Thursday, 27 September 2018

Barkers Hypothesis

Critical review of the foetal origin of disease hypothesis

Louise Usher

David Barker CBE, born 1938, was a physician and epidemiologist. 
Prior to his death in August 2013 saw him argue the next generation do not have to suffer from diseases such as heart disease and diabetes. Rather that the diseases are not mandated by the human genome.  As such diseases were not in existence 100 years ago to the levels of the turn of the millennium, Barker hypothesised we could prevent them should we have the will to do so. 

During Barkers position in 1984 was director of Medical Research Council Environmental Epidemiology Unit (now renamed MRC Lifecourse epidemiology unit), he began to observe maps of the UK. Each county in 1910 and 1920 showed mortality rates of neonatal and post-natal correlated to 60 and 70 years later a higher death rate from coronary heart disease. 
Barker began at this stage to suggest an adverse environment within the uterus may mean chronic disease later in life. (Hanson., 2015)

2006 saw him awarded a CBE for his work. (Pincock., 2013)

Barkers hypothesis proposed in 1990 that low birth weight, premature birth and intra uterine growth retardation have a causal relationship to the origins of non-insulin dependent diabetes, hypertension and coronary heart disease in middle age.  A historical cohort study saw the hypothesis as it was derived. Significantly, an association of hypertension and coronary heart disease in middle age and low birth weight, along with premature birth was ascertained as an association. (Hanson., 2015)

Socio-economic status has a bearing on the support of the hypothesis.  Evidence from low income counties sees low birth weight and intrauterine growth retardation highly prevalent and therefore could not support this study for fear of skewed results.  In conjunction, hypertension and coronary heart disease are less prevalent by a significant number than in higher income countries. (Barker., 1986)

Barker presents the evidence within his book Fetal and infant Origins of Adult Disease (1992)  

* * * * * * * 

Universally it is known and accepted a malnourished mother will give birth to low birthweight babies (Hales et al., 2001).  As the babies mature into children often they are further undernourished (Rayhan and Khan., 2006).
The cycle of poor nutrition leads to cognitive and health issues. Hence maternal malnutrition needs to be prevented (Paneth and Susser., 1995).
The prevalence of adult onset hypertension and type 2 diabetes mellitus have been linked to a slow rate of growth in years 2-3 of childhood (Rosenbloom et al., 1999).

Seemingly there is much evidence to support Barker in his hypothesis.  However, he does not explore further into the possible other causes, for example, should a mother carry a bigger baby due to gestational diabetes, could this be a preventative for the future of the child? Possibilities are endless yet not explored currently under the hypothesis. What might make the fetus a larger born child that might have a preventative effect on the later life of the adult?  Of course, the reverse may be true. Would something to cause a lower birth weight baby cause them to be more prone to chronic disease later in life?

The Thrifty phenotype hypothesis

Hales and Barker studied the associations of increased risk of impaired glucose tolerance and the metabolic syndrome in 2001 in the Thrifty phenotype hypothesis.

Epidemiological findings are concurrent across ethnic group and populations (Hales and Barker., 2001).  Validity of these findings is therefore widely accepted as a general rule.  Debating the extent of the underlying causes posed the question of the mechanisms of causal agents.  Was this genetic or environmental? 

Rarely, genetic causes of insulin secretion are found in association with poor fetal growth yet as insulin is a major fetal growth hormone this is a difficult position to prove.  While changes in glucose metabolism may be linked to genetic polymorphisms yet this will be less conclusive than the association with lower birth weights.  Every human characteristic may possibly be suggesting within Hales and Barkers paper that type 2 diabetes mellitus resides within a mix of both genetic and environmental.  Leaving the question if a genetically disposed fetus might overcome the risk factors slightly should the environmental situation be more favorable.
This hypothesis proposes that indeed environmental factors are a dominant cause of type 2 diabetes mellitus.  Other influences have a part to play of course.  Maternal and placental factors may lead to poor fetal nutrition
(Muthayya, S., 2009) which gives rise to the under development of pancreatic beta cell mass (Garofano et al., 1998).  The islets of Langerhans vasculature may be compromised in these fetus’ according to Nielsen et al (1999), which will contribute as a key element to later life type 2 diabetes mellitus.

