Mind & Body · Saturday, 12 September 2026

01 Briefing what happened

Your enamel has no living cells, so it cannot heal a hole - but before the hole it can be rebuilt from the outside

Enamel is the hardest thing in the body, and there is nothing alive inside it. It cannot repair itself, so every repair it gets is chemistry arriving from the saliva and the paste on the outside - and a protein gel from a team in Britain has now grown new crystals on eroded human teeth.

3.1 of 3.4 GPa

the hardness the coated human teeth reached, against 3.4 for untouched enamel

acid had dropped the same teeth to 1.1 gigapascals before the protein went on [1]

54%

less tooth decay where fluoride varnish was applied quarterly, in younger children and those with a dry mouth

pooled from 13 randomised trials and 4,784 participants, with unwanted effects under 5% [7]

44.3%

of appendicitis patients given antibiotics who had the appendix out within ten years

253 of the 257 Finnish patients first randomised were still being followed a decade on [8]

16 of 20

sunscreens sold in Australia as SPF 50 or above that tested below their label

the consumer group CHOICE ran the test in 2025 and got readings in the forties, thirties and twenties [9]

The lead story — what happened

Tooth enamel is the hardest and most mineralised tissue in the body, and it cannot regenerate, because there is nothing living inside it to do the rebuilding. [1]
It is made of packed crystals of a mineral called hydroxyapatite, stacked into rods about four to eight thousandths of a millimetre thick. [1]
Those crystals dissolve when the liquid around the tooth turns acid and re-form when it does not, so enamel is losing and gaining mineral all day. [2][3]
Decay is what happens when the losing runs ahead of the gaining for long enough. [2]
Saliva is the supply line: it dilutes and buffers the acid and carries calcium and phosphate back to the surface. [3][4]
Fluoride adds no cells. It joins the crystal and makes a tougher mineral, fluorapatite, which needs a stronger acid to dissolve than ordinary enamel does. [5][2]
A team led by the University of Nottingham in Britain coated eroded human teeth with an engineered protein that works as a scaffold, and new crystals grew on it in the pattern enamel normally has. [1][6]
Acid etching had cut those teeth from 3.4 to 1.1 gigapascals of hardness; after the coating they measured 3.1. [1]
The work was published in the journal Nature Communications, and the teeth were extracted samples in a laboratory, not teeth in anybody's mouth. [1][6]
Alvaro Mata, the biomedical engineering professor who led it, said the team hoped to have a first product out the following year. [6]
About 3.7 billion people have some form of oral disease, and the World Health Organization counts enamel breakdown as a large part of that. [6]
None of this reaches a tooth that has already collapsed into a hole, where a filling is still the only way to close the gap. [4][3]

Who is involved

Alvaro Mata

a biomedical engineering professor at the University of Nottingham in Britain; he led the team that made the enamel-growing coating
Paul Hatton

a biomaterials professor at the University of Sheffield's dental school in Britain and a member of the British Dental Association's science committee; he called the result an exciting breakthrough
Streptococcus mutans

the mouth bacterium that turns dietary sugar into acid; it is the organism most often blamed for tooth decay
The World Health Organization

the United Nations' health agency; it lists fluoride varnish among the medicines every country should keep in stock

How it unfolded

Before the tooth appears the enamel is built and finished, and afterwards it cannot regenerate
Every day acid pulls mineral out, saliva puts mineral back
Early decay mineral is lost under a surface that is still whole, and can still be replaced
After it collapses the hole is permanent, and only a filling closes it
Next the Nottingham team says it hopes for a first product the following year

Where this points

No one has yet tested the coating on a tooth inside a living mouth. Every result so far comes from extracted human teeth in a laboratory, and the team says it hopes for a first product within about a year. [1][6]

What is pushing on the whole day

The bar and the word are our reading of how hard each one is pushing today. The arrow is where it is heading. The evidence is in the stories below.

Treating without cutting Building↑

A protein coating grew new crystals on eroded human teeth and took their hardness from 1.1 back to 3.1 gigapascals. [1] Silver fluoride painted on children's first adult molars left 88.1% of them with no visible decay after six months. [10] Antibiotics let 73% of appendicitis patients avoid an operation in the first year. [11]

Gum trouble reaching the heart High→

Treating gum disease lowered the upper blood pressure number by about 4.6 points across randomised trials. [12] Across 17 studies covering 146,001 people, those with gum disease had 84% higher odds of a heart attack. [13] A review by the American Heart Association, a US doctors' body, found no link with heart events at all. [14]

Protection that wears off Steady→

The World Health Organization found two applications of fluoride varnish a year beat one, and silver fluoride is usually painted on twice a year too. [15] In a meta-analysis of 4,784 children, the largest reduction, 54%, came where varnish was applied quarterly. [7] Most people never put on or renew enough sunscreen to get the protection printed on the bottle. [16]

Labels ahead of the tests Building↑

Sixteen of 20 Australian sunscreens sold as SPF 50 or above came in below their label. [9] Fewer than 2% of the extra ingredients added to sunscreens have been tested in people, and only 18 are approved. [16] A fluoride-free toothpaste sold on rebuilding enamel matched an ordinary fluoride paste over 27 months in 1,063 children, with no untreated group in the trial at all. [17]

The rest of the day

53 more stories on this beat.

