sometimes data not given)

behaviour modification –if so what and how frequent. ?eating cues,? Rate
of eating,? Record keeping, ?rewards given – if so what and

counselling – if so by whom, frequency, nature length etc

psychiatric appraisal and how followed

? diet
education – if so how much, what etc

medication – if so what. Frequently not stated at all

? how good
is compliance actual loss/week cf expected

? exercise
– if so what type, how often, ? compliance

?any time
in hospital/clinic – if so conditions applied

loss – how expressed

? as %
excess weight change; ? as BMI; ?as median of group, ?as mean of group
(?+SE); ? as kg change

Some times
the weight loss is expressed in different units from the pre-treatment
situation making it impossible to translate one to the

Change to

? sudden;
?gradual change if so details of rate of change;? Specific foods/food
types allowed or restricted;


? goal
setting ? target – if so what and how expressed

behaviour modification maintained – if so what and how

counselling – if so how often, for how long, by whom etc

? seen at
all . ? contacted by telephone – by whom, how, frequency etc

? exercise
– if so ? advised or undertaken with group, what type, how frequently, how
controlled etc

? dietary
advise – if so in form of avoidance, ? strict diet. ? calorie counting,
?”sensible eating pattern” etc

intake allowed as component – if so under what conditions, ? redieting
allowed as necessary during follow up

? regular
weighing – if so what frequency, under control or at home, ? what to do in
event of change

? medicine
– if so what type and how controlled

Spouse/family/lay friends etc
involvement ? group care

Educational and work

probable reason for excess weight been dealt with


How deal
with dropouts – sometimes not even mentioned

How long;
? goal set; ?what form of diet: ?food, formula, ? calories, ?macronutrient
levels (sometimes data not given)

behaviour modification –if so what and how frequent. ?eating cues,? Rate
of eating,? Record keeping, ?rewards given – if so what and

counselling – if so by whom, frequency, nature length etc

psychiatric appraisal and how followed

? diet
education – if so how much, what etc

medication – if so what. Frequently not stated at all

? how good
is compliance actual loss/week cf expected

? exercise
– if so what type, how often, ? compliance

?any time
in hospital/clinic – if so conditions applied

loss – how expressed

? as %
excess weight change; ? as BMI; ?as median of group, ?as mean of group
(?+SE); ? as kg change

Some times
the weight loss is expressed in different units from the pre-treatment
situation making it impossible to translate one to the

Change to

? sudden;
?gradual change if so details of rate of change;? Specific foods/food
types allowed or restricted;


? goal
setting ? target – if so what and how expressed

behaviour modification maintained – if so what and how

counselling – if so how often, for how long, by whom etc

? seen at
all . ? contacted by telephone – by whom, how, frequency etc

? exercise
– if so ? advised or undertaken with group, what type, how frequently, how
controlled etc

? dietary
advise – if so in form of avoidance, ? strict diet. ? calorie counting,
?”sensible eating pattern” etc

intake allowed as component – if so under what conditions, ? redieting
allowed as necessary during follow up

? regular
weighing – if so what frequency, under control or at home, ? what to do in
event of change

? medicine
– if so what type and how controlled

Spouse/family/lay friends etc
involvement ? group care

Educational and work

probable reason for excess weight been dealt with


followed up ? telephone, ? questionnaire; ? seen – if so is advice given
at same time, frequency etc

How deal
with dropouts during follow up.

How is
result defined ? in relation to target; ?in relation to lowest
weight/weight at end of diet phase. How dealt with when gradual change to

See also
other problems under pre-treatment and during

As if this
situation were not daunting enough, the individual papers do not attempt to
specify even a limited proportion of these confounding features, nor is it
possible to find standard answers to even a limited list.

However, while
bearing all the concerns about validity in mind, I have taken a random selection
of the results and expressed them in the form of graphs. Since it seems that the
greatest relevance lies in the percentage change from the original weight that
is achieved at each stage, we have expressed the graphs in this form so far as
possible. We have accepted the figures as reported in the original paper and not
attempted to correct for dropout level (where this is stated) since there are
various ways by which dropouts could be corrected.

Specifically we
have selected papers (see figures 2.2 to 2.10) which indicate that while the
general proposition is true, namely that stopping control of the subjects means
a return to their original state, demonstrate that there are a many studies in
which this has been avoided, by long-term close control. Moreover even in those
groups in which recidivism is the rule, there is a proportion of the population
who have sustained a substantial weight reduction. The information which has
been presented, shows we believe that the long term results have nothing to do
with the precise means of weight reduction or maintenance, but depend on the
amount of effort that is put into long-term management. This is scarcely
surprising for a psycho-social disorder.

Figure 2.2. A
diagram taken from Hensrud et al (1995) showing the effect of a study with an
800kcal food based diet in moderately overweight women. At the end of the
dieting period no further action was taken until the subjects returned at the
end of 4 years. The result is compared with a control group of normal
weight women to show that the normal weight does rise with time. The failure of
weight maintenance is typical

Figure 2.3.
Diagram from Bjorvell & Rossner (1985). This compares a control group who
were given instructions about how to lose weight but then left to look after
themselves. The next (dotted) line is that for a food based 600kcal food based
diet . In the maintenance phase, the subjects could take part in a regular
advisory programme if they wished The lowest (dashed line is that for jaw wiring
followed by a regular voluntary advisory service . Note that with the advisory
service there was a reasonable weight maintenance, in this study apparently
better for VLCD than for jaw wiring


Figure 2.4 This
is a diagram based upon the information in the paper by Anderson et al (1992).
They used a 500kcal VLCD and achieved a good weight loss. The subjects were
encouraged to undertake a weekly advisory programme during the 24 month follow
up with self monitored exercise , but only a proportion did.

Figure 2.5
This is a diagram from the Pasman et al (1999) study. This treated the whole
group with a 460kcal diet for two months. All subjects took part in an endurance
programme for the first four months. Then one group (solid) continued with the
exercise for the rest of the period while the others acted as a control
group. In this study there was no apparent difference as a result of the
exercise regime used.

Figure 2.6
This is a diagram from the study by Torgerson et al (1997). It compares a non
VLVD group (hypocaloric food diet throughout) with a group who took VLCD
(400-500kcal) for 12 weeks followed by a hypocaloric diet for the rest of the
period. The final result for women shows no difference, but that for men a
greater weight reduction and then a lower end point. It is interesting that men
show better results in most of the papers. This diagram shows that there are
specific reasons for different responses, not just the use of VLCD

Figure 2.7 This
diagram by Miura (1989) shows the effect of VLCD alone, behaviour modification
alone and a combination of the two This particular behaviour modification
programme appears to be effective – others do not.


Figure 2.8 This
is a diagram from Ohno et al,(1990). Like Figure 8 it shows an effective pattern
with VLCD plus behaviour modification but not with VLCD alone.

2.9 This is the study by Pavlou et al (1989). This study, in
contradistinction to others shows a beneficial effect of exercise on the
long-term results with both 800 kcal food and formula diets and with a 420kcal
VLCD. I am puzzled that the non exercise hypocaloric food diet was so effective
in reducing the weight.

Figure 2.10 This
diagam comes from Dittchuneit et al (1999) who compared the effect of either a
food based diet (1500kcal approximately) or a diet in which two of the meals
were replaced by a formula diet for 3 months. For the 24 months
maintenance phase all the subjects consumed a maintenance programme diet which
substituted one of the three meals by a formula diet. There was a monthly
weighing programme but no behaviour modification was attempted..


During the 1980s two
fundamentally opposing views developed concerning the nature of the body
composition changes which occurs when weight is lost and the influence exerted
by the composition of the diet on the body compositional changes. This is
exemplified by the differences to be seen in the COMA (1987) report and that for
example in the SCF (1990) and Codex Alimentarius (1995) reports.

The first view was that
propounded by Webster et al (1984), Garrow et al (1985) which supports the older
view if James et al (1978). This held that when weight is lost as a result of
any energy deficit
with a diet which provides adequate macronutrients, be it at 400 or 1200kcal
intake per day, protein is naturally and necessarily lost at the same time as
fat, the accepted proportion being about 75% fat: 25% protein.