Should an individual continue to be poorly nourished as they grow, therefore remaining thin, the insulin secretion functional capability and capacity would not be a detrimental factor.  
Typically, within these findings, Barker and Hales concluded that fetal malnutrition led to insulin resistance.
Glucose intolerance would be triggered by obesity.  Calories imbalanced as the individual had a lower calorie expenditure, higher calorie intake and therefore gained weight.  Genes were accepted within this paper to play a part in type 2 diabetes mellitus development yet was encouraged to consider fetal growth and development.

Below, figure 1 shows 64-year-old men given a ratio for risk of development of impaired glucose tolerance or type 2 diabetes.  Figure 2 shows metabolic syndrome. However, an age is not stated so the tables are difficult to compare with the differing types of diagnoses.

Figure 3 gives a clear indication of the pathway Hales and Barker were considering for the development of the metabolic syndrome within the Thrifty phenotype.

Conclusions stated within this paper ascertained the genetic versus environmental factors were conclusive towards determining growth and development of type 2 diabetes mellitus and metabolic syndrome.  Within the conclusion Hales and Barker mention the use of identical twins with the respect to conclusively showing the importance of fetal environment.  However, this does not state in what way. Could future work lead a study considering twins of equal nutritional status in utero and yet contrasting environment to discover the development of type 2 diabetes or metabolic syndrome in later life? Hales and Barker finalized with a statement that this is a stage to consider their finding as a useful framework for further study.

Syndrome X

1993 saw Barker et al conducting studies to question the prevalence of syndrome x in lower birthweight babies, shown in table 2. Syndrome X being the development of Type 2 Diabetes mellitus, hypertension and hyperlipidaemia.  The 407 British men from Hertfordshire were born between 1920 and 1930. 

Later on, studies were performed to test the theory of correlation between lower birth weight and the incidence of Syndrome X. In the town of Preston, UK, health visitors recorded the weight of the males babies mentioned above. Between birth and one year old, details of weights were accurately kept. As 64-year-old men, revisited, these subjects who were of a birth weight of 6.5lbs or less showed a significant 22% had been diagnosed with syndrome X.  Subjects with birthweights of more than 9.5lbs showed a ten times lower risk factor.
The second study also carried out in Preston was both sexes. Between 1935 and 1943 (including the war years which may have a bearing on nutritional status of the mothers), (Winter, JM, 1983). 266 subjects were also measured and the results comparable of the original findings of Barker and Hales, (1993).
Confounding variables such as smoking, alcohol consumption and socio-economic status was an independent factor.
Those diagnosed later in life with syndrome x had small head circumferences noted and eruption of teeth was later as seen in table 1. Barker and Hales stated confidentially that syndrome x and type 2 diabetes have originated from the less favorable conditions in utero.
Interestingly, hypertension in adults rose by a mean of 15mmHg in systolic pressure as placental weight read less than 1lb as measured in table 3. Those with greater placental weight of 1.5lb saw a fall by 11mmHg of mean systolic pressure.
Highest blood pressures were recorded in small babies who were born alongside a larger placenta. The adaptation of circulation may contribute to this finding.  Barker and Hales (1993), state that hypertension may be dependent on improving health and nutrition of mothers.  However, with little evidence except the facts of measuring and assessing later in life this seems a broad statement of a fact.

Could those children catch up?

Pampanini et al, (2017) very recently carried a study on pregnant rats. Assessing of intrauterine growth restriction (day 19 of gestation) would affect the developments of the gonads in the fetal rats.  Uterine artery ligation was performed on the postnatal rat testis. Several offspring were killed at day 5, 20 and 40 after birth.  At this time, one gonad was preserved within liquid nitrogen, processed for RNA and steroid extraction. The other, formalin fixed for histology.
Hormones testosterone, serum gonadotrophins and estradiol were measured.  The control group had shown the growth restricted rats had 30 genes dysregulated.
By 40 days post partum, the weights of the testis were beginning to catch up in comparison to those at days 5 and 20.