Each with its own sources. None of these is a link to the story above.

02
Fluoride makes a tougher mineral, not new tissue

Ordinary enamel is hydroxyapatite, which starts dissolving when the liquid around it falls to about pH 5.5. When fluoride is present, some of it swaps into the crystal and makes fluorapatite, which holds out until about pH 4.5. [5] Fluoride also slows the bacteria down: inside them it blocks enolase, an enzyme they need to make energy and acid. [5] So fluoride works from outside the tooth, on the mineral and on the microbes, never on any living part of the tooth. [2]

Why it matters — It explains why fluoride is painted on rather than taken as a course, and why stopping it moves the balance straight back.
03
Hydroxyapatite pastes matched fluoride in a dish

Researchers made early decay on 105 blocks of cattle enamel by feeding a bacterial model 10% sucrose three times a day for four days. They then brushed the blocks with pastes containing natural hydroxyapatite, synthetic hydroxyapatite or fluoride. Mineral recovery was 29.2% for the natural hydroxyapatite paste and 27.1% for fluoride, against 9.6% for artificial saliva alone. [18] These are blocks in a rig, not teeth in children.

Why it matters — Fluoride-free pastes are sold on exactly this comparison, and the comparison has so far been made outside the mouth.
04
Two minerals together beat either alone

A second laboratory study put cattle enamel through 14 days of acid and recovery cycles with four toothpastes. A paste holding both calcium hypophosphite and hydroxyapatite restored 89.7% of the lost hardness. Calcium hypophosphite alone managed 75.4%, hydroxyapatite alone 62.4% and standard 1,450 ppm fluoride 60.3%. [19] Each group improved from its own starting point; the differences are between the groups.

Why it matters — It points at combinations rather than single ingredients, and at the same time shows how far these results still are from a child's mouth.
05
A peptide that gets under the surface

A white spot on a tooth is decay that has taken mineral from beneath a surface that is still unbroken. A self-assembling peptide called P11-4 is designed to soak into that space and give new crystal somewhere to form. A review of seven controlled clinical studies found P11-4 did better than fluoride on subsurface repair in every one, with laser readings of lesion depth falling by 23% to 41%. [20] The studies were small and mostly in people wearing braces.

Why it matters — This is one of the few places where the new materials have been compared in actual patients rather than in extracted teeth.
06
A fluoride-free toothpaste tied with fluoride

A double-blind trial enrolled 1,063 children aged three and four from 12 kindergartens in Hubei province, China. Half were given a fluoride-free toothpaste containing 7.5% bioactive glass; half got a normal paste with 800 parts per million of fluoride. After 27 months there was no significant difference in how much new decay appeared, and the same was true at 12 months. [17] There was no group using nothing.

Why it matters — A tie can mean both worked or neither did, and without an untreated arm the trial cannot tell those apart.
07
An intensive varnish protocol on baby teeth

A clinical study followed white spots on children's primary teeth for a year, checking them by eye and with a laser fluorescence meter at three, six, nine and twelve months. An intensive protocol using Curodont Repair Fluoride Plus had 6.5 times the odds of arresting decay compared with a standard Duraphat varnish, and nearly 20 times the odds of turning active lesions inactive. [21] A third product, MI varnish, was no better than Duraphat.

Why it matters — It is one of the clearer patient results in this field, and it still measures lesions rather than teeth saved.
08
Nanosilver rinse and white spots in braces

Fixed braces trap plaque where a brush cannot easily reach, and white spots are the common result. A review of human trials found that after six months, 9.5% of teeth developed a white spot among people using a nanosilver mouthwash, against 24.4% for both fluoride and chlorhexidine rinses. [22] The upper right lateral incisor was the worst-affected tooth, at 38.1%.

Why it matters — Orthodontic patients are the group where prevention and damage run on the same two-year clock.
09
Acid drinks strip enamel with no bacteria involved

Erosion is the chemical loss of tooth surface to acid that never passed through a microbe, and it is common: roughly 30% to 50% of children and 20% to 40% of adults. [4] The acid comes from fizzy drinks, fruit juice and energy drinks, or from stomach contents in reflux. [4] In one laboratory comparison, carbonated drinks roughened enamel the most, and brushing straight after an acid exposure made the loss worse. [23]

Why it matters — It is a separate route to the same damage, and it does not respond to anything aimed at bacteria.
10
Stomach acid and kefir, tested on real molars

Researchers took 80 baby second molars and 80 adult premolars and soaked them for 72 hours in gastric acid at pH 1.2 or in kefir at pH 4.5. They then treated the samples with three commercial repair agents for 14 days, with artificial saliva alone as the control. [24] Reflux disease, which sends stomach contents back up the gullet, affects an estimated 10% to 30% of people worldwide. [24]

Why it matters — It sets the size of the problem for anyone whose acid comes from inside rather than from a bottle.
11
Silver fluoride arrested nearly nine in ten molars

A blinded trial randomised 165 children aged six to twelve by school. One group had 38% silver diamine fluoride with potassium iodide painted on early decay in their first adult molars; the other had a 5% fluoride varnish. After six months, 88.1% of the silver-treated teeth scored as sound, against 65.6% of the varnish ones. [10] How far the molar had erupted made no difference either way.