The alternative view,
which depended largely on the observations of Forbes (1987) was that the
proportion of fat to protein in the weight which was lost varied depending upon
the proportion of the fat in the body. Thus it was held that for those who were
very obese a substantial proportion of the weight loss consisted of fat while
for those of lesser levels of excess weight (and therefore fat) there was a
significantly higher proportion of lean fat loss. This would have the effect
that not only would there be increased danger of protein deprivation in those of
lesser excess weight, but in this group the loss of the additional lean mass
would also have a greater lasting effect on future ability to maintain the lower
weight due to the reduction in the basal metabolic rate. It was further argued
that in the overweight the loss of lean body mass would be replaced by fat
during re-feeding.

These alternative views
have such a vital effect on our understanding of the body composition effects of
dieting that it was felt imperative to examine the extensive recent literature
on the subject to determine where the truth lies. To this end the following
matters were reviewed.

The level of accuracy and
reproducibility of the various techniques which have been used for the study of
body composition changes.

The studies that have been
undertaken on body composition changes during weight loss and their

3.1 Examination of the body composition determination

3.1.1 Reliability of the analytical methods.

There are now a
substantial number of papers which deal with the reliability of various
analytical methods for determining the composition of weight losses during
dieting. A qualitative overview of these is given in the paper by Lukaski (1987)
(Table 3.1).

Kjeldall method for
nitrogen determination

One of the
methods not considered in the Lukaski paper is that of nitrogen balance by
Kjeldall analysis, a method which was widely used in earlier studies including
some of those quoted by Forbes. Because it was so widely used and quoted in the
1980s literature, a study of the reliability was undertaken in Cambridge.(Kreitzman
& Beeson 2001). This
serves well as an example of one of the difficulties in the whole body
composition area:

“Until recently the
“Kjeldall method” of nitrogen determination was the only method for direct
measurement of protein balance. There are a substantial number of potential
errors arising, for example from inappropriate corrections for unmeasured
nitrogen intake and loss. However less has been published about the reliability
of the method itself and it was therefore felt desirable to check

Samples (from 24 hour
collections of urine) from eighteen subjects who were undertaking a VLCD weight
loss study were submitted for analysis to a widely recognised and extensively
used commercial laboratory. The results, shown in (Figure 3.2) as the left hand
(unshaded) blocks represented a single analysis for each sample.

Each sample was at the
same time pipetted in triplicate into sample bottles and labelled randomly as 54
sequential samples. These were then submitted blind to one of the senior UK
academic laboratories whose results have figured extensively in UK nitrogen
balance studies over many years. Each sample was analysed in duplicate by the
laboratory and the results are presented as an average (shown darker
hatched on the charts (Figure 3.1).

When the code was
broken, the differences between the academic and commercial laboratories on the
same sample were substantial, with each commercial figure representing a
substantially higher daily protein loss. However even more surprising was the
variation between identical samples tested blind in the same academic
laboratory. It is important to stress the importance of the size of the
differences within this laboratory. In the worst case, these differed by as much
as 5g nitrogen per litre. This would be interpreted as more than 30g protein
lost per litre urine

Figure 3.1 The results of the Cambridge study of the
reliability of the Kjeldall measurement of nitrogen balance. For details see the

In the particular
dieting study, the twenty four hour samples that were being analysed generally
amounted to 3 litres total volume. Therefore a difference of 5g/litre would have
meant differences of about 100g/day of lost protein, purely on the reliability
of the method in the laboratory. It is clear that such a difference would render
the nitrogen balance meaningless.

It is fully accepted
that this just represents the results in one laboratory, albeit one of the
reputed best in the UK. The only interpretation which should be applied is that
for any laboratory presenting nitrogen balances based on micro-Kjeldall
estimations, there should be a blind study at regular intervals of the
reliability of the method in their laboratory and preferably a blind audit
across a group of laboratories”.

In this respect
it is worth pointing out that the problem with a graph of the Forbes/Prentice
type which takes results from various laboratories, at different times, is that
the cross reliability between laboratories is largely or completely unknown.
This concern also applies to the Ballor & Poehlman (1994) widely quoted
paper on the influence of exercise on the FFM loss, since this paper utilises
information from various laboratories the cross reliability of which is

3.1.3 Reliability of indirect methods of
estimating the body protein economy.

It is important
to stress that the vast majority of the methods used in papers which purport
to determine protein balances during weight loss do not measure nitrogen,
but set out to estimate a representation of the protein content of the body from
other measurements. The estimate which is most widely presented used to be
called “lean body mass (LBM)” but is now better called “fat free mass

Contrary to
popular medical belief FFM does not represent the protein component but consists
of at least 6 compartments (intra-cellular water, extra-cellular water,
glycogen, bone, minerals, protein). Each of these compartments can change
independent of the other to a greater or lesser extent during physiological and
pathological conditions (including dieting). For example, the physiological
conditions which have a profound effect on indirect body composition estimations

Changes in glycogen stores which result from pre-study food choice

Hormonal changes e.g. the menstrual cycle and menopause; stress; insulin


Ambient temperature

Inactivity – not only bed rest but also restriction e.g. plaster cast on a

It is important
to stress the importance of the glycogen compartment in this whole discussion.
The glycogen store itself is about 400-500g, but each g of glycogen has
associated with it between 3 and 5 g of water. Hence with dieting (or
re-feeding) there will be a change in the first few days in the glycogen
compartment amounting to anything up to 2kg. Thus any current indirect
measurement of body compositional change must take account of this substantial
component. This particularly applies to the first few weeks of dieting (or
re-feeding). This is why it is vital to ignore studies of less than about 4
weeks and also to ignore those in which the post-diet determinations have been
made after even a brief period of “maintenance”.

There are
several older studies that have investigated the variations from one technique
to another (e.g. Yang et al, 1977; Vaswani et al, 1983; Garrow, 1990) However
during the past 10 years a substantial literature has been published on
technical aspects of neutron activation analysis of various chemicals, a
substantial proportion of these papers emanating from the Heymsfield group. This
is currently the only method by which chemicals within the living body can be
measured directly. Among these chemicals is nitrogen. Neutron activation can
determine directly the nitrogen status within the body. Even then it can not
measure the protein economy itself since protein is only one of the nitrogen
containing body components, albeit the largest one. Unfortunately neutron
activation analysis is expensive and there are relatively few units which can
currently undertake this determination. In consequence, though neutron
activation analysis is the current “gold standard” it is still necessary to rely
heavily on indirect estimates of the body composition. Interpretation of the
indirect methods must be guarded and the assumptions questioned

As a consequence
it is important to determine not only the reliability of these various methods
in their own right but how far they cross correlate, one with the other, not
only under stable conditions but under variable physiological and experimental
conditions. There have been many recent papers which have reported such cross
comparisons though usually with only a few methods in any one study. These cover
studies in normal humans, the aged etc. However one study in the USA (Albu et
al, 1992), one in the UK (Kreitzman et al, 1993) and one in Spain (Valtuena et
al, 1995) are directly relevant to the present situation and appear to be the
best to indicate factors of current importance.

The Albu study
(which comes from the Heymsfield group), looked not only at various recent
methods, but also how these would be converted to FFM estimates, using different
equations and different numbers of compartments. They studied 10 dieters, taking
a 600kcal VLCD for 24 weeks and Figure 3.2 shows the dramatically different
estimates for fat and FFM that emerge in each individual dieter when different
study methods are used. It is important to note from this figure that the
variation is not uniform for any individual method (look, for example at the
figures for 40K water dilution (2C-TBK) compared with those for
tritiated water dilution (2C-HD)).