Harper et al (2015), explored the effect of food restriction in mice during early pregnancy. The mice were subject to a 50% restriction of calorie intake from day 1.5 to 11.5 of pregnancy. While placental weights were reduced, little effect continued into adulthood.  Liver gene expression and reduction in adipose tissue (in males only) was demonstrated.  Irreversible effects on the placenta into adulthood was doubted. By day 18 global gene expression was non-remarkable compared to the control group. This study saw the conclusion that alterations in the placenta caused by restricting nutrients (it remains unclear which nutrients) early on within pregnancy may in fact be reversible.

Bonel et al (2010), blindly tested the apparent diffusion co-efficient (ADC) of the placenta in the paper Diffusion-weighted MR imaging of the placenta in fetuses with placental insufficiency. If the fetus birthweight was predicted to be in the 10th percentile or less, placental insufficiency was diagnosed.  Interestingly, when a Doppler of the umbilical artery was performed, abnormal findings were recorded.  Conclusion of the results showed an accuracy of 99% that placental dysfunction associated with growth restriction is associated with restricted diffusion and reduced ADC.  Early markers used ADC as an indication of pregnancy complications such as intra uterine growth retardation.  Yet still, no causal factor was examined as to the placental dysfunction.

Barker stated in his research Fetal Origins of coronary heart disease (CHD), (1995), active research needed to continue.  Blood pressure, insulin response to glucose, cholesterol metabolism, blood coagulation and hormonal setting are beginning to show something within the underlying causal factors relating back to fetal undernutrition.  What specific type of nutrition, we do not know.  Also is this purely due to calorific restrictions of more specific to nutrition intake and possibly bio availability from mother to fetus? During mid to late gestation, fetal growth seems to go some way to programming CHD later in life. Once again, placental size comes into discussion within this paper.  Relation of birth size to placenta affects the outcome of later diseases.  Yet within this paper, quality of placenta is not assessed

Toxic exposures?

Rogers, (2006) reviewed Barkers Hypothesis more recently in 2006. While this paper is now dated, at the time Rogers stated new discoveries were suggestive of the ability of toxic exposures to also impact fetal development. Post-natal and during the intrauterine period, metabolic programming may be affected due to sensitivity to endogenous and exogenous influences. Animal studies he looked at showed low protein and high fat and high carbohydrate diets linked to adverse metabolic profiles.

Later still, Thomas (2012), began to look deeper into Barkers hypothesis as he subjected individuals to an activity questionnaire.  Those with a greater activity level showed a lower propensity for type 2 diabetes. This gives questionability to wondering if there could be a reversal of type 2 diabetes and perhaps other chronic diseases which may have been prevalent in this cohort yet with prior knowledge and adjustment to lifestyle, could this effect be reversed and prevented from development. 

Dutch famine

During the Dutch famine (Roseboom,. 2006) in 1944-1945 some mothers were limited to a low calorific diet of 400-1000 kcal/day.  Within the mothers who were pregnant and their fetus’ endured famine early on in its development were born with an atherogenic lipid profile and higher body mass index. 
Those who were mid to late pregnancy while enduring the famine were more likely to be impaired with relation to reduced glucose tolerance.
What causes such differences? This is something we currently do not know.

However, it is proven (Ong and Loos, 2006.,) rapid weight gain should not be promoted in small birth weight babies as this can have a central obesity and insulin resistant effect on health over time (Ibanez et al, 2006). Ibanez et al state the importance of understanding the underlying predisposition of adversity could aid preventative interventions.

Is this evidence conclusive?

Many scientific papers have looked at many numbers of people and aiming to prove or disprove Barkers hypothesis.  Yet most seem to draw a similar conclusion.  Fetal development and low birth weights seems to link to a higher prevalence of cardiovascular disease, hypertension, diabetes type 2 (non-insulin dependent), hyperinsulinemia and hyperlipidemia.  With even stronger evidence showing large placenta linked to low birth weight may be more suggestive.

