"Current evidence indicates many chronic diseases can be largely prevented or treated by adhering to a plant-based diet, making health conscious lifestyle modifications and utilizing nutraceutical therapy as and when appropriate" – NutriSophic
The first recommendations on carbohydrate intake were proposed in the 1980’s and 90’s by COMA which has since disbanded. Since then overwhelming evidence has mounted which shows carbohydrate consumption to be associated with many of today’s current health problems. More specifically, the type of carbohydrate and the consumption of simple sugars and refined carbohydrates has become an increasing concern. High sugar intake is implicated as a significant risk factor for diabetes, fatty liver disease and obesity and receives a large amount of focus for current health initiatives and government policy on the recommendations for sugar intake.
Prevalence of weight related disease
In the UK 57% of adults are overweight and obese which is predicted to reach around 70% by 2034 (Public Health England Obesity Knowledge and Intelligence team, 2016). Children in the UK are following a similar trend with 25% of them being over weight and obese. The prevalence of doctor-diagnosed diabetes in adults increased between 1994 and 2014 from 2.9% to 7.1% and 1.9% to 5.3% for men and women respectively. The cost of obesity to the NHS is £5.1 billion (Scarborough et al., 2011) and the cost of treating diabetes and the complications that result from it in 2010/11 was £9.8 billion a year which is projected to be over £16.9 billion by 2035/36 (Hex et al., 2012). However, the NHS has refuted claims about potential bankruptcy in the future (Nhs.uk, 2012) despite such claims circulating in the media (Google.co.uk, 2015).
Actual sugar consumption has fallen over the past 40 years while consumption of sugar-sweetened beverages and foods have risen. Children ages 4-10 are said to consume on average just over 60g of sugar a day, equating to 5,543 sugar cubes or 22kg of sugar in one year (Gov.uk, 2016). Sugar consumption is highest among school age children and low income families. However, a high consumption of sugary foods is not justified by a low income when you consider a bag of bananas or apples can be purchased at a lower price which contains natural sugars, as well as vitamins and minerals. The biggest source of sugar for kids are juices and soft drinks, although for ages 19-64 one of the biggest sources of sugar comes from table sugar. However, this may be attributed to Britain’s cultural obsession with Tea.
Parents perception of child weight status and health
The fact that 42% of parents do not recognise their children to be overweight or obese when they are (Public Health England, 2015) also contributes to the problem. A study showed parents of overweight and obese children considered happiness, diet and activity level to be more important than body weight as an indicator of health, despite the physical and mental health implications of being overweight or obese (Syrad et al., 2014). The same study found that parents also didn’t find the BMI scale to be a credible indicator of a child’s health, because according to parents it didn’t take into consideration the child’s lifestyle. This shows that despite the implicated health risks of being over weight or obese, parents do not acknowledge body weight to be a significant risk factor to their child’s health. This is a dangerous misperception that needs to be immediately corrected. A strategy to give parents a more accurate perception of ‘overweight’ as well as education on the diverse effects that being overweight or obese has on their children, must be part of the health initiative. Failure to do so will not address the wider context of the problem
Current health initiatives
Health initiatives are currently in place across Britain to reduce sugar intake. Public Health England compiled an evidence based report called “Sugar consumption: The evidence for action” (Public Health England., 2015) which expresses the need to drastically reduce sugar intake across the population, which even the British Dental Association stated would be reckless to ignore (BDJ Team., 2015). Change4Life has issued a new campaign that focuses on educating parents to be “sugar smart” and even encourages parents to download the new Sugar Smart app that measures the sugar content of every day food and drink (Nhs.uk., 2016). Action on Sugar have also proposed an evidence based, six point sugar reduction plan to David Cameron (Cameron’s Plan: A comprehensive approach to prevent obesity, 2015) and are also backing TV chef Jamie Oliver’s obesity plan too (Actiononsugar.org, 2015). Some of the actions proposed by Action on Sugar involve a 50% sugar reduction within the next five years starting with soft drinks, ceasing the promotion and all types of marketing of unhealthy food to children and adolescents and a 20% duty on all sugar sweetened soft drinks and confectionery. They also began promoting sugar awareness week between the 30thNov-6thDec (Actiononsugar.org, 2015). All health initiatives proposed involve the proposal of a sugar tax with 53% of the public being for it. Educational behavioural strategies
In review of five educational school intervention programmes that aim to reduce sugar-sweetened beverage consumption and investigate changes in body mass, three showed long term success (Avery et al., 2014). After 12 months, one of which found the percentage of overweight and obese children decreased while the control group increased by 7.5% (Stockman., 2006). Sugar tax doesn’t address the root causes or take into context the bigger picture. Research has also suggested calorie intake has dropped but activity levels have dropped further (Prentice et al., 1995). Evidence investigating marketing strategies such as the four P’s (promotion, price, product, place) framework is shown to influence consumption and purchase of sugar (Sugar Reduction: The evidence for action Annexe 3, 2015). These same principles can be applied to the marketing of healthy foods, but need to be marketed with equal if not more vigour than the marketing strategies used to promote unhealthy foods.