Figure 3.2. Effect of different methods of
determination on the estimated fat loss (from Albu et al, 1992)

In the Kreitzman
et al (1993) study, not only was the change in body composition of the eleven
dieters using a 405 kcal diet for 10 weeks measured by twelve different
observations, but for four of the methods, studies were made in entirely
independent units, namely:

3 laboratories

2 laboratories

Skinfolds 2

Impedence 2 laboratories

Thus this study
provides information on both the reliability and reproducibility of the
individual methods of indirect estimation but also cross laboratory

One method of
demonstrating the degree of variability within methods and between methods is to
calculate the FFM changes for each, the ratio
DFFM/DFAT and the mean fat weight i.e. the
values used for the Forbes and Prentice diagrams. The ratio which would arise
for each subject using each estimate is shown in the graphs in Figure 3.3 (next

Once again while
the variation in the means is not very great, the individual variations are
large and as irregular as those of the Albu study. With such individual
variability it is clear that it is

Figure 3.3 The results of the study of the
DFFM/DMean Fat Wt ratio in 10 of the 11
subjects who undertook the experimental 10 week VLCD diet. The body composition
of each of the 10 subjects was estimated with 8 main methods (many in
duplicate/triplicate in different units). The details of the studies are to be
found in “The Swansea Trial” Eds Kreitzman SN & Howard AN Smith-Gordon &
Co Ltd 1993. Note that the eleventh subject is not included because she was not
able to undertake the densitometry measurement.




10 –

not possible to
reliably recalculate the estimate in any individual patient for one method on
the basis of another method.

The third study
is that of Valtuena et al (1994), graphs showing the results of which are shown
in Figure 3.4. Their results are very similar to those of both Albu et al and
Kreitzman et al, though with fewer methods studied.

Figure 3.4 The results of a study by Valtuena (1995)
of the
DFFM/DMean Fat Wt ratio determined in nine
dieters, each studied by three different methods.

It was hoped
that it would be possible to determine whether there was any correlation between
these studies to indicate whether any characteristic of the subject might show a
correlation with deviations in an individual method. Unfortunately it was not
possible to do so because of major differences in the methodology. Indeed it was
not possible to use the Albu data further because it included a variable
maintenance period (24 – 33 weeks). There was an extra problem in further
analysis of the Albu study because only 7 of the 10 dieters were studied post
diet, but the paper does not indicate which they are.

An overall
representation of the variation which derives from the use of different study
methods is shown in Figure 3.5

Figure 3.5 Comparison of the body composition
results using five different methods in four different studies. Densitometry
results are taken as 100 and the results of the other methods expressed as a
proportion of these.

In part the
different results given by the various methods may be explained on the basis of
different degrees of obesity. Thus Gray et al (1989) showed that when the body
fat was over 48% of the total weight, impedance overestimates FFM when compared
with the results from densitometry. In part it depends on other physiological
variables which can change, with time in the same person. For example the
observations recorded by de Groot et al (1989) using diets of very similar
composition show wide fluctuations in the
DFFM/DWt ratio (0.09, 0.37, 0.18, 0.47; see
record 24A to 24D in the summary table ***).

Other studies
that have examined the variation in the FFM which results from the use of
different indirect methods include Murgatroyd & Coward (1989); Heymsfield
& Waki (1991); Ballor & Poehlman (1994); Houtkooper et al (2000); Piers
et al (2000).

3.1.4 Variation introduced by different
formulae for conversion using indirect methods.

From what has
been written here it should be clear that each of the indirect methods for
estimating FFM require fundamental assumptions to be made in order to calculate
FFM (or fat and hence FFM by subtraction). The body compartment which is
determined and some of the assumptions that are made for representative indirect
methods are shown in Table 3.2.

Table 3.2 The compartment which is
determined and some assumptions that are made for some of the common body
composition estimation methods.



& conditions that create false estimates


Exchangeable body

Constant hydration
of FFM (1)

Stable hydration
state (2)

Oedema fluid


Body potassium

Dietary intake of
K uniform (e.g. milk, fruit etc) (4)

Constant ratio of
K/N (5)

Uniform body
terrain (6)


Average body

Very sensitive to
hydration (1)

Water confident

Dietary status

Sensitive to
bladder and gut contents

Variable equations
which do not always agree


Total body water

hydration of FFM (1)

Stable hydration
state (2)

Oedema fluid


Local fat

Uniform fat
distribution – subject variability

Does not measure
visceral fat

Constant hydration
(1) (2) (8)



hydration of FFM can not be assumed since total body and compartmental
fluid status is variable at different stages of diet and also varies from
subject to subject. The test converts TBW into FFM based upon the assumption
that FFM is 73% water which is not universally true

hydration state within and between subjects is assumed and is not true under
different study conditions. Hydration is influenced not only by the intake and
excretion of fluids but also by food, hormones, temperature, activity levels,
drugs etc both before and during any study.

fluid is different between subjects especially when obese subjects are compared
with the non-obese. Loss of this fluid may be sensitive to macronutrient

potassium intake will reflect in 40K measurement, e.g in study of
formula diet in which the calories are raised with milk to compare with lower
calorie water. Milk is potassium rich which is measured in total body potassium
pool and would wrongly suggest increased FFM.

studies show that potassium can change independently of nitrogen. Changes in
fluid balance will change potassium without any change in nitrogen.

The measurement of body potassium assumes a constant source to detector distance
and uniform absorption path. Human bodies do not comply, especially when they
are changing shape during weight loss. Also varying fat distribution will
influence readings.

confidence. The test involves underwater weighing of the subject in a confined
tank and if subjects are obese, external weights are needed to keep subject
submerged. Total exhalation is required. The procedure is less problematic in
no-obese subjects.

fluid contributes to weight and loss of this fluid will change body weight by a
greater proportion than that shown by skinfold measurements, not least because
the areas where skinfold measurements are made are not those where oedema fluid
would be expected to be marked. This will therefore suggest higher FFM loss per
weight loss but not related to a loss of protein

But even this is
not the limit of variation because many of the estimates include “correction
factors”. These are not the same from one study to another, even
when the same method is used (as an example see Table 3.3.)

Table 3.3. The effect of different prediction
equations on the conversion of hydrostatic measurements to body fat estimates
(from ***)

But even without
variation introduced by the use of different formulae, there is evidence that
the calculations can not be applied across different levels of obesity. Thus
Lohman (1977) showed that for subjects with over 30% fat, the Siri equation for
the calculation from densitometry measurements yields higher values for FFM that
does that of Brozek.

Summary of
the reliability of composition estimates.

To summarise the
situation, the accuracy of each method of body composition estimation depends

The limit of the reliability
and reproducibility of the method per se

Accuracy of measurement in
the individual laboratory

Biological variations
influencing the interpretation of indirect methods when these actually measure
independently variable body components

Different formulae for
converting the observations into a measurement of reputed fat mass, fat free
mass etc.

Variation of conditions
within and between the studies

It must be
appreciated that for weight loss studies these problems are further complicated
by the fact that the tests are undertaken both before and after the diet. Each
has its own level of inaccuracy and each is influenced by physiological
variables, including those that arise from endocrine changes resulting from the
diet and the stage of the diet itself (e.g. first week of

Even then there
are further complications, for it has been demonstrated clearly by Saris that
exercise during dieting can influence the preservation of lean body

3.1.6 Significance of these variations in
relation to the Forbes/Prentice graphs.

If every single
point in the Forbes/Prentice graph was based upon a determination of the same
body component using the same technique and converted to FFM using the same
formula, there would still be the problem that results from individual
variation. However the situation is far less clear than this. Of the studies
quoted by Forbes (1987) and Prentice et al (1991) as the source of their data
for the graphs which we have examined carefully, the data is probably derived
from the following techniques

Densitometry (some variation in
16 studies

40K counting (with
4 studies

3 studies

3 studies

1 study

We have used the
words “probably derived” because some of the studies have used more than one
technique and it is not clear which result has been taken for the
Forbes/Prentice graph. It has been assumed that when there was a densitometry
estimate available this was the one that was used, but there is no direct
evidence that this was the case.

On the basis of
what has been presented above, it is submitted to the Working Party that, as
presented, doubt must be cast on the accuracy of the overall graph as shown in
Figure 11b of the Prentice et al (1991) (see Figure 3.6 of this discussion
paper). That graph was based on different indirect methods of estimation,
undertaken in different laboratories and applying different formulae to derive
the body composition.

Figure 3.6 Figure 1 from the Prentice et al (1991)
paper which the Working Party asked to be re-examined.

