All content of this blog is my own opinion only. It does not represent the views of any organisation or association I may work for, or be associated with. Nothing within this blog should be considered as medical advice and you should always consult your Doctor.

Infants, Vitamin D & The Truth About Diet

ALL infants need vitamin D supplement in the UK, anyone in the Northern hemisphere is deficient! As rickets reappear, so do generalised guidelines - and parents are often told that diet can't provide much vitamin D, instead it's all about sunshine and supplements.

Official Guidance

The NHS say:
"Vitamin D only occurs naturally in a few foods, such as oily fish and eggs. It is also added to some foods, such as fat spreads and breakfast cereals. The best source of vitamin D is summer sunlight on our skin. 
It's important that young children still receive vitamin drops, even if they get out in the sun.  All babies and young children aged six months to five years should take a daily supplement containing vitamin D, in the form of vitamin drops. This helps them to meet the requirement set for this age group of 7-8.5 micrograms (mcg) of vitamin D per day.  Babies who are fed infant formula don't need vitamin drops if they are having 500ml (about a pint) of formula or more a day. This is because formula is already fortified with the vitamins they need.  If you are breastfeeding your baby and didn't take vitamin D supplements during your pregnancy, your health visitor may advise you to give your baby vitamin drops containing vitamin D from the age of one month."
So I thought it might be interesting to explore just how much D lurks in food and what contribution this could realistically make to intake.

First we need to talk briefly about the different types of vitamin D.  There are 6, but D2 and D3 are the types sold as supplements.  D3 is generally considered superior to D2 but again it gets more complicated because not all studies nor experts agree.

It's also not easy to tease things apart, as many studies use synthetic supplements, whilst in nature other compounds that work in synergy (if you want to get techy read more here) are also found. 

Some studies that make the case against D2, highlight more is needed to generate the same circulating levels and it has a much shorter life after a single ingestion when studied over the next 28 days, however when it comes to infants they concede:
"Despite early evidence of differences in potency between the 2 vitamin D forms on a per weight basis, it must be highlighted that the widely practiced addition of vitamin D2 to milk in the United States and Europe in the 1930s served to successfully eradicate rickets as a significant health problem.  Additionally, fortification of milk with either vitamin D2 or vitamin D3 to this day has proven effective in the elimination of infantile rickets in North America. 
To prevent infantile rickets, a minimal intake of 2.5 μg (100 IU) vitamin D/d in infants with little sun exposure was shown to be efficacious (10). Thus, despite potential differences in the dose equivalence of vitamin D2 and D3, it is likely that vitamin D2 is currently provided at a high enough dose per kg infant body weight to maintain adequate bone mineral metabolism." here
In short, in "real life" either appears to protect against rickets, in a lab D3 sometimes looks better on paper - particularly when discussing supplements..

They're often quotes as offering a little, but not much D.  But what if that depends on the egg?

An independent study showed that UK eggs today have 70% more vitamin D3 than in the 1980's.  Birds also need sunlight or food sources of D and the reduction in caged hens and increase in free range and organic who see daylight,  plus improvements to their diet mean things have changed.

How much?
Well one medium sized egg can now contain as much as two-thirds (66%) of the RDA for an adult according to EU labelling regs.

At the time several, including the director of the "British egg information service" (made me chuckle) called for this significant egg finding to drive industry use (Pinchen H., Roe M., Finglas P. M., Buttriss J., Grey J., Cryer A.2012)

So, the EU lists adult RDA of 5µg and the NHS states that 1-5 year olds have a requirement of 7-8.5µg.  If one egg provides 66% of adult RDA, each egg provides roughly 3.3µg.  I wouldn't call nearly 50% an insignificant contribution would you?  

Fish can be a good source of D3.  This study though found farmed salmon contained 75% less than vitamin D than wild did.  As farmed fish is now the supermarket standard, you can see why some conclude it's not always easy to obtain D from food.

Furthermore cooking method impacts; baking salmon retains almost all the vitamin D, whilst frying in vegetable oil reduced the content by half.

What this paper also highlighted was that type of fish, diet, environment all impacted on vitamin D levels. You can see a list of the vitamin D value of fish here - although researchers concluded that the lists were out of date and new tests were needed.

Mushrooms are a huge vitamin D secret mainly because they can be hacked (by exposing them to bright sunlight), to have a higher D level either during after picking, Maitake for example, when grown in the sun can boast as much as 28.1µg per 100g, with 1 cup serving providing 20µg of D.

This has been dismissed by some as it's D2, however along with what we learnt about about D2, a 2011 study specifically explored mushrooms.