Why it matters — Silver fluoride stains the treated spot black, which is why it is used most where a filling is not available.
12
Silver and sodium fluoride compared again

An updated review pooled randomised trials comparing silver diamine fluoride with plain sodium fluoride in children under six. Silver had higher odds of stopping a lesion, at 1.41, but no measurable advantage on the count of decayed, missing and filled surfaces. [25] Untreated decay in baby teeth affected about 532 million children in 2017, the tenth most common condition in the world. [25]

Why it matters — Stopping a lesion that already exists and preventing the next one are two different jobs. Silver did better on the first and no better on the second.
13
Varnish four times a year, and the number that follows

A meta-analysis screened 2,315 records and analysed 13 randomised trials covering 4,784 participants. Fluoride varnish cut decay across the pooled group. The largest effect was in younger children and in those with a dry mouth, where quarterly applications were associated with a 54% reduction and unwanted effects stayed below 5%. [7] Variation between the trials was high, which the authors put down to inconsistent application protocols. [7]

Why it matters — The dose here is a schedule, not a quantity, and the benefit is counted per visit.
14
The health agency put varnish on its essential list

The World Health Organization's guidance on mercury-free dental products reviewed ten systematic reviews of fluoride varnish. It reports that twice a year beat once a year for preventing early childhood decay, with a mean caries increment 3.57 surfaces lower after a year in one study. [15] It found no treatment-related adverse events in the varnish trials, though few of them collected that information. [15] Varnish is on the agency's model list of essential medicines. [15]

Why it matters — Being on that list is what makes a treatment something health ministries are expected to stock rather than something patients buy.
15
What varnish costs per cavity prevented

An economic model followed Brazilian preschoolers over four years in six-month cycles. Adding fluoride varnish to standard care prevented cavities in four children out of every 100, at an average cost of 33 Brazilian reais a child a year. [26] The full incremental cost came to R$6,929 per cavitated lesion prevented. [26] The model assumed each child who developed decay developed only one lesion.

Why it matters — It is the number a health ministry actually decides on, and it is a different number from the trial result.
16
How common decay is by seventeen

A review of 14 randomised trials across different countries and income levels pooled data from more than 13,000 children given fluoride varnish. Its background section sets the scale: decay affects around 40% of seven-year-olds and about 85% of people by the age of 17. [27] The review cites reductions of roughly 37% in baby teeth and 47% in adult teeth. [27]

Why it matters — Decay reaches almost everyone, so the practical argument is about getting varnish to children rather than about finding a new treatment.
17
The bacterium that turns sugar into acid

Streptococcus mutans lives on tooth surfaces and ferments dietary sugar into lactic acid. It also builds sticky sugar chains called glucans that glue it to enamel and hold the film together, and it can keep working at a low pH that silences its neighbours. [5][28] Sucrose matters most, because the glue is made from it. [28] A healthy film contains species that buffer acid instead of making it. [29]

Why it matters — The film is not a dirt layer to be scrubbed off but a community, and which members dominate it is decided partly by what arrives.
18
A sweetener that starved the film

Researchers built a test platform to measure how cariogenic a sugar is, then compared allulose, a rare sugar used as a sweetener, against sucrose. Habitual refined sugar reduces the variety of microbes in the mouth and favours the acid-makers. [28] Allulose did not support the same biofilm growth. [28] The work was done in a laboratory model of the mouth, not in people.

Why it matters — Sugar substitutes are usually sold on calories; this is the other thing they change.
19
Stevioside cut the sticky matrix

Stevioside, the sweet compound from the stevia plant, was tested against Streptococcus mutans. The bacterium builds its film using an enzyme, glucosyltransferase, that turns sucrose into glue, and it defends itself against acid with a tolerance response. [30] The extract interfered with biofilm formation and with those virulence traits. [30] Non-sugar sweeteners are being looked at for this second job rather than for sweetness.

Why it matters — If a sweetener cannot be turned into glue, the film has less to hold on with.
20
A sugar from breast milk blocked the film

Sialyllactose is one of the complex sugars in human milk that babies cannot digest. Researchers grew Streptococcus mutans and mixed streptococcal species in the laboratory and tested those milk sugars and a fragment of them against biofilm formation. [31] The mouth holds more than 700 bacterial species and about 100 million to a billion cells in every millilitre of saliva. [31] Inside a film, bacteria are shielded from antibacterial agents and from immune cells. [31]

Why it matters — It is one reason the film is hard to treat once formed, and why the work keeps returning to stopping it forming.
21
Mouth bacteria found further down

Forensic scientists sampled 50 bodies aged from newborn to 94 and looked for Streptococcus mutans along the gut. They found it in the mouth in 14 cases, 28%, in the gullet in three, in the stomach in one, in the small intestine in one and in the large intestine in four, 8%. [32] Oral bacteria are swallowed constantly with saliva and food. [32] The study reports where the organism was, not what it did there.