3.2 Re-examination of the old data and examination of new
data relating to body composition changes

Re-examination of
the Forbes/Prentice graphs.

Despite all the
problems that have been identified, it appeared to be desirable to examine each
of the papers cited by Forbes(1987) and Prentice et al (1991) to determine the
method used and other relevant information.

In addition a
search has been undertaken for other relevant papers over the period from about
1960 to 2000. Over 100 papers which were available for detailed analysis could
be identified.

From these we
have attempted to identify those studies which must be eliminated because they
were invalid and to indicate why (Appendix 4). Ideally only those studies should
be included which are based on formula diets, the exact composition of which
could be verified. Unfortunately this removed almost all the studies of
800-1200kcal diets since the vast majority of these are food based. We therefore
modified the criteria maintaining a category based on the following

formula based diets for which the composition was clear and which

studied for 4-16 weeks without

with either no exercise or low level

where the rate of weight loss per week
suggested reasonable compliance

and densitometry determinations were

These are marked
“Accept” in Appendix 3.

We also added a
further criterion (marked “Provisional” I Appendix 4) for

food based diets between 800 and
1200kcals/day, which were

studied for 4-16 weeks without

with either no exercise or low level

where the rate of weight loss per week
suggested reasonable compliance

and densitometry determinations were

There were a
certain number of these studies which were quite clearly inappropriate
(hydrolysed collagen diet, starvation, use for only a few days etc) and these
have been totally rejected. For the remainder, including those that have been
rejected for other reasons (e.g. method of estimation of the composition) we
have shown all the actual raw data, the basis of the calculations and the
DFFM/DWt ratio and mean fat weight in Appendix
4. From this table it was possible for any member of the Working Group to check
the data. They can then determine whether they feel that the plots of
DFFM/DFAT and mean fat weight which have
been made are valid. The ratios and mean fat weight of those studies that have
been regarded as “acceptable” and “provisional” as bold in this table to make it easier to
distinguish them.

It is
disappointing to find how few valid observations are available from some 40
years of studies worldwide. Of more than 60 papers examined only about 20
contain valid data. This is clearly the only data on which we can try to
determine whether

the FFM component of weight loss is dependent on the body fat mass.

the use of VLCD produces a higher FFM loss than does an 800-1200Kcal

From this
“valid” data we have shown on separate Figures (Figures 3.7 and 3.8 – next page)
the ratios plotted against MFW for the use of formula based VLCD 400 to 800Kcals
(Figure 3.7) and formula and food based diets between 800 and 1200 kcals (Figure
3.8). We have also plotted the information for the individual dieters in
those studies (Deurenberg 1989: Kreitzman & Howard 1993; Valtuena et al
1995,) in which there are enough observations at various body fat levels
(Figures 3.9, 3.10 and 3.11 – two pages on).

On the basis of
the information given in Appendix III and plotted in Figs 3.7 to 3.11 it is
submitted that there is no current evidence for either of the above widely
publicised views, namely that the composition of the weight which is lost
depends on the body fat level or that VLCD produce a higher proportion of FFM
loss that do higher energy providing diets.

Hence there is
no evidence that VLCD are more dangerous than other diets when used in the
overweight as opposed to the obese. We have sought to determine whether these
views can be supported by statistical analysis but the data is too limited. In
any case the use of statistical methods must be suspect when the data is liable
to such a high level of error.

The figures
which follow have not been re-labelled from those presented to the Working

3.2.2 The body composition studies expressed in
terms of BMI status

In the above diagrams relatively little
of the information has been expressed in terms of the original or finishing BMI
level, but information expressed in this way was requested by the Working

Unfortunately, the body composition data
(by any method) expressed in terms of BMI, are not available for all the
studies. Forbes expressed his results in terms of mean fat weight and most
subsequent authors followed this pattern. However, if it is accepted that a MFW
of 30kg is broadly equivalent to a BMI of 30 then it is clear from Appendix 4
that there are a substantial number of individuals in the range <30 MFW for
diets of <400kcal, 400-600kcal 600-800kcal and above 800kcal.

For some of the studies it is possible to
examine the
DFFM/DWt ratio for individual subjects above
and below MFW 30. Therefore although it is not possible to compare with other
studies (due to different methods), it is possible to assess the situation
within the same study. We would specifically draw attention to the fact that not
only do these cover patients whose pre-treatment BMI (or MFW) is below 30 but it
is clear from the data presented that some at least of the subjects were reduced
to BMI levels between 20 and 25

The body
composition studies expressed in terms of the energy value of the

The data in Appendix III covers a wide
range of diet energy content viz:


Number of











There is no indication that the energy
value of the diet used influenced the body composition changes with weight

The Keys (1950)
Minnesota Study – an appraisal

This study, which is always quoted
concerning the effect of “semi-starvation” clearly influenced the Forbes
analysis of changes in body composition with changes in body weight during

It was undertaken on a group of 32 young
male volunteers. At the start of the study the mean BMI was 21.9. As a result of
24 weeks dieting this was reduced to a mean of 16.9. Body composition studies
were undertaken at time 0, 12 weeks and 24 weeks by hydrodensitometry. The exact
technique differs somewhat from modern methods and the results can not be
compared directly with those quoted in Appendix 4.

The ratio of DFFM/DWt loss for the first 12 weeks (BMI
change from 21.9 to 18.7
) is 0.63. The ratio for the second twelve
weeks (BMI change from 18.7 to 16.9) is 0.57. Thus the lower the BMI the less
was the protein lossas opposed to the opposite determined by Forbes.

However it is our opinion that the Keys’
study should be discounted as of no relevance to considerations of VLCD dieting
for the following reasons:

The average BMI at the start
of the Minnesota dieting period was 21.7 (i.e. low area of normal) and not a
level at which dieting should be contemplated.

The dieting took the BMI
down to average 16.9 (the pictures within the book show how emaciated they
were), the residual fat averaged only 3.4kg according to their calculations and
this is substantially below any target weight for therapeutic

Three different food diets
with substantially different proportions of fat, carbohydrate and protein were
used on different days.

The average energy intake
per day over the 24 weeks and 32 subjects was no less than 1569 kcal, but this
hides a range of means for individual subjects between 1213 and 1833 kcal. The
range between individuals by weeks stretched from 608 to 2095 kcal. The diet was
adjusted individually each week to achieve a theoretical weight loss curve. The
energy value and composition of the diet was changed depending on the previous
week’s weight loss. The adjustment was mainly by additional carbohydrate and
hence the glycogen stores would have changed erratically.

A high enough energy
expenditure to achieve the required weight loss with the high energy intake was
achieved by daily exercise mainly outside in the bitter cold (Minnesota in
the winter!)

“The weight loss was
complicated by clinical oedema and
relative increase in interstitial fluid volume” Keys attempted to adjust
the composition to allow for this fluid accumulation. The adjustment which he
applied changes the ratio for the second 12 weeks to 0.34. This is even further against the
Forbes effect

Interestingly one of the volunteers in
the Kreitzman study had a starting and finishing BMI almost equal to the mean in
the Minnesota study but with a ratio of 0.36, well within the ordinary
densitometry range in that study

A re-appraisal of the
Forbes and Prentice graphs

On the next page we have reproduced the
Forbes and Prentice graphs as they were shown in their original papers.
(shown as Graphs 3.12 a & b)

However it is clear that the two points
to the far left of each of these diagrams can not represent figures determined
from a regular dieting programme since they represent subjects whose mean body
fat wt is under 10kg (i.e. a sub-normal mean BMI).

If then we accept all the other points on
these graphs as being valid (and it will be recalled that in the discussion
above (page * et seq) we drew attention to problems in accepting them) we can
derive two revised graphs (shown as Graphs 3.13 a & b)

There is then no indication from visual
inspection that there is any increase in the proportion of fat free mass loss at
lower mean body fat levels.