Body composition has not been broken down within the newborn babies to ascertain if there may be an influential factor within the make-up of the body at this early stage. Could adipose tissue perhaps be a higher percentage within malnourished fetal growth? If so, might this give a casual factor to type 2 diabetes mellitus, CHD and hypertension? Current studies show these chronic diseases contribute to atherosclerosis, (Luehmann et al., 2017) leading to a further prevalence of disease and fatality.  Could body composition be influenced by maternal diet in the fetus and early child?  Studies might be conducted with a simple test of when a child holds its head up, suggesting early development of muscular system, (Bri and Sabatier, 1986.)  Watching these children into later life may be another opportunity for further work.  Many studies leading this research forward is of the utmost importance as Barker began to scratch the surface of something revealing. Most studies in relation to this have agreed with the hypothesis of development of chronic disease linked to lower birth weight babies.  However passionate Barker appeared in relation to this research, was he perhaps also bias? Hoping to find something deeper than he already had discovered does give way to a bias although with many other respected scientists confirming Barkers hypothesis goes some way to realising his claims.

Most of Barkers early evidence was correlational.  Potential confounders were not addressed.  Smoking cessation, alcohol, mothers nutritional status all were not adjusted for.  How the baby was fed from birth was not considered as a factor while evidence shows (Bonel et al, 2010.) the benefits of breastfeeding over other means. During breastfeeding, should the mother be exposed to toxins, eat well, sleep well and keep stress low?  Any of these factors may contribute to the child and their body composition as well as nutritional status.

What are the latent effects of such a hypothesis? How would the mother benefit from being forced to eat a healthy diet while pregnant, would she comply, and would she suffer psychological stress which may be passed on to the baby? (Lsarais et al, 2006).

To conclude

Li et al, (2017) have begun to go further into Barkers Hypothesis recently. Questioning the chances of other factors becoming influential within this study.
We know that a developing female embryo will begin to lay down the foundations for her own daughter within the ovaries as she starts very early in the embryonic stages (Laraia et al, 2006.)  Therefore, it could be suggested that the maternal mother in pregnancy may not only affect her daughters health but that of a future grandchild.

Changes in current food culture needs inspiration for change. Health at a population level must become a priority as we head into the future as disease must turn into a lower incidence. 

As a species, the health of our nation is currently being compromised worldwide.   The effects of what todays expectant mother subjects her baby to during pregnancy can quite clearly be seen to have an impact on their long term health. Carrying a daughter will mean many years of damage will be done which seemingly is very hard to undo. Over such a long period of time, the nation will become sicker which puts a financial pressure on the economy as we aim to try and fix these diseases and keep the public healthful.

Barker clearly highlighted an amazing and conclusive subject. Yet without further work and of course education to the mothers for them to see the levels of which they are able to influence the future of the health of the nation, the chances of change are very limited.  While this sounds bleak, developed countries are becoming more aware of choices of lifestyle affecting them in their day to day lives.


Hanson, M., 2015. The birth and future health of DOHaD. Journal of developmental origins of health and disease6(5), pp.434-437.

Pincock, S., 2013. David Barker. The Lancet382(9899), p.1170.

Barker, D.J. and Osmond, C., 1986. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. The Lancet327(8489), pp.1077-1081.

Hales, C.N. and Barker, D.J., 2001. The thrifty phenotype hypothesis. British medical bulletin60(1).

Rayhan, M.I. and Khan, M.S.H., 2006. Factors causing malnutrition among under five children in Bangladesh. Pak J Nutr5(6), pp.558-562.

Paneth, N. and Susser, M., 1995. Early origin of coronary heart disease (the" Barker hypothesis"). BMJ: British Medical Journal310(6977), p.411.

Rosenbloom, A.L., Joe, J.R., Young, R.S. and Winter, W.E., 1999. Emerging epidemic of type 2 diabetes in youth. Diabetes care22(2), pp.345-354.

Poulter, N.R., 2001. Birthweights, maternal cardiovascular events, and Barker hypothesis. The Lancet357(9273), pp.1990-1991.

Barker, D.J., Hales, C.N., Fall, C.H.D., Osmond, C., Phipps, K. and Clark, P.M.S., 1993. Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia36(1), pp.62-67.

