Category Archives: Nutrition

Cow’s milk protein/allergy intolerance

Allergy, General paediatrics, Immunology, Nutrition

A common issue for babies and infants.  But not that common – in EAT study, symptoms (vomiting, colic, eczema) related to milk reported by 13% of parents, but only found in 0.7%!

“Intolerance” suggests that cow’s milk causes adverse effects (generally gastrointestinal) but without committing to an underlying mechanism. 

If there is reason to think the adverse effects are immune mediated (because there are signs/symptoms outside the GI tract, for example) then it is preferable to use “cow’s milk allergy” (which then divides into type 1, non type 1, or mixed). 

Can even affect exclusively breast fed infants if sufficient milk proteins transmitted in breast milk, but probably over diagnosed (as challenge after 2-4 weeks not done).

Not the same as lactose intolerance – lactose is a sugar, intolerance to it is due to malabsorption and effects of undigested sugar in colon eg bloating, diarrhoea.  NOT rash, vomiting.  Usually post-gastroenteritis, transient.  No useful test other than lactose restriction for 2 weeks then rechallenge.

Some parents feel milk leads to more respiratory problems – there is some evidence that milk allergy is associated with more respiratory/GI infections and that an elimination diet (although supplemented by pre/probiotics) lead to reduced infections and less antibiotic use.

Cow’s milk allergy

Can be IgE mediated (immediate, histamine release, potentially anaphylaxis), else non-IgE mediated (typically more chronic, delayed symptoms, predominantly gastrointestinal, possibly a threshold level below which a patient is asymptomatic) but can be both. Non-IgE mediated symptoms include:

  • Eczema
  • Colic
  • Gastro-oesophageal reflux
  • Constipation [NOT green or mucuous stools]
  • Eosinophilic oesophagitis
  • Allergic Proctocolitis (FPIAP – see below)
  • Growth failure
  • Enterocolitis (FPIES)
  • Enteropathy – no blood, and longer recovery time (weeks)

Note that the first 4 problems are very common and cow’s milk protein intolerance may only be a factor in a small proportion of such patients. Best predictor of whether symptoms are due to milk allergy appears to be the background of the health care professional, not the history, age or family history of atopy! See Imperial College review of evidence (Munblit and Perkins 2020).

ESPGHAN 2023 guidance does detail trial of exclusion for reflux. For colic, very strict – only when Rome IV research criteria satisfied (3hrs per day, without obvious cause, cannot be prevented or resolved by care givers, 3 days a week, confirmed with prospective diary) AND suspected on basis of additional symptoms.

In patients with eczema, a mixture of IgE mediated and non-IgE mediated reactions can be seen (and immediate reactions may be seen on re-introduction even when only delayed reactions seen initially).

Food protein induced allergic proctocolitis

Well baby with blood +/- mucus in stool, usually in first few weeks of life. Associated with eczema and family history of food allergies. Mixed feeding appears to protect. Benign – in exclusively breast fed infants, ESPGHAN says no dietary intervention for first month. Even for formula fed babies controversial, as large study in Boston found elimination increased risk of later type 1 milk allergy by factor of 5!

DRACMA 2022 guidelines from WAO quote small Brazilian study showing 80% tolerant by 6 months so earlier reintroduction presumably possible if you do exclude. Calls for more research.

So depends on severity/frequency – and if you eliminate, definitely challenge early.

Diagnosis

Prescriptions for specialist formulas increased massively in early part of century – 10-12x higher than expected in England, for example. Estimated prevalence is 1% in the UK, less than 0.3% in Germany and Greece.

With delayed reactions, diagnosis depends on history, and then dietary exclusion followed by re-challenge after 2-4 weeks. In the case of FPIES, re-challenge may need to be done in hospital. Sometimes the diagnosis is only made at endoscopy.

Dietary exclusion has been shown to affect long term taste preferences. Also significantly restricts diet, with potential impact on calcium intake (and also riboflavin, niacin, zinc).

For immediate reactions, skin prick testing (SPT) more specific than IgE blood testing. 3mm SPT wheal considered positive in infants, but low specificity; when doing IgE/SPT tests, also check egg allergy (high cross-reactivity) and soy (for formula substitution). If IgE/SPT negative, needs challenge (ideally double blind).

Substitute Formulas

  • Breast feeding mothers may need to exclude dairy in their own diet.  Daily requirement of calcium (1250mg) and Vitamin D (10mcg), so supplement and fortified alternative dairy products needed.
  • Because of theoretical risk from phyto-oestrogens in soya, use extensively hydrolysed formula (EHF) instead of soya formula if under 6 months. Soya cross reactivity is reported in up to 25% of young infants with non IgE allergy but this varies widely. Soya milk usage is also associated with increased risk of subsequent peanut allergy (RR=2.6)!
  • ESPGHAN says you can also use hydrolysed rice formula – available in UK? Reported arsenic values are within WHO limits.
  • About 10% of infants will not tolerate even extensively hydrolysed formula (eHF) and may require an amino acid based formula; anaphylaxis has been described even with hydrolysed formula.  AA formula should be used first line if:
    • anaphylaxis,
    • severe non IgE (eg PR bleeding leading to haematological disturbance, severe skin disease, FPIES),
    • faltering growth (says ESPGHAN but controversial).
  • eHF potentially better than other types of formula, and potentially added benefit from probiotics – in trial of N=260 (42% IgE mediated, non-randomised) tolerance after 12 months 79% for EHF & Lactobacillus rhamnosus GG (LGG), cf 43% for EHF. 23% soya, 18% AA. Associated with IgE mechanism (negatively, OR 0.12), and EHF (4.41) or EHF & LGG (29) [Canani, European lab for food induced diseases, Naples. PMID 23582142].

Challenge

Cow’s milk must be tried again to prove it is the causal agent, unless type 1 symptoms, or severe non-type 1 (FPIES).  If symptoms return then continue elimination diet for at least 6 months, else 1yr of age, then re-introduce gradually. ESPGHAN says do IgE for milk first if type 1! Highlights that boiling more likely to hydrolyse proteins than baking, but ignores matrix idea. No evidence for further challenges but suggests every 6 months.

Prognosis

Exposure does encourage tolerance. In studies, after 6 months of oral desensitization, 11% had had positive food challenges cf 40% for abstainers. And in the abstainers, the threshold of sensitivity tended to be lower, and symptoms more severe [Eur Ann Allergy Clin Immunol. 2007 39:12-9. PMID 17375736].

Almost all non IgE milk allergy and most type 1 resolves by 1yr after diagnosis.

Reintroduction is typically done according to a “ladder” of 4 or more steps – baked milk, then boiled milk, then yogurt, then fresh raw milk. Baked milk is less allergenic due to the matrix of wheat – if wheat allergic, then gluten free cheese oatcakes (Nairns) or shortbread (Walkers/Asda).

