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These comments were prompted by a suggestion made by scientists at the University of Buckingham
Claire Williamson, Nutrition Scientist, British Nutrition Foundation, said:
“Leptin is a hormone that is synthesised in adipose (fat) tissue which appears to signal how much fat is stored, thus helping to regulate appetite. Researchers in the past found that when leptin was injected into specially bred mice, the mice ate less, burned food faster and lost significant amounts of weight.
“However, the precise details of the leptin system and its physiological significance in human weight control still remain to be fully understood.
“The research in rats supplemented with leptin is in its very early stages and needs to be replicated by further studies. Furthermore, results from animal studies cannot be assumed to apply to humans, so it is much too early to say whether this could be a possible way to prevent obesity in humans.
“Obesity is a complex disorder with a diverse range of causal factors, which makes it a complex and challenging disorder to tackle. Both genetic and environmental factors come into play in the causes of obesity. However, one incontrovertible fact is that for an individual to become obese, energy intake (i.e. energy from food) must exceed energy expenditure (i.e. through physical activity) for an extended period of time.”
Christine Hancock, European Director of the Oxford Health Alliance, said:
“These new foods must be treated with caution. If children grow up thinking they will remain thin, regardless of their lifestyle, they might be dissuaded from engaging in regular physical activity and maintaining a healthy diet, especially in their adult years. This is worrying, as such activity can help prevent a number of chronic diseases, such as heart disease, hypertension and many cancers – as well as type 2 diabetes.”
Steve O’Rahilly, Professor of Clinical Biochemistry and Medicine, University of Cambridge, said:
“Leptin is a very important hormone, normally produced in fat cells, that goes to the brain and keeps it informed about the amount of fat stored in the body. Humans who lack the leptin gene feel hungry all the time and become very obese. Leptin injections cure this. However most fat people have lots of circulating leptin and it seems that their brain do not fully recognise the leptin signal. Recent work has suggested that, early in life, leptin might have effects in the brain areas controlling feeding that are permanently etched and continue to exert effects as an animal grows up. Several workers have suggested that exposing animals to higher leptin levels during early life might have long-lasting benefits in terms of protection against later obesity. This still needs to be firmed up. The notion that leptin in baby milk will prevent human obesity is currently in the realms of wildly optimistic science fiction for a number of reasons. Firstly, leptin is a large peptide and most of it will be broken down in the gut ; secondly there is no evidence whatsoever that this “early life” imprinting effect of leptin is at all relevant for humans. On the contrary, when humans who have totally lacked leptin due to a genetic lesion for over 40 years are given leptin injections, they rapidly return to a normal body weight. If this “early exposure” were a critical event, you would not expect that to happen.”
Keith Frayn, Professor of Human Metabolism, University of Oxford, said:
“First, of course it is not easy to deliver peptides (as leptin is) by ingestion. They are broken down by the normal processes of digestion into amino acids. That’s why people with diabetes have to inject insulin rather than taking it in pills. So either the Buckingham scientists have developed a clever way of protecting the leptin from digestion (which has never been achieved for insulin) – or perhaps they intend to deliver it to very young infants (neonates) whose gut is somewhat permeable to proteins (that’s how breast milk delivers antibodies to the baby).
“Secondly, there is the question of whether leptin would work to suppress appetite in humans as it does in rodents. Clinical trials with injection of leptin as a treatment for obesity have been very disappointing. It seems that in humans, delivering more leptin than is already there doesn’t do much to appetite. Leptin is really a signal of starvation: when leptin levels fall below normal, hunger is stimulated. Hence the only real leptin-related condition in humans in leptin deficiency (identified in a very small number of children who are massively obese). But this is such a rare condition (only about 10 I think identified world-wide) that it cannot be the intention of the Buckingham scientists to treat them.
“So I think we need much more convincing that (1) the leptin in food will reach the bloodstream and (2) even if it does, it will have any effect in suppressing appetite.”
Dr Nick Finer, Clinical Director, Wellcome Clinical Research Facility, Addenbrookes Hospital, Cambridge, said:
“The importance of leptin (and other hormones) at determining the development of brain circuits that control energy balance is an area of current research interest. The leap to a functional food being effective or safe is enormous. All obesities result from an excess of energy intake (food) over energy expenditure (basal metabolism and the costs of activity and exercise) so any treatment must have effects on either or both arms of the equation. Most human obesities are thought to result from altered appetite rather than energy expenditure. In the rare children with leptin deficiency, replacement mainly results in a dramatic decrease in appetite rather than increased energy expenditure. We also know that leptin is only one of many signals to the brain informing it of the body’s energy stores. Even if this approach is shown to be valid in humans, extensive clinical trials would be needed to allow the right dose to be chosen and to show that the approach was safe. The concept that adding something to a food that could permanently alter brain development is exciting but at the same time so scary that it would mean a wholly new approach about how such treatments can be tested and approved for use. Would the first trials be in newly born children?”
Amelia Lake, Post doc research fellow in obesogenic environments, Newcastle University, dietitian, and registered public health nutritionist, said:
“Obesity is a complex problem, which is the result of an energy imbalance. While we are making headlines with new scientific discoveries the facts are simples: too much energy in and too little energy out equals overweight and often obesity.
“Our society is obesogenic, which means it encourages us to consume energy dense foods and to be fairly inactive. In order to address the obesity epidemic we need to tackle the obesogenic environment.
“This work, while interesting, is based on animal models and not on real-life situations with social cues for eating as well as cultural contexts for behaviour.”
Dr Ian Campbell, Hon. Medical Director of Weight Concern, said:
“Without evidence that this works in humans, it is pure flight of fancy that those consuming leptin from infancy will never get fat. I’d be surprised if this product could be advertised or marketed with these extraordinary claims.
“To date, leptin has proved to be a great disappointment. Most of us have plenty and true deficiencies are rare. In fact, obese people tend to have higher than normal levels.”