“I think the first thing that people fail to appreciate is what a valuable evolutionary step it was to be able to store fuel,” says Randy Seeley, who researches energy balance and metabolism at the University of Michigan. “If you’re not able to do that, you’re a filter feeder: you have to swim in your food.”

But while many organisms possess some form of body fat, in mammals, it has evolved into something much more complex than just a kind of meaty bubble wrap, says Seeley. “It also now becomes integrated into the overall regulation of blood glucose, body temperature and other physiological functions, including bone health.”

Controlling hunger

The first clues that we were underestimating our body fat came in the 1990s with the discovery of leptin. This hormone, secreted by fat cells, acts on the brain to suppress appetite and boost energy expenditure. On the flip side, when people quickly lose fat, leptin levels drop, which the brain interprets as a sign that energy stores might be running low. It responds by ramping up hunger signals and reducing energy expenditure to help you regain that lost fat.

The discovery of leptin cracked open a hidden communications network between fat and the rest of the body. Since then, we have discovered that fat cells release many more hormones and other signalling molecules, some of which communicate with tissues nearby, while some travel much further afield. Together, they are known as adipokines.

What’s more, this communication isn’t only chemical – it’s also electrical. We now have evidence for networks of nerve fibres extending deep inside adipose tissues, forming a direct, two-way line of communication between the brain and our fat.

“The nerve supply in adipose tissue enables a bidirectional and fast communication route with the brain,” says Kristy Townsend, a neuroscientist at The Ohio State University who studies fat. As well as sending messages about energy and metabolism, nerves allow fat to quickly communicate its health status, for instance, whether it is injured or inflamed.

Fat and immune health

Immune cells may also join these conversations, relaying information about inflammation or injury and releasing molecules that help nerves survive and grow. “If you look at the tissue in between all the adipocytes, there’s pretty much every immune cell you can imagine – so fat is also an immune organ,” says Townsend.

In short, fat doesn’t just store energy; it speaks. And together, these adipokines, immune cells and nerve fibres form the vocabulary of an unexpectedly sophisticated organ.

The far-reaching impacts of fat are only now coming to light. Its best-documented role is in energy balance (see “Your unappreciated organ”, below), telling the brain when reserves are full or depleted. But fat’s communication with the brain also seems to extend to our moods. While mood disorders such as depression or anxiety are complex, and stigma or poor body image may also contribute to this, evidence is increasingly linking obesity – particularly metabolically unhealthy obesity – to these conditions.

While the mechanisms are still under investigation, the leading idea is that inflammation within adipose tissue triggers brain inflammation, which in turn alters the balance of neurotransmitters and triggers behavioural changes. Altered levels of leptin may also influence brain reward circuits and mood regulation.

And our fat plays a crucial role in fertility, too. Without a minimum level of body fat, for example, menstruation won’t start or will stop, which makes sense, because entering pregnancy without sufficient energy to sustain a developing fetus could be catastrophic for both mother and child.

“People forget that fat is metabolically really important. Without fat, we have issues with hormonal control, infection immunity,” says Louise Thomas, a professor of metabolic imaging at the University of Westminster in London.

When fat turns bad

So if fat is such a crucial factor in our health, why does it get such a bad rap? The first issue is its location. White fat makes up more than 95 per cent of our total stores and is found both under the skin (subcutaneous fat) and wrapped around internal organs (visceral fat). “Our organs are often sitting in a sea of fat,” says Thomas.

That internal sea can turn toxic. Excess visceral fat is linked to a higher risk of type 2 diabetes, high blood pressure, heart attacks and certain cancers. Growing evidence also suggests it may affect brain function and contribute to conditions such as Alzheimer’s disease.

What triggers this shift from cooperative organ to rogue state is a major focus of research. While white fat cells in both subcutaneous and visceral deposits can expand and contract depending on the body’s storage needs, those surrounding internal organs appear especially vulnerable to the harmful effects of excess fat.

In obesity, these fat cells enlarge and are prone to dying once they reach a critical size. Part of the problem is that their blood supply can’t keep up with their growth. Stressed and suffocating, they release inflammatory molecules as distress signals, attracting immune cells to clear dead or dying cells.

These immune cells intensify the inflammation, with effects reaching far beyond the fat itself. The chemical signals interfere with insulin – the hormone that regulates blood sugar – raising the risk of type 2 diabetes. They are also linked to cognitive changes seen in obesity such as memory and attention problems, and may create conditions that foster tumour growth. Obesity is a risk factor for many kinds of cancer, and often people who are obese tend to have worse outcomes.