IgE disease less likely to resolve if asthma, rhinitis, severe reactions or strongly positive results.  Median age of tolerance 5yrs.  According to Thermofisher, positive IgE Casein (Bos d 8) means less likely to tolerate baked milk or outgrow, as protein (casein) more heat stable (no consensus on component testing in ESPGHAN 2023).

You could argue for early introduction of weaning foods but this is only briefly mentioned in ESPGHAN 2023 and not yet recommended.

Final adult height has been shown to be reduced in milk allergy – this could be related to co-morbidities (asthma, eczema, steroid use, sleep disruption etc) or feeding difficulties (associated with elimination diets).

Prevention

EAACI task force recommends against use of milk formula top ups in first week of life in breast fed babies. Low certainty, though. Also recommends avoidance of allergens (including milk but not limited to) in pregnancy and during breast feeding!

ESPGHAN discusses too. In a multivariate model, independent factors associated with milk allergy were family history of allergy (OR = 2.83), avoidance of dairy products during pregnancy or breastfeeding (OR = 5.62), and formula given at the maternity hospital (OR = 1.81). In an RCT of daily 10ml formula supplementation (n=504 breast fed) cf only soya formula if required, performed between 1 and 2 months of age, daily formula ingestion prevented nearly 90% of later milk allergy confirmed by OFC at 6 months (RR: 0.12). EAACI neutral on this – and regular top ups would never be supported by breast friendly clinicians. Overall however, ESPGHAN group decided there was insufficient evidence for any of these things.

See also EAT study, and GINI study.

Treatment

66% of kids grow out cow’s milk allergy, even if they completely avoid it. But rate rises to nearly 90% if baked milk introduced. And less restrictive diet good for everyone, of course.

Salmivesi RCT from Finland 2012 – n=28, age 6-14. 81% using daily milk 6400mg protein at 12 months. First dose milk 0.06mg – 8 further observed doses (0.12mg day 8; 0.24mg day 15; 2.0mg day 36 [big jump!]; 4.0mg day 38 [2 days later!?]; 8.0mg day 42; 40mg [big jump again!] day 57; 80mg day 64; and 160mg on day 78) with other dose increases done at home. Monitored for 2hr in clinic. Final dose of 6400mg (=200ml) was given at home (!) on day 162.

Oral immunotherapy (OIT) for severe milk allergy (IgE >85 or low eliciting dose):  at 1yr 36% tolerated 150ml, 54% 5-150ml (good enough for accidental exposure). 10% could not complete protocol. [reference?]

DRACMA update on milk immunotherapy (2021) mostly fresh milk used in research. Randomized trials looked at kids aged 2-14, mean 8. Non randomized had wider range. 67% tolerated 150ml (cf 2.2% of controls), 78% tolerated 5-150ml (=swig protection) (cf 3.3% of controls). Anaphylaxis rate of 5.5 per person-years (although not always defined, and not always usual definition). 63% used IM adrenaline!?

6.9% developed EOE but rarely biopsy confirmed. No deaths.

2–8 weeks after discontinuation of successful OIT, tolerance of cow’s milk persisted in only 36% (20%–91%). So you have to persevere life long, probably.

Quality of life badly reported – only 5 studies. 1 study found parents reported better QOL in 37%, worse in 26%, and unchanged in 38%! 2 conference abstracts reported improved QOL or at least reduced anxiety in general and reduced fear of unexpected reaction. Some studies found worse QOL! Certainty of evidence overall v low…

Only 1 trial and 2 non randomized studies of baked milk OIT! In the 1 RCT of baked milk, 73% achieved tolerance at 12 months (cf none of control group) – other studies did not find evidence of effectiveness however (meta-analysis of Anagnostou. Tolerance to heated or baked milk may be temporary and diminish within a few years. Dantzer. 20% required adrenaline! Only some children assessed for QOL, with evidence of benefit – of the parents studied, no improvement in QOL! [Dantzer and Dunlop 2021]. Low desensitization rate for unheated milk means persisting concern about exposure in real life despite less frequent adverse reactions (8%–33%).

Other studies did not find this relationship, which is consistent with the meta-analysis results of Anagnostou et al. (41). Tolerance to heated or baked milk may be temporary and diminish within a few years. Dantzer et al. found that a protocol involving gradually increasing doses of baked milk was effective in promoting desensitization (73% achieved end dose of 4000mg cf 0% of controls).  Mean age 11. “This suggests that the initial dose [and then building] may influence the efficacy of desensitization.” 

[Yan Wang, China – Front. Immunol., 04 June 2025]

4% rate of biopsy proven EOE – note EoE typically emerges approximately 2.8 years after initiating the maintenance phase so many studies will miss…

Longer duration better. None of the studies reported on sustained unresponsiveness.

Only Dantzer study reported quality of life! 

Highlights “a dire need for a standardization in outcome assessment and reporting,” and that successful completion of OFC needs to be validated as a predictor of “real world” success. [Natasha trial will hopefully clarify further…]

Separate article on OIT recommendations – apart from balancing risks and benefits, recommends using omalizumab (monoclonal anti-IgE) in advance and in initial stages of oral immunotherapy with unheated cow’s milk. Inferring from limited evidence (use in other food allergies, mostly) that risk of anaphylaxis reduced (RR0.34 but not significant!). Not really any downside? (But costs at least £256 per dose, maybe double? Lasts a month?). Plus, does not recommend baked milk OIT as very low certainty of benefit. More evidence on effect, risks, QOL benefit obviously required.  

Sublingual/epicutaneous immunotherapy (SLIT) for milk? Not much evidence – low rate of success and high rate of relapse.

[EGPHAN 2023, Frontiers in Pediatrics 2019; BMJ cmpa article sept 2013]

Rush study from Japan used microwaved milk – microwaved for 100s at 550W (!). Dosing was 2–4 times a day in hospital for several days (frequent adverse events) aiming for 200 mL dose (total daily, I assume). If not achieved, dose increases changed to 1ml per day. At 200ml, dosing changed to once a day. After 2 months of maintenance, length of time in the microwave gradually reduced.

Another Japanese study looked at using heated milk powder (3 mins at 125degC) vs unheated milk. Rush protocol (5 days in hospital) up to maintenance of just 3ml daily. At 1 year, 35% and 18% in the HM group and 50% and 31% in UM group passed the 3 and 25 mL OFCs, respectively, so not great efficacy. Rates of moderate or severe symptoms significantly lower (halved) in the heated milk group however.

Natasha Trial is looking at Peanut or cow’s milk OIT in UK – groups are Peanut age 6-23yrs, Peanut age 2-3yrs, Cow’s milk age 3-23yrs. Using everyday food products. Final results expected 2027.