This is not to say that at

Low levels of protein and perhaps
carbohydrate in the diet there may be serious changes in composition of the body
weight loss

At low levels of BMI (below BMI 20) there
may be changes too

Figures 3.12 a & b The original Forbes and Prentice

Figures 3.13 a & b. The Forbes and Prentice graphs with the
two left hand points, which can not represent regular weight reduction results

For a better
view of figures 3.12 and 3.13 click here

3.5 Further data relating to body
composition changes during weight loss with VLCD.

There are two extensive individual
studies (Hoie, Bruusgaard and Thom, 1993; Donnelly, Jacobsen and Whatley,1994)
which provide excellent information relating to the question of whether the loss
of fat free mass is greater at a lower BMI level.

In that undertaken by Hoie et al, (1993)
body composition analysis was undertaken by near-infra-red interactance (Futrex
5000). It was conducted on 82 women and 45 men and a 430kcal diet containing
61.5 g high quality protein and 30.5g carbohydrate was consumed daily for eight
consecutive weeks. Dr Hoie has very kindly provided me with the summary of the
original data on which his paper was based, (unfortunately the data on each
individual dieter has been lost in the intervening 10 years). Nevertheless the
information in his original paper and that in the summary tables is adequate to
reach substantial conclusions.

Thus, the proportion of the total group
in the various BMI categories at the start of dieting and after 8 weeks as
calculated from his data is shown in Table 3.4. From this it is clear that as a
result of an average loss of some 3.9 BMI units for women and 4.8 units for men
some 20% of the group came into the normal weight category (BMI 20-25) at the
conclusion of the 8 weeks diet with a further 30% now having a BMI between 25
and 30.

Table 3.4 Number (%) of dieters in each BMI range
at start and end of an 8 week diet (Hoie et al (1993)

BMI Range

Number (%) time 0

Number(%) time 8



25 (20%)


7 (6%)

19 (15%)


19 (15%)

19 (15%)


101 (79%)


The ratio of FFM/Wt loss overall was 0.25 with
no significant difference between men and women. Without the records for the
individual dieters it has not been possible to construct a scatter diagram of
this ratio compared with the initial BMI but Hoie et al (1993) found that the
ratio did not differ significantly over the whole range from 51 down to 25 (r =
-0.03; P = 0.75).

The study by Donnelly et al (1994) on the
other hand was conducted only in women (116) using a diet providing
520kcals (protein 50g, carbohydrate 79g) for 12 weeks and with body composition
determined by hydrodensitometry (Brozek et al equation).

For the Donnelly et al study, Table 3.5
indicates the number and percentage of subjects who fell into different BMI
categories before and after the diet. Before dieting the lowest BMI was 27, the
highest 64 (mean 37.6) and with a mean fall of 20.2kgs over the 12 weeks, the
mean BMI level at the end of dieting was 30.2 with no less than 16 (14%)
achieving a normal weight (BMI<25) (range 21.9 – 52.1)

Table 3.5 Number (%) of dieters in each BMI
range at start and end of 12 week diet. (Donnelly et al, 1994)

BMI range

Number of dieters (time

Number of dieters (12


0 (0%)

16 (14%)


9 (8%)

48 (41%)


37 (32%)

37 (32%)


39 (34%)

8 (7%)


20 (17%)

4 (3%)


11 (9%)


Figure 3.13 shows the relationship
between the ratio of the FFM/Wt loss and the BMI level. The mean FFM/Wt loss
ratio was 0.19 (r = -0.9 x 10-7) confirming that there is no
difference in the FFM proportional loss at different BMI levels. It is worthy of
note that the level of compliance to the diet was excellent with only 4 dieters
showing a weight loss per week of less than 1kg. Each of these four with poor
compliance recorded a FFM/Wt loss ratio that was substantially out of line
including both those at the extremes.

Figure 3.13 A scatter diagram of the ratio of FFM to
weight loss compared with the initial BMI in 116 women dieting for 12 weeks on a
520Kcal VLVD (Based on data from Donnelly et al, 1994)

Although the
Hoie et al (1993) study used near infra-red interactance to measure the body
composition, while Donnelly et al (1994) used densitometry, the proportion of
fat lost to weight lost was of the same order in both studies. Moreover the
study by Hoie et al was based on a relatively high daily protein ketogenic diet
while that of Donnelly et al involved a non-ketogenic diet with more modest
protein content.

3.6 Summary of the
body composition study determinations.

From the information derived from the 20
studies involving a relatively limited number of dieters (using VLCD and LCD)
coupled with that from the two extensive studies which examined
ketogenic/non-ketogenic VLCD and the two genders, it can be concluded that there
is no difference in the proportion of fat which is lost during

between LCD and VLCD,

between men and women,

between ketogenic and non-ketogenic diets

throughout the whole range of initial BMI levels from about 60 down to

and finishing BMI levels in the normal range (20 –25).

3.7 Submission related to the matter of positive and negative
nitrogen balances

In an earlier portion of this submission we have examined the
accuracy, reliability and reproducibility of Kjeldall determinations in general
(Section 3.1.2). Investigation of the current literature in those areas where
there are economic considerations (e.g. studies of protein in animal carcasses
for commercial exploitation) indicate that the Kjeldall method has been largely
abandoned. This is not to say that with appropriate control and care it is not
possible to determine the nitrogen balance by the use of Kjeldall
determinations. However it does stress the need for such careful controls and
means that balance studies which use this technique must be examined carefully
to determine what controls have been applied.

This is particularly relevant in the light of some of the
discussion papers which have been presented to the Working Group concerning the
nitrogen balance during weight loss as a result of dieting. Many of these are
quoted as showing either a positive nitrogen balance or alternatively a negative
nitrogen balance in the early stages which subsequently becomes positive after a
period of some three to four weeks. There is a fundamental problem here.

While weight is being lost with any weight
reducing programme, there is no possibility that there can be a zero, let alone
positive nitrogen balance
This was established and accepted by the authorities as long ago as 1987 (see
Appendix F of The COMA Report (1987) on the Use of Very Low Calorie Diets
in Obesity). This appendix was prepared by John Garrow in response to the
Cambridge Nutrition calculation of protein losses (see page 38).

It stems from the fact that
when adipose tissue is lost or gained, a significant proportion consists of fat
free mass (FFM). This FFM contains protein. In the calculation given by Garrow
(which uses the proportion 25%FFM/75%fat for adipose tissue) this “allowable”
protein loss (as Garrow calls it) amounts to 4.75% of the total weight lost.
Although there are some differences of opinion about the exact proportion of the
weight lost which consists of FFM the acceptance of this principle implies that
there must be nitrogen loss when weight is being lost. This has been discussed
in detail in an earlier sections of this present paper (3.1 to 3.6). Since this
nitrogen loss is always present in weight loss, we would prefer to refer to it
as “obligatory” rather than “allowable”

Hence what we must look at during
weight reduction is not the nitrogen balance as calculated, but whether nitrogen
losses are greater than the “obligatory nitrogen losses”.

We have accordingly examined as much of the nitrogen balance
literature as we can find to determine whether at a level of 50g of
quality protein intake per day in the form of a VLCD, the nitrogen losses are
greater than the obligatory nitrogen losses.

4. We
have excluded several of the papers because at 50g protein intake per day, they
report a positive nitrogen balance per day even when the matter of the
obligatory nitrogen loss is ignored. These include those of Apfelbaum et al,
1967; Winterer et al, 1980; Blackburn et al, 1975; Bistrian et al, 1977a;
Bistrian et al, 1976; Marliss et al, 1978 ; Bistrian et al, 1977b; Hoffer et al,
1974; Genuth, 1979; Phinney et al, 1988; Vasquez et al, 1985. In these papers
the positive nitrogen balance occurred at various levels of carbohydrate intake
above about 30g available carbohydrate per day.

5. There
is a further group which should be rejected from analysis because the length of
the study was substantially less that 4 weeks or there was no nitrogen balance
or there were obvious fallacies in the design. (Hoffer et al 1984 – No nitrogen
balance provided; Genuth et al, 1974 – No absolute values for nitrogen; Yang
& van Itallie, 1976 10 day experiments only; Baird et al 1974 – Short
periods only with various diets; Aoki et al, 1975 – 7 day experiments only;
Howard et al, 1978 100g CHO – 5 day balance only; Hendler et al 1988- 21 day
only on CHO; Greenberg et al 1976 – not dieting; post operative;
Bistrian 1977 – unable to find paper).