Why it matters — Finding a bacterium somewhere does not show it does anything there. Most claims linking mouth microbes to the rest of the body still rest on where organisms were found.
22
What the mouth's 700 species live on

The mouth's microbes divide the territory: some prefer tooth surfaces, some the tongue, some the pocket between tooth and gum. [33] Helpful species such as Veillonella, Actinomyces and Neisseria can crowd out the harmful ones, and some produce their own antibacterial proteins. [33] A systematic review of 22 studies, eight of them randomised trials, found diet is a major determinant of which species dominate. [34] More than 80% of Americans have had a cavity by their mid-thirties. [33]

Why it matters — The tooth surface is the one part of the body where the resident population and the mineral balance are the same story.
23
Cleaning under the gum moved blood pressure

A meta-analysis of randomised trials measured what happens elsewhere in the body after gum disease is treated. Systolic blood pressure fell by an average of 4.64 millimetres of mercury and diastolic by 1.84. C-reactive protein, a general marker of inflammation in the blood, fell by 0.58 milligrams per litre. [12] The treatment is mechanical cleaning of the tooth root below the gum line.

Why it matters — The change is made on a tooth surface and shows up in a blood vessel, which is what makes this a whole-body finding rather than a dental one.
24
Gum disease and heart attacks, in 146,001 people

A meta-analysis pooled 17 studies covering 146,001 participants and 3,199 heart attacks. People with periodontitis had 84% higher odds of a heart attack, an odds ratio of 1.84. [13] Publication bias was detected; correcting for it brought the figure down to 1.26, still above one. [13] Bleeding when the gum is probed carried an odds ratio of 2.90 on its own. [13]

Why it matters — The authors' own correction moves the number a long way, which is the honest size of what is known.
25
Heart failure risk 58% higher

A separate review pooled long-running cohorts with follow-up between 5.4 and 13 years and mean ages from 43 to 65. Gum disease was associated with a 58% higher risk of heart failure, a crude relative risk of 1.58. [35] Heart failure affects about 1% to 2% of people and more than 10% of those over 70. [35] The proposed route is bacteria and inflammatory signals entering the bloodstream from the gum. [35]

Why it matters — It is the same suspected mechanism as the heart attack finding, measured on a different outcome.
26
Atrial fibrillation, and what recovery did to it

A review of cohort studies found gum disease associated with irregular heart rhythm, with adjusted hazard ratios from 1.03 to 1.31. Severe disease carried the top of that range. [36] In people whose gum disease had recovered, the extra risk disappeared, with a hazard ratio of 1.00. [36] Gum disease affected about 951 million people in 2021 and accounted for 6.2 million years of healthy life lost. [36]

Why it matters — The extra risk disappeared in people whose gum disease had cleared up. That is as close to a test as an observational study gets.
27
The heart body that says there is no link

Meta-analyses of epidemiological work put the extra relative risk of a cardiovascular event at between 12% and 59% after adjusting for the usual risk factors. [14] A review by the American Heart Association, a US doctors' body, found no association between gum disease and cardiovascular events. [14] The authors state plainly that there is no conclusive evidence either way on whether gum disease is an independent risk factor. [14] More than 40% of adults over 30 in the United States have gum disease. [37]

Why it matters — Two sets of experts read the same studies and came to opposite conclusions. Nobody has run the trial that would settle it.
28
A gum bacterium and the brain's barrier

Porphyromonas gingivalis is the organism treated as the keystone of chronic gum disease, because it tips the whole microbial community out of balance. [38] Its outer coat contains lipopolysaccharide, which can enter the bloodstream, bind receptors on the cells lining brain blood vessels and make that barrier leakier. [38] Chronically raised inflammatory signals are proposed as the route to nerve damage in older people. [38] This is a proposed mechanism, not a demonstrated cause.

Why it matters — It is the same inflammation argument as the heart work, aimed at a different organ and standing on weaker evidence.
29
Diabetes and gums pull each other

A clinical review screened studies and kept 110 covering diabetes, gum disease and heart disease together. High blood sugar produces advanced glycation end-products, which bind receptors on immune cells and raise inflammatory signalling. [39] People with poorly controlled diabetes have more and worse gum disease, and people with gum disease tend to have worse blood sugar control. [39] Treating the gums produced modest gains in blood sugar control. [39]

Why it matters — High blood sugar makes gum disease worse, and gum disease makes blood sugar harder to control. Each one keeps feeding the other.
30
Ten years after antibiotics for appendicitis