Colic = Cry-Fuss Behaviour

Common, General paediatrics, Nutrition, OPD

Cry-fuss behaviour (=colic etc), mean is just short of 2hrs per day for first 6 weeks, reduces to 72 minutes by 10-12 weeks.

“Colic” suggests that there is a bowel issue, usually suspected due to drawing legs up, passing wind – but these could be considered normal for crying and distress, of any cause.  Reflux (GORD) is often blamed, yet international consensus states there is no evidence to support an empiric trial of acid suppression as a diagnostic test in infants and young children, even though symptoms tend to be less specific [Vandenplas, J Pediatr Gastroenterol Nutr. 2009 Oct;49(4):498-547. doi: 10.1097/MPG.0b013e3181b7f563]!

Cause

Mums with an anxiety disorder prior to pregnancy are at higher risk of having a child with excessive crying at 2, 4 or 16 months postpartum compared with mothers without an anxiety disorder.  Risk increased further for mothers who developed an anxiety disorder during pregnancy.

So does maternal anxiety lead to “intrusive” parenting, in turn increasing infant crying ?[Arch Dis Child 2014;99:800–6]. Else fetal programming?  Genetics?

What’s the influence of fathers!?

Surprisingly, maternal depressive disorders, cf anxiety, experienced before or during pregnancy, did not predict maternal report of excessive infant crying.  Is the difference withdrawal, rather than intrusiveness?

Reflux

Consider 2 week trial of anti-secretory eg ranitidine (but NOT PPI – increase risk of infection esp respiratory and GI, associated with parietal cell hyperplasia, and possibly food allergy!).  But don’t assume improvement due to response!  Or investigate with pH monitoring.  Or stick to supporting parents!   Even if arching and refusing to feed, no evidence of effectiveness.

Infection

5% have UTI retrospectively, but in absence of other signs, investigations not routinely required.

Associations

Crying that lasts more than 3 h per day, for more than 3 days per week and for more than 3 weeks in a row—is associated with child abuse and maternal depression!  Higher scores on PND scale persists at 6/12 even if crying resolves…

6% of parents retrospectively admit physically abusive behaviours towards baby when crying.

Predicts shorter duration of breast feeding.

Persistent problems with cry-fuss behaviour at 5/12 associated with later behavioural problems (metanalysis, but confounded by psychosocial risk factors).

Management

Reassure the parents/carers that infantile colic is a common problem that should resolve by 6 months of age.

RCTs of behavioural sleep intervention under 3/12 did not decrease crying.  So encourage parent-infant reciprocity (ie responding to crying) until old enough to suit Gina Ford type regimented sleep regimes.

Encourage the parents to try relaxed cue based care, sleeping in the same room as the baby (not the same bed – beware SUDI) , offering physical contact esp skin to skin contact, and ensuring the baby gets lots of rich sensory experiences during the day.  This,  combined with average 10 hours of physical contact per 24hr (even if asleep), associated with 50% less crying and fussing. Only 37% of 3/12 babies sleep 8hrs straight at night.

Night waking is associated with co-sleeping and breast feeding, but breast feeding does not equate with less total sleep for parents over the whole 24hr period (quality, however, may be inferior).

Over sensitive babies may benefit from OT/Physio, but beware removing sensory stimulus as associated with neurodevelopmental problems.  Massage, wrapping may help, little evidence for chiropractic, craniosacral, nutritional.  Offer diverse sensory stimulation (through parents’ own social life and activities).

If symptoms are severe (subjective, of course) or persist after 4 months, consider an alternative underlying cause for symptoms.

NICE says seek specialist advice from a paediatrician if infant is not thriving, or symptoms are not starting to improve or are worsening after 4 months of age.

Caveat for GPs is “Seek specialist advice if Parents/carers feel unable to cope with the infant’s symptoms despite reassurance and advice in primary care.”

 

Feeding

Feed refusal is often linked, often impaired mutual regulation of feeding that result in entrenched patterns of difficult feeding esp breast feeding issues.

The following suggest a feeding problem –

  • 4 heavy disposable nappies per day minimum
  • 3-4 yellow curdy stools if breast fed minimum
  • Nipple/breast pain, attachment problems
  • falling asleep within 10 minutes, feeding longer than 30 minutes (active feeding ie not including dozing, interacting) regularly
  • clicking sound, gurgly sounds, absence of swallowing sounds
  • Increased resp effort

Expect 125g per week growth average in first 3 months.  Tongue tie only really relevant to breast feeding babies.

Babies who have infrequent large feeds are not necessarily abnormal, and cue based feeding rather than scheduled 3-4hrly feeds often works better.

So offer feed calmly, unless already full blown crying, in which case calm holding eg skin to skin until more settled.  Cochrane review concluded that pacifier use does not interfere with breast feeding in mothers who are motivated.

Some evidence for trial of hydrolysed formula. RCT of 107 breast fed babies with colic excluded dairy, soy, wheat, nuts, fish and shortened duration of crying, but only CMPI really substantiated.  Probiotic has helped in RCT but roles of feed management, lactose overload etc need to be elucidated first?

Functional lactose overload? – as feed progresses, fat level usually increases so transit time slows.  If insufficient fat, rapid transit leads to lactose fermentation in colon (lower cholecystokinin levels seen).

Parent Support

The self-help support group Cry-sis for families with excessively crying or sleepless children, has a website and runs a national telephone helpline (0845 122 8669).

There’s also parent info including a video at http://www.nhs.uk/Conditions/Colic/Pages/Introduction.aspx

 

[https://cks.nice.org.uk/colic-infantile#!scenario]

[Clinical review BMJ 2011;343:d7772  doi: http://dx.doi.org/10.1136/bmj.d7772]

Vitamin D

General paediatrics, Nutrition, OPD, Orthopaedic

=colecalciferol.  Essential for bone health.

Obtained from sun exposure to the skin.  Only a few dietary sources – oily fish, cheese, egg yolk, fortified cereals. Diet more important for calcium, of course. Once you apply sun screen, you don’t make vitamin D any more so there is a conflict with the potential for skin solar damage including cancer.

Children under 5 considered a high risk group, along with pregnant, pigmented skin, northern latitudes, wearing concealing clothing, being housebound etc.

2021 Scottish government advice is that everyone consider taking a Vitamin D supplement, particularly between October and March, but that all year round supplementation should be taken by:

  • all pregnant and breastfeeding women
  • all infants and children under 5 years old
  • people who have low or no exposure to the sun, for example those who cover their skin for cultural reasons, are housebound, confined indoors for long periods or live in an institution
  • people from minority ethnic groups with dark skin such as those of African, African-Caribbean and south Asian origin, who require more sun exposure to make as much vitamin D

2017 chief medical officer (CMO) advice – all babies from birth up to one-year-of-age should be given a daily supplement of 8.5 to 10μg vitamin D with Healthy Start vitamin drops being the recommended choice of vitamin, other than babies who are formula fed getting at least 500ml per day, as infant formula already has added vitamin D.