Conclusion Overall the dynamics of sugar consumption and its effects on the health of the population is complex. As such, this surely warrants an equal response and an approach that mirrors it’s complexity. The food industry needs to become a part of the solution and not part of the problem to shift the favour towards the goals of the initiatives. Whilst the government needs to do its part in enforcing change and aggressively working towards fulfilling the goals of the initiatives. However, reducing sugar consumption is just one step towards tackling a multi faceted problem. There are many other factors affecting the health of the public besides sugar. Significant, long term improvements in public health and reductions in dietary related diseases will ultimately be accomplished at an individual level without tactics of coercion. This change will come from parents having; realistic nutrition and bodyweight perceptions, better food awareness, practical guidance on calorie balance and portion control and education on the effects of overnutrition. This all of course needs to be followed up with parents putting knowledge into practice and implementing long term positive behaviour changes such as moderating portion sizes or increasing purchases of foods that contain natural sugars such as fruit, whilst decreasing or eliminating the purchase of foods that contain ‘free sugars’.
Actiononsugar.org. (2015). ACTION ON SUGAR BACKS JAMIE OLIVER’S OBESITY STRATEGY AND LAUNCHES ITS OWN EVIDENCE-BASED ACTION PLAN TO SAVE LIVES AND THE NHS. [online] Available at: http://www.actiononsugar.org/News%20Centre/Press%20Releases%20/2015/167492.html [Accessed 17 Mar. 2016].
Actiononsugar.org. (2015). Sugar Awareness Week. [online] Available at: http://www.actiononsugar.org/sugar-awareness-week/Sugar%20Awareness%20Week%202015/167198.html [Accessed 15 Mar. 2016].
Avery, A., Bostock, L. and McCullough, F. (2014). A systematic review investigating interventions that can help reduce consumption of sugar-sweetened beverages in children leading to changes in body fatness. Journal of Human Nutrition and Dietetics, 28, pp.52-64.
BDJ Team (2015)2, Article number: 15157. Ignoring Public Health England report on sugar reduction would be reckless. BDJ Team, 2(10), p.15157.
Butland B, Jebb S, Kopelman P. (2007). Tackling obesities: future choices – project report 2nd Ed. London: Foresight Programme of the Government Office for Science, 2007.
Cameron’s Plan: A comprehensive approach to prevent obesity. (2015). [pdf]. UK: Action on Sugar. Available at: http://www.actiononsugar.org/News%20Centre/Press%20Releases%20/2015/167492.html [Accessed 16 Mar. 2016].
Google.co.uk. (2015). diabetes threatens bankrupt NHS UK 2015. [online] Available at: https://www.google.co.uk/gfe_rd=cr&ei=e3PpVo_DEenS8AesxIKIDg&gws_rd=ssl#q=diabetes+threatens+bankrupt+NHS+UK+2015 [Accessed 16 Mar. 2016].
GOV.UK. (2016). 5 year olds eat and drink their body weight in sugar every year – Press releases – GOV.UK. [online] Available at: https://www.gov.uk/government/news/5-year-olds-eat-and-drink-their-body-weight-in-sugar-every-year [Accessed 15 Mar. 2016].
Hex, N., Bartlett, C., Wright, D., Taylor, M. and Varley, D. (2012). Estimating the current and future costs of Type 1 and Type 2 diabetes in the UK, including direct health costs and indirect societal and productivity costs. Diabetic Medicine, 29(7), pp.855-862.
Nhs.uk. (2012). Massive rise in diabetes costs predicted – Health News – NHS Choices. [online] Available at: http://www.nhs.uk/news/2012/04april/Pages/nhs-diabetes-costs-cases-rising.aspx [Accessed 16 Mar. 2016].
Nhs.uk. (2016). Let’s get Sugar Smart! Download the Change4Life Sugar Smart app for free today. [online] Available at: https://www.nhs.uk/change4life-beta/campaigns/sugar-smart/sugar-facts [Accessed 15 Mar. 2016].
Obesity Knowledge and Intelligence team. (2016). Public Health England. [online] Noo.org.uk. Available at: http://www.noo.org.uk/slide_sets [Accessed 4 Mar. 2016].
Prentice, A. and Jebb, S. (1995). Obesity in Britain: gluttony or sloth?. BMJ, 311(7002), pp.437-439.
Public Health England. (2015). [pdf]. Sugar Reduction: The evidence for action. Available at: https://www.gov.uk/government/publications/sugar-reduction-from-evidence-into-action [Accessed 15 Mar. 2016].
Scarborough, P., Bhatnagar, P., Wickramasinghe, K., Allender, S., Foster, C. and Rayner, M. (2011). The economic burden of ill health due to diet, physical inactivity, smoking, alcohol and obesity in the UK: an update to 2006-07 NHS costs. Journal of Public Health, 33(4), pp.527-535.
Sugar Reduction: The evidence for action Annexe 3: A mixed method review of behaviour changes resulting from marketing strategies targeted at high sugar food and non-alcoholic drink. (2015). 1st ed. England: Public Health England, pp.pg 7-8.
Stockman, J. (2006). Preventing Childhood Obesity by Reducing Consumption of Carbonated Drinks: Cluster Randomised Controlled Trial. Yearbook of Pediatrics, 2006, pp.407-408.
