Your Nutritionist Recommends

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How to reduce your risk of obesity and cardiovascular disease
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How to reduce your risk of obesity and cardiovascular disease

You have the short-term or the long-term option

Maria Cross's avatar
Maria Cross
Oct 20, 2024
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How to reduce your risk of obesity and cardiovascular disease
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The UK Government is determined to tackle the nation’s obesity crisis and has come up with a cracking solution: provide free weight loss jabs on the National Health Service.

The NHS chief executive, Amanda Pritchard, agrees, saying that the drugs could also reduce the risk of diabetes, heart attack and stroke.

The real reason for this experiment, sorry, initiative, is to get the fat, sick and idle back to work. According to the Prime Minister Keir Starmer, the Government must “think differently”, what with the dire economic situation we’re in. So here’s different thinking in action.

We need to increase revenue, because obesity-related illness, including cardiovascular disease, costs the NHS £11 billion a year and the loss in productivity amounts to nearly £100 billion.

The scheme is a win-win opportunity, at least for the Government and for the maker of the jab, the world’s largest pharmaceutical company Lilly. Plans have been announced of a five-year trial of the drug, Mounjaro, involving nearly 250,000 people.

Like similar injectable weight loss drugs, Mounjaro works by increasing production of insulin and keeps you feeling full for longer. It is seen as a rival to the better known Ozempic and Wegovy, made by Novo Nordisk. These two drugs are classified as semaglutides and work by mimicking the hormone GLP-1, which creates a sense of fullness and stimulates insulin production. Mounjaro is classified as a tirzepatide and works in a similar way.

Wegovy is already available to some people on the NHS through specialist weight management clinics. It has also been approved as a drug to lower the risk of heart attack and stroke in people considered at risk.

What these drugs do is tackle metabolic syndrome. This is a pre-diabetic condition, characterised by a cluster of symptoms that constitute a serious risk of developing cardiovascular disease, stroke, and diabetes. Those symptoms include overweight and obesity, high blood pressure and poor blood sugar management.

The scheme seems like a dream come true, but like all dreams it’s short-lived, unless you stay on the drugs for the rest of your life. The consequences of doing so are unknown. And you’ll have to stump up, too: these drugs are costly, and the NHS will only cover the cost for two years maximum. Once you stop, expect your appetite to return with renewed vigour. That’s if you can still tolerate the side effects: nausea, diarrhoea or constipation and in more serious cases gall bladder disease and kidney issues.

Which brings us to the second, long-term option, which works in a surprisingly similar way to the first, and produces similar results.

There are several hormones involved in appetite regulation, other than GLP-1. The two main ones are ghrelin and leptin. Ghrelin is produced in the stomach and, via the vagus nerve, tells the brain that you are hungry. Leptin does the opposite: it suppresses ghrelin by informing your brain that you have had enough. It is secreted predominantly by fat cells and by the small intestine.

Another hormone, cholecystokinin (CCK), is also secreted in the small intestine, once you’ve had something to eat.  Like weight-loss injections, CCK slows down the rate at which food leaves the stomach, so you stay full for longer. It also suppresses ghrelin and stimulates another appetite-suppressing hormone, PYY.

Production of PYY increases after eating and decreases during fasting. PYY also increases energy expenditure and the rate at which you burn fat.

This orchestra of hormones keeps food intake at the ‘normal’ setting. But how well they work, and how long for, depends on what you eat.

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