Dying or overstuffed fat cells also release fatty acids, or lipids, into their surroundings – and in excess, these can be toxic to surrounding cells. Over time, this lipotoxic stress can damage the network of nerves threaded through fat, a condition known as adipose neuropathy. Obesity, type 2 diabetes and ageing are all linked to this loss of peripheral nerves, which further disrupts metabolism by impairing communication between the brain and fat.

Protecting bone health

Misfiring fat signals can also play havoc with our bones. Most of the time, oestrogen produced by adipose tissue can help protect against excessive bone resorption – where old bone tissue is broken down faster, then new bone can replace it. However, growing evidence suggests that excess fat, particularly visceral fat and fat accumulation within bone marrow, can impair bone quality and increase fracture risk. This is partly because inflammatory cytokines released by adipose tissue can stimulate osteoclasts, the cells responsible for bone resorption, which, in turn, promotes bone loss.

Despite the downsides of dysfunctional fat, adipose itself isn’t the enemy – we need it. And efforts to get rid of it can backfire. Studies of liposuction, a cosmetic procedure that removes targeted fat, suggest that the extracted fat may simply reappear elsewhere. “You may want to remove fat from some locations, but you may like even less where you get it afterwards,” says Seeley, who has been involved in some of this research. “If you remove subcutaneous fat, you’re probably going to end up with more visceral fat in the long run, and that probably leaves you in a worse place than where you were before.”

Not everyone with obesity is unhealthy, either. Between 10 and 30 per cent of people classified as obese based on body mass index seem to escape the usual health effects, such as insulin resistance, high blood pressure and unhealthy cholesterol levels – at least in the short term. This so-called metabolically healthy obesity has intrigued researchers like Matthias Blüher at the University of Leipzig in Germany.

About 15 years ago, Blüher and his colleagues began comparing fat tissue from people with obesity who developed insulin resistance – often a precursor to the development of type 2 diabetes – and those who didn’t. They found that where excess fat sits and how it behaves are both crucial: people with more visceral and liver fat tended to be metabolically less healthy, while those whose adipose tissue contained smaller fat cells, fewer immune cells and a healthier secretion pattern of adipokines appeared to be more protected.

Different types of fat

More recently, the researchers have taken this investigation down to the cellular level, analysing which genes are active in different fat deposits across dozens of people with healthy and unhealthy obesity. Their results, published earlier this year, reinforce that not all visceral fat is equal. “Even within the visceral cavity, it makes a difference where the fat is located,” says Blüher. The highest risk is associated with fat that sits outside of the intestine, although, for now, they aren’t sure why this is the case.

The fat also looks different in people with healthy obesity: their fat cells are more metabolically flexible – able to switch efficiently between storing and burning energy – pump out fewer inflammatory signals and host fewer immune cells. Their visceral fat also contains mesothelial cells, which can transform into other cell types, perhaps enabling their fat to expand more smoothly without triggering excessive inflammation. Why some people have more of these metabolically healthy cells is probably down to genetics, although lifestyle factors such as diet and exercise may play a role.

Either way, Blüher thinks that these insights could help doctors identify which people with obesity are at the highest risk of complications, and then tailor treatment accordingly.

Reprogramming fat for health

His longer-term dream is to find a way to restore fat’s healthy function – perhaps even transform “unhealthy” obesity into a permanently more benign form. Encouragingly, this may not require dramatic weight loss. Many of the benefits of modern weight-loss drugs and bariatric surgery seem to stem not from the amount of weight lost, but from improving fat distribution and function, says Blüher. “In bariatric surgery, even if people don’t lose a lot of weight, the health benefits start almost immediately.”

Achieving this would be revolutionary, not least because it would prompt a rethink of what a healthy body shape looks like.

And if fat could be reprogrammed to behave more healthily – or the cellular memories of its bloated heyday erased (see “The yo-yo effect”, below) – many more of us might live longer, healthier lives without obsessing over size.

Whether obesity begins in the adipose tissue or the brain is still debated, but it is clear that when communication between the two falters, the whole system drifts off-kilter.

Seeley likens the situation to an orchestra: “All of these organ systems – your liver, pancreas, adipose tissue, muscle and gastrointestinal tract – are all talking to your brain, and your brain is talking to all of them. If your symphony conductor isn’t doing a good job, then even if all your instruments are OK, it won’t sound great.”

In other words, fat isn’t necessarily the problem; it’s an instrument playing slightly out of tune in a misdirected symphony. Many of us have been conditioned to try to shrink, remove or hide our body fat. But the real task is to understand it – to coax this creamy, talkative organ back into harmony with the rest of the orchestra. Because when it plays well, it helps keep the whole body in tune.