Syrad, H., Falconer, C., Cooke, L., Saxena, S., Kessel, A., Viner, R., Kinra, S., Wardle, J. and Croker, H. (2014). ‘Health and happiness is more important than weight’: a qualitative investigation of the views of parents receiving written feedback on their child’s weight as part of the National Child Measurement Programme. Journal of Human Nutrition and Dietetics, 28(1), pp.47-55.
Our understanding of the human genome has improved exponentially over the past century. With the completion of the human genome project in 2003 humans have sequenced the entire molecule of life, deoxyribonucelic acid (DNA), estimating the presence of 20,500 genes and 1.42 million single-nucleotide-polymorphisms (SNP’s) (Sachidanandam, Ravi et al 2001). This of course has led to a much clearer understanding of our genes and with it, a deeper cognizance for the information stored within them. Because of this, we are now able to much more thoroughly interpret our own genetic information which may hold the key to the future door of human health. Genetic analysis can be used to indicate an individuals susceptibility to specific diseases by identifying certain SNP’s that are associated with a persons risk of developing that particular disease. Similarly a person can even become familiar with their bodies own capacity to metabolise certain drugs and learn how well they respond to them. People are also able to build a social network with long distance relatives through the analysis of the ethnic composition of ones genome. However concerns have been raised regarding the interpretation and use of personal genetic information by the general public. This article will discuss both positive and negative implications of the use of a genetic analysis service 23andMe, as an accessible health screening device for the general public.
Genetic analysis from 23andMe can indicate an estimated risk of disease according to the identification of mutation SNP’s and could be used effectively to encourage healthier behaviour patterns in the right minded individuals. This could lead to an individual taking preventative measures to reduce their disease risk (Milne et al 2000) and thus resulting in positive health improvements. However, such information can also be misinterpreted and misleading for some, creating panic and anticipation about a disease that may never occur. This could create a rush for unnecessary screening and testing in healthy asymptomatic people that may never develop disease especially with regards to those who test positive for BRCA mutation genes associated with breast cancer. Conversely in the case of Rita Rubin, she found out through genetic analysis 23andMe that she had a smaller chance of developing Crohns disease than the average person but yet had lived with the condition all her life (Nextavenue.org). Genetic testing could also lead an individual into a false sense of security promoting an indulgence in unhealthy behaviours that may actually encourage disease, even though they are not genetically susceptible to it (Chapman and Bilton 2004) . Some of the disease susceptibility included in the service are diseases for which there is no cure or effective treatment. A concern remains in the question of whether psychologically and emotionally unstable individuals will respond well to finding out they are at a high risk for developing a disease they can not manage or treat. Conversely a strong minded and proactive individual being made aware they have a small chance of developing a disease will most likely take preventative actions to minimise their risk and make positive lifestyle changes.
Positive implications also exist for the testing of genetic variations that indicate drug metabolism. For example patients that use drugs to prevent heart attacks or blood clotting may benefit from knowing how well they respond to a certain drug and how sensitive they are to it. This information of course could potentially save lives, but may have to be used, in the context of public health, under the guidance of all relevant qualified health care professionals including emotional counsellors (Allyse and Michie 2013).
Data from genetic analysis can be both useful and detrimental to a persons physical and psychological welfare, depending on the individual and their interpretation of the data. Although data from such an analysis can not be currently used to determine exhaustive and definitive susceptibility to disease, it can nonetheless serve as a platform for the progression of this type of technology so more accurate interpretations can be made from this type of data in the future. Also until the reliability of the data from genetic analysis improves and its interpretation can be given more accurately, it should serve as ‘information of interest’ for the public, rather than a tool to discover the fate of one’s health. It should be made explicit to anyone using genetic analysis that genetics are only one factor in disease risk and not the only factor. Genetic analysis could ensue more concern and worry for some than the significance and reliability of the data deserves credit for. It does, however, have the ability to prosper as a device used for public health screening and for personalised health improvement at an individual level.
References Allyse, Megan, and Marsha Michie. (2013). ‘Not-So-Incidental Findings: The ACMG Recommendations On The Reporting Of Incidental Findings In Clinical Whole Genome And Whole Exome Sequencing’. Trends in Biotechnology 31.8 (2013): 439-441. Available from: http://www.nature.com/gim/journal/v15/n7/full/gim201373a.html [15 March 2015]
MILNE, S et al (2000) ‘Prediction And Intervention In Health-Related Behavior: A Meta-Analytic Review Of Protection Motivation Theory’. J Appl Social Pyschol 30.1: 106-143. Available from: file:///C:/Users/User1/Downloads/JASP-PMTMeta.pdf[15 March 2015]
Nextavenue.org. (2013) ‘The Pros And Cons Of Genetic Testing’. N.p. Available from: http://www.nextavenue.org/article/2013-04/pros-and-cons-genetic-testing [15 March 2015]
At least 2 billion people worldwide are currently affected by micro-nutrient deficiencies and despite the UK being a developed country with high food availability, some British children still suffer deficiencies. During pregnancy and childhood where physiological growth occurs at a rapid rate, its well known an intake of Vitamin D is required in sufficient amounts during these crucial periods of growth. Mothers with low 25-OHD serum levels who fail to intake or supplement the recommended amounts of vitamin D during pregnancy and who breastfeed past 6 months without supplementation are the biggest causes of childhood vitamin D deficiency. Other factors that affect vitamin D status in children is inadequate UVB exposure and/or low intake of dietary sources include fortified foods or supplements. Vitamin D deficiencies seems to be a problem of our awareness about the importance of nutrition and of the availability of supplementation or food sources that could be improved with fortification rather than a problem of race and age.