They found "the bioavailability of vitamin D2 from vitamin D2-enhanced button mushrooms via UV-B irradiation was effective in improving vitamin D status and not different to a vitamin D(2) supplement"

And a 2013 study again exploring vitamin D and mushroom consumption/bioavailability noted several things. 

First that the D2 in mushrooms was as bioavailable as that in a supplement. Furthermore the D2 in mushrooms was as effective at raising and maintaining blood levels of D as a supplement of either D2 or D3.

Second that D4 had been found in mushrooms as early as 1937. Therefore they decided to test a range including oyster, portabella & shiitake and found all contained varying levels. Another study continued their research exploring the D4 and again found this linked to light exposure.

Further examination revealed some also provided D3 whilst "Shiitake mushrooms not only produce vitamin D2 but also produce vitamin D3 and vitamin D4"

Leading them to conclude:
"The observation that some mushrooms when exposed to UVB radiation also produce vitamin D3 and vitamin D4 can also provide the consumer with at least two additional vitamin Ds"

Hack my shrooms

Some mushrooms like button, grow in the dark and so naturally have lower levels of vitamin D. However this study found a short short exposure to sunlight increased the vitamin D levels from 5µg to 374µg per 100 grams.

And the more exposure, the more vitamin D.  Putting Shiitake mushrooms with 40 IU of vitamin D into the sunlight for eight hours with the gills upward (ie sun-drying) resulted in 46,000 IU of vitamin D2. Another six hours (14 hours in total) of sunlight exposure boosted levels to an astonishing 267,000 IU of vitamin D per 100 grams."

In addition, researchers found that one year later, the sun-dried mushrooms retained a large amount of vitamin D; therefore sun-dried mushrooms could be stored and used in winter months.

Some feel more data is needed about mushrooms however because of one particular study in which researchers gave "sun-treated" or untreated mushrooms to a group of adults.  They found vitamin D2 supplementation via mushrooms didn't help overall, as the participant's vitamin D3 levels reduced to compensate - thus giving no-overall effect.  The massive flaw in this study as I see it is that these were healthy adults who started with totally normal serum levels, and maintained totally normal levels.  Yet it appears well accepted when giving a D supplement that the blood level does not keep increasing even with ongoing supplementation. It rises into the ideal range and then it stabilises. Vitamin D is consumed by the body, it is utilised and then inactivated (Dr David Grimes, Consultant physician and gastroenterologist)

You can see a table here of the different values recorded in meats in different studies.  As you can see beef offal packs a huge punch.

Our shift in what meats we choose to eat has also likely reduced our vitamin D intake:

This review finds numerous studies linking fat and vitamin D and says it was:
"significantly associated with the fat content of whole cuts, and in the cuts 8 to 10 times more vitamin D-3 and 2 to 3 times more 25(OH)-D-3 was found in lard and intramuscular fat than in the lean parts."
Fatty whole joints slow cooked used to be pretty standard as they were cheap (now often called "traditional cuts").  Many locally recall their parents home rendering lard and "dripping" which was even eaten on bread for lunch.

Then came the fat phobic/convenience era and lean steaks with the fat removed that could be cooked in minutes increased in popularity.  Use a Griddle so you make sure you strain as much of the evil arterty clogger away.   Liver was left behind, the overcooked dried offerings presented as school dinners etched on our brains, mingled with a fear of overdosing on vitamin A.  Lard and tallow were replaced with vegetable and sunflower oils and without realising we also waved goodbye to fat soluble vitamin D.

The problem with the convenience era, is that animals don't grow 33 leg chops and chickens don't have 20 breasts.  We therefore need many more animals to meet demand than when "nose to tail eating", that is consuming as much of the animal as possible rather than selecting choice cuts.

The trouble is if nobody wants a huge chunk of the animal, the parts we do want become more in demand - this drives down price and producers need to find cheaper and more economical ways of raising animals. 

Hello factory farming; feeding animals low grade foods, keeping them in low grade conditions provides cheap meat and fish. But at what cost?

Turns out raising animals in substandard conditions leads to substandard meat.  What the animal is fed impacts on what nutrients it provides, to quite a large degree.  It also turns out that animals, like humans need sunlight themselves to produce adequate quantities of vitamin D, or they need their feed supplementing too.

PART 2: Shame on the British Media! What Really Happened?

After posting this blog, I was made aware that the devastating story of Landon's life, portrayed by the media - may not be entirely accurate.

These posts sent to me, were from a PUBLIC forum:

Some points that may be relevant:

1)  Baby had experienced a difficult delivery,  with concerns for oxygen levels and heart rate following compression of the umbilical cord - resulting in 14 medical staff and an emergency section.