6. We
have equally excluded from the analysis those with a carbohydrate level below
30g/day (since the 1970s it has been known that these levels are inappropriate)
and where the protein level is less than 30g (for a similar reason). (Yang &
van Itallie, 1984 – mixes groups with no CHO and high CHO; Bistrian et al, 1977.
CHO below 30g/day; Marliss et al, 1978 CHO less than 30g; Koppeschaar et al,
1983 25g protein and 25g CHO; Wynn et al 1985 Various CHO values mixed; Fisler
et al, 1982 – CHO below 30g/day; Vasquez et al, 1992 – only 10g CHO/day)

This leaves a total of 15 published papers which can be used
for further analysis, namely:

Howard & Baird, 1977

Wilson & Lamberts, 1979

Hanefeld, 1987a

Hanefeld, 1987b

Ditshuneit et al, 1985a

Ditshuneit et al, 1985b

Alban Davies & Baird, 1987

Wechsler et al, 1984

Wechsler et al, 1984

10.Bistrian et
al, 1981 – 21 days only

11.Vasquez et
al, 1992
Haven et al, 1980 – 21 days only

13.Morgan et
al, 1993

14.Henry et al,

15.Henry et al,

These are analysed in Table 3.6

Table 3.6 Nitrogen balance
studies (for details see text)



Wt loss /week

Prot intake g/day

CHO g/day

Balance a

Balance b

Obligatory loss

Balance c








































































































































Balance a = as presented in
paper (cumulative g protein)

Balance b = as re-calculated
for any additional losses not included in the paper (i.e.
nitrogen loss in faeces = 0.7g nitrogen/d = 5g protein
/day; miscellaneous losses = 0.4g nitrogen/day = 3g protein/day)

Obligatory protein loss 0.475% (weight loss –
2.5kg). This is the Garrow Formula (see COMA Report (1987) (cumulative g

Balance c. The theoretical
balance for an intake of 50g/day protein rather than that used in the paper
(cumulative g protein)

* Note:
with studies less than 4 weeks it is far from clear whether the Garrow
obligatory protein loss formula applies. We have accordingly excluded all the
studies lasting substantially below 4 weeks, but included those at 3 weeks with
this caveat.

It will be seen that for many of these studies the total
protein loss (Balance b) is not much greater than the obligatory loss even at
the lower protein intakes. There are 2 studies of 4 weeks or more and a protein
intake of 50g or more and in both these balance b does not show a greater loss
that the obligatory loss. When a theoretical calculation is made to adjust to an
intake of 50g/day the loss is nearly always no greater than the obligatory

We fully accept that this is not an ideal presentation. In
previous sections we have already suggested that nitrogen determinations by the
Kjeldall method are suspect. Moreover the re-calculation to an intake of 50g has
no scientific support. Nevertheless there are no current observations of
nitrogen balances determined by neutron activation. Hence, we submit that if Kjeldall determined nitrogen balances
are to be considered (and they are discussed in other papers submitted to the
working group and included in the draft SCOOP Report), then adjustments of the
type given in Table 3.6 are the only possible way of presenting the picture.

3.8 Studies which provide information on the desirable
carbohydrate level.

It is vital to appreciate that the safety of 40g+
carbohydrate is confirmed by the fact that some 90% (45,000) of the patients
studied in the published trials were at daily carbohydrate levels between 30 and
45g. Hence the clinical effects are well known and the safety well established.
with VLCD with carbohydrate levels substantially below 50g/day (but over

The substantial majority (almost
90%) of the published papers which demonstrate the safety of modern VLCD (see
Table 2.1) were concerned with diets containing less than 45g/day carbohydrate.
Such diets produce a mild ketosis in the majority of the dieters. The mean
plasma ß-hydroxybutyrate with 40 to 45g available carbohydrate per day is
1mmol/L with a maximum in a group of 491 dieters tested after over two weeks
continuous dieting 5mmol/L (Tiessen & Weinkove, personal communication).
From the early studies (Baird & Howard, 1974) it has been apparent that when
the available carbohydrate is less than 30g per day the level is inadequate to
prevent mineral losses and increased uric acid levels. However all the clinical
biochemical investigations at levels above 30g/day have failed to show
abnormalities. Moreover, in the United Kingdom and several other countries, the
carbohydrate level for some years was under 35g/day and the practical clinical
results were good at this level. On the other hand there is virtually no
published experience with carbohydrate levels in excess of 50d/day (Table

There are two arguments in favour
of a mildly ketogenic diet, namely appetite suppression and a greater sparing of
lean body mass. Search of the literature shows that there is an almost even
split between those who favour a mildly ketogenic one and those who favour a
higher carbohydrate level which renders the substantial proportion of dieters

We would submit that unless it
can be shown that there is clear evidence presented that the non-ketotic
solution has substantial benefits for the maintenance of the protein economy, it
would be better to leave it open that VLCD with available carbohydrate levels
above 40g/day are safe. If a higher value is given, it is important to determine
precisely how powerful is the evidence for the necessity, or even benefits of
non-ketotic diets. I note incidentally that the minutes specifically ask that
any evidence showing that above 50g carbohydrate/day is safer than 50g/day
should be circulated, but no such evidence was circulated.

The biochemical argument for the
merit of ketone bodies is that other than glucose, they are the only compounds
that can be metabolised by the brain and indeed are preferentially used by that
organ. Hence when glycogen stores are depleted, under any circumstances, the
production of ketone bodies means that protein breakdown is less necessary to
provide glucose. Thus the phenomenon of protein sparing has been described not
only in starvation, (e.g. Cahill, 1976; Sapir and Walser, 1977) but also under
surgical stress (Williamson et al, 1977; Rich and Wright, 1979; Crowe et al,
1989). We would draw attention to the protein balance data shown in Table 3.6.
This indicates that even at levels of protein intake below 35g/day many of the
papers show that protein losses are no greater that the obligatory losses during
weight reduction by any means. Unfortunately this evidence is not as powerful as
it might be, because there are virtually no observations with non-ketogenic
carbohydrate levels.

As further support for this view,
we would draw attention to the paper by Fery et al (1996). They conclude (page
E829) “The present study, based on the prolonged suppression of FFA and KB or of
FFA alone, suggests that both compounds participate in the conservation of the
protein mass during fasting and indicates that this process is operative after
only a few days of food deprivation” and then “During fasting the elevated
levels of both FFA and KB exert a suppressive action on gluconeogenesis, they
maintain glucose concentration at low levels and they protect the protein
stores”. A similar conclusion is reached in the review of the subject by Tessari
et al (1996), which provides a substantial number of further references. What
many of these papers, referenced in this review by Tessan et al point out is
that there is not just one factor which is responsible for the pattern. It
depends on a balance of the level of the substrates and the balance of the
influence of the many hormones which, as shown in various discussion papers for
the Working Group are substantially changed during the administration of VLCD as
the sole source of nutrition.

It has been argued that the paper
by Halliday et al (1993) speaks about “this apparent sparing of protein is
solely due to the increased rate of protein synthesis”. This is exactly what one
would expect to see (Williamson et al, 1977; Nair et al, 1988; Crowe et al,
1989; Halliday et al, 1993). In this respect we would draw attention to the
paper by Nair et al (1988) which appears to be particularly pertinent.

There is a constant flux of amino
acids from tissue proteins, a flux that is increased during weight loss. When
glucose levels are low, but there are adequate levels of ketone bodies and FFA
available to provide for both brain and muscle metabolic needs, gluconeogenesis
decreases and free amino acids in the circulation encourage protein synthesis
producing exactly the effect that have been described by several groups and to
which attention has been directed

The main evidence advanced by
those who favour the non-ketogenic solution are the Vazquez papers. The Vazquez
et al (1995) paper is quoted as demonstrating that the cumulative nitrogen
losses are lower in the high carbohydrate groups. Unfortunately the Kjeldall
nitrogen observations must be treated with reservation (see section 3.1.2 for
discussion on this aspect). Specifically, in the Vazquez et al (1995) study, by
day 28 the subjects receiving 70g/day were in positive nitrogen balance which is
impossible during weight loss (see sections 3.2-3.6).