Micro-nutrients are organic and inorganic substances composed of vitamins and minerals that we need from our diet which are necessary for cellular function, physical growth and tissue repair during all stages of life (Merson, Black and Mills, 2012). At least 2 billion people worldwide are currently affected by micro-nutrient deficiencies (Unitedcalltoaction.org, 2016) and despite the UK being a developed country with high food availability, some British children still suffer deficiencies. Currently many children and adolescents across the whole of Europe including Britain have all shown the same consistent deficiencies of at least six micro-nutrients (Kaganov et al., 2015).
Micro-nutrient deficiencies can affect all age groups but children are a particularly vulnerable group, especially those from low income families (Casey et al., 2001). The social and economic costs of micro nutrient deficiencies in women and children are also thought to be significant (Darnton-Hill et al., 2005). During pregnancy and childhood where physiological growth occurs at a rapid rate, it is well known an intake of micro-nutrients are required in sufficient amounts during these crucial periods of growth. Adverse effects from nutrient deficiencies are well documented (Viteri and Gonzalez, 2002) (SCN.,2004) and the effects of a prolonged deficiency is catastrophic.
One micro-nutrient deficiency that has made a come back since the industrial revolution is vitamin D. Deficiencies in vitamin D results in serious physical growth deformities (Abrams., 2002). Vitamin D deficiencies (VDD’s) are now being frequently observed children as a result of poor intake, inadequate sunlight exposure or because of a deficiency in the mother during pregnancy or breastfeeding. The long term outcomes from these deficiencies can lead to limitations in the quality of a childs future. So the importance of an adequate intake of vitamin D during pregnancy and childhood cannot be overstated, although requirements are often not being met. Therefore the focus of this review will be based on the prevalence and causes of vitamin D deficiency during pregnancy and among British children. This review will derive from recent research mainly within the last 15 years.
Vitamin D intake and recommendations
Two main forms of vitamin D exist as vitamin D2 (ergocalciferol) which can be attained predominantly from animal foods and vitamin D3 (cholecalciferol) which is photochemically synthesised cutaneously in human and animal skin. Vitamin D converts into one of its active forms 25-hydroxyvitamin D (25-OHD) of which serum levels can be measured and is the main clinical method used for assessing vitamin D status. Clinical deficiency is classed as a 25-OHD serum level of <25 nmol/L and a vitamin D insufficiency <50nmol/L, both inadequate levels for good health (Thurston et al., 2015). VDD (vitamin D deficiency) is now proving to be associated with many health problems (Macneil, 2008) (Gominak and Stumpf, 2012) (Zoler, 2012) (Reid, 2015) but is more widely known for effects on bone metabolism. This is important particularly for children and adolescents as 90% of bone density is laid during the first two decades of life (Eufic.org, 2014).
Vitamin D measurements and recommendations of intake can be confusing too as food labels and recommendations often use both µg and IU of units of measurements, which both have different equivalences. To avoid confusion it’s important to remember that every 1µg of vitamin D is equivalent to 40IU of vitamin D. Recommendations on vitamin D intake was set out by the Committee on Medical Aspects of Food and Nutrition Policy (COMA) in 1991. It was based on the assumption that the population would receive sufficient vitamin D intake in the summer resulting in sufficient stores for winter. Therefore, reference nutrient intakes (RNI’s) were only issued for vulnerable groups such as Infants and children aged under 4 years, who were advised an intake of 7-8.5µg/day (280-340IU/day), and pregnant women and breastfeeding women, advised an intake 10 μg/day (400 IU/day) via supplementation (Panel on Dietary Reference values of the Committee on Medical Aspects of Food Policy., 1991). However, these dietary values are not being met by these groups today and may also not be in line with the lifestyle and cultures of today’s population who spend more time indoors or out of sunlight exposure and inactive than is recommended (Matsuoka et al., 1993) (Certain and Kahn, 2002).
Young women in the UK, from mixed ethnic backgrounds, also only average a daily intake of only 3μg of vitamin D and less than 1% of young women consume more than the RNI of 10μg/day (Marriott and Buttriss, 2003). This is worrying considering 10μg/day is the recommended intake advised during pregnancy and breastfeeding to prevent deficiency which can lead to growth impairments or osteoporotic bone injuries later on in life. Mothers with low 25-OHD serum levels who fail to intake or supplement the recommended amounts of vitamin D during pregnancy and who breastfeed past 6 months without supplementation are the biggest causes of childhood VDD (Thomas et al., 2011) (Aljebory, 2013). Nutritional rickets is regarded as a disease of VDD which results in serious bone deformity and the prevalence of rickets, is currently at its highest since 1963 (Goldacre, Hall and Yeates, 2014).
Vitamin D deficiency in cultural and ethnic groups
Culture and ethnicity are other factors that exacerbate childhood VDD prevalence in the UK, especially when dietary intake of vitamin D is already low and British weather is notoriously unreliable as a sustainable source of sunlight (UVB) exposure. Six Infants aged 10-28 months born in the UK of mothers that failed to supplement vitamin D during pregnancy and during breastfeeding were referred to a paediatric clinic. All infants presented with low serum 25-OHD levels and were subsequently diagnosed with florid rickets as a result of VDD. Some of the mothers were postgraduate students and some were immigrants but most of the mothers were traditional Muslims who concealed their skin in public for religious reasons (Mughal et al., 1999).