2) Being " a bit dehydrated" after birth, typically occurs when there has been excessive blood loss such as placental abruption, which isn't noted above.  I suspect what actually happened is they tested baby's blood sugars, which due to the difficult delivery were low enough to warrant immediate IV intervention whilst still in recovery.  
"Treatment depends on how severe the low blood sugar is in your baby and on your baby’s feeding skills. In some cases, frequent feeding is enough to correct the problem. In other cases, the doctor or advanced practitioner caring for your baby may provide extra sugar in a mixture that is given through a tube placed in the baby’s nose or mouth. In severe cases, sugar (called glucose) is fed right into the baby’s bloodstream through a needle placed in the infant’s vein. This is called an intravenous line or IV. The baby may need an IV for several days, but he or she can usually still feed from the mother’s breast or bottle during this time."
3.  The next few days in hospital don't give detail as to what happened with regard to doctors monitoring baby following this.  Normal protocols following this type of delivery and early IV required, would be that blood sugars and hydration levels would be checked constantly during this period; ensuring baby had stabilised.   This means either baby was hydrated with good blood sugar levels during his stay (and he was feeding well and crying for another reason, perhaps linked to delivery), or that inadequate checks were made during this period.

4.  There is no mention of distress when they returned home - in fact far from the media reports of constant crying, or sleeping as one would expect in a dehydrated infant, parents report they enjoyed "playing" with their baby.

5.  Only a few hours later at 2.15am did mum discover the tragedy - there isn't enough time here for a baby to have become severely dehydrated since their discharge at tea-time.

6.  Doctors immediately discussed seizures and SIDS.  And with good reason.  If we look at
"What causes neonatal seizures", we can see the most common causes listed here, the first being:
  • lack of oxygen before or during birth because of problems such as placental abruption (premature detachment of the placenta from the uterus), a difficult or prolonged labour, or compression of the umbilical cord.
In fact as this paper from the Department of Clinical Neurophysiology, Great Ormond Street Hospital, London outlines, 30-53% of seizures are as a result of such labour complications - compared to 0.1-5% as a result of low blood sugars.  As low sugars are also linked to complicated deliveries like the above, this makes things more complex.

"Seizures in the neonatal period are also the most common neurological emergency and are associated with high mortality and morbidity 1,2."
6.  Baby Landon survived several weeks in hospital, following his re-admittance - where he received expressed breastmilk.

6.  There is no mention of any link associated with feeding and the initial episode until 2015, when Christie del Castillo-Hegyi, founder of the "fed is best" movement, and recipient of questionable healthcare pertaining to her own infant, contacted this family.

It appears a not entirely unbiased mother (an A&E doctor, not a pathologist), went through the autopsy results of another, and concluded it was lack of breastmilk that caused the seizure that resulted in Landon's death.


Do you think the media representation accurately depicted the mother's words?

    Shame on the British Media! The Starving Breastfed Baby - Fact V Fiction

    1. I've watched in horror as the British media including the Sun, Mirror and Metro have covered the tragic story of a newborn who died from dehydration, in the inaccurate, irresponsible, scare-mongering style only they can.

    Headlines have included:
    "If I Had Given Him Just 1 Bottle, He'd Still Be Alive"
    Which the cynic in me struggles to believe isn't a play on one of breastfeeding's most hard hitting papers "Just One Bottle Won’t Hurt” -- or Will It?".
    "Cluster Feeding Led to Newborn's Death"
    This one irks me as "cluster feeding" is a totally normal, typical part of feeding - yet parents everywhere will now be terrified, but perhaps that was the plan?  This baby wasn't "cluster feeding" - when a term, healthy baby feeding well and typically several weeks old, takes a number of feeds back to back over two or three hours, in order to fill up their tummy and support a longer sleep stretch of 5 or 6 hours.  

    This baby wasn't "clustering", he was starving.  He was trying constantly to get food - he didn't die from cluster feeding, no "feeding" was taking place, he died from insufficient milk intake.

    The level of ignorance from doctors who have been quoted on the subject goes beyond cringe-worthy, to downright shocking - although it's no surprise the press have jumped to support the "fed is best" campaign, when it's all about readership not facts.

    Until I started reading studies and facts from other sources, I don't think I would have believed how much manipulation goes on to sell the desired angle to the audience - click bait headlines and half the facts, deliver a very different picture to the truth.

    So let's talk about the story this week.

    Indeed tragically a breastfed baby died due to insufficient milk intake.  This much is true.

    However a number of key details that parents should be aware of:

    1) This was the USA FIVE years ago!

    Practices and protocols surrounding infant feeding and hydration in the UK are completely different. The risk of hypertraenemic dehydration in some US hospitals is recorded as relatively high, particularly in comparison to the UK.

