Wednesday, 6 May 2020

Can you reverse type 2 diabetes?

My opinion is, as always, it very much depends on the patient. What we do know is that health can be affected by diet and lifestyle and type 2 diabetes is definitely a big player in that hypothesis. 

I found this video and really wanted to share it. Personally, I would recommend keeping an eye on your blood glucose levels as it's easy to do, inexpensive and a key to better health if you are bordering on unhealthy blood glucose levels. 

Some patients will be in a pre-diabetic state long before they head into the diabetes threshold and this is the crucial time when you could potentially lower blood glucose levels. I will speak more in depth about this on an other blog post (make sure you subscribe for the updates) but watch the video and make up your own mind. 

We will, as always on this website, share some science data so you can clearly see the people who beleive they have reversed type 2 diabetes.  But you can always lower your blood glucose levels unless you have type 1 diabetes which is a totally different case. I'll also write in another post about the difference between type 1 and type 2.

Blood glucose monitoring kits are inexpensive and easy to use.

Feel free to let me know your thoughts by emailing here

Tuesday, 21 April 2020

Public Health England re-issues advice on vitamin D as Government response to Covid 19

Today, Public Health England (PHE) has re-issued existing advice on the NHS UK website.

Within this advice, PHE has made it clear that this is not in relation to preventing Covid-19 but due to the role vitamin D has always played in the optimum health of bones and muscle. 

As we are staying at home following Government advice, many people will be indoors for the majority of the day. This is a time of year within the UK when we begin to get vitamin D from sunlight. 
The body creates vitamin D when the skin is exposed to sunlight during spring and summer.  

Public health advice suggests if you are not outdoors at this time, you should consider supplementing with 10micrograms of vitamin D. 

They were clear to state on the NHS website that the advice is not in relation to preventing Covid 19.

Vitamin D supplements can be bought at most pharmacies and supermarkets and the PHE is advising not to buy more than is needed. 

The advice statements can be found at:

The website is highlighted in yellow to point out that there is no evidence that the risk of coronavirus can be reduced with vitamin D. Even though there have been some reports about it. 
(see the video within this link )

Listed on the NHS website are the risks for taking too much vitamin D and when to seek medical advice in relation to taking the supplement.


Sunday, 5 April 2020

Dr Berg’s ‘take’ on vitamin D and the Coronavirus

For several years I have watched Dr Bergs’ YouTube videos and my opinion is he talks a lot of sense.

Currently, the pandemic climate is victim to many hypothesise being flaunted to the public and as a registered nutritionist, I feel ill equipped to try and share another. So I won’t.

However, one thing we do know is that a healthy immune system is paramount in all health related matters. And one thing we can all try to do during lockdown is to improve immunity. Something which can have a pretty fast effect on the immunology of the world is food, Including vitamin D (which in the UK we can now also get from the sun as its availability is April-October due to how close we are to the sun). 

Have a look at dr bergs videos, make up your own mind. Possibly try and improve health at this time when you can cook properly, sleep better, chose wiser foods. If not now, then when?


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.

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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.

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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.

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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. 

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