Since VDD is particularly prevalent among sunlight deprived individuals, such as women practising religions that require skin concealment, the current dietary recommendations may be inadequate for these individuals to attain sufficient 25-OHD levels who receive little to no UVB exposure (Glerup et al., 2000). Results from a UK study on 78 women aged 18-36 of South Asian origin showed 94% of these women to have VDD evident by low serum 25-OHD levels (Dobson, 2007). Further research supports the UK recommendations of UVB exposure in the summer to be inadequate for adults of South Asian ethnicity (Farrar et al., 2011) which means compensations must be made through dietary intake. Repeated research has also shown children of ethnic minority groups tend to be at a higher risk of vitamin D deficiency than caucasians (Shaw, 2002) (Brenner and Hearing., 2007) with high prevalence of VDD among Somali children (Modgil et al., 2010) and asian children (Zlotkin and Blumsohn, 1999). This obviously raises concerns for children born in the UK of mothers who are of a particular religion or ethnicity and of Mothers who are likely to have VDD before, during and after pregnancy while breastfeeding, unless of course specific dietary needs are met.
Vitamin D deficiency in Caucasians and general population
Many Caucasian women and children of the population however despite differing levels of ethnic susceptibility to VDD are still vitamin D deficient and studies have even shown even those in sunlight rich countries are susceptible to VDD (Bettica et al., 1999) (Gannagé-Yared et al., 2000) .
A study involving 1414 Caucasian women has shown females in the UK with fair skin have lower serum 25-OHD levels than Caucasian females with dark skin (Glass et al., 2009). This outlines variability in responsiveness to UVB exposure which ultimately affects vitamin D status and since the effects of VDD on bone health in Caucasian and non-Caucasian women are the same (SA, 2011) the prevalence of VDD in Caucasian women should not be overlooked either.
A longitudinal study involving 99 British Caucasian women who were pregnant showed 44% of the women were vitamin D deficient (25-OHD <25nmol/L) at 20 weeks gestation and 96% of women were vitamin D insufficient (25-OHD <50nmol/L) at 12 and 20 weeks . All women seemed to have improved vitamin D status by 35 weeks compared to 12 weeks gestation, but even then 16% were still vitamin D deficient and 75% still had insufficient levels. Some women also took vitamin D supplements which led to higher serum 25-OHD levels than those who didn’t, but vitamin D insufficiency was still present even with supplementation (Holmes et al., 2010).
A study conducted on children born of vitamin D deficient mothers showed all children were born deficient in vitamin D. However, vitamin D status in the infants quickly normalised after receiving an intake of 10μg/day (400 IU/day) at 2 weeks of age (Bergström, Blanck and Sävendahl, 2013) which intake is the RNI recommended for pregnant and breastfeeding women. Research shows that when baseline serum levels from groups were < 75 nmol/L, for every 1μg of vitamin D supplemented 25-OHD levels are raised by 2 nmol/L. However, when groups were clinically deficient (<25nnmol/l 25-OHD) or insufficient (<50nnmol/l 25-OHD) in vitamin D, there was significant value in providing an additional 10μg per day of vitamin D.
In a longitudinal UK study nearly a third of women studied had insufficient maternal 25-OHD levels (<50nmol/L) and 18% had maternal levels of 25-OHD levels indicative of deficiency (<25nnmol/L). These low 25-OHD levels during pregnancy resulted in reduced bone mass in their children at the age of 9 (Javaid et al., 2006). A cohort study showed the same results of reduced bone density observed in their offspring at 20 years of age born of mothers who were vitamin D deficient during pregnancy (Zhu et al., 2014). This highlights the need for national preventative and educational strategies aimed at the entire population with particular focus towards UK women of child bearing age.
Given the current rise in VDD It seems logical to make vitamin D supplements available to pregnant women through their GP in the same way folic acid is, although it was concluded by The National Institute for Health and Care Excellence in 2003 that vitamin D should not be routinely administered to all pregnant women (NICE, 2003). Since then though clear relationships between maternal 25-OHD status and offspring health have been made apparent (Sabet, 2012) (Young et al., 2012) (Rebecca et al., 2013). Research has shown doses of 50μg/day of vitamin D supplementation taken by mothers during pregnancy and during breastfeeding has shown to protect infants from being born into deficiency and up until 8 weeks of age (March et al., 2015). Firm recommendations on vitamin D supplementation intakes as high as the maximum upper tolerable level (UL) to prevent deficiency has also been suggested (Holick et al., 2011). However others state the evidence is still insufficient to support definitive clinical recommendations of vitamin D supplementation during pregnancy (Harvey et al., 2014) even though supplementation does raise serum 25-OHD levels to recommended amounts, larger randomised controlled trials have been prompted (Pérez-López et al., 2015).