    A 2013 study analysing almost 1,000,000 births in the UK and Ireland found just 62 cases of severe neonatal hypernatraemia, equivalent to just seven in every 100,000 births and an individual risk of 0.007%. No baby died, had seizures or coma or was treated with dialysis or a central line. At discharge, babies had regained 11% of initial birth weight after a median admission of 5 (range 2-14) days and none had long-term damage. (3)

    2) This was medical ignorance; numerous warning signs were ignored by healthcare providers:

    In startling parallels with the story of  Dr Christie del Castillo, founder of the "Fed is Best movement", whose son also developed hypertranemic dehydration (and was inappropriately re-hydrated leading to life-long consequences) - numerous flags were raised here too.

    According to newspaper reports, the baby cried for abnormally long spells:
    "Mother whose baby cried all day didn’t realise he was starving to death"  (Mirror)
    And had lost a concerning amount of weight even prior to discharge:
    "Landon was discharged from hospital on the third day of his life, having lost 9.7 per cent of his body weight - considered 'routine' and 'unremarkable'."
    Considered "routine" and "unremarkable" by whom?

    The American Academy of Pediatrics states:
    “Weight loss in the infant of greater than 7% from birth weight indicates possible breastfeeding problems and requires more intensive evaluation of breastfeeding and possible intervention to correct problems and improve milk production and transfer.” 
    The International Lactation Consultant Association and the Registered Nurses' Association of Ontario specify that:
    A loss of more than 7% of birth weight, continued loss after day 3, or failure to regain birth weight within a minimum number of days (i.e., 10 days or 2–3 weeks, respectively) are signs of ineffective breastfeeding.
     The Academy of Breastfeeding Medicine advises:
    "Possible indications for supplementation in term, healthy infants [include] weight loss of 8% to 10% accompanied by delayed lactogenesis (day 5 or later).” (1)
    So we have a concerning situation - a baby with a bigger than typical weight loss, who is crying excessively, being discharged without any feeding plan to ensure adequate intake.  This was a huge gamble.

    If my child was in hospital showing every sign of kidney failure and a team of kidney specialists all failed to recognise this -you can bet I'd be looking for answers as to how on earth they were so incompetent they missed the blooming obvious.  I'd be campaigning not that we should all be given artificial kidneys, but that those paid and employed to care for those with kidney conditions, could a) identify when they were failing, b) know the safest course of action to take should this arise.

    The debate surrounding the number of women with "failed lactation" is thrown about - but in terms of saving lives, knowing a figure isn't key to outcome; even one baby suffering a preventable condition as a result of poor practice is too many.  As long as we have trained healthcare professionals who can then educate caregivers, we can save lives - it's not an invisible situation where baby goes from fine to desperately ill without warning.

    3) Neither the British media, nor fed is best have made parents aware that far more babies die as a direct result of infant formula e.g bacterial contamination and as a result of not being breastfed.

    Bacterial Contamination

    In April 2016, the CDC released a new report, warning of a bacteria called Cronobacter Sakazakii, one of the most lethal contaminants found in paediatric food and/or milk formula, with an estimated mortality rate as high as 80%.  This bacteria has been isolated from items in the home such as vacuum cleaner bags - and thus often contamination of the powder can also occur once the tin has been opened.  Using recommended protocols to reconstitute the powder significantly reduces risks - trace levels of bacteria are unlikely to cause harm, but multiplying in warm milk can significantly increase the load.

    This information isn't new. 

    In 2008 the CDC Morbidity and Mortality Weekly Report covers two cases and states:
    "Previous investigations have found Cronobacter spp. cultured from prepared formula, unopened Powdered infant formula (PIF) containers, and the environment where PIF was reconstituted, clearly implicating PIF as the source of outbreaks. "
    Infants throughout the world consume PIF, some exclusively. PIF preparers should be aware that PIF is not sterile and can contain pathogenic organisms (e.g., Cronobacter spp.). Preparers also should be aware that PIF can be contaminated extrinsically (although mechanisms for such contamination are not well defined) and that bacteria can multiply rapidly in reconstituted PIF. Consequently, WHO has developed guidelines for preparation of PIF, including reconstitution with water hot enough to inactivate Cronobacter organisms (3). Universal adoption of these guidelines can aid in implementation of safer PIF preparation, storage, and handling.
    Yet we don't know is what prompted the 2016 safety update...

    In June 2016, just two months later, 27 day old Axel Burnett tragically succumbed to the meningitis & sepsis caused by Cronobacter bacteria.

