Children and adolescents

Atherosclerosis does not begin in middle age. Fatty streaks are present in the arteries of children, and autopsy series in adolescents and young adults who died of other causes have found early lesions whose extent tracks with the cholesterol, blood pressure, weight and smoking status they had at the time. The disease this whole guide is about starts decades before anyone measures anything.

That fact sits awkwardly against UK practice, which does not screen children's cholesterol. This chapter sets out what is actually done, the case for doing more, and the reasons the UK has decided against — because a page arguing for a change of policy that did not explain why the policy exists would not be worth reading.

1. What the UK does now

There is no universal childhood lipid screening in the UK. What exists is targeted case-finding, and it is aimed almost entirely at one condition.

Familial hypercholesterolaemia affects roughly 1 in 250 people. It is a single-gene condition causing lifelong high LDL from birth, and the cardiovascular risk it carries is a function of how many years the arteries have been exposed — which makes it the clearest case in medicine for finding something early. NICE guidance is that children at risk because a parent is affected should be tested by about age 10, before puberty complicates the lipid picture, and that where a family mutation is known, genetic testing gives a clean answer.

That is cascade testing: start from a diagnosed adult, work outward through the family. Each first-degree relative has a one-in-two chance. It is efficient, it has a clear question, and it avoids testing large numbers of people at low prior probability.

The problem with cascade testing is arithmetical. It can only find the children of adults who have already been diagnosed — and most adults with FH in the UK have not been. A strategy that starts from index cases inherits the failure rate of index-case detection. If the majority of parents are undiagnosed, the majority of affected children are unreachable by design.

2. The case for screening children earlier

This is a real argument made by serious people, and several countries act on it. The United States recommends universal lipid screening once between ages 9 and 11 and again between 17 and 21. Slovenia screens universally at age 5. The reasoning runs as follows.

• Childhood is the one window where FH separates cleanly. Between about 1 and puberty, LDL-C in an affected child is distinctly higher than in an unaffected one, with relatively little overlap. In adults the distributions blur, because ordinary lifestyle-driven hypercholesterolaemia becomes common and obscures the genetic signal. The test is at its most discriminating precisely when nobody is doing it.
• Cumulative exposure is the thing that matters. The relationship between apoB and events depends on both the height of the level and the number of years lived with it — the argument set out in the misconceptions chapter. Twenty years of untreated FH before diagnosis is twenty years of exposure that cannot be given back. Treating from adolescence, rather than from a heart attack at 45, is the difference the condition turns on.
• Screening the child finds the parent. This is the argument that makes universal childhood screening more efficient than it first looks. A child with FH has an affected parent by definition, and usually an undiagnosed one. So paediatric screening runs cascade testing in reverse — sometimes called reverse cascade — and can reach the adults that adult case-finding has missed.
• The treatment is established and tolerated. Statins in children with FH have been studied for over two decades, including long-term follow-up showing that early treatment substantially reduces cardiovascular events in adulthood, with growth and development unaffected. This is not an intervention searching for a justification.
• The test is cheap and the condition is not rare. At 1 in 250, FH is more common than most conditions already screened for at birth.

3. Why the UK has not adopted it

The National Screening Committee has considered childhood lipid screening and has not recommended it. The objections are not trivial and are worth stating properly.

• A screening programme is not a test. It is a test plus a follow-up pathway plus a treatment decision plus the consequences of being labelled, applied to an entire population of well people. The bar for that is deliberately higher than for offering a test to someone at known risk, and it is the bar the UK applies to everything.
• False positives fall on healthy children. A raised reading in a child usually is not FH, and the interval between an abnormal result and a definitive answer is spent by a family believing their child has a serious inherited disease.
• Treatment timing is genuinely uncertain even once FH is found. Statins in childhood are supported, but exactly when to start — and whether starting at 8 rather than 18 changes lifetime outcome enough to justify a decade more of medication — has not been settled by trial.
• Insurance and labelling consequences are real, and fall on someone who cannot consent to them.
• The alternative is not nothing. The UK position is that better cascade testing from adult index cases would find most of the same children at lower cost and lower harm — and that the failure is not the absence of childhood screening but the under-diagnosis of FH in adults, which is fixable without screening any children at all.

4. The part that does not depend on screening at all

Whatever happens with lipid testing, the larger point stands independently: the habits formed in childhood are the ones that operate for the following sixty years, and they are formed far earlier than most people assume.

Taste preferences, portion expectations, the normal sweetness of a drink, whether vegetables are a food or a punishment, whether movement is something you do or something you were made to do at school — these settle young and are hard to shift later. Nothing in adult cardiovascular prevention has anything like the leverage of not having to undo them.

And the childhood risk factors are increasingly not theoretical. Type 2 diabetes in adolescents, once nearly unheard of, is no longer rare; childhood obesity tracks strongly into adulthood; blood pressure in childhood predicts blood pressure in middle age. The metabolic story in the glucose chapter and the liver chapter increasingly begins in the teens.

What actually helps is unglamorous and mostly not about the child:

• What is in the house is what gets eaten. The decision is made in the supermarket, not at the table, which is where an argument about it will otherwise happen.
• Drinks are the highest-yield single change. Sugar-sweetened drinks are the largest avoidable source of free sugars in UK children's diets, and water instead is a change that costs nothing and requires no negotiation about food.
• Eat the same meal. Separate "children's food" teaches that ordinary food is for other people, and it is the habit most often regretted later.
• Do not moralise about it. Framing food as good and bad, or as something to be earned through exercise, has its own well-documented risks in adolescence, and a page about cardiovascular prevention should be the last place to encourage it.
• Activity beats exercise. Walking, cycling, playing and sport that is actually enjoyed all count, and the step from nothing to something is where nearly all of the benefit sits — the same shape as in adults.

Eating for the heart has a chapter specifically on children, which goes into the dietary side properly.

Both positions in section 2 and section 3 have a cost, and it is worth being explicit about which cost you are choosing. Screening universally means a number of well children and their families spend weeks believing something serious, to find the affected ones earlier. Not screening means a knowable number of children with FH are found in adulthood instead, after twenty years of exposure. Neither is a free option, and anyone presenting their side as obviously correct is leaving out the other column.

One boundary worth naming. The evidence that childhood habits track into adulthood is strong. The evidence that any particular parental intervention reliably changes those habits is much weaker, and the gap between the two is where a great deal of guilt-inducing advice lives. Do the cheap, structural things; do not treat a child's future cardiovascular risk as a measure of your parenting.