Nonetheless, breastfeeding is preferred – supplementation needed for breastfed infants given lack of sunlight in the UK (probably only useful sun exposure in Scotland between April and September, and between 11 and 3pm).

Children aged 1-4 years old should be given a daily supplement containing 10mcg of vitamin D.

“Healthy Start” vitamins preferred – made for  NHS,  available free to those on income support,  contains recommended dose (approx 300 units) .

Standard prevention dose is 300-400u (10mcg) (neonates), between 400u and 1000u (over 1/12) per day.  Over the counter multivitamins often contain surprisingly little Vitamin D.  Drops, tablets, sprays all available.

Many vitamin D preparations around this dose contain calcium, which may improve efficacy in fracture prevention, but some people won’t like.  Fultium D3 capsules have 800u (20μg) vit D and no calcium.

Symptoms

Aches and pains, delayed walking, seizures and tetany, genu valgum/varum, muscle weakness (incl cardiomyopathy).  The classic features of rickets are bowed legs, rachitic rosary (expanded costochondral junctions), pectus carinatum, curvature of the spine, expansion of the metaphyses at the wrist/ankle, poor dentition.

Testing

Historically deficiency defined as 25hydroxyVitaminD below 25nmol/L. But debated what is optimal.  NICE CKS uses this figure, and defines ‘insufficiency’ as between 25 and 50 nmol/L.

Treatment

Vitamin D3 preferred – D2 sometimes used.

If rapid correction needed eg deficiency with symptoms, fixed loading dose used for 8-12 weeks:

  • 1-5 months: 3000 IU
  • 6 months -11 years: 6000 IU
  • 12yr+: 10 000IU. Single/divided oral dose totalling 300 000IU can be considered if compliance issues.
  • After that, standard prevention dose as above unless significant lifestyle changes to improve Vitamin D status.

Otherwise 400-600IU daily from age 1 month to 18 years. Buy over the counter unless for chronic condition that leads to deficiency.

Assess need for calcium supplementation eg milk allergy. Online calcium calculators available.

Colecaciferol liquid available (3000u/ml), tablets come in 1000u doses and higher.  The combined VitD/Cal tablets tend to have lower Vit D doses and may not be tolerated.

Weekly doses, or single megadoses (30x daily dose) have been recommended where compliance a concern. Intramuscular ergocalciferol 7.5mg (300,000 units, 1ml) can be given in special situations.

Alfacalcidol is used in chronic kidney disease, needs specialist advice and careful monitoring.

Monitoring

Repeat measurement of serum 25 OH vitamin D is not usually necessary, and certainly not within 3 months of starting treatment unless agreed with the duty biochemist.  Check compliance eg empty bottles?

Continue supplementation until child has stopped growing.

Vitamin D deficiency in children | Health topics A to Z | CKS | NICE

Anorexia nervosa

General paediatrics, Mental health, Nutrition

Eating disorders categorised as:

  • Anorexia Nervosa (IDC-10, DSM-IV)
  • Bulimia Nervosa (IDC-10, DSM-IV)
  • Eating Disorder not otherwise specified (EDNOS)
  • Binge Eating Disorder (without the compensatory behaviours of bulimia eg vomiting, exercise)
  • Selective/Restrictive Eating

DSM-IV Criteria for Anorexia Nervosa

  • Body weight at or below 85% of that expected
  • Fear of gaining weight or becoming fat, even though underweight
  • Disturbed perception of body weight or shape
  • Amenorrhea, at least 3 consecutive cycles
  • Disturbance in way one’s body shape is experienced (?)

ICD-10 adds a couple of things:

  • BMI < 15
  • Weight loss caused by food avoidance, self induced vomiting, purging, excessive exercise (not in DSM)
  • loss of libido in men
  • Pubertal delay if early onset

For children, these strict criteria can overlook significant disordered eating – wide variation in weight and height gain through puberty; menses not present else irregular.  Levels of cognitive development obviously vary.  Abnormal food behaviours eg slow eating, hiding may have been present from a young age. One type of eating disorder can change into another.

Interest in healthy eating and exercise may initially give impression that child is well. Dieting is miserable for most people, but for some it appears to relieve anxiety, which can lead to a vicious cycle. Sometimes it is specific foods that are feared.

BMI <2nd centile prob more useful for kids.  GOSH Criteria (Nicoles, Chater & Lask 2000) talks about determined wt loss, abnormal cognitions about weight/shape but also morbid preoccupation.  Similarly, Bulimia Nervosa defined as Recurrent binges and purges, Sense of lack of control, Morbid preoccupation with weight or shape. Purging is any behaviour to prevent weight gain including self induced vomiting, fasting, dieting, excessive exercise, misuse of medicines such as diuretics or laxatives.

Questions:

  • What did you eat yesterday? Are there foods you don’t eat any more?
  • Are you more interested in food and cooking?
  • Are you trying to cut back?
  • Does it ever feel like your eating gets out of control?
  • What happens if you can’t exercise?
  • Have you been making yourself sick? Do you drink water to prevent hunger?
  • What do you see when you look in the mirror? (Body dysmorphia = perception of shape, size that is unrelated to reality). Is there a weight you would like to be? What sort of things do you look at online?
  • Explore mood and risk of self harm.  Anhedonia (inability to enjoy anything) common. Ask direct questions about abuse or neglect (explain this is routine).

Clinical features:

  • short stature,
  • hypothermia,
  • dry lips/mouth,
  • ketosis,
  • scaphoid abdomen,
  • pallor/carotenaemia/acrocyanosis,
  • lanugo, thinning of scalp hair,
  • dry skin and brittle nails,
  • evidence of self harm,
  • Flat affect, mood changes, impaired concentration/memory,
  • hypotension, orthostatic HR/BP changes,
  • SUSS test – stand, squat, stand (without using upper limbs); sit up from lying
  • cardiac failure,
  • peripheral neuropathy.
  • Callus on back of hand (Russell’s sign) in bulimia

Associated with depression, anxiety, obsessive/compulsive disorder and alcohol misuse.

Differential

Beware diabetes, hyperthyroidism, Addison’s, coeliac, malignancy.

Treatment

Early intervention associated with better outcomes.  Poor outcome in anorexia if patient does not receive effective treatment in first 3 years. 