The Vazquez & Adibi (1992)
study has no relevance to the discussion. The ketogenic diet which they used
contains only 10g available carbohydrate per day. Since the pioneer studies of
the 1970s (e.g. McLean Baird & Howard, 1974) it has been known that at
carbohydrate levels below 30g/day, there is substantially greater protein
breakdown than above 30g. At the other extreme, they used 86g/day for their
non-ketogenic diet. Since they did not study any intermediate carbohydrate
intakes (e.g. between say 30g and 45g/day) it can not be concluded that this
would not be just as beneficial as the 86g/day.

The Vazquez also relies heavily
on leucine data. Leucine data has been criticised at various times as not being
fully representative of the protein economy. For example in the study by Bowtell
et al (1998) on the modulation of total body protein metabolism by variation in
dietary protein it appeared that leucine oxidation is very dependent on leucine
availability rather than on other factors.

This is supported by the further
study by the Bowtell group (2000) which demonstrated that the sparing effect of
glucose on leucine oxidation appeared to be dependent on a previous high protein
intake. In that particular study their low protein intake at 0.7g/kg/day (as
opposed to the high intake of 1.8g/kg/day for the high protein group) and this
low protein intake would be broadly that used in the VLCD studies. Another
observation that raises doubt about relying too heavily on leucine tracer
studies is that of Pannemans et al (1997). They used both 15N-glycine and
–[1-13C]-leucine in the same protein balance study and found that in fasting
elderly women who were consuming a 20% rather than a 10% protein diet, protein
turnover (both anabolic and catabolic) was higher as measured by glycine but
equal in both diets as measured by leucine. Furthermore, in the Halliday et al
(1993) paper which has already been quoted, further differences are high-lighted
between glycine and leucine measurements, though not in the same study.

We would therefore submit that
there is no uncontroversial evidence that there is a protein sparing effect with
the higher carbohydrate level which will ensure an absence of ketosis. With the
very substantial amount of evidence that at levels below 45g/day available
carbohydrate, there is no justification

3.9 Observations made
after the circulation of the first draft of the report to the working

“1. I am
very concerned about having section 6.3 (on nitrogen balance), in the present
form and section 7.3 on the ratio between the fat mass/fat free mass ratio
being constant in the same document. If you accept section 7.3, the protein mass
is reduced by about 25% for any weight loss. This means that there can not be a
positive nitrogen balance during any weight loss period of more than the few
initial days (glycogen and water loss). Yet section 6.3 is based on the concept
of achieving positive nitrogen balance. These two concepts are
scientifically mutually exclusive. To put both concepts in the same report
without drawing attention to the scientific contradiction would in my opinion,
lead to considerable doubts about the validity of what is in most other respects
an excellent report

2. There
is clearly still a dispute in the Working Group about the question of whether
ketogenic or non-ketogenic diets are preferable. You will note that the vast
majority of the experimental and general use experience relating to safety is at
levels which would be mildly ketogenic. The Group has already accepted that in
practice VLCD at carbohydrate levels per day over 40g (perhaps even over 30g)
are safe. The other considerations leading to a higher suggested carbohydrate
level are theoretical and largely depend upon analytical techniques which are
known to be suspect. Nevertheless, I do not believe that it is necessary to
argue this further. If the working group concludes that carbohydrate below
40g/day is undesirable, but above, say 45g/day is, in practice, reasonable and
safe this will mean that those who favour a mildly ketogenic diet can continue
to use it while those who favour a non-ketogenic one can add more

Section 8.4 deals with the matter of dietary fiber. It does not reach a
conclusion on content, but in the conclusion this becomes translated into
“Fiber: 10 g to max. 30g as an ingredient” I agree that it is now desirable to
define a fiber content, but believe that the what is meant by “fiber” for VLCD
use should be clear. I equally submit that only the ‘minimum’ amount per day
about 10g should be given for the following reasons:

Insoluble fibres, particularly those that can chelate and those with a
high phytate content can block at least mineral absorption. The reduction in the
availability of Ca and Mg and other minerals may be dangerous. Very little work
has been done on this in relation to high fiber use with VLCD. I would prefer
the term “insoluble or soluble fibre” which would avoid this mineral
availability problem.

5. A high
content of soluble fibre (e.g. 30g/day) without other food is very likely to
produce severe diarrhoea either by the osmotic effect or by the substantial
alteration in the intestinal flora. Other recent work with which I have been
involved suggests that this is very likely to be a problem.

Examination of the fiber content of current VLCD in Table 4.2 indicates
that there is virtually no information on the effects above about 10g/day
soluble fiber. The prime role of the SCOOP report is to provide
data. I believe that this recommendation of 10 – 30 g/day goes well beyond

7. If the
minimum is defined as “10 g soluble fiber” it would not stop those who
want to use more from doing so.

8. If we accept the
concept that there should be a “soluble fiber content of 10g/day” this provides
broadly about 5 g ‘available carbohydrate’ (perhaps more under certain specific
conditions). If therefore we reach a conclusion that the content should be “a
minimum of 50 g/day available carbohydrate” this equals the CODEX
content but based on 45g normal carbohydrate and 10g soluble fiber. The use of
the word ‘minimum’ would mean that those who prefer more could use more.”


The evidence
presented in this report demonstrates that the safety of formula diets does not
depend upon the energy content but on the macronutrient and micronutrient
levels. There is, therefore, no valid reason for imposing an entirely arbitrary
lower limit on products that are available to assist those who need to lose
weight. It would be scientifically irrational to expect that energy intake per
se, as opposed to the composition of the diet would affect safety. In all
humans, the daily nutrient and energy needs are made up from both stored
deposits and dietary sources. So far as energy is concerned, even a thin 60kg
‘reference woman’ has some 115,000 kcals available from her body fat
alone. This equates to enough energy to provide for her total requirement for
some 80 days.

This discussion
paper establishes beyond reasonable doubt that the overall safety of VLCD is of the same order as that of LCD in the
800-1200 kcal range. It is difficult to be more precise than this about the
relative safety of the different energy levels of the formula diets because,
whereas the VLCD have been subjected to very extensive study over several years
the number of formal studies of the safety of LCD in the range 800 – 1200kcal)
is by comparison small.

The literature examining the use by
health clinics, and the use by consumers who obtained VLCD on free sale confirms
that they can be regarded as a valuable means of weight reduction and as an
adjuvant for the maintenance of a lower weight. But no only are VLCD as good and
safe as LCD and food based diets but they have advantages in some subjects,

It is widely accepted that
food-based diets (even those devised by dietitians) are far fRom ideal, both in
energy content (Stordy, 1992) and micronutrients (Fisher & Lachance, 1983).
Formula diets on the other hand provide the energy, macronutrients and
micronutrients that are required, bearing in mind that the adipose tissue
contains a very substantial energy store. Formula diets have been shown to be
more effective than normal food based diets as judged by compliance during
weight reduction- Accordingly, it should be no surprise to see that a high
proportion of recent papers, even those that advise behaviour modification and
exercise, advise food replacement with a formula food. Of these current evidence
suggests that VLCD are among the most effective diets for weight reduction and
weight maintenance..

There is no perfect single
weight reducing method and a variety of diets to suit differing desires and
prejudices is desirable, providing such diets do not carry additional health
hazards. This is particularly valid for diets, like VLCD, which have been
extensively studied over at least 25 years and which can be shown to exert
positive health benefits (see below).

There is recent evidence
that the rapidity of weight loss confers additional positive health benefits
independent of the actual amount of weight which is lost, when compared with
food-based diets or higher energy level formula diets. This applies

the management of some
cardiovascular disorders (particularly hypertension where anti-hypertensive
drugs could be withdrawn, Kreitzman & Beeson, 1996)

but particularly with
non-insulin dependent diabetes mellitus (see, for example Lean et al., 1990;
Henry & Gumbiner, 1991; Wing & Greeno, 1994; Wing et al, 1994;
Hernandez-Bayo et al, 1985) in which metabolic control and lipid profile is
markedly improved by the rapid fall in weight using VLCD.