    On her Facebook page his mum Jamie says:
    "We are so mad and so upset that Enfamil Gentlease would not put a warning label on the label knowing this could happen! Our baby boy got tooken from contaminated formula, did we know this would happen? No, why? Because NO ONE WARNED US!"
    His mum tried to raise awareness of the issue online, founding a "Justice for Baby Axel" page, which has received over 11,000 likes.  Despite this still no major news station or parenting site has covered the story.
    "This bacterium is an emerging opportunistic pathogen that is associated with rare but life-threatening cases of meningitis, necrotizing enterocolitis, and sepsis in premature and full-term infants. Infants aged <28 days are considered to be most at risk. Feeding with powdered infant formula (PIF) has been epidemiologically implicated in several clinical cases."
    One study found:
    "The presence of Enterobacter sakazakii and other Enterobacteriaceae was surveyed in 82 powdered infant formula milk (IFM)

    Although Enterobacteriaceae were enumerated from one powdered IFM sample (Klebsiella ozaenae, 200 cfu/g), 7/82 had detectable Enterobacteriaceae after enrichment in EE broth."

    Do you know how many babies die per year of Cronobacter from infant formula?  No?  Neither does anyone else.  As the CDC explained in 2008in the United States; formal surveillance and reporting systems exist only in Minnesota. 

    Yet parents are still not aware how important safe formula preparation is, we only have to look at how popular products like the "Perfect Prep" machine are.  Despite concerns the small amount of water released in the "hot shot",  may rapidly fall below 70 when it hits the powder, not sustaining the temp for 2 minutes to effectively eradicate all bacteria present - nobody appears to have examined this further.

    Lack of breastmilk & formula use

    A review published in the journal Archives of Disease In Childhood titled, “Marketing breast milk substitutes: problems and perils throughout the world,” suggests:
    "Currently, suboptimal breastfeeding is associated with over a million deaths each year and 10% of the global disease burden in children"
    In her article with over 100 references - Dr Folden Palmer estimates over 9000 US infant lives are lost each year due to lack of breastfeeding.  She says:
    "The final relative risk for formula feeding comes out to 2—that’s double the risk of death for American infants who are fed with formula, compared with babies who are fed naturally.
    A multitude of studies demonstrate that when breastfeeding is accompanied by formula supplementation, illness and death rates are much closer to those of babies who are fully formula-fed. Studies also reveal conclusively that the longer breastfeeding lasts, the greater the measurable difference in illness and death rates."
    A 2010 a study published in Pediatrics quoted 1000 lives:
    "The United States incurs $13 billion in excess costs annually and suffers 911 preventable deaths per year because our breastfeeding rates fall far below medical recommendations," the report said.
     There's also a whole heap of interesting studies and reading on risks of not breastfeeding here.

    We need to realise this one sided approach from our media, is purely to appease their readership. The "Fed is Best" campaign is anti-feminist, paternalistic propaganda, to try and convince parents how they feed their baby doesn't really matter.  It does.

  • Enterobacter sakazakii: An Emerging Pathogen in Powdered Infant Formula 2006
  • Marketing breast milk substitutes: problems and perils throughout the world 2011


    This blog: 

    Upper Lip Tie Treatment in Infants - Informed Choice, Risks & Efficacy

    In all the noise about lip ties, is there risk of misdiagnosis?  And are parents really making an informed decision?

    We acknowledge there are risks to most things - from getting out of bed, to taking a paracetamol or treating a tongue tie. We typically weigh up what the benefits may be, what risks are involved and we (hopefully) get the chance to make an informed choice. 

    When it comes to treating tongue ties, we have (thanks to diligent practitioners and researchers) over 20 years of studies under our belts.  NICE have explored the research, discussed this with experts in the field and drafted guidelines.  These tell us (among other things) that frenulotomy (treatment for tongue tie), is a procedure of minimal risk for most healthy neonates.  

    Risks & Benefits need examining both short and long-term.

    Short-term risks of tongue tie treatment would include for example infection in the wound site, baby bleeding more heavily then expected following the procedure or perhaps later in the day after the event.  Long-term risk may include say keloid scarring at the wound site, if you're genetically predisposed.

    In short - aside from discussing the potential benefits and effectiveness of tongue tie treatment, we've also established what the potential knock on associated effects may be, and we can examine rates to discuss risks.

    Recently some seem to have made the leap of logic to assume it's also therefore safe and beneficial to release other oral frena babies have too - if it is considered "tied".  Tied means that the frenulum is shorter, thicker or placed abnormally compared to a typical frenulum.

    So here are the things I think we need to know:

    1)  What is a normal infant upper lip frenulum & what is its function?
    2)  How do we diagnose an abnormal infant upper lip frenulum?
    3)  What problems can an abnormal upper lip frenulum cause?
    4)  When & how should we treat it?
    5)  What are the benefits, risks and outcomes of treatment?