Principles –

  • Give diagnosis – may not be appreciated. Anosognosia = inability to see weight loss or failing health (and therefore others with that viewpoint are irrational or unkind)
  • Strengthening family relationships away from food (in many families tends to be around meals, snacks, eating out, and many conversations around favourite foods etc)
  • Conceptualising the eating problem as being separate from the young person.  Eating problem as “bullying voice”. Avoid discussions of weight or body image (“you look healthier” can be misinterpreted as “you look fat” by eating problem).
  • Not a choice, not rational. Alexithymia (inability to express feelings) common. Genetic heritability accounts for approximately 50–80% of the risk of developing an eating disorder, often pre-existing tendencies towards anxiety, inflexibility, difficulties with emotional regulation, enhanced sensitivity towards punishment. [Proposed mechanism here]
  • Families are not to blame!
  • Food is medicine. Enforcing regular, balanced meals and snacks (3 of each daily) as a family improves mood, behaviour as well as physical symptoms. Terrifying at first, of course. Metabolism often ramps up once refeeding begins, so a huge increase in intake is often required to achieve restoration of healthy weight (and catch up growth) in anorexia. For bulimia, regular pattern of eating more important.
  • Don’t allow meal choices or negotiation, discourage involvement in or observation of food preparation, which reinforces disordered thinking. Reduces anxiety when not required to make “difficult” choices about problem foods.
  • Avoid regular weighing and other forms of body checking
  • Full recovery is possible, especially when detected early eg months rather than years.

Can be helpful to offer option not to be told weight.  Beware concealing weights on body, water loading before weighing day.  Praise honesty, highlight confidentiality, agree sharing of information with parents.

Parents can become used to “new normal” of disordered eating, and might not appreciate risks.  Alternatively, young person might feel threatened by alliance between doctor and parents.

Target weight is tricky – what is required for normal bodily function? What was growth/puberty trajectory before eating restricted? So healthy thoughts about food, normal periods (often 9 months or more), return of premorbid personality etc. Fluctuating weight gain may be due to metabolism, fluid shifts, concealed weights or water loading, concealed purging (silent exercise eg crunches in bed).

Where food refusal is an issue, energy dense food is required – increase fat content, avoid water or diet drinks, leave fruit/veg till after other foods eaten. Smoothies or milkshakes often better tolerated. Bloating and nausea with refeeding common initially but should improve.

Family based treatment is recommended by NICE as first line. Emphasises that parents initially take back responsibility for feeding, then gradually handing it back to the young person.  Minimisation of blame.  If ineffective then CBT.

Psychotropic medication not recommended – metanalysis found no benefit from antidepressants in anorexia.

No evidence based guidelines for re-introduction of nutrition/energy in adolescents!

For the majority of patients, 40kcal/kg/day (1200kcal/day) appears to be safe – don’t start a meal plan with less calorific content than they were receiving prior to admission, although difficult when history of the amount taken is unclear.

  • The meal plan should comply with normal macronutrient guidelines (10-15% protein, 30-35% fat, 50-60% carbohydrates).
  • Increase the meal plan by 200kcal/day until 2000kcal/day is achieved.

Fluid 50ml/kg/d for 15yr+, 55ml/kg/d 11-14yr (Shaw et al).  GOSH use standard paediatric fluid requirement calculations.

Promote weight gain 0.5kg/week (NICE 2004, Junior Marsipan 2012).  Ignores malnutrition, of course.  Percentage weight for height used, but easiest to divide BMI by median BMI for age/sex – 85% is underweight, 90% is satisfactory.

Check electrolytes, calcium, phosphate, magnesium, liver function, vit D on admission.  QTc must be calculated MANUALLY (to find end of T, draw tangent through steepest part of curve).

All patients should be prescribed prophylactic dose of Vitamin D at a dose of 800IU/day whilst waiting for Vitamin D levels to be reported.

Prophylactic phosphate should not be routinely prescribed, however it should be considered where:

  • There has been a previous history of re-feeding syndrome.
  • Multiple risk factors

Consider Thiamine where starvation has been very prolonged (e.g. greater than one year at very low weight and poor intake) or there is a concern about vitamin deficiency.

A low phosphate (<1.1 mmol/L) before initiating feeds is unusual (see below) and should be corrected as soon as is possible on the day of admission:

  • Low phosphates should be discussed with the responsible consultant.
  • Give two sandoz-phosphate tablets and commence TDS regular phosphate regime.
  • Recheck U&E in 12 hours and monitor clinically (see below).
  • Do not make any increases on the feeding regime until phosphate has been corrected.
  • If phosphate is still low at 12 hours then consider repeated double dose, or IV correction. This is unusual.
  • Other causes of low phosphate should be excluded – in particular Vitamin D deficiency and hypoparathyroidism: check PTH and Vitamin D with next set of bloods (if hasn’t already been checked). These bloods should not hold up commencing of feeding once phosphate is normalised.
  • If phosphate is significantly low (<0.5) consider IV replacement – this will generally mean transfer to a medical ward.
  • Phosphates that are potentially dangerously low (<0.3) should be managed on a medical ward/PICU and discussions should occur with the consultant and CSPs about transfer before commencing feeding.

Refeeding syndrome

Biochemical abnormalities AND cardiovascular and neurological findings.  Onset is in first 48 hours, up to first five days of initiating feeding (cases up to 18 days later described -consider at risk for up to 20 days).  Cardiac arrest has occurred.

Early finding is drop in phosphate (increased requirement as body switches back to carbohydrate metabolism, plus chronic phosphate depletion due to starvation). Potassium, Mg also fall. 

All patients considered at risk of re-feeding syndrome should be monitored for clinical signs of the re-feeding syndrome:

  • Resting tachycardia (differential for this includes anxiety).
  • Oedema or swelling, especially in the legs.
  • Confusion or altered conscious state (always check glucose in this case).

Patients should have:

  • Daily inspection for any signs of oedema (in particular peripheral oedema) for first five days.
  • Three times/day resting pulse and lying and standing blood pressure for first five days.
  • Monitor for biochemical/blood parameters of the re-feeding syndrome:
  • Daily urea, creatinine, sodium, potassium, phosphate, magnesium daily for five days. The drop in phosphate seen when re-feeding will normally occur within 48-72 hours.

[http://www.gosh.nhs.uk/health-professionals/clinical-guidelines/refeeding-guidelines-children-and-young-people-feeding-and-eating-disorders-admitted-mildred-creak]

Current GOSH study, issue may be more the degree of malnutrition than the rate of re-feeding, so perhaps guidelines excessively cautious.

