Associated with range of negative outcomes.
Adverse childhood experiences increase probability of smoking in adulthood. Physical harm in Eastern European countries increases the probability of heavy drinking by about 3.4%, but not in other regions. Exposure to child neglect (little understanding) increases the probability of alcohol abuse by 2.7% in Nordic Countries but not other macro-regions. The experience of a poor relationship with parents is a strong predictor of alcohol abuse for the female subsample in Latin countries (2% higher).
While ACE does not appear to have a substantial effect on excess weight in any macro-region, childhood trauma (physical harm) appears to have a major impact on the likelihood of being obese later in life. Obesity has a more obvious impact on chronic illness than poverty, smoking or alcohol.
Children growing up on farms are less likely to develop allergies and asthma. Farming has been part of human culture for probably 7000 years.
It is widely accepted now that a symbiotic relationship with a diverse population of microbes in the environment, on the skin, in the gut and in the lung is necessary for a healthy immune system (“microbiome“). These microbes influence the balance between inflammation and immune tolerance. That relationship needs to be developed in early life, and nutrition is a major part.
Big European cross sectional studies – PARSIFAL and GABRIEL. Amish and Hutterites in US are genetically similar but Hutterites use industrial rather than traditional farming techniques (and have 4-6x the rate of hay fever and atopic sensitization).
Prenatal maternal exposure to farm animals is protective against eczema in the first 2 years of life, and against asthma symptoms pre-school.
Farm milk consumption in the first year of life is protective against respiratory allergies. Not clear what it is about it – more whey? Higher levels of cytokines or polyunsaturated fatty acids?
In children, exposure to cows and hay was protective against asthma. Some evidence for pigs, but risk seems to go up for sheep.
Mediators thought to potentially be N-gylcolylneuraminic acid (animals/pets) and arabinogalactan (plants).
Lipopolysaccharide (endotoxin) is widespread in the farm environment. Levels in mattresses inversely associated with hay fever, atopic sensitisation and asthma.
Lack of gut microbial diversity in first month of life predicts school age asthma.
Dietary diversity in first 2 years of life protects against asthma and allergic rhinitis. The link between gut microbes and lung health is thought to be short chain fatty acids, such as acetate and butyrate.
[Ped Allergy and Imm 2022
Contains a range of different sugars, aromatic oils, also pollens and bee proteins. Royal jelly and beeswax related, of course.
High fructose content can cause GI intolerance in some.
Allergic reactions can happen, often unrecognised, mostly due to specific pollens (depending on what flowers the bees feed on), in minority to bee proteins. Commercial honey tends to contain v low amounts of pollen, due to production techniques. IgE test for honey is available, but you may need to skin prick test with the specific honey if negative.
Honey eaten all year round is rumoured to prevent hay fever symptoms because of the pollens it contains, but this has not been proven, although it’s a nice idea related to immunotherapy. Depends on getting the right pollens of course – bees don’t like grass and birch flowers, probably. In some it may just trigger allergy symptoms.
Cross reaction between honey and bee venom is reported, not surprisingly, but not automatic.
Plant toxins can be present in sufficient quantities in honey to cause poisoning eg rhododendrons (some species).
Botulism reported in infants – failure to thrive, hypotonia, cranial nerve palsies. Clostridium and other bacteria cannot grow in honey due to the high sugar content, but spores can be present. So advice is not to give honey to infants.
Sources are animal products including meat, fish, dairy and egg.
For vegans, yeast products (eg Marmite) or fortified breakfast cereal are the only places you get it.
High levels often seen in teenagers. Appears benign, although high levels reported with lymphoma and hypereosinophilic syndrome, plus liver disease.
Like many things, low red cell count can be problem of production, loss or destruction.
So causes include:
- Bone marrow failure or infiltration (leukaemia, Fanconi’s, Blackfan Diamond, erythrovirus/parvovirus)
- Nose bleeds, gastrointestinal losses eg Meckel’s, gastritis, heavy periods
- Haemolysis eg G6PD deficiency, hypersplenism, autoimmune
- Iron, folate or B12 deficiency
In children, one of the most common causes is excessive milk consumption, which appears to lead to a low level colitis. Pica is often the presenting problem.
- Blood film – Howell Jolly bodies if hypersplenism. Leucoerythroblastic reaction (with immature red cells, as well as immature white cells) can be due to malignancy but can also be due to infection and haemolysis. Spherocytes or other abnormal forms may suggest a hereditary haemolytic condition. Sickle cells in sickle cell disease.
