The Diet Myth by Tim Spector dismantles the conventional wisdom behind dieting, replacing simplistic calorie-counting and fat-phobia with a science-led understanding of how individual our bodies truly are. Drawing on his work with identical twins, Spector shows that even people with the same DNA can have radically different waistlines, proving that genes alone cannot explain the obesity epidemic — UK obesity rose from 7% in 1980 to 28% by 2018, far too fast for genetic adaptation, which needs roughly a hundred generations.
The book's central argument is that our bodies and our gut microbiome are deeply personal. Taste itself is genetically unique: we carry dozens of variants for bitter, sweet, and umami detection, influencing what we eat and crave. Spector repeatedly challenges nutritional dogma with evidence:
Spector weaves in fibre-rich regimes, soy isoflavones and their epigenetic effects, and citizen-science microbiome testing to argue that there is no single right diet. Instead, dietary diversity, fermented foods, and feeding a varied gut ecosystem matter more than any fad. The takeaway is liberating but demanding: ignore the myths, distrust one-size-fits-all rules, and pay attention to your own microbial and genetic individuality.
Our bodies simply seem to adapt to the new reduced calorie intake and do what they are programmed by evolution to do. It appears that the dull monotony of most exclusion diets is overridden by the body’s impulse to hold on to our fat stores. Once someone has been obese for a while, a whole series of biological changes transpire to maintain or increase their fat storage and the brain’s reward mechanisms for food.3 This is why most diets fail.
In fact, identical twins can sometimes have very different waistlines despite having identical genes, and we are studying these special pairs in great detail to find out why. These genetic factors alone don’t explain the massive changes seen in the population over the last two generations. In the UK in 1980 only 7 per cent of men and women were obese – in 2018 it was 28 per cent. Genes, made up of variations in DNA, cannot change that fast and traditionally need a minimum of around one hundred generations to adapt by natural selection.
that allows anyone with access to the internet and a postal service to test their own microbes and share the results with the world.6 I
In 1931 a Dupont chemist found out by chance in his lab that 30 per cent of people cannot taste a substance called PROP that 50 per cent of people find bitter and 20 per cent intensely unpleasant. Here was clear proof that our taste experiences are unique. We probably have hundreds of different taste genes, and more variants are being discovered every year. Most of those found so far belong to two gene families (called TAS1R and TAS2R). There are at least three gene variations for sweet-taste detection (for fruit), over five for umami (as a marker of protein), and at least forty for bitter tastes (toxins). Which gene variants we have influences not only our appreciation or dislike of foods but also our fat, vegetable and sugar intakes. The bitter and sweet receptors are also present in our noses and throats and unexpectedly play a role in signalling to our immune systems when to expect a microbial infection.
proportionally there is nearly three times as much of the lipid cholesterol in ‘healthy’ foods like lobster, crab meat or fish oil as in ‘unhealthy’ lard, beef or pork.
The cheese group didn’t increase blood lipid levels or cholesterol at all, whereas the butter group did, showing that not all saturated fat is the same.9 The results now seem clear, particularly if you separate cheese from butter consumption. Far from being a risk for heart disease, full-fat cheese (but not butter), despite the saturated-fat content, now shows not only no harmful effects but a consistent protective effect on heart disease and mortality.
The anxiety and stress were consistently reversed by giving them lactobacilli probiotics, which suggests that yoghurt, not crisps, should be our treat after going swimming.
The committee announced their findings in the New England Journal of Medicine in 2013. It was a knock-out blow for the high-fat diverse diet advocates and against the low-fat traditionalists.8 Both Mediterranean diet groups with high fat consumption had 30 per cent fewer heart attacks and fewer strokes, as well as improved lipid and cholesterol levels and blood pressure.
the gruel contains a mixture of oats, adlay seeds, buckwheat, white bean, yellow corn, red bean, soybean, yam, big jujube, peanut and lotus seeds. Some patients get bitter melon too. The regime provides around 1,350 calories per day plus masses of fibre for nine weeks, followed by a maintenance diet for a total of five months. Most of the volunteers showed lowered levels of blood inflammation and insulin resistance, and the average person lost 5 kg while only 9 per cent failed to lose weight.
We now know that the isoflavones in soy don’t affect oestrogen levels directly but do stimulate oestrogen receptors and have gene-modifying (epigenetic) effects.
Based on Glasp's analysis of highlights from 3 readers, this is a myth-busting, evidence-driven look at nutrition whose passages cluster around genetics, the microbiome, and surprising fat science.
Glasp AI analysis based on highlights from 3 readers.
Readers frustrated by failed diets and conflicting nutrition advice will find clarity here. It suits anyone curious about the gut microbiome, the science of taste, and why fat and cholesterol guidelines have shifted. Health-conscious eaters, popular-science fans, and those interested in twin studies or personalized nutrition will benefit most. A basic interest in biology helps, but no specialist knowledge is required — Spector explains the research accessibly.










Import your Kindle highlights to review, organize, and share the ideas that matter most to you.
Get the free browser extension