Admission criteria

  • %IBW <75%
  • Dehydration
  • Electrolyte disturbance (hypokalaemia, hypocalcaemia, hypomagnesaemia)
  • Cardiac dysrhythmia (can occur even in absence of electrolyte disturbance)
  • Syncope / Seizures
  • Cardiac failure
  • Pancreatitis
  • Severe bradycardia
  • Hypotension
  • Hypothermia
  • Acute food refusal
  • Failure of OP treatment
  • Uncontrollable binging and purging
  • Suicidal ideation
  • Acute psychosis
  • Co-morbid diagnosis that interferes with treatment eg OCD

Hypokalaemia can be due to vomiting, diuretic/laxative misuse. 

“Check bloods regularly” – ? Responsibility

Multivitamin and Thiamine 100mg bd for 10/7

[BMJ 2017; 359 Helen Bould]

Junior MARSIPAN: Management of Really Sick Patients under 18 with Anorexia Nervosa.  January 2012.

Patient information

Obesity

General paediatrics, Nutrition

See Management, Treatment and Prevention.

Obesity is more than a number.  As defined by the Obesity Medicine Association, it is a “chronic, relapsing, multi-factorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences”. It is therefore not “cured” simply by the numbers getting better.

Obesity is associated with a range of problems, including slipped upper femoral epiphysis and sleep apnoea that are clearly related to being overweight, plus psychological issues related to self image.  But there are also unexpected complications such as higher rates of admission and longer hospital stays after road traffic accidents, and higher mortality with asthma (not necessarily due to worse asthma), and SARS-CoV2 (2.1x – but not an increased risk of getting it).

It does appear that adipose tissue produces inflammatory cytokines.  The insulin resistance that can be associated with obesity also increases endothelial and platelet dysfunction, which increases the risk of vascular and thrombotic conditions.   

Hazard ratios for healthy lifestyle factors and BMI - BMJ 2016

It’s also true that BMI is only one factor in health – if you have one or more healthy lifestyle factors, you could well have better life expectancy than someone with normal BMI but high waist circumference and no healthy lifestyle factors. [BMJ 2016] Evidence that moderate/high levels of cardiorespiratory fitness appear to attenuate or even eliminate the risks.

Some US states reporting declines in rates of childhood obesity. Australia has plateaued. The COVID pandemic was bad for obesity with figures from NHS England and Public Health Scotland showing a sharp increase – obesity prevalence at reception age (4-5yrs) is up from 9.9% in 2019/20 to 14.4% in 2020/21, and Year 6 (age 10-11), from 21.0% to 25.5%. 

Ethnicity is a major risk factor – Black and Asian have higher rates than whites, Chinese lower.  Boys outnumber girls slightly in both age groups.  Risk at least twice as high in most deprived areas cf least deprived.  In London, 30% of 10-11yr olds now obese.

Obesity and Child Protection

Growing evidence linking adolescent and adult obesity with childhood sexual abuse, violence and neglect. In US preschool children, obesity linked to neglect and physical punishment even after controlling for socioeconomic group.

Wouldn’t be surprising if food became a way of dealing with stress (or feeding a way of dealing with distress) but obvious confounding.

A study of obese children in care found only 1% of the obese children were obese when taken into care, and risk increased with time in care. So can hardly be argued that putting children in care likely to help severely obese children!

So probably not itself a child protection concern, but may be part of wider concerns. Development of obesity and then failure to tackle also 2 different things. Consistent failure to engage with lifestyle changes or outside support IS a sign of neglect. Parental capacity is important. Environment often very unhelpful.

If looked at from children’s rights perspective, health can be seen as shared responsibility of the state, parents, and child themselves – note right to health, play, safe spaces, clean air etc. [ 2016]

Obesity Detection

About half of parents of overweight/obese children fail to recognise it. Particularly true for young children.  Doctors are not great at perceiving obesity visually either – in small study of 100 patients, 19% of obese were underestimated, and 25% of overweight [BJMP 2012;5(2):a520]. When presented with photos, GPs incorrectly assessed the majority of obese and about half the overweight patients presented in photographs. To be fair, this poor performance is probably true of the general population too.

BMI vs Fat

There are probably different obese phenotypes.  BMI is only a moderately good predictor of adiposity in children, and poor in younger children.  It is also true that there appear to be ethnic differences, for example Indian boys tend to have relatively higher percentage fat at all BMI levels.

Abdominal circumference in adults probably more important when it comes to metabolic (type 2 diabetes) and cardiovascular risk. Triceps skinfold thickness centiles available, over 14-15mm 95th centile for under 8 boys, 15-20mm for under 8 girls, 16-23mm for over 8 boys and 21-30 for over 8 girls.

When it comes to monitoring, changes in BMI have reasonable sensitivity but poor specificity when it comes to changes in adiposity – so beware over intepreting [BMC Ped 2018].

Weight (self) Perception

Weight (self) perception has a complicated relationship with actual weight, and whether young people engage in extreme weight management practices.  People who were underweight or overweight were mostly aware of their weight (80%, 96%), but bizarrely over 80% of those of healthy weight and obese inaccurately assessed their weight. Overassessors with healthy weight more likely to have extreme weight management practices, and even more true if underweight and female (OR 12.6, 95% CI: 3.4–46.6). [n=14,722 US high-school students, J PedGN 2014]

40% of men don’t recognise that they are overweight/obese (cf 19% of women), esp lower social class and ethnic minorities (“visual normalisation”). And seems to be getting worse over time.  [England, Obesity 2018]

Factors

Sleep deprivation

Associated with short duration of sleep in several cross sectional studies.  Longitudinal study in NZ 3-5yrs old found longer sleep reduced BMI at age 7 by 0.48 per extra hour, with a 61% reduction in risk of being overweight.  Controlled for physical activity, diet etc.  BMJ 2011:342:d2712.  Late bed times (after 9pm) an independent risk factor (for waist measurement) in age 2-6 [Sweden, Peds 2020].

Screen time

More TV time associated with increases in BMI from ages 14-18 in White middle class American kids with starting BMI average or above average.  Obesity 2013 Mar; 21(3): 572–575. doi:  10.1002/oby.20157]

Having TV sets in bedrooms associated with excess weight gain.

  • In France, in boys only. Explained 26-42% of body adiposity, other leisure activities didn’t make much difference. [Obesity 2017]
  • In US, boys and girls. 30% higher risk of being >85%, even after controlling for TV time! [Peds 2002]

Interventions to reduce screen time have also reduced obesity (not because more physical activity – less snacking!) [2yr study of age 4-7.  Success higher in lower social class] Epstein LH, Arch Pediatr Adolesc Med. 2008;162:239-45.]

These things all go together of course –

  • The cluster with the most screen time, shorter night-time sleep duration, average dinner timing and outside playtime had the highest overweight/obesity prevalence (15.1%)
  • This cluster also had the highest proportion of irregular mealtimes and the most screen time for both parents.
  • Cf cluster with the least screen time, the longest sleep duration, the earliest dinner timing and average outside playtime (4.0%).
[Japan, BMJ Open 2016]

Physical activity

Most people overestimate their own levels of activity, compared with accelerometer recordings.  Fitness helps boost mood, which can positively influence diet adherence.  Muscle mass will increase calories burned even at rest.