The APPAC trial in Finland randomised adults with appendicitis confirmed on a scan to surgery or to antibiotics, and has now reported ten-year results. Of 257 patients given antibiotics, 253 were still being followed. Appendicitis came back, confirmed on tissue, in 37.8% of them, and 44.3% had had the appendix removed by ten years. [8] The treatment was three days of intravenous ertapenem then a week of tablets. [8]

Why it matters — It is the longest randomised follow-up available on treating an organ rather than removing it, and the recurrence keeps accumulating.
31
What the first year looked like

In APPAC's first year, 73% of patients with scan-confirmed uncomplicated appendicitis avoided an operation on antibiotics alone. [11] By five years the cumulative operation rate was 39.1%, with no rise in burst appendixes or serious complications among those who went on to surgery. [11] Complications overall were lower in the antibiotic group, 6.5% against 24.4% in the surgical group. [11]

Why it matters — The trade is fewer complications now against a running chance of the operation later, and the trial reports both halves.
32
Three treatments ranked at once

A network meta-analysis compared surgery, antibiotics and a newer keyhole technique that clears the appendix from the inside through a colonoscope. On complications the endoscopic route came out best and surgery worst. On recurrence surgery came out best and antibiotics worst, with an odds ratio of 0.06 for surgery against antibiotics. [40] A separate review of ten studies in 1,372 children found no significant difference in recurrence between the endoscopic route and the comparison groups. [41]

Why it matters — Each option wins on a different measure, so the choice depends on which failure a patient and a surgeon mind most.
33
A stone in the appendix changes the odds

A meta-analysis of six randomised trials covering 2,101 adults found 34% of antibiotic-treated patients needed an operation within a year, and a quarter of those turned out to have complicated appendicitis. [42] Patients with an appendicolith, a hardened lump blocking the appendix, did much worse: 49% needed surgery, with significantly higher complication rates. [42]

Why it matters — It is the closest thing in this cluster to a rule for who the antibiotic route suits.
34
Sent home on tablets

A single hospital reviewed every patient diagnosed with uncomplicated appendicitis between 2020 and 2022 who was discharged from the emergency department on oral antibiotics with no admission. Of 99 patients, 76% were still free of surgery at one year, and 70% at a median follow-up of 34 months. [43] Four in five of the operations that did happen came within the first ten months. [43] A separate cohort followed for a mean of 64 months reported a 95.7% success rate. [44]

Why it matters — The two cohorts disagree by a wide margin, and neither was randomised.
35
The first new sunscreen filter in the United States in 25 years

The US Food and Drug Administration has approved bemotrizinol, the first new active sunscreen ingredient cleared there in more than 25 years. It was first proposed more than 20 years ago. The United States regulates sunscreen as an over-the-counter drug, while the European Union treats it as a cosmetic, which is why filters available elsewhere have not been sold there. [9]

Why it matters — What kept those filters out was the legal category sunscreen sits in, not a finding about the filters themselves. It decides which bottles reach which shelves.
36
Sixteen of twenty sunscreens missed their number

The Australian consumer group CHOICE tested 20 widely sold sunscreens in 2025, from brands including Neutrogena, La Roche-Posay, Cancer Council and Banana Boat. All were labelled SPF 50 or above. Sixteen came in below the claim, with readings in the forties, thirties and twenties. [9] SPF measures how much longer skin takes to burn with the product on than without it, tested on small patches of skin. [9]

Why it matters — People pick a bottle by the number on the front. That number comes from small patches of skin under careful application, and 16 of the 20 products did not reach it.
37
The trial that showed sunscreen cutting a cancer

The Nambour Skin Cancer Prevention Trial, run in a town in Queensland, Australia, randomly assigned 1,621 people to use sunscreen above SPF 15 every day or as they chose, over four and a half years. Daily use was associated with 39% fewer squamous cell skin cancers by the end, and 38% fewer after eight years. [45] It remains the largest population trial of its kind. [45]

Why it matters — Almost everything else about sunscreen is measured on skin markers; this is one of the few results counted in tumours.
38
What melanin does, and what nobody has tested

In a study simulating sunlight across skin types, the melanin in the darkest skin gave about 60 times the protection against DNA damage in a deeper layer of skin compared with fair, European-origin skin. [9] The epidemiologists behind the Nambour trial say its result cannot simply be extended to people with darker skin, and that there is no trial evidence that sunscreen prevents cancer in them. [9]

Why it matters — Advice given to everyone rests on evidence collected in one group, and the people running that trial are the ones saying so.
39
Sunscreen changed what the skin's genes did

Thirty-two female volunteers across four skin types were given repeated moderate doses of ultraviolet light, with samples taken from untreated skin, unprotected exposed skin and skin covered with sunscreen first. [46] Repeated low doses that never redden the skin still switch on DNA repair, inflammation and stress responses. [46] Sunscreen substantially reduced those molecular changes. [46]

Why it matters — It measures the damage that arrives below the level of a sunburn, which is the part nobody can feel.
40
Iron oxides block the light the filters miss