Vitamin D status among children
Apart from mothers with low maternal vitamin D status during pregnancy and breastfeeding and ethnic susceptibility, other factors that affect vitamin D status in children are inadequate UVB exposure and/or low intake of dietary sources including fortified foods or supplements (Hartman, 2000). Excessive sunscreen use has been recognised as a factor in causing VDD in Caucasian children (Galibois, Rhainds and Gagné, 2001) which unfortunately mimics the same problem ethnic groups face who have low UVB absorption rates due to dark skin pigmentation and its use on children has been put into question (Norval and Wulf, 2009). This makes dietary intake or supplementation of vitamin D seem like the only plausible option for achieving ample vitamin D status. Although intakes of dietary sources among children are poor especially in countries where optional or no mandatory fortification policy is in place (Prentice, 2008). The diets of 755 children aged 18 months-3.5 years from the Avon Longitudinal Study of Parents and Children (ALSPC) in the UK were analysed. It was found that all of the childrens diets were low in dietary sources of vitamin D and were all below the recommended intake for vitamin D. It also found that milk was the main source of what little vitamin D they did consume and it was suggested that an increase in fortification levels of vitamin D would most likely help children receive adequate intakes (Cribb et al., 2014). In a study involving 252 Irish children and adolescents, more than half had 25-OHD serum levels at <50nmol/L which is considered insufficient (Carroll et al., 2014). Educational methods and health promotion have proven effective at increasing intakes of dietary sources of calcium and vitamin D among children (Spence et al., 2013) (Pampaloni et al., 2015) and may work in concert with a similar educational programme aimed at parents that could reinforce what’s being taught in children.
Children pay the price because of their Mothers inadequate nutritional intakes during pregnancy and breastfeeding and largely because of their Mother’s lack of awareness about the importance of vitamin D. Awareness and education early on in pregnancy may lay the foundations for a vitamin D sufficient future for future generations in the hope that the message of vitamin D importance is passed on to prevent an issue of the past and present becoming an issue of the future. An improved national fortification policy aimed at frequently consumed foods may help resolve vitamin D deficiency, as will national supplementation recommendations on vitamin D during pregnancy and breastfeeding which has shown to improve vitamin D status. Research is showing vitamin D deficiencies and rickets to be on the rise and vitamin D deficiency is clearly being observed in pregnant and breastfeeding women and in children of all ages and ethnicities. Vitamin D deficiencies seems to be a problem of our awareness about the importance of nutrition and of the availability of supplementation or food sources that may be improved with fortification rather than a problem of race and age.
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For muscle-building to occur certain physical stresses and dietary requirements needs to be adhered to. Our bodies aren’t really designed to be as muscular as some men are or want to be and to maintain that kind of physique it requires a lot of discipline from the dietary side and plenty of hard work from the physical side on a consistent and regular basis to continue to maintain or build that muscle. The correct blend of nutrients alongside the correct training for your genetic build, coupled with enough R&R, will equate to gains in muscle mass as far as your genetics will allow.
First of all, lets start with the diet! Calorie intake for muscular hypertrophy is kind of a reversed fat loss diet. For fat loss, you consume fewer calories than what you expend each day to lose fat. For muscle to grow, however, there needs to be a calorie surplus, more calories than you expend daily. These extra calories are what provides your body with the energy to grow new lean muscle tissue. Make no mistake, if you aren’t consuming enough calories, you won’t grow, plain and simple. Even if you are consuming enough calories you will at some point need to increase them to keep new gains coming. I kid you not when I say building serious muscle naturally can require some serious eating. For me, 4000 calories a day is standard if I’m sitting at around 205lbs in total body weight. On the other hand, more calories doesn’t necessarily mean more muscle, only unnecessary fat gain. With possibly the exception of a typical hard gainer, a true “ectomorph”, anything over around 400-500 calories above what it takes to maintain your weight will likely pose a risk of new unwanted fat gain.
Uh-oh, so what does this mean…calorie counting? what!? seriously?
If you want to be accurate and want to minimise fat gain, whilst maximising muscle gain, I think it’s a necessity unfortunately. As a general rule, for fat gain susceptible “endomorphs”, a modest 300 calorie surplus is all that is needed to provide enough calories to grow on, while an ectomorph may need a 600 calorie surplus (or more) while the mesomorph could gorge on a 600 calorie surplus and will probably still get crazy shredded gains (bastards). So if your currently eating 2600 calories and have been for a couple weeks and you haven’t even gained half a pound, then its safe to say you need more calories. Therefore, increase your calories by roughly 300 (ie, 2 protein shakes and a banana or a handful of nuts and an apple or a peanut butter sandwich) until you can gain around 1-2lb in 2 weeks. Maintain this caloric intake until you no longer gain 1lb every 2 weeks. This is the trial and error method. Another simple way to eat for muscle gains is to simply start by eating 18 calories per lb of body weight and adjust from there depending on whether or not you’re gaining or losing weight each week.
Drip fed protein
When you lift heavy weights you break the muscle down and cause micro trauma, tiny tears in the fibers that when combined with enough sleep, calories and protein equates to new thicker stronger muscle fibers. To save you an essay eat 2g of protein per kg of body weight throughout the whole day, you weigh 90kg = 180g protein. Regular eating patterns should be incorporated to maximise protein synthesis, eating every 3 hours works well for me and that feeding time interval has some good research behind it too, 30-40g of protein for women and men is more than enough per meal.