Moreover, meal replacements
of various types, not specifically aimed at slimmers and therefore not
restricted under current legislation, are widely available at energy values
under 150kcal. Most of these have an inadequate nutrient content both for
essential amino acids and micronutrients. These “snacks” which are readily and
freely available can be, and are, used extensively as meal replacements for
weight reducing purposes even though they can not be advised for this use. It is
therefore highly desirable to make nutritionally complete and safer alternatives
like VLCD equally readily available

Additionally, in some cases,
unscrupulous claims are made for protein-rich foods supplemented with various
levels of vitamin and minerals. There is currently no means by which their use
can be controlled and the risk of inadequate nutrition is clear.

There is a view that a
proportion of the obese are dependent on food – probably specifically fat. With
any dependence it is vital to wean the subject off their substance of dependence
as the first stage in effecting a change in behaviour This clear benefit of
formula VLCD over traditional food-based diets has proved to be a valuable
adjunct to weight maintenance in some people.

It is therefore submitted that modern
nutrient-complete formula VLCD have an important place in weight reduction and
their availability under the same regulations as other formula diets (of
800kcals and above} is fully justified


5.1 Medical precautions for
the use of VLCD.

There is no
dispute that like many weight loss programmes VLCD should only be used as the
sole source of nutrition by those in otherwise good health, unless the dieter is
under the advice or supervision of a medical practitioner.

A list of
contraindications has been published in most examples of the current
legislation. For some physiological and pathological conditions, we submit that
the contraindication should be absolute, that is, VLCD should only be used by
those with considerable expertise in the field. For the remainder, in our
opinion the ultimate responsibility for deciding on the balance of benefit/risk
lies with the medical practitioner, who will be best able to judge the overall
needs of the individual patient. In those circumstances we submit that VLCD
should only be used with the explicit agreement of the practitioner.

We would draw
attention to the fact that some specialist out-patient clinics have used VLCD in
a number of obese patients suffering from disorders in the list of medical
contraindications. They have encountered no problems and a high success record
(Weinkove et al., 1987. Shapiro et al., 1989 Paisey et al, 1998; Miles, Cavan
& Kerr , 2000). However, it is important to stress that considerable
experience of the use of VLCD is essential for such use.

In particular the changing attitude
towards the use of VLCD in NIDDM should be noted. This condition was originally
placed by many authorities in the list of contraindications. Recent studies
(Fukuda et al 1989. Wing et al 1991; Kelley et al 1993; Wing et al 1994; Brown
et al 1996; Gumbiner et al 1996; inter alia) have shown that VLCD (probably
intermittent use, and obviously under medical supervision) has considerable
value in the management of NIDDM. The extent of these successful studies raises
questions about the validity of the report from Koffler and Kisch (1996) in just
one unit that VLCD can lead to diabetes.

Advice that any form of dieting should be used only
under the supervision of a medical practitioner also applies to those who are
receiving an established list of prescribed medications and this list is widely
quoted in current legislation. There is little dispute about the medications in
this list. Since many patients are unaware of the nature of the medication which
they are being prescribed, we believe that the sensible advice is that any patient receiving prescribed
should only undertake any form of dieting under the direction of
or after receiving clearance from their medical practitioner.

A list of
contraindications to any form of effective dieting is as follows:


Children and adolescents Pregnancy and

The elderly

Illnesses and disorders

Type 1 diabetes

Recent myocardial infarction

Cardiac arrhythmias

Recent stroke or serious heart

Renal disease

Major psychiatric disorders or substance




Insulin and oral hypoglycaemic


5.2 Medical supervision of individuals
apparently clinically healthy apart from excess weight

It is our view
that, while medical advice may be desirable for all forms of weight loss, it is
not actually essential for those who are overweight or moderately obese though
otherwise healthy.

Indeed the question must be raised
whether medical supervision has great merit in the management of the ” otherwise
normal overweight and moderately obese”.

It is clear from many
comments by patients that the medical profession in general, while accepting the
problems associated with obesity, have little interest in supervising treatment
which they regard as unrewarding. The standard medical approach is still
reported as being “You need to lose weight. Here is a diet sheet. Come back when
you have lost 15 kilos”

Non qualified advisors with
interest in the subject are probably just as good and careful about safety
aspects (Atkinson & Kaiser 1981; Cox et al 1990; Blackburn 1993).

12 of the 17 “liquid protein
death” patients had been under the direct care of medical practitioners. The
evidence in the original reports suggests that the standard of care they
provided was entirely appropriate. It is just that with an inappropriate
formulation there were not early signs that could be recognised more readily by
medical practitioners. It is just not true that “if only they had been under
appropriate medical care the tragedy would have been avoided”]

Surveys referred
to in various official reports suggest that some 30% of those who use VLCD in
conditions of free-sale consult their practitioners before starting the
diet, a proportion well above that for all other forms of dieting. The
information provided in this report con6rms that there is no evidence of a
relationship between safety and the energy intake. It is the composition of the
diet which affects the safety.

W e therefore
submit that logically, all diets, including those published in the lay media
should require medical advice for use by healthy individuals or none should. It
is however suggested that attention should be directed to the fad diets and
nostrums which are widely advertised and available in the European Union with no
controls, no benefits.

The information in this discussion
paper does however support the view that for those who suffer from certain
illnesses or disorders, for those receiving defined medications, as well as
those needing to lose substantial weight by any method there should be
requirement that they seek medical advice



In order for weight loss programmes to be successful, it is essential to conduct post-diet monitoring and provide the overweight patient with long-term support. The Lipotrim pharmacy-based programme, therefore, encourages an interactive approach with GPs to ensure successful, sustained weight management

it seems easy to justify practice time and resources to assist overweight and obese patients lose weight. The link to type 2 diabetes alone is sufficient. With rapid weight loss, normalisation of blood sugar levels is achieved in days. With further weight loss, the disease can be held in remission.
Better long-term glycaemic control is achieved with rapid weight loss, even after some weight regain, than is achieved by losing the same amount of weight more slowly. Almost 50% of hypertensive patients can reduce drug treatments with weight loss. Surgical interventions can be scheduled when substantial weight is lost. Fewer antidepressants are required and overall, the frequency of GP visits is significantly lower for leaner patients.
There is no shortage of choice to meet the weight loss needs of individual patients: drugs, both current and promised for the future; dietetic referral; exercise on prescription and pharmacy-based treatment programmes. Each has a place depending upon the specific clinical needs of the patient. An exercise prescription may not be the best choice for a 40-stone patient who may struggle simply to walk, which at this weight is considerable exercise.
While willpower can often help people lose weight over a short defined period, upholding control for the months, years or even decades required for maintenance is quite a different story. Loss of weight by any means confers absolutely no lasting legacy for weight maintenance. Weight loss, however achieved, is only the beginning of the treatment, not the end point. When the drug therapy is discontinued, when the counsellor moves on, when the patient is “cured” of excess weight – this is the point at which a dieter requires the maximum attention and assistance.
Weight management requires control of eating behaviour over a sustained period of time. A difficulty comes with justifying practice time and resources for a patient who has achieved weight loss and is now both healthier and at a normal weight. The expectation that this patient will sustain the weight loss without considerable help is naïve.

Lipotrim pharmacy-based programmes are ideal for the varying weight management needs of patients. Obesity prevention is part of the pharmacy complement of health promotion services, dealing with excess weight before it reaches obese levels and exacerbates comorbidities. The care of patients during weight loss is advantageous when monitored by the pharmacist, who understands the implications of other drug treatments that may interact with the weight-loss programme. But it is at the post-diet stage that the pharmacist is best equipped to provide essential long-range guidance, support and education that will increase the length of time that the weight loss is maintained.
Both the new GP and the pharmacy contracts strongly encourage interactive efforts to deal with a range of health problems, most of which have weight-related implications. Weight loss is vital for management of cholesterol, blood lipids, diabetes, hypertension and asthma. It even impacts upon programmes for smoking cessation. The success of the Lipotrim pharmacy-based programmes in dealing with weight loss and maintenance should not be overlooked.

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