Chait, A. and Brunzell, J.D., 1990. Acquired hyperlipidemia (secondary dyslipoproteinemias). Endocrinology and metabolism clinics of North America19(2), pp.259-278.

Pampanini, V., Germani, D., Puglianiello, A., Stukenborg, J.B., Reda, A., Savchuk, I., Kjartansdóttir, K.R., Cianfarani, S. and Söder, O., 2017. Impact of uteroplacental insufficiency on postnatal rat male gonad. Journal of Endocrinology232(2), pp.247-257.

Harper, J.L., Caesar, G.A., Pennington, K.A., Davis, J.W. and Schulz, L.C., 2015. Placental changes caused by food restriction during early pregnancy in mice are reversible. Reproduction150(3), pp.165-172.

Roseboom, T., de Rooij, S. and Painter, R., 2006. The Dutch famine and its long-term consequences for adult health. Early human development, 82(8), pp.485-491.

Ferrannini, E., Haffner, S.M., Mitchell, B.D. and Stern, M.P., 1991. Hyperinsulinaemia: the key feature of a cardiovascular and metabolic syndrome. Diabetologia34(6), pp.416-422.

Barker, D.J., 1995. Fetal origins of coronary heart disease. BMJ: British Medical Journal311(6998), p.171.

Rogers, J.M., 2006. The Barker hypothesis: implications for future directions in toxicology research. Current Opinion in Endocrinology, Diabetes and Obesity13(6), pp.536-540.

Thomas, N., 2012. Beyond the Barker hypothesis and the thrifty genotype-The womb, ethnicity, genes and the environment-Recent perspectives on the evolution of diabetes and the metabolic syndrome in India. Indian journal of endocrinology and metabolism16(Suppl 2), p.S142.

Li, X., Zhang, M., Pan, X., Xu, Z. and Sun, M., 2017. “Three Hits” Hypothesis for Developmental Origins of Health and Diseases in View of Cardiovascular Abnormalities. Birth Defects Research.

Laraia, B.A., Siega-Riz, A.M., Gundersen, C. and Dole, N., 2006. Psychosocial factors and socioeconomic indicators are associated with household food insecurity among pregnant women. The Journal of nutrition136(1), pp.177-182.

Luehmann, H., Detering, L., Gropler, R.J. and Liu, Y., 2017. CC Chemokine Receptor Type 2 (CCR2) Targeted PET Imaging of Early Atherosclerosis.

Muthayya, S., 2009. Maternal nutrition & low birth weight-what is really important. Indian J Med Res130(5), pp.600-8.

Garofano, A., Czernichow, P. and Breant, B., 1998. Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat. Diabetologia41(9), pp.1114-1120.

Nielsen, J.H., Svensson, C., Galsgaard, E.D., Møldrup, A. and Billestrup, N., 1999. Beta cell proliferation and growth factors. Journal of molecular medicine77(1), pp.62-66.

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Bonel, H.M., Stolz, B., Diedrichsen, L., Frei, K., Saar, B., Tutschek, B., Raio, L., Surbek, D., Srivastav, S., Nelle, M. and Slotboom, J., 2010. Diffusion-weighted MR imaging of the placenta in fetuses with placental insufficiency. Radiology257(3), pp.810-819.

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Wednesday, 30 May 2018

Probiotics and microbiota

With yesterday as World digestive health day , this is a great time to talk about gut health and the impact it can have within many areas of our biology.

 My research has taught me more about the importance of probiotics than I already knew.

Microbiota is the name given to the microbe population living in our intestine. Making up 90% of our cells! Containing 100s of trillions of microorganisms including at least 5000 different species of bacteria. The microbiota are important in nutrition, immunity and the brain.
The Microbiome is the combined genetic microorganisms in a particular environment.
Millions of years of co-evolution have moulded this human microorganism interaction into a symbiotic relationship where the gut bacteria contribute essentially to human nutrient metabolism and in return occupy a nutrient rich environment.