Carbs = bigger fuller muscles
Since we know carbs draw around 2.5 g of water in with every gram of carbohydrate you eat it becomes very easy to gain weight and create a more muscle-building environment when your carb intake is high. I personally choose to have most of my carbs in the meals after training, around a good chunk for breakfast. Having most of your carbs post workout and for breakfast is a better use of carbs as your muscles will be more sensitive to the effects of insulin meaning you can be sure your muscles will soak the carbs instead of your fat. It should go without saying that carb sources throughout the day in any meals (with the exception of post workout nutrition) should be high in fibre and as unprocessed as possible carbs of a slow release nature. A good rule of thumb when trying to gain muscle is to start at around 1.5g-2g of carbs per lb of bodyweight. For example If weighed 190lb I will go for around 380g of carbs in a day, broken up. Generally, try to get the bulk of your carbs in at breakfast, pre workout, post workout and post post workout.
Pre and post workout are arguably the most crucial times to feed your muscles with nutrients.This really is the make or break time where nutrition really matters. Think of it like this, going to the gym and training without having a post workout shake is like giving a builder the blue-prints to build a house without providing him any raw materials. The tools are there, but without bricks, cements and materials, there is nothing to build with. You can’t build a house out of air just like you can’t build muscle out of air. DO NOT UNDERESTIMATE THE IMPORTANCE OF POSTWORKOUT NUTRITION.
Men and women really want between 20-40g of protein with around 60-120g of refined, high glycemic, sugary carbs (glucose/dextrose/maltodextrin) fairly soon after your last set or straight before training. For hard-gainers I would shoot for the higher end regardless of body weight.
After many years of hard lifting and big eating your bound to hit what I call the genetic wall. Everyone has genetic limitations but if you are aware of your body type and can and eat in a way that reflects your body type then you can to an extent learn to override these limitations to make gains in strength and size with time.
There are 3 basic body types, these 3 body types are referred to as somatotypes and they are Endomorphs, Ectomorphs and Mesomorphs. Each somatotype has its own physiological differences that define their natural body composition…
Endomorphs tend to be stocky with a tendency for fat gain, they usually have tree trunk legs big calves and can build muscle at an easy rate, but again their downfall being their susceptibility to fat gain
Ectomorphs tend to be skinny and sometimes lanky, they usually have a thin skeletal frame, skinny wrist and generally a thin stature, they tend to be lean but skinny and find it hard putting on weight (me!)
Mesomorphs have the best of both worlds, great genetics, naturally lean and builds muscle easily, very athletic (so jealous)
Although somatotypes are really a truncated explanation for the genetic differences between people. It can be helpful to guide you towards a training and eating regime that fits your frame.
Train like a pro bodybuilder to look like a pro builder… No!
First of all I just want to dispel something, I’d imagine there maybe some guys reading this that would like to get as big and as freakishly muscular as Ronnie Coleman or Jay Cutler? Or some guys just want guns like Arnie? Or maybe you’d like to attain a more aesthetic look like that of Serge Nubret with his pleasingly muscular yet athletic look similar to most bodybuilders in the golden age?
Well, I definitely had the same wishes at one point in my life. I remember reading these magazines in my young teen years and thinking if I train like these guys and take the supplements they recommend maybe I could get like them. If you are one of them guys and your heart is set on growing until your 240lbs+ and 6% body fat you’re probably aiming a little high unless you know you have great genetics. Generally speaking, for an “average” drug-free person, that kind of build and size is not attainable. It’s a pipe dream that you’ll soon realise is limited by your natural ability. If you want arms like Arnie’s or you want to be as wide a Heath, stop dreaming it’s probably not going to happen.
For most people, with typical jobs, with typical social lives and typical genetics, following the routine of a pro bodybuilder will most likely result in over-training. Take from them their training concepts, philosophies and adapt it to suit your own build and lifestyle by decreasing either the volume or frequency.
Now you’re aware of what’s realistic and you have a good grasp on reality, you’re now ready to achieve a decent amount of muscle in proportion to your frame and you’re ready to get the most out of your body and reach your genetic potential. Building a great physique naturally if tough and requires consistency and hard work, but the results are far more satisfying.
You can’t gain much more than a lb of sold muscle a month, and this probably a generous estimation. Muscle building can be a painstakingly slow process especially for those who are highly trained. Realistically I look to build 1lb of lean muscle per month if muscle-building is my goal. Fortunately, if you are relatively new to training or you have had over 6 months off training or have come off from a long dieting stint, it’s actually possible to build muscle at a much faster rate while burning off body fat at the same time.The only exception may be if you are bulking up straight after a cut and you are carb depleted or you are new to training altogether whereby it is possible to get quick noobie gains. Those are the only exceptions when it might be seen as acceptable to gain more than 4lbs a month. But remember, most of this may just be mainly be muscle water weight from an increase in carbohydrate intake. Even after that though, once your glycogen levels fill up you are looking for 0.5-1lbs of lean muscle a month couple with a lb or two of water weight. Sounds pretty disappointing right? It’s not. Over a year of consistent training this can accumulate to impressive gains. Fast forward a year later and you have packed on 15lbs of weight most of which is lean tissue. You can reassure yourself you have earned it these gains. Naturally built muscle with consistency and hard work gives you a sense of satisfaction and achievement. Hold your head up high and be sure that your muscle’s won’t deflate like a balloon and do not require anything other than what you did to build it for it to be maintained.