When it comes to losing weight, physical activity really needs to be at the high intensity level to be effective, especially if dietary changes are limited.

The concept of regular exercise or sport is both alien and inconvenient to the majority of the UK population. In recent years, rhetoric has
switched from sport to physical activity.

Stigma

People who identify themselves as overweight have worse mental health, for example greater risk of depression and reduced quality of life.  Not sure if there is any evidence for this in children but this presents a major problem when it comes to trying to improve health outcomes. [ObesRev 2017]

Obesity among Health care professionals

In England at any rate, nurses are no more likely to be obese than people in non-health professions (25%) but more likely to be obese than other health care professionals.  Unregistered care workers have the highest rate of obesity (31%) [BMJOpen 2017].

Health professionals of normal weight are more confident in their weight management practice, perceive fewer barriers to weight management and have more positive outcome expectations, and have a stronger role identity.  But also have more negative attitudes towards obese individuals.

Being female and having  knowledge and clinical experience of weight management appeared to predict positive attitudes towards obesity/obese patients and high self-efficacy in weight management. [ObesityReviews 2011]

Obesity treatment

General paediatrics, Nutrition

Limited quality data to recommend one treatment program over another, but combined behavioural lifestyle interventions appear to be better than “standard care” or self-help. Mean benefit of 0.3 Z score in children under 6.

Poor evidence for “parent only” interventions. Poor evidence that interventions to change behaviour of health professionals or the organisation of care (dietician, doctor, combined etc) makes any difference!

In obese adolescents, orlistat, metformin, and sibutramine should be considered as an adjunct to lifestyle interventions, but balance against potential for adverse effects. Average BMI benefit of 1.3, high drop out rate (25%) although only 5% due to adverse effects. [Cochrane 2016]

Surgery produced mean loss of 34.6kg in adolescents in Australia.  28% required further revisional surgery. Only 1 RCT! At 2 years, only benefit in 2 of 8 QOL measures. [Cochrane 2015]

Research needed into psychosocial determinants for behaviour change, strategies to improve clinician-family interaction, and cost-effective programs for primary and community care.

Cochrane 

Obesity prevention

General paediatrics, Nutrition, Psychology

Childhood obesity can be prevented – Cochrane updated evidence 2011!

Most effective interventions change social and physical environments and norms, not just individual behaviour.  Policies for healthy eating and physical activity in schools and early childcare settings, support for teachers to do health promotion, parent support and home activities that encourage children to be more active, eat more nutritious foods and spend less time in screen based activities.  Esp 6-12yrs but heterogeneous.

Fast food patronage is a frequent reality for many children and their parents. Although there are increasingly healthier alternatives for popular menu items (apple slices instead of French fries), they are infrequently selected.

Lifestyle factors cluster of course.  Boys’ adherence to a healthy lifestyle pattern (combining a nutrient‐dense diet and limited screen time) at 5 years was positively associated with prosocial behaviours (β = 0.14; 95% confidence interval [CI] 0.01, 0.26) and inversely related to hyperactivity‐inattention symptoms (β = −0.12; 95% CI −0.23, −0.01) at 8 years. But in the EDEN cohort, there was no association with BMI, and for girls, a mixed lifestyle pattern (sugar or artificially sweetened beverages, high screen, physical activity and low sleep times) was still associated with prosocial behaviours (β = 0.12; 95% CI 0.01, 0.23). [DOI:10.1111/ppe.12926]

What would Batman eat? Priming

Study of 22 children presented with 12 photos of 6 admirable and 6 less admirable models incl Batmand and Superman.  Asked, ‘Would this person order apple fries or French fries?’ In the health prime condition, the same children were shown 12 photos of 6 healthy foods and 6 less healthy foods and asked to indicate if each food was healthy or unhealthy.

Results

When children were asked what various admirable people – such as Batman or Spiderman – would eat, 45% then chose apple slices over French fries (cf 9% in control group).  Incidentally, knowing which foods were healthy or not made no sigificant difference to food choice.  [Wansink et al,  Pediatric Obesity, 7: 121–123. doi: 10.1111/j.2047-6310.2011.00003.x]

Weight talk in the home—parents talking to their children about their weight, shape or size— is associated with many negative health outcomes in children and adolescents, although the majority of research has been with adolescents.   Most psychological (e.g., emotional problems) and social (e.g., peer problems) outcomes differed significantly by race/ethnicity!

  • no significant associations between weight talk and biopsychosocial outcomes were found for Hmong and Latino children;
  • negative association (e.g., less healthy functioning) was found for African American and Somali children;
  • a positive association (e.g., healthier functioning) was found for Native American children. [DOI:10.1007/s10826-022-02351-9]

Food protein–induced enterocolitis syndrome (FPIES)

Allergy, Gastro, General paediatrics, Immunology, Neonatology, Nutrition

Non–IgE-mediated severe gastrointestinal food hypersensitivity, typically presents in early infancy with repeated vomiting, dehydration, lethargy, metabolic acidosis (even mimicking sepsis).  Watery diarrhoea (sometimes with blood and/or mucus) can develop in some cases. The severity is really what makes it worthy of a distinct name, debatable if it is actually distinct from other non-IgE mediated food allergy.

Probably underdiagnosed.

A few unusual features cf type 1 allergy.

The most common offending foods are cow’s milk and soy in young infants; in older infants, there are a range of food triggers including some foods usually not considered allergenic eg rice, oat, chicken, sweet potato!  Egg an unusual cause in some countries!  Cases in breastfed infants have been reported, even severe hypotension requiring intensive care.

Acute symptoms occur 1 to 5 hours after ingesting the offending food.  Lasts up to 24 hours. Not always consistent, which might suggest co-factors important.

In Europe, rare to get multiple food FPIES but in UK/US/Australia about 25% (English speaking!?).

Diagnosis

Diagnosis is based, predictably for a non-IgE condition, on clinical history and food challenges. Leucocytosis and methaemoglobinaemia are associated but low specificity/sensitivity.  

2017 Consensus out of date but diagnostic criteria still used – 

  • Major – vomiting at 1-4 hours in absence of type 1 skin/resp symptoms.
  • Minor – at least 3 minor criteria eg second episode of repetitive vomiting after same food; extreme lethargy; hypotension; need for hospital care or IV fluids; etc

Probably mild, mod and severe! Proposed BIO-FPIES criteria includes abdominal pain, nausea, increase in neutrophil count (but 3 points for second episode of repetitive vomiting after same food).

