the condition yourself, no matter what you do. And genetics is generally too complex a subject to be able to make very accurate predictions. So any recommendations regarding eating certain foods to prevent disease should read something like this: “ Eat such-and-such food, and you may be able to make a slight difference to your overall risk of developing the condition, unless your genes say otherwise, and who can tell if this is the case?” It seems that almost every day a new association between diet and health is discovered. Certain food groups have been shown in reliable studies to decrease the risk of various conditions; for example, the high lycopene content of tomatoes helps to prevent prostate cancer, and calcium-containing foods such as yoghurt and broccoli delay the onset of osteoporosis.

Other foods have been shown to cause, or aggravate, particular conditions. People with high blood pressure are routinely advised to cut down on salt intake. Gout sufferers are all too aware of the impact that some foods, especially drinks like beer (even alcohol-free beer!) have on their joints.

The problem with these food-health relationships, is that they are not very specific, or predictable. How many tomatoes must you eat, and for how long, for it to have a protective effect on your prostate? Assuming, of course, that you are a man and therefore would have one of these. And how much yoghurt and broccoli should you eat to help delay the onset of osteoporosis? Nobody seems to know the answers to these problems, and so it is generally recommended that we eat as much of the protective food types as we can, while avoiding the less favourable things like salt and saturated fats.

Recommendations like these seem to be a bit too vague for my liking. In this era of precise measurements and percentages, it could be expected that someone would be able to prescribe a daily or weekly portion of the particular food group required to decrease the risk of having a condition by a precise percentage. But this is just not possible. Confounding factors such as genetics need to be taken into account; if you have a family history of an illness you may have a genetic predisposition to having the condition yourself, no matter what you do. And genetics is generally too complex a subject to be able to make very accurate predictions. So any recommendations regarding eating certain foods to prevent disease should read something like this: “ Eat such-and-such food, and you may be able to make a slight difference to your overall risk of developing the condition, unless your genes say otherwise, and who can tell if this is the case?”

People with high blood pressure are routinely advised to cut down on salt intake. Gout sufferers are all too aware of the impact that some foods, especially drinks like beer (even alcohol-free beer!) have on their joints.

The problem with these food-health relationships, is that they are not very specific, or predictable. How many tomatoes must you eat, and for how long, for it to have a protective effect on your prostate? Assuming, of course, that you are a man and therefore would have one of these. And how much yoghurt and broccoli should you eat to help delay the onset of osteoporosis? Nobody seems to know the answers to these problems, and so it is generally recommended that we eat as much of the protective food types as we can, while avoiding the less favourable things like salt and saturated fats.

Recommendations like these seem to be a bit too vague for my liking. In this era of precise measurements and percentages, it could be expected that someone would be able to prescribe a daily or weekly portion of the particular food group required to decrease the risk of having a condition by a precise percentage. But this is just not possible. Confounding factors such as genetics need to be taken into account; if you have a family history of an illness you may have a genetic predisposition to having the condition yourself, no matter what you do. And genetics is generally too complex a subject to be able to make very accurate predictions. So any recommendations regarding eating certain foods to prevent disease should read something like this: “ Eat such-and-such food, and you may be able to make a slight difference to your overall risk of developing the condition, unless your genes say otherwise, and who can tell if this is the case?”

of course, that you are a man and therefore would have one of these. And how much yoghurt and broccoli should you eat to help delay the onset of osteoporosis? Nobody seems to know the answers to these problems, and so it is generally recommended that we eat as much of the protective food types as we can, while avoiding the less favourable things like salt and saturated fats.

Recommendations like these seem to be a bit too vague for my liking. In this era of precise measurements and percentages, it could be expected that someone would be able to prescribe a daily or weekly portion of the particular food group required to decrease the risk of having a condition by a precise percentage. But this is just not possible. Confounding factors such as genetics need to be taken into account; if you have a family history of an illness you may have a genetic predisposition to having the condition yourself, no matter what you do. And genetics is generally too complex a subject to be able to make very accurate predictions. So any recommendations regarding eating certain foods to prevent disease should read something like this: “ Eat such-and-such food, and you may be able to make a slight difference to your overall risk of developing the condition, unless your genes say otherwise, and who can tell if this is the case?”

liking. In this era of precise measurements and percentages, it could be expected that someone would be able to prescribe a daily or weekly portion of the particular food group required to decrease the risk of having a condition by a precise percentage. But this is just not possible. Confounding factors such as genetics need to be taken into account; if you have a family history of an illness you may have a genetic predisposition to having the condition yourself, no matter what you do. And genetics is generally too complex a subject to be able to make very accurate predictions. So any recommendations regarding eating certain foods to prevent disease should read something like this: “ Eat such-and-such food, and you may be able to make a slight difference to your overall risk of developing the condition, unless your genes say otherwise, and who can tell if this is the case?” the condition yourself, no matter what you do. And genetics is generally too complex a subject to be able to make very accurate predictions. So any recommendations regarding eating certain foods to prevent disease should read something like this: “ Eat such-and-such food, and you may be able to make a slight difference to your overall risk of developing the condition, unless your genes say otherwise, and who can tell if this is the case?” Some prediction!

However, there is one condition where lifestyle and diet will always have a predictable impact on its severity and course, and that is insulin resistance.

“What?” you say. “Never heard of it.” And most people haven’t heard of it, despite the fact that it is one of the most prevalent conditions in the world today. It is more common than diabetes; in fact, insulin resistance is the cause of type 2 diabetes, and has been estimated to affect about one in four people.

So what is insulin resistance?

The answer is not a simple one: insulin resistance is a complex entity, which involves a spectrum of conditions ranging from excess weight around the waist, to type 2 diabetes mellitus. It is the single cause of conditions such as metabolic syndrome, polycystic ovarian syndrome and type 2 diabetes, and is strongly associated with high blood pressure, cholesterol abnormalities, gout, and most frighteningly, sudden death, especially in middle-aged women. In short, it is a medical time bomb.

Its origins are not always clear-cut either. Insulin resistance tends to run in families – although not everyone in the same family is necessarily equally affected. A brother may never show any symptoms of the illness, while his sister may have significant weight problems and go on to develop type 2 diabetes at the age of forty. Or vice versa. Why this happens is not always apparent, although diet and lifestyle do play very significant roles in the progression of the condition.

Insulin resistance may also be “acquired”; in other words it develops in an individual with no family background of insulin resistance and its associated conditions. This usually occurs in people who are overweight for whatever reasons. It has bee