Children born vaginally get much needed microbes as they pass through the vaginal canal from the mother.  Yet those who are born by cesarian section tend to suffer more with asthma, allergies and leukaemia, (Neu, 2011.) Breast fed children have an intake of  sugars containing sialic acid which promotes infant growth through healthy microbiome, (Nestle Nutrition Insitiute), due to feeding the microbes.

Seratoin production is thought to be produced to the massive quantities of 90% within the gut, (Yano et al., 2015) which gives evidence to show those with altered microbiome will suffer further with depression and mental health issues, (Evrensel and Ceylan, 2015). A major role is played by the gut microbiome in bidirectional communication between the gut and brain. The Brain - gut axis communicates its systems between the Central Nervous System and Gastero Intestinal Tract, (Burokas, 2015.) As Burokas published in Science Direct, the gut microbiota can be a key regulator of mood, cognition, pain and obesity.
The immune cells are stimulated by a population of microbiota.  Those with impaired microbiome shows dendritic cells are reduced in the ability to stimulate pro inflammatory T cell responses.

Short chain fatty acids (SCFA) are produced in the gut and this aids the body immune systems and metabolic functions. When dietary fibre is fermented in the colon, short chain fatty acids are produced. They have many physiological roles in body functions.  Butyrate is important for colon health and is a  SCFA which arises from the bacterial fermentation of dietary fibre.  Produced by the probiotics, Butyrate is an important food for the cells lining the colon (colonocytes). Increasing the energy production and cell proliferation, there may be a protective element against colon cancer. The colonic inflammatory response if mediated by the presence of Butyrate. 70% of the energy needed for colonocytes is provided by this SCFA.  It is beleived there is a preventative and therapeutic potential to counteract inflammation mediated ulcerative colitis and colorectal cancer by the increase of modulation of the immune response and inhibiting tumour genesis.

Non starch polysaccharides  feed the microbiome.  Contributing to the host digestion (us).
Polyphenols are phytochemical fund in vegetables, legumes, chocolate, cranberries and green tea.  The consumption of these carries a reduced risk of chronic disease.  The low absorption rate in the upper gasteroinstestinal tract will benefit the colon.  Once the microflora break them down, they may change into bacteria themselves and possibly play a prebiotic role to modify the microbiota favourably.

Wu et al, (2011) studied the long term diet and the association with the microbiome.  Gut health is important.  As 70% of the immune system is in the gut, we need to know the factors affecting the microbiome. 
The largest affect is the host species, body mass, age, lifestyle and smoking.
Medium affecters: Antibiotic use
Medium-small: Drugs, exercise, genetics, pet co-habitation.
Small affect: Short term dietary intervention.

Can a daily supplement help?  I would say the best bet is to take one, while the stomach acid is quiet (IE not before or after food but about 2 hours either side) and definitely without adding any hot drinks. Heat will kill the important bacteria within the supplement.  Try it, you might be surprised how amazing you feel. 


Sunday, 13 May 2018

Vitamin D and the fortification of milk

1941 saw the exposure of solar exposure and cancer risk.  Later studies found associations with low vitamin D levels associated with type 1 diabetes mellitus, autoimmune issues such as inflammatory bowel disease, MS and animal studies supported low vitamin D causing increased inflammation and cancer.

Adequate levels of 25 hydroxyvitamin d (OHD25) is considered a level of about 50nmol/L at the end of winter and 10-20nmol/L higher at the end of summer. The institute of medicine vs the endocrine society state the guidelines inappropriately conclude the benefits of vitamin d are at 75nmol/L 25OHD and above. Mistakenly concluding all persons with serum 25OHDlevels below 50nmol/L are deficient.

UK DoH recommends a plasma concentration of 25nmol/L

In 2016 public health england published a report advising that 10 micrograms are advised daily to support bones, teeth and muscle. This advice was published in line with recommendations from SACN to suggest this safe level for everyone over 4 years old. SACN did not take into account the vitamin D from sun exposure as the synthesis of the vitamin through the skin is complex. PHE advises that throughout the months from March until October the majority of the public gain enough vitamin D through sunlight and a balanced diet.  During the winter, dietary sources are relied on.  IT is difficult for people to meet the 10 microgram recommendation. Fortification of foods will assist with those who are less likely to get out in sunlight and those who do not consume enough naturally through diet.