    Language that features below:

    Frenulum/Frenum/Frena/Frenula:  The "string" that attaches to the top lip or tongue (or bottom lip/ cheeks)

    Maxillary/ labial fraenumUpper lip frenulum
    Diastema:  Gap in the front teeth

    Babies should have an upper lip frenum that attaches to the gum or palate.  Seriously I want to drive round with a loudspeaker on the top of my car simply repeating this phrase.

    These pictures below show you normal infant placement.  Infant upper lip frena are supposed to be "low sitting".

    These babies had no feeding problems, reflux, wind or any other issues.

    The confusion as to why everyone at the moment thinks these are ties, is I believe is explained well here.  It's because they can see the low sitting frenum.  As I discuss in this piece 93.4% of babies do, as the frenum attaches to the gum or palate.


    The frenulum acts as a spacer for teeth.  People are concerned their child has a gap in their teeth, and yet this is exactly as it should be.  

    Here we can see a normal ADULT MOUTH:
    In contrast let's look at the ideal INFANT MOUTH:
    Image Glenn Carty Orthodontics 

    See how different it looks?  And note the low sitting frenulum. Glenn Carty Orthodontist tells us:
    "Did you know that Adult front teeth are 2-3 mm wider than baby front teeth? Adult front teeth therefore occupy more space than baby front teeth. A young child's smile should appear very different to that of an adult's. The smile should resemble a picket fence. The baby front teeth should be spaced. While this might not look pretty, the extra space is needed for proper alignment of the adult front teeth"
    The frenulum moves up the gum-line in the first 10 years of life, until it sits in the adult position. The gap closes as second teeth align - as per the photo below.

    Same child: shows normal frenulum regression and appropriate dental development during childhood
    This spacing also makes teeth easier to keep clean.

    A 2011 paper states:
    The superior labial frenum is triangular in shape and attaches the lip to the alveolar mucosa and/or gingiva. It extends over the alveolar process in infants and forms a raphe that reaches the palatal papilla. Through the growth of alveolar process as the teeth erupt, this attachment generally changes to assume the adult configuration. [1] Taylor has observed that a midline diastema is normal in about 98% children between six and seven years of age, but the incidence decreases to only 7% in persons 12-18 yrs old. [2] But in some instances, the infantile arrangement is retained.
    So normally they regress but sometimes this doesn't happen and the frenulum remains lower on the gum. Sometimes a gap (or a diastema) can be seen.  A very famous example of this being of course, Madonna:

    Diastema is heavily prevalent in some cultures - for example Nigeria has incredibly high rates.  In turn it's considered extremely attractive and surgery exists to create the gap.  In contrast it's very uncommon in other areas such as china.  

    What criteria are we using to diagnose tied versus normal?  How was this established and is it reliable?

    When it comes to tongues we look at what normal presentation and function is, and we establish (or we should) how far away from that each baby is.

    When it comes to lips, there seems to be a lot of confusion and inaccurate information shared.

    The advice many are given is to push the lip back and see if there is blanching, that if it pulls tight and there is a "notch" this will create a gap - and as such removing the frenulum prevents the risk of a diastema.  

    But is this true?

    It's not just as simple as the skin you can see...

    Initially it was assumed the frenulum caused the gap, it seems obvious - we can see a thick meaty piece of skin between the teeth, which we know acts as a "gap holder" for infant teeth.  Thus it was assumed that the frenulum not regressing at the expected age, was the root cause of a persistent gap into adulthood.   Interestingly as researchers began exploring further, they discovered it wasn't quite so clear cut.

    Some concluded that when the normal regression of the frenulum didn't happen, it wasn't the frenulum causing the gap, but the gap that resulted in the frenulum remaining low.   Another study found a cleft in the bone was associated with some gaps, and others found removing the frenulum did not alone, appear to make a difference to the gap compared to those that remained untreated;10 years later there was no identifiable differences between he two groups.   Some theorised certain types of frenulum could cause a gap, but researchers decided ultimately this wasn't so.  They noted gaps with frenula and frenula without gaps.  They also noted wide variance in the normal frenulum in terms of visual presentation - thickness and so on.

    A 2012 review outlines the evidence concerning the cause of a persistent gap, and the possibility of closing it by removing the frenulum:
    "At the beginning it was thought that the labial fraenum interfered with the closure of the midline diastema. This belief resulted in misdiagnosis and unnecessary surgical intervention of the fraenum 13,14.
    They then outline all the papers and their findings - I've linked below if you want to look in more detail.