To summarise again:
Muscle growth key points
Be aware of how many calories your consuming
Create a 300-600 calorie surplus through diet (approx 20cals/lb body weight)
Eat every 2-4hours
Daily protein intake should be at least 2g/kg of body weight (eg 90kg = 180g protein a day)
Pre/post workout and breakfast are important opportunities to build muscle so make these meals >700cals
Women and men should eat around 400-700 calories in each meal which should include a complete protein with a decent amount of complex carbohydrate
Use a programme that reflects you natural genetic ability
Train progressively heavier each week
Sleep for at least 8 hours each night, you grow when you are not training so learn to relax outside of the gym
Water! being well hydrated means hydrated cells = hydrated muscles = more muscle growth
I hope this information helps and isn’t too overwhelming. Hopefully you can apply these tips and start making some gains!
Nutrition consists of the functional components in food that an organism must obtain in order for it to grow and flourish. Nutrition simply put is a collective term for all of the nutrients required by an organism to sustain life and promote health.
“Nutrition is the intake of food, considered in relation to the body’s dietary needs. Good nutrition – an adequate, well balanced diet combined with regular physical activity – is a cornerstone of good health. Poor nutrition can lead to reduced immunity, increased susceptibility to disease, impaired physical and mental development, and reduced productivity.” – (World Health Organisation)
Nutrients are the organic and inorganic substances found in plant and animals material deemed biologically functional to an organism’s physiological demands. Simply put, nutrients support the functioning of an organism on a cellular level. There are two types of nutrients; Essential nutrients, of which the body cannot biosynthesize (or can but in inadequate amounts) which must be obtained from diet and non-essential nutrients, of which the body can biosynthesize in sufficient quantity.
“Food provides a range of different nutrients. Some nutrients provide energy, while others are essential for growth and maintenance of the body. Carbohydrate, protein and fat are macronutrients that we need to eat in relatively large amounts in the diet as they provide our bodies with energy and also the building blocks for growth and maintenance of a healthy body. Vitamins and minerals are micronutrients which are only needed in small amounts, but are essential to keep us healthy. There are also some food components that are not strictly ‘nutrients’ but are important for health, such as water and fibre.” – (British Nutrition Foundation)
There are six main essential nutrients carbohydrates, fats, protein (the macronutrients), vitamins, minerals (the micronutrients) and water which is also considered an essential nutrient.
Macro-nutrients are generally obtained from the diet in amounts ranging anything from tens of grams to hundreds of grams. For example the protein requirements are based on the “RNI” (Reference Nutrient Intake) and for an average UK adult is 0.75g per kg of body weight, which is 53g for a 70kg adult. Compare this to carbohydrate requirements, based on “DRV’s” (Dietary Reference Values), which are 50% of total energy intake which would be 313g on a 2500 kcal diet.
Micronutrients however, are required in far smaller amounts and are measured in milligrams and micrograms. Intakes are based on the RNI’s and are based. The dietary recommendations for intakes of B12 for example are so small the amount needed would fit on the tip of a pin since only 1.5 micrograms is required.
Non-essential nutrients are nutrients which do not need to be directly obtained via the diet since they are indirectly obtained via substrates and can be synthesised endogenously (within the body). Non-essential nutrients mainly consist of the non-essential amino acids, but also nutrients such as inositol (vitamin B8) and certain minerals are also considered non-essential, although this does not undermine the importance of these nutrients for our health.
Phytochemicals There are of course very important components of foods that do not get official recognition as “essential nutrients” although their exclusion from this category might mislead one to think they’re not as important. They are, and arguably more so when the aim is to optimise health. Phytochemicals are beneficial non-nutritive components of foods such as vegetables, fruits, whole grains, herbs, nuts and seeds. These plant chemicals include phenols, terpenoids, sulfurs compound, pigments and other antioxidants, all of which have shown to promote significant health benefits and may have specific preventative implications for certain disease including cancer and cardiovascular disease.
Is diet enough to obtain all the nutrition we need?
Absolutely. Most people should be able to get all the nutrients they need by eating a healthy, varied diet, including multiple colours and fruit and vegetables. However, there are a few exceptions where supplementation may be wise or even necessary. For example, if a woman is planning to conceive a child it is recommended they take a folic acid (vitamin B9) supplement to prevent congenital birth defects. Unless of course you can consistently consume at least 300 mcg of dietary folate, supplementation is a sensible option. Spina-bifida can occur in Mothers whose B9 intake is insufficient before conception and particularly during the first 12 weeks of pregnancy. Vitamin D is another vitamin in which it is difficult to obtain in sufficient amounts all year round from food and sunlight alone. This is even more the case for vulnerable groups such as pregnant women, the elderly, Muslims who veil the skin, those with dark pigmented skin such as Asians and Africans, children and also Caucasians with fair skin. Current research now supports the idea that most people would benefit from vitamin D supplementation as current intakes and levels of UVB exposure are inadequate, especially for building reserves for winter. Moderate to high dose supplementation may also be a necessary requirement for those or are clinically deficient as to consistently raise serum levels from deficiency status into adequate ranges, which even then could take months.
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