But there is also an acquired form that sneaks up on people later in life, diabetes 2. (Today there are researchers looking into whether there may also be a number of intermediate forms between diabetes 1 and 2, but we’ll leave that aside here for the sake of simplicity.)
To sketch out a simple explanatory diagram for this process, when you eat sugar and your blood sugar level rises, a signal is sent to the pancreatic gland, which releases insulin. The insulin is sluiced out and ‘opens up’ the cells in order to sluice in the broken-down sugar, along with proteins and fat.
When the body constantly takes in large amounts of sugar and insulin levels have to stay elevated in order to shuttle the sugar out of the bloodstream and into the cells, it creates a so-called insulin resistance. In other words, there is insulin in the blood that’s supposed to deal with the sugar, and that makes the insulin attach to the cells, but something goes wrong in the communication between the insulin and the cells. The cells simply lose their ability to react to the presence of insulin. The number of people who have metabolic syndrome is growing rapidly, because more and more people eat the wrong kind of food, have a sedentary lifestyle, and/or suffer from stress and other psychosocial problems.
The above-mentioned triple combination, with diabetes/belly fat/high blood pressure, used to be a medical condition that affected mainly older people. But now it’s increasing even among younger men and women. Altogether it’s estimated that one quarter of the adult population in the United States, Canada and Europe have metabolic syndrome. In short, we are talking about an epidemic that is increasing like an avalanche in the Western world, an enormous threat to public health.
In the past, each of these diseases was studied separately. But Inger Björck and many other researchers worldwide are now beginning to realise that the diseases are in fact connected.
‘Then you have to wonder, how can suffering be prevented?’ she says.
Inger Björck is carrying out innovative research in this area. For example, she’s studied mice that have been fed either a high-fat or a low-fat diet. In addition to that diet, the mice were given different berries and fruits like lingonberries, raspberries, prunes and currants. It turned out that the mice who ate berries – especially lingonberries – maintained the same weight regardless of whether they ate a high-fat or low-fat diet. The lingonberry group actually lost some weight, even with a high-fat diet.
Björck believes that the risk of diabetes 2 and coronary artery disease can be decreased by means of an entirely new method, a new category of food in which berries are part of a larger food group.
‘These foods are called anti-inflammatory,’ she says.
I make a note of the name. It calls to mind what I read about in Dr Perricone’s books ten years earlier.
Then Professor Björck begins to explain how these new foods can affect the whole person, not only blood pressure and cholesterol levels but also cognitive ability, or the brain function that includes a person’s intelligence, in the broad sense of the word – our capacity to think, remember, solve problems and learn new things. This research sounds both creative and worthwhile, and so far I’m following her presentation with interest. This is worth supporting, my professional self acknowledges in an observant yet slightly distant fashion.
But when she shows us the list of the foods the researchers have been using to achieve these results in people, I get a shock. A slow-motion lightning bolt strikes my brain, and I sit at the very edge of my chair, suddenly wide awake.
First, there are things like decreasing sugar, doing away with white flour, increasing the intake of all kinds of berries, increasing the amount of vegetables and fatty fish, and adding vinegar and probiotic supplements. But then comes a concrete list of foods, and it looks like . . . Rita’s food list?
My heart does a quiet leap of recognition and time stands still. I gaze around me at the old meeting room, with its view of the university library’s stepped gable in brick. The great linden trees shimmer with fresh new leaves in the spring evening.
What is this? Have I unknowingly been eating anti-inflammatory foods and thus affected my body much more deeply than I had realised?
The effects I’ve felt are exactly the ones that Inger Björck describes in her test subjects. They grew stronger, reduced their waistlines, expanded their mental capacity and developed more of a zest for life.
Or is it just an amazing coincidence?
After the talk, we are served an anti-inflammatory buffet that the researchers have designed themselves. They’ve even baked their own bread, similar to Danish rye bread, using whole barley. There are salads, fatty fish and nuts, and everything is delicious. Over one of the salads, I share my insight with another woman. I lean forward confidentially, almost a little embarrassed.
‘I’ve actually been eating like this for a few months. Or at least trying to.’
‘I thought you looked energetic, somehow,’ she says, looking at me appraisingly.
I go up to Professor Björck and tell her that there are in fact people who live like this every day but who haven’t quite made the scientific connection to anti-inflammation that Björck’s team has. They just do it because they’ve discovered that it works.
‘Who are they?’ she wonders.
‘Well . . . fitness people in the United States and Canada,’ I say.
She looks surprised. We agree to stay in touch. And that’s where my own journey of knowledge begins.
Inflammation and anti-inflammation. What is this all about? I have to learn more.
I begin racking my brain for long-ago facts from my university studies in immunology. I think I took that course in the red building at the old Veterinary College in Frescati in Stockholm, if I remember correctly, and we learned something about the two forms of inflammation – because inflammation is not always a bad thing.
The first type of inflammation is purely positive, a helping process. Imagine a cut from a kitchen knife, a finger squeezed in the car door, a urinary tract infection or a sore throat. When you’re injured or infected, your immune system starts producing inflammation as a defence mechanism. A teacher I once had used this image to describe it: imagine a land that is being attacked by an external enemy and wants to defend itself. That’s how the immune system works. The outer injury is the external enemy, the immune response is the country’s government and defence, and the inflammation is part of what you have to do to defend yourself. There are a number of different foot soldiers who help. These soldiers in turn have many different specialist functions, just like in a regular army, with bridge builders, telegraph operators, explosives experts and intelligence agents.
In human blood, the blood platelets constantly wander around looking for problems in the blood. The blood platelets gather around the problem – the cut, the bruise or the infected body part – and then send a chemical signal to the immune system.
‘Problem at g, come here right away,’ say the blood platelets.
The signal is intercepted by the white blood cells, who answer, ‘On our way.’
An advanced line of defence is set up, with many different types of foot soldiers. They’re called cytokines, leukotrienes, prostaglandins, chemokines, thromboxanes and so forth, and they function like support troops, where each one sets out with its own task. They expand the blood vessels at the site of the affected tissue and make the area around it more ‘transparent’. This means that more cells from the immune system can reach the injury,