Visible light makes up nearly half the solar spectrum, and the blue end of it drives pigmentation, oxidative stress and photoaging through a receptor on pigment cells. [47] Ordinary chemical UV filters do almost nothing beyond 400 nanometres. [47] Tinted sunscreens containing iron oxides and pigmentary titanium dioxide cut high-energy visible light by 80% to 97%. [47] In one trial in 20 people with darker skin types, a tinted product held pigmentation steady where unprotected skin darkened. [48]

Why it matters — It matters most for people whose main complaint from the sun is patchy darkening rather than burning.
41
Most of the added extras are untested

Sunscreens increasingly carry non-filtering ingredients meant to add protection, from antioxidants to DNA repair enzymes. A review counted them and found that fewer than 2% of the candidate ingredients have been clinically validated, and only 18 are approved for use in sunscreens. [16] It also notes that real-world protection falls short because people do not apply or reapply enough. [16]

Why it matters — The claim on the front of the bottle is usually about the extras, and that is where the evidence is thinnest.
42
Ultraviolet light rises with altitude

Ultraviolet strength is not a fixed quantity. It rises by roughly 10% to 12% for every 1,000 metres of altitude, because there is less atmosphere above to absorb it. [49] Near the equator the ultraviolet index regularly passes 10 or 11, which the World Health Organization classes as very high, while temperate regions peak lower and seasonally. [49] Thinner ozone raises the shorter-wavelength UVB share. [49]

Why it matters — The same bottle behaves differently in different places, which is part of why national rules on SPF differ.
43
Antibodies against blood you have never met

Blood group A, B and O are sugars on the surface of red cells, and the ABO system is the only one where people make antibodies against the groups they lack without ever being exposed to them. [50] Babies start producing them at four to six months and reach a peak by about ten. [50] Around 20% of group A people of European descent belong to a weaker subgroup, most often A2, and some of them make antibodies against the stronger A1. [50][51]

Why it matters — It is why blood typing is done twice, once for the cells and once for the serum, and why the two answers can disagree.
44
When the lab's two answers disagreed

A hospital transfusion department collected every case over three years where the control tube in reverse typing clumped when it should not have. Eleven patients turned out to carry anti-M antibodies. Nine of the eleven had produced a discrepancy between the two halves of the blood typing test. [52] Seven were transfused with blood from donors lacking the M antigen, all raised their haemoglobin and none had a reaction. [52]

Why it matters — The mismatch between the two halves of the test is what tells the laboratory to look further. The patient is not treated for it; a different donor is found.
45
Learning to reject after nine bags of blood

A five-year review looked at people with sickle cell disease who were transfused and had no previous antibodies. Of 805 patients, 325 qualified. Fifty of them, 15.4%, developed a new antibody after a median of nine units of red cells, and 14% of those went on to make more. [53] The commonest were anti-C, anti-E and anti-K. [53] In a separate single-centre series of 241 patients, anti-E was found in 20% and anti-C in 15%. [54]

Why it matters — Each new antibody narrows the pool of blood that person can safely be given for the rest of their life.
46
Matching five Rh markers instead of one

Routine crossmatching checks the RhD marker, the one that makes blood positive or negative. The Rh system also carries C, c, E and e, all capable of provoking antibodies. [55] Evidence in people needing repeated transfusion links extended matching across all five, and genetic typing of the underlying genes, to fewer new antibodies. [55] Mismatches can also complicate organ transplants, where graft survival suffers in ABO-incompatible cases. [56]

Why it matters — It is prevention by bookkeeping: nothing is done to the patient, the donor unit is simply chosen more narrowly.
47
A third of the dummy group got better

An individual-patient meta-analysis pooled 1,703 people from nine trials of advanced drugs for ulcerative colitis, a long-term inflammation of the large bowel. In the induction phase, 33% of people given placebo responded and 9% went into remission. In maintenance trials the figures were 28% and 14%. [57] Those are the rates a new drug has to beat, not zero.

Why it matters — It sets how large a real effect has to be before a trial can see it at all.
48
Placebo response fell as country income rose

Researchers analysed 51 trials in psoriatic arthritis, covering 6,843 patients, and 43 in plaque psoriasis, covering 5,671. They matched each trial's placebo response against the national income of the countries where it recruited. Placebo response fell as income rose, by about 5.7 percentage points for every 10,000 international dollars in psoriatic arthritis. [58] The same direction held in the psoriasis trials, more weakly. [58]

Why it matters — Where a trial recruits changes the number it reports, before any drug is involved.
49
Active dummies barely changed the answer

An active placebo is a dummy designed to produce the same side effects as the real drug, so participants cannot guess which arm they are in. A meta-epidemiological study gathered 67 reviews, 123 meta-analyses and 1,698 trials to see whether ordinary placebos inflate drug effects. On average they did, by about 2%, which the authors call slight. Variation between meta-analyses was considerable. [59]

Why it matters — A long-standing worry about trial design turns out, on the largest look at it so far, to be small on average.
50
The sham group's gain did not vanish when they were told

REDUCE LAP-HF II randomised heart failure patients to a shunt implanted in the heart or to a sham procedure, and unblinded everyone after two years. Among 421 participants, the sham group's quality-of-life score had improved by 9.3 points at two years, and fell by only 1.7 points in the year after they learned which arm they were in. [60] The estimated placebo component was two points or less.