- Low MCV suggests lack of iron, but may also be due to thalassaemia.
- Reticulocyte count – indicates on going red cell production, may be high if recovering from low production
- White cell count and platelets – if low too, suggests bone marrow failure but parvovirus can knock off all cell lines too.
- Coagulation – deranged coagulation with low platelets suggests disseminated intravascular coagulation (DIC), usually due to sepsis, but can also reflect haemophagocytosis syndrome (due to sepsis or rheumatological disease)
- Renal function – haemolytic uraemic syndrome (usually with diarrhoea and bloody stools, but not always)
Iron is found in red meat, pulses, green leafy vegetables, wholemeal bread, nuts, dried fruit, fortified breakfast cereals.
Processed meats in particular linked with cancer. Probably the nitrites that are nearly always used.
Increases risk of colorectal cancer. As does alcohol. Dairy products, fruit/veg, fibre all prevent.
Genetic cause of short stature, often prenatal growth retardation too. Characteristic triangular face with relative macrocephaly.
Chromosome 11p15. But 10% due to maternal uniparental disomy 7.
Longitudinal research shows association between progressively higher glycaemic index diet and incidence of depressive symptoms. Experimental exposure to diets with high glycaemic load increases depressive symptoms in healthy volunteers, with moderately large effect.
Mechanism could be repeated and rapid changes in blood glucose, triggering counter regulatory hormones such as cortisol, adrenaline, growth hormone, glucagon.
Appears to be an inflammatory response to high glycaemic index foods too. Adherence to Mediterranean diet reduces markers. Mood disorders have been linked to heightened inflammation, although only in a minority. Observational studies show people with depression score higher for “dietary inflammation” viz trans fats, refined carbohydrates, lower intake of omega 3 fats. Mediated through polyphenols, polyunsaturated fatty acids?
Diet also affects microbiome, which interacts with the brain in bidirectional ways using neural, inflammatory and hormonal signalling pathways. High fibre, polyphenol, unsaturated fats promotes microbial taxa that generate anti-inflammatory metabolites such as short chain fatty acids.
Study of probiotics in healthy volunteers found altered response to a task that requires emotional attention, and may even reduce symptoms of depression.
But no benefit in large trial of Medierranean diet with subclinical depressive symptoms, only small trials of current depression showed benefit. Note context of people’s expectations regarding food/diet, which will likely have a marked effect on wellbeing.
Danger too of stigmatisation if trying to change an individual’s dietary choices.
[Joseph Firth, BMJ 2020;369:m2382]]
Freka PEG tube can only be removed orally. Good if v active, combative patient. But risk of mucosal burying, so weekly push and pull. Corflo can be removed by traction. Need replacing every 18 months.
Button preferred now, tube can be disconnected as required, replace every 12-18 months. 40% mortality at 5yrs post fundoplication where CP. 40% had no improvement in gagging symptoms. Only 1 in 8 need subsequent fundo if PEG only done first, so tend not to be done at same time.
Alternatives – jejunal tube via PEG (needs
continuous feeds) or jejunal button (less retching but more tube problems eg
Jejunostomy via Roux en Y potentially primary procedure. Risk of volvulus.
Oesophagogastric disconnection – (Manchester)
stomach detached from oesophagus, which gets plumbed on to Roux en Y
Bridles for NG/NJ skin fixation issues.
Blended diet for growth issues, feeding tolerance issues, failed jejunal, to avoid fundoplication. Currently not done via NG/NJ.
Actually 3 different gene defects possible, most commonly Galactose-1-Phosphate uridyl transferase deficiency (GALT, or Gal-1-PUT). The others have different phenotypes.
Presents in the newborn period after initiation of milk feeding, most commonly with jaundice, which can be unconjugated in first week but becomes conjugated thereafter. The other features listed below are seen in only a minority:
- poor feeding
- Cataract – can be present at birth, but more usually after a week or two.
- Sepsis – esp E coli septicaemia
Lab findings include hypoglycaemia, deranged LFTs, coagulopathy, metabolic acidosis, abnormal urine aminoacid excretion. Urine for reducing substances is not sensitive or specific. The definitive test is RBC Gal-1-PUT activity, but if a transfusion has been given alternatives are genotyping or testing the parents for carrier status.
Management is by diet. Nonetheless, neuropsych problems usually develop in adolescence and ovarian failure often occurs. Some debate about whether galactose can be tolerated from age 2-3yr.