    They continue:
    "Since there is no evidence concerning the fact that the maxillary labial fraenum is the main causative factor for a midline diastema, some orthodontists propose the following therapeutic methodology 37,45: Initially, it is necessary for the dentist to make a diagnostic trial, in order to find out whether the fraenum is implicated in the pathogenecity of the diastema. 
    1. Positive “blanch test” of the incisal papilla, when pulling the lips forward. By pulling the upper lip and exerting pressure on the fraenum, if there is a blanching, it is safe to predict that the fraenum will unfavourably influence the development of the anterior occlusion; 
     It is important to emphasize the fact that frenectomy has clinical validity only after the eruption of all 6 permanent teeth if it failed to close the diastema, and then only in conjunction with orthodontic treatment. So after the eruption of all 6 permanent teeth, 9,14,16,20,34,36,37 orthodontic appliances are used to close the diastema. A frenectomy is carried out, so as the scar tissue will hold the teeth together 16,20,27,33,37,39,48. During the primary dentition phase, surgical intervention of the labial fraenum is not recommended7."
    This clarifies blanch tests etc are a tool that may be useful as a diagnostic tool once 6 permanent teeth are in.  They weren't designed for, nor tested in terms of accuracy or reliability, in babies and young infants who are expected to have a low sitting frenulum.

    The above paper continues to explain the different opinions held by dentists and oral surgeons.

    Surgeons tend to prefer removing the frenum and following immediately with orthodontics (so they have good, clear access to the tissue), some dentists agree; other dentists feel a better result is obtained by pushing the teeth together first with orthodontics, and then removing the frenulum, or only removing it if the teeth "drift" back apart again - so any resulting scar tissue holds the teeth together. The last group don't feel there are any benefits to frenectomy.

    What all seem to agree on, is the risk of removing tissue from the gum when there are no teeth to push together, suggesting that this may at times result in scar tissue on the gum that makes it impossible to completely close the gap. They continue:
    "In the orthodontic community there is unanimity on this issue 37. Orthodontists support that the fraenum should be maintained until the age of the eruption of all 6 permanent anterior teeth. After that, and only if the diastema remains the same, a frenectomy is indicated, with subsequent orthodontic closure of the diastema 9,16"
    "Oral surgeons suggest that in case of a maxillary midline diastema, a small intervention of the fraenum is useful. In this way, the closure of the diastema is facilitated and the orthodontic treatment is not affected 9,2 "
    So the "unanimous" view is that 6 permanent teeth should be in before the frenulum is removed - ie this is the optimal time for removal along with orthodontics.

    What are the risks and benefits therefore to removing it earlier than this, or before the top teeth have even appeared?

    I couldn't turn up any studies exploring this.

    Here we can see the progression of teeth following lip tie removal in a child who should still have a low sitting frenum, as they do in the first picture:

    We can see the child has typical spacing in the first picture, similar to that we saw above.  These pictures have been shared as evidence removing a tie removes a gap - and in this instance it seems clear that removing the "spacer" indeed rapidly resulted in adult dentition and lack of spacing between the teeth.

    However we know already this is what happens in the majority of people with time, so what benefits and risks of hastening this process?  How will this impact on adult teeth spacing long-term?  

    Interestingly we can note the top lip still looks thin and pinched.  There also appears to be slight yellowing between the teeth on the last photo, although I'm not sure whether that is just this particular photo and the light.

    One mum has expressed concern her child's top teeth have come in crossed following his upper tie removal (he had no teeth at the time of the procedure):

    Will this self correct as other teeth align and a correctly functioning tongue exerts appropriate pressure? Is this linked with premature removal of the frenulum and something parents need to factor their decision making process?

    Without studies we're working from anecdote, which is non-transparent and unreliable.

    Mr Sheehan (ENT) Manchester, proposes that as part of the role of the upper lip frenum is to stabilise the top lip, removal of the upper lip tie may also allow over extension when smiling in some people, perhaps those with naturally longer gums.

    Helen Marshall (IBCLC) shares similar concerns:
    "I had my upper tie removed at around 10 or 11 years old because of a gap in my teeth.  My lip pulls higher up and exposes more of the gum when smiling, and which started post-revision. You can see where it attached to my lip and gum, and my smile would not be the same if it hadn't been cut - --my lips wouldn't be able to ride up and uncover my gums"

    Assessing an infant for lip tie.

    Even if we were to establish the blanch test above may accurately determine the lip is tight, does that mean we can assume the cause is the length of the frenulum?  We talk about assessing function not appearance, but even this isn't straightforward.