Why it matters — Patient-reported scores are often dismissed as soft; this design tested that directly and found the softness small.
51
Melatonin did not prevent delirium

A double-blind trial gave hospitalised patients aged 65 and over nightly melatonin at 5 or 8 milligrams, or a placebo, for up to five days. It was stopped early for futility with 109 patients analysed. Delirium appeared in 3.64% of the melatonin group and 1.85% of the placebo group, a difference that was not significant, and sleep duration, 28-day deaths and readmissions did not differ either. [61] The authors say the low event rate left the trial underpowered. [61]

Why it matters — A negative trial stopped early answers less than it looks, and the authors say so themselves.
52
A stroke drug beat placebo by five points

TASTE-2 randomised 1,362 people having a stroke caused by a blocked large vessel, all of them due for a procedure to pull the clot out. They received edaravone dexborneol or placebo before the procedure and twice daily for 10 to 14 days. At 90 days, 55.0% of the treated group were functionally independent against 49.6% on placebo, a difference of 5.4 percentage points with a p value of 0.05. [62]

Why it matters — It is a result sitting exactly on the conventional line, which is the kind that gets argued about for years.
53
Two more trials, two different answers

OLINGUITO is a phase 3 programme of two randomised studies in axial spondyloarthritis, a form of spinal arthritis. Filgotinib beat placebo in both. In the first, 39.5% of 258 patients reached the main response target against 20.9% on placebo; in the second, 34.5% against 17.8%. [63] In HypoBar I, a crossover trial in people with low blood sugar after weight-loss surgery, neither acarbose nor canagliflozin reduced time spent below the threshold compared with placebo. [64]

Why it matters — Both trials used the same design and the same kind of control, and the control is what makes the two answers comparable.
54
Doctors using a dummy that announces itself

An open-label placebo is a dummy pill given to someone who has been told it is a dummy. A systematic review assessed 15 randomised trials, nine with some concerns and six at low risk of bias. It reports that 77% of family doctors in Britain use open-label placebos, on the grounds that they cost little and carry no drug side effects. [65] Placebo responses engage brain networks handling pain, emotion and reward. [66]

Why it matters — It removes the deception that made placebos an ethical problem, and leaves the question of what is actually happening.

02 Lesson why it matters

A tooth cannot heal itself. What repairs it is the liquid around it.

Enamel has no living cells, so nothing inside the tooth rebuilds it; the minerals come from the saliva and paste outside.

The twist

A part with no living cells in it still gets its mineral back. The calcium and phosphate come from the saliva and the toothpaste outside, because nothing inside the tooth can supply them.

How it works

Enamel is finished before the tooth appears, and holds no living cells
So nothing inside the tooth can rebuild it
But enamel is a crystal, and crystals dissolve and re-form
Acid in the mouth pulls calcium and phosphate out of it
Saliva, and whatever is put on the tooth, pushes them back in
So the repair is done by the surroundings, and stops when they stop

The same force, elsewhere today

Where this chain is also running, in today's other stories.

Silver fluoride arrested nearly nine in ten molars

the tooth does nothing; a liquid is painted on the surface, and it has to be painted on again about every six months
The trial that showed sunscreen cutting a cancer

skin can repair its own DNA and cannot keep up, so the protection that worked was a layer applied on top and renewed daily
Ten years after antibiotics for appendicitis

nothing is removed and the conditions inside are changed instead, and the same repeat-it problem shows up as 44.3% coming back for the operation
Cleaning under the gum moved blood pressure

the work is done on the outside of a tooth root and the change appears in a blood vessel, which is the same outside-in route

Where you've seen this

Old paper

paper cannot repair itself, so conservators bathe a book in an alkaline solution and the chemistry does the work

Roads

tarmac has no way to close its own cracks, so the surface is laid again from above

Stone walls

the stone does not grow, so the mortar between it is raked out and replaced

The catch

This only works while the enamel over the lesion has not broken. Once it caves in and leaves a hole, no amount of mineral in the saliva puts it back, and the tooth needs a filling.

And the whole of it

A dentist sees the tooth twice a year and reads a score. What happened in between was thousands of small swings in one direction and then the other, and nobody watched any of them, including the person the tooth belongs to.