Deficiency  - corresponds with blood levels with clinical evidence of bone disease such as rickets or osteomalacia. Once levels are below 20-25nmol/L a very high risk is present.
Insufficiency is a biochemical term. No clinical evidence of disease is present. PTH levels may be elevated in the blood.
Some studies do not differentiate yet the differentiation will really determine a change of numbers reported on the studies.

A large number of studies exist to show low 25OHD is associated with increased risk of cardiovascular disease, hypertension, type 2 diabetes mellitus, cancer, autoimmune disease and increased mortality.

Is vitamin D simply a good marker for health? Were the randomised control trials started early enough? Were these studies including looking at calcium?

Vitamin D toxicity is rare but potentially serious.
HypervitaminosisD is not caused by diet or sum exposure but rather intake of a supplement at levels of 60,000 IU a day for several months.  As the body regulates the vitamin D produced from sun absorption really very well, fortification may be an excellent answer to gain better status levels from the diet.  Fortified foods do not contain major amounts of vitamin D and are regulated closely.
Toxicity from vitamin D has a main consequence of hypercalcemia in the blood. Symptoms noted are nausea, increased urination and weakness.  Possible progression pathways are into bone pain, kidney problems and the formation of calcium stones. Treatment includes stopping vitamin D intake and restricting calcium in the diet.

Naturally occurring vitamin D can be found in fatty fish and fish liver oils.  A plant source of vitamin d is mushrooms although this is vitamin d2 yet animal products contain vitamin d3.

The largest source of dietary vitamin d is fortified foods.  Namely milk, orange juice and cereals.
Vitamin D is essential to bone metabolism and calcium absorption.
Vitamin D deficiency is common among older adults as they have impaired ability to synthesise vitamin d from the sun


Monday, 12 March 2018

Do you have a simnel cake image?

My magazine column will see me post a recipe of simple cake prior to Easter.

I need images!

Do you have any nice photos of your simnel cake you would allow me to use for my publication?  You will get the credit and retain the copyright.  Please send them to my email

You see, this year I have simply run out of time to bake and take a photo of a simnel cake.  I would love your help!

Thank you in advance


Wednesday, 28 February 2018

Deciding to heal

Deciding to heal.

Medical intervention is life saving.  We know this.  Those who save lives are totally incredible and we need eternal gratitude for all those who have been touched by these lives.

There is zero doubt in my mind about this.  There are times, we simply need help.
My final year of my degree has highlighted the importance of taking control of ones own health, mind, body and as always, spirit (although that’s not often mentioned in my science degree.)  Biochemistry, physiology and the body is a miracle.  How does everything work together so synchronously for us to thrive as humans?  Honestly, I believe a certain degree of miracle must be present.  Being designed so beautifully, our cells and organelles are factories for our health, without them, no oxygen. Without oxygen, no life.  Without lungs, no oxygen… see my point.  Symbiosis is truly ever present and when things go wrong, we sometimes need to ask why.

Laying blame is wrong.  No one wants to be sick.  No one chose to make himself or herself ill.  Yet the chronic diseases we see so prevalent in this world are often preventable. This is a fact.  Yet do we know how?  Why do we suffer such illnesses?  Can they be reversed?
Research, research, research.
The information is out there.  Sadly, often our doctors simply do not have the time to go through finer details and we could be left in wonder of what to do next.

Finite details might just switch on the knowledge or motivation for change.
I have a story rather like this.

Forever a sick child,  we were given antibiotics on most occasions. There was a time the primary reason for visiting the doctors was to ‘get some antibiotics’. Now we know this is not the best route to take in all occasions, yet life saving in others.  Finally we know that antibiotics are to fight bacterial infections, hence the name.  My teenage years were also troubled with health issues which carried on through infertility, hormonal and other chronic pain manifestations.
My symptoms here will not be described in detail but please be aware of a few descriptions approaching. 
Many surgeries, all non specific and seemingly unrelated, followed and a general feeling of not being my best came to a head in 2009. Shocking issues from the gut we stopping me in my tracks. Putting on the brakes of life until the symptoms were so bad I was heavily loosing blood all day, every day.  The GP seemed to think more surgery might be needed and gave me a follow up appointment which was definitely not treated as urgent.  Things got worse, I ended up in the hospital and after surgery and biopsies I was told they were looking for harmful tumors. 
How could I share this with my parents?  They already buried my brother and there was only me left.  You can’t help but think of the worst-case scenario but I should have worked harder on relaxing inside as much as my outer appearance seemed.