Phenotype switching

Egg and nut FPIES often go on to develop IgE sensitisation (about 20%), less for others. Of those, about 30% of milk FPIES will switch to type 1 phenotype, 15% for egg, less for other foods. But overall, unlikely to make much of a difference to care (and doesn’t help predict resolution).

Management

No role for antihistamine/adrenaline!

BSACI has FPIES plan.

Family support at www.fpiesuk.org.

For introducing weaning foods, when known FPIES to one food, start with low risk foods, supervise common triggers eg rice/egg.

Challenge

Challenge is necessary to decide whether things are getting better or not. Consensus is that 12-18 months after last reaction is a good balance between chances of things being better, and risk of causing severe reaction.  

50% milk/soya resolve by age 3-4, more like 4-5 years for other foods. 

Traditional protocol is 0.3g/kg protein, divided into 3 doses over 30 mins.  But unrealistic for low protein foods eg fruit. And doesn’t really make sense to split dose when you don’t expect a reaction for hours (but risk of switch to type 1 allergy for egg/nuts).

2 day protocol (25% portion then whole portion next day) had less severe reactions. 

25-30% of age appropriate portion triggers reaction in most children. [Baked???] Over 50% react after at least 2 hours. 

Beaudoin 2024 has home challenge protocol but brave… 

[Marta Vazquez-Ortiz systematic review]

[BSACI FPIES grand round – Marta Vazquez-Ortiz (Imperial/St Mary’s, BIO-FPIES research network)] [2025 Shaker shared decision making] [2024 Anvari]

Obesity management

Common, General paediatrics, Nutrition, OPD

Public health surveillance use 85th centile as definition for overweight, and 95th centile for obesity (UK says “at risk of obesity”…). Clinical definitions (SACN/RCPCH 2012, NICE) however are different: (UK 1990, use special BMI chart)

  • Obesity = BMI >98th centile for age (2 standard deviations, one tail)
  • Overweight = >91st centile (1.3 SD)

Growth charts then label:

  • Severe obesity = 99.6th centile (2.67 SD)
  • Morbid obesity = 3.33 SD.  High probability of co-morbidity, unlikely to improve by age 16.
  • (some guidelines use Extreme = 4 SD)

Cut off for overweight/obesity high in babies, starts at 18/20 age 2, nadir of 17/19 at age 5, rising to 20/24 at 10 then usual 25/30 at age 18. Girls same as boys, slightly fatter after 10 yrs. [International data, BMJ 320:1242.] Charts are available at the RCPCH.

Centile charts show centile spaces that are equivalent to 2/3 of a standard deviation.  When you get to high centiles, you need something better than “above the 99.8th centile” so you use Z score, which is the number of standard deviations above the mean

Calculators available to calculate BMI and Z-scores eg Phsim.man.ac.uk/SDSCalculator

So secondary referral for:

  • extreme, or
  • ?secondary obesity, eg
    • under 2 yrs with severe (>99.6th centile) obesity
    • short for age
  • co-morbidity eg strong FH type 2 DM, sleep apnoea, idiopathic intracranial hypertension, orthopaedic probs
  • psychological comorbidity,
  • safeguarding.

2nd care history –

  • menstrual hx,
  • sleep eg Chervin questionnaire (adds anything?)

Examination

  • acanthosis nigricans (neck, flexures) – highly associated with insulin resistance
  • buffalo hump.  Striae and obesity as only signs of Cushings v rare. Striae in Cushings more intense red!?
  • Mid-Parental Height – endocrinopathy unlikely if normal growth
  • Waist circumference
  • Goitre – hypothyroidism
  • BP
  • Peak flow
  • Syndrome eg BWS
  • Acne, Hirsutism – polycystic ovary syndrome
  • Telangiectasia

Investigations

Little evidence for investigations, not routine.

  • Fasting glucose, insulin, lipids
  • FBC, U&Es, LFTs
  • TFTs
  • HBA1c
  • SHBG (marker of insulin resistance)

For more severe cases, consider:

  • OGTT – 2hr glucose >11.1=diabetes, 7.8-11.1 = impaired glucose tolerance.  Esp if S Asian, other signs/risks of insulin resistance.
  • ECG
  • Sleep study
  • Molecular genetics (EDTA) eg Prader Willi, Bardet-Biedl syndrome, Cohen syndrome, MOMO syndrome.
  • Urinary cortisol/creatinine
  • Low dose dexamethasone test (more sensitive than above but needs overnight admission) – cortisol should suppress below 100, else suggests Cushings
  • CT head (if suspicion of raised intracranial hypertension

Homa-IR >4.5 for insulin resistance [Score = (Fasting insulin)*(Fasting glucose) / 405, measuring in mg/dl].  Transient increase in insulin resistance seen in puberty, independent of BMI.

Total choles:HDL 3.6 95th, 4.3 99th but no great paed data.

ALT>70 twice should proceed to USS to look for fatty liver, >100 urgent (for differential more than anything, although non alcoholic fatty liver disease can be progressive).

Communication

Delicate! Moral issue too – for example:

  • uncertain benefits on physical health
  • negative psychosocial consequences including uncertainty, fear, stigmatization
  • aggravating inequalities
  • disregarding the social and cultural value of eating
  • infringement upon personal freedom regarding lifestyle choices and raising children

Addressing these issues may avoid resistance [Erasmus medical centre, Obes Rev. 2011 Sep;12(9):669-79. doi: 10.1111/j.1467-789X.2011.00880.x. Epub 2011 May 4]

PHE “All our health” has child (and adult) obesity thread– use opportunistic moments to open up conversations around weight. “Let’s talk about weight” = short conversations guide.

  • Initiate a conversation. Anticipate defensiveness
  • Discuss “healthier weight” concept
  • Positive, non-judgmental language
  • Terms such as ‘obese’ are not generally well accepted by parents/carers

Opportunistic is good, but probably sensible to check that this is a good time, or at least create an invitation to start this conversation. And then, do more questioning and listening than advising.

What works?

The above section may already have brought up issues of low self-esteem and poor motivation. Building a therapeutic relationship, using motivational interviewing skills, is key then, especially where parents/children may have sensed discrimination and bias in the past.

General advice should include: (SIGN)

  • Healthier eating, and decreased calorie intake
  • At least 60 mins of moderately vigorous activity per day, pref habitual eg brisk walking! Given that evidence that moderate/high levels of cardiorespiratory fitness appear to attenuate or even eliminate the risks, just as important to emphasize fitness as weight loss? 
  • Max 2 hours screen time per day!

But as indicated above, probably more important to ask about the blocks, than to say “eat less, move more”.

OSCA 2012 Viner, arch dis child educ (paeds network)

See Prevention and Treatment.