03 Truth what's really going on

What is really going on

Dentistry is moving from drilling tooth away to putting mineral back, and almost all the evidence for the new pastes, peptides and gels comes from extracted teeth in laboratory rigs rather than from people. [1][18][19][20] Where anyone has followed real patients a long way, the picture is harder: ten years after Finnish patients took antibiotics instead of having the appendix out, 44.3% had had it out anyway. [8]

Why it works on us — A hardness reading taken on an extracted tooth before and after treatment is a real measurement, and it reads like a cure, because nothing in that picture shows the mouth the tooth would have had to survive. [1][18]

Who gains

The Nottingham team and whoever licenses the coating — A laboratory result in Nature Communications is the step that lets a product be developed, and the group says one is about a year off. [1][6]
Makers of fluoride-free toothpaste — Laboratory papers now report hydroxyapatite pastes matching fluoride on mineral recovery, which is the claim the packaging rests on. [18][17]
Health ministries running varnish programmes — The Brazilian model puts the cost at about 33 reais a child a year, and the World Health Organization lists varnish as an essential medicine, which is what gets it into budgets. [26][15]
Hospitals treating appendicitis without an operating theatre — One unit discharged 99 patients on tablets from the emergency department, and 70% had still avoided surgery at a median 34 months. [43]
Sunscreen makers selling in the United States — Bemotrizinol is the first new active filter approved there in more than 25 years, opening a category that had been closed since the 1990s. [9]
Dental product firms with peptide and silver formulas — Silver diamine fluoride arrested 88.1% of early lesions against 65.6% for standard varnish, and a peptide beat fluoride on subsurface repair in all seven trials reviewed. [10][20]

Who pays

Anyone whose decay is found after the surface has collapsed — Remineralisation only reaches a lesion while the enamel over it is still whole; after that a filling is the only option. [4][3]
The 44.3% of the Finnish antibiotic group — They had the drugs, the follow-up and then the operation. The cumulative rate was 39.1% at five years and 44.3% at ten, so it was still climbing. [11][8]
People with sickle cell disease on repeated transfusions — 15.4% made a new red-cell antibody after a median of nine units, and each one narrows the blood they can safely be given afterwards. [53]
People buying sunscreen above its real strength — Sixteen of 20 Australian products tested below their label, so the protection people paid for and planned around was not there. [9]
People with darker skin given advice built on other people's data — The Nambour trial recruited in Queensland, and there is no equivalent evidence for skin types where melanin already gives about 60 times the protection against deep DNA damage. [45][9]
Children in places with no varnish programme — Decay reaches about 40% of seven-year-olds and 85% of people by 17, and untreated decay in baby teeth affected roughly 532 million children in 2017. [27][25]

What nobody knows yet

Open questions from across today’s stories — ours included.

01

Whether the enamel coating does anything in a living mouth.

Every test published so far was on extracted human teeth in a laboratory, and no trial in patients exists. The team says it hopes for a product the following year. [1][6]
02

Whether hydroxyapatite pastes prevent cavities in people.

The comparisons with fluoride were run on cattle enamel blocks in acid-and-recovery rigs, which is not a mouth. [18][19]
03

Whether gum disease causes heart disease or simply travels with it.

Meta-analyses put the extra relative risk at 12% to 59%, while a review by the American Heart Association found no association with cardiovascular events, and the authors say there is no conclusive evidence either way. [14]
04

Which appendicitis patients are in the 44.3% who come back.

The Finnish ten-year report gives the rate but not the profile. A separate meta-analysis found 49% of patients with a hardened lump blocking the appendix needed surgery, against 34% overall. [8][42]
05

Whether sunscreen prevents skin cancer in people with darker skin.

The only large randomised trial was run in one Australian town, and its own investigators say the result cannot be extended to people of colour. No trial in that group exists. [45][9]
06

What a bottle's real SPF is.

Sixteen of 20 Australian products labelled SPF 50 or above tested lower, and the test itself is done on small patches of skin under controlled application. [9]
07

Why placebo response falls as a country's income rises.

The association held across 51 psoriatic arthritis trials and 43 psoriasis trials, and the analysis reports the pattern without establishing what produces it. [58]
08

Whether the fluoride-free toothpaste result means both worked or neither did.

The trial in 1,063 children compared bioactive glass with fluoride and had no untreated group, so a tie cannot be read either way. [17]
09

Whether mouth bacteria found further down the gut do anything there.

The forensic study reports Streptococcus mutans in the large intestine of 8% of 50 bodies. It measures presence, not effect. [32]
10

How long a cohort's appendicitis results hold.

One hospital cohort reports 70% free of surgery at 34 months and another 95.7% success at a mean of 64 months. Neither was randomised and they disagree widely. [43][44]

04 Hope carry this

In younger children and in those with a dry mouth, fluoride varnish applied four times a year was associated with 54% less tooth decay, pooled across 13 randomised trials and 4,784 participants. It sits on the World Health Organization's list of medicines every country should keep in stock.

Also true today

An engineered protein coating grew new crystals on acid-damaged human enamel and took its hardness from 1.1 back to 3.1 gigapascals, against 3.4 for a tooth that had never been touched.
In the Australian town of Nambour, 1,621 people were randomly assigned to use sunscreen every day or as they chose. After four and a half years, squamous cell skin cancer was 39% lower in the daily group.
Ten years after the Finnish appendicitis trial, 55.7% of the people given antibiotics had still never had the operation.