During the surgery, I was informed that my colon was heavily ulcerated.  They suspected ulcerative colitis.  Immediately I began research.  Specifically into Inflammatory bowel conditions.  It’s known as IBD and is the collective term for crohns and colitis.  Being inflamed anywhere in the body is not a good place to be. Yet already I was motivated and determined to do what I could to help myself.

Results were in. The biopsies showed Crohns disease.  A disease from anywhere from mouth to anus in the digestive system.  It will also have the ability to penetrate right through the tissue layers which is life threatening.  Alongside gastritis, a hiatus hernia and flattened villi (showing Coeliac disease – a gluten allergy).  So, while this sounded a pretty grim story and the potential need for lots of surgery, I became determined.

Burning candles at my desk late into the night, I was busy reading more and more, going deeper and deeper while I waited for more medical appointments.  Finding a diet detailing The Specific Carbohydrate diet, I read a book by Elaine Gottschall “Breaking the Vicious cycle” and read it cover to cover in one sitting.  Why had I never heard of all this stuff?  You can heal from your nutrition?  You can heal your gut and it changes everything, even mindset! I was astonished. 

Immediately I requested an appointment with a dietitian at the local hospital and I began eating the way the book instructed instantly. 
Science moves on quickly and I’m pleased to say that today, the NHS does now recommend the low FODMAP diet for those struggling with digestive health which is not too dissimilar to the Specific carbohydrate diet.  Yet in 2009 I left the dietitian clinic in floods of tears when they spoke to me of ‘a varied and balanced diet’ and showed me the Eatwell Plate full of grains and starches.  Inside I was screaming but remained polite.   I knew this was wrong as I had already begun eating bone broths and eliminating sugars as well as the gluten which had been harming my body all these years through allergy.
My gastroenterologist gave a long list of prescriptive medicine for me to use.  Two of them were essential at the time but turned me inside out with pain so I got off those as soon as I could possibly do safely.  We had a heated conversation; I was frustrated – his exact words, “You can’t deal with crohns without medication or surgery.”  I cried.  I would. I was determined.  I knew what I had read.  Keeping an open mind to what he said was unthinkable.

Continuing to spend much time in the kitchen with careful preparation of my nutrition, continuing to research, beginning to wear bikinis in case he was right and I needed abdominal surgery….everything changed.
Beginning a running regime I was determined to run a race in totality.  Just 5k, that would do.  Dance has always been my passion and I began to compete, doing great with my amazing dance partner and ending up finalists of the nationals from 160 couples down to 5.  We didn’t win but that didn’t matter.
My body transformed unrecognizably.  I was feeling fit and well, my horrific symptoms I saw before surgery disappeared within 3 weeks. 
The following summer, for the first time, I had no hay fever.  My constant ear infections which also needed previous surgery and I lost my hearing bones in one ear, had gone.  Totally.
Never in my life had I felt so amazing.

More difficult conversations with the gastroenterologist led to a place of ‘agreeing to disagree’.  I knew then that diet was the key to making significant improvements.  While this was a dramatic way of eating, it was necessary to heal.  Being transparent, things have slipped since and I can feel it. But easily, I pull things back and see the same wonderful results over and over.

They say you are what you eat.  You definitely are a product of your absorption.  While my degree has taught me much about the systems of metabolism I feel the important lesson to pass on is to listen to your body.  This far, 9 years later I am blessed to still be in better health without surgery or medication.  My crohns went into remission after 3 weeks and that is where it has stayed.

* If you have any health concerns I would always recommend seeking the advice of a health professional as well as listening to your body.

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