    Tongue ties can cause tension through the lips that makes them tight:

    The above baby had incredible tension pulled through his mouth by his tongue tie. When we "flipped his lip", it didn't flip at all - instead it blanched and felt incredibly tight.   His parents commented they didn't know where he got his mouth shape as they both had full, plump lips. After the tongue was released and baby turned to his parents, the first thing they both noted was the phenomenal difference in his lips and mouth shape.

    The little girl below didn't just have her lips bound down by her tongue tie, her whole chin and jaw was pulled back too.  We saw her chin move forward when feeding immediately post revision, and function was completely changed.

    Something as simple as being hungry can cause a baby to tighten their lips. When we assess hungry infants post feed and note tightness, this often presents different when baby is full and relaxed.

    Therefore in order to accurately hope to assess function, don't we need to release the tongue first?

    What people also often don't understand is that if baby is in a shallow latch on the breast or bottle, the top lip can sometimes curl under when feeding, appearing as though it can't do anything but - to try and compensate.  

    Image Milk Matters - tongue tied baby compensation
    This is extremely common in tongue tied babies as this post demonstrates. However as anyone who fully understands the mechanics of milk transfer and has observed thousands of dyads will know - it is not desirable for the top lip to flange outwards when feeding either -  it should be neutral as the post above highlights (and the image below shows), flange suggests anything from slightly shallower to very shallow latch.

    Below is the same breastfed baby as above with the curled under top lip, immediately after tongue tie release:

    Image Milk Matters 

    If we just treat the lip, do we sometimes just allow for more or better compensation?

    "The added ability to fully flange the top lip will allow a baby to compensate for continued poor positioning or tongue function issues. But of course this is treating a symptom and not the underlying cause. Improving positioning, tongue –tie division, tongue exercises and suck training to promote effective tongue mobility would be more appropriate. "(Oakley 2016)"
    And of course, again without studies - what about possible negative consequences? 

    One mum on Facebook explained how her journey developed.

    Her son had a tongue tie, he had learnt to feed gripping extra hard with his top lip - just like the babies above.  However they were unable to find anyone who would release the tongue and so only the lip was treated.

    Following this, he was no longer able to adequately grip with the excess force he had been doing to compensate, and was no longer able to breastfeed.

    This proved an extremely traumatic time for all involved and mum feels more studies are needed.

    Lack of Guidance

    We have no NICE guidance pertaining to lip tie, nor recommendations from any other recognised authority.

    Nobody has (in any official capacity), questioned whether the procedure is beneficial to infant feeding, or for the prevention of diastema; whether it has the desired outcome or when the best time for treatment is. Whether the area needs numbing and if pain relief afterwards is required.  Whether both tongue and lip should be released together, given not only the change in presentation post tongue tie release, but because of the difficult or discomfort baby may have feeding with two sore areas in the mouth.

    At the moment different practitioners use different lasers (some use heat to cauterise the area, others use intense water jets to vapourise tissue).  This paper discusses that scarring can occur, and describes a surgical technique combining the frenectomy with a "laterally positioned pedicle graft", to give the best aesthetically pleasing response- are infant frenectomies different?  Which method is safest, most effective?

    Best practice should surely be based on best for baby, not "we've travelled a long way so may as well just do both..."

    Perhaps most importantly,  nobody seems to have explored whether there could be any unintended risks associated with the procedure.  Some argue those who treat would have observed problems should that be the case - however long-term risks can be very difficult to identify in practice rather than research, especially if we're approaching with a bias, and we're not clarifying what "normal" is.

    Abnormal lip frena of course exist, and whilst those promoting removal of the ULT claim we in the UK are "behind" and "ignorant" when it comes to diagnosis and treatment, I'm not entirely convinced.

    I've found when there is truly abnormal presentation (such as a excessively wide, tight frena that have bound down the lip) the NHS have treated.

    Interestingly they tend to release the tissue up where it is attached to the lip, not touching tissue on the gum margin.  In the private sector I have seen both methods used, suggesting we also need assessment and standardisation of this area too. 

    However, when presented with normal low sitting frena being called a tie, the NHS (as evidence supports), recommend reassessing again age 8-10 and treating if appropriate.

    This is why controlled studies are key.

    We need to start asking questions, so that we continue to push for studies and evidence to support guidance for practice.  Simply accepting the word of those performing the procedure is not enough.

    Some charge as much as £500 for a consult and release lasting around 15 minutes, enabling them to see 4 per hour.  A 7 hour day that's potentially £14,000, or £70k per week, 280k per month, and so on. Further charges may be applied for feeding support, which many parents report is often needed. 

    That's of course not to say there aren't situations where removal may be beneficial - lack of evidence isn't lack of efficacy, but we need to know more!

    Parents need facts on which to base a decision, as do those supporting infant feeding.