|Year : 2013 | Volume
| Issue : 2 | Page : 86-90
Nutritional risk factors in endocrine diseases
Sukhminder Jit Singh Bajwa1, Esha Sethi2, Randeep Kaur2
1 Department of Anaesthesiology and Intensive Care Medicine, Gian Sagar Medical College, Banur, Patiala, Punjab, India
2 Department of Anaesthesiology and Intensive Care Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India
|Date of Web Publication||6-Jul-2013|
Sukhminder Jit Singh Bajwa
House No-27-A, Ratan Nagar, Tripuri, Patiala, Punjab
Source of Support: Only departmental support, Conflict of Interest: None
Nutrition plays a role of great magnitude in the pathogenesis and progress of endocrine diseases. Traditionally, the nutritional risk factors such as over- and under-nutrition in the context of endocrine diseases have been described alone in their individual capacity. However, the current subject of interest is how these risk factors interact with genetic variations and affect nutritional programming. Also, the role of endocrine disrupter chemicals that are consistently being ingested in routine diet is being evaluated in the causation of current epidemic of endocrine disorders such as diabetes and obesity. The present review aims at highlighting the important nutritional risk factors that have impacts on various endocrine disorders.
Keywords: Adipokines, endocrine disease, endocrine disrupting chemicals, nutrition, obesity
|How to cite this article:|
Bajwa SJ, Sethi E, Kaur R. Nutritional risk factors in endocrine diseases. J Med Nutr Nutraceut 2013;2:86-90
| Introduction|| |
Nutritional care has become an essential part of modern intensive care and clinical practice. Majority of the endocrine diseases can flare up due to nutritional imbalances because functioning of endocrine organs is closely interlinked to the nutritional status. For a long time, it has been known that diet plays an important role in the pathogenesis of important endocrine diseases such as diabetes, obesity, bone, and thyroid disorders and those dietary modifications can influence the progression and evolution of these disease processes. In fact, dietary habits have been shown to program the mechanisms associated with obesity, adiposity, and diabetes during early developmental phase of intrauterine fetal life and infancy itself. ,, However, it is only recently that research has started to uncover the finer nuances behind these gross connections. Animal and human behavioral and molecular and genetic research is in progress to reveal the mechanisms behind linkage of nutrition and endocrine system.  These mechanisms are complex and attempts are underway to unravel these associations so that the nutritional risk factors in development of endocrine diseases can be better defined. Currently, much is known regarding these risk factors, but the means and mechanisms are not completely understood. The present review aims at highlighting the important nutritional risk factors that have possible impact on various endocrine disorders.
The endocrine diseases that are relevant in context of nutrition are those related to obesity, pancreas, thyroid, parathyroid, bone and growth disorders, and reproduction. ,,,, Grossly, over-nutrition is associated with the risk of obesity, diabetes mellitus, and metabolic syndrome. , Diets with excessive iodine or deficient iodine or selenium are associated with an increased risk of goiter, hypothyroidism, autoimmune thyroid disorders, and hyperthyroidism, respectively.  Bone and dental health is dependent upon an adequate intake of calcium, vitamin D, and proteins. Risk of diabetes mellitus type 1 and β cell autoimmunity has also been associated, although weekly, with early life dietary factors.  Reproductive hormone disorders are linked with endocrine disrupter chemicals and increased adiposity.  Currently, prevalence of endocrine disorders related to excess nutrition is on rise. It is a matter of investigation whether apart from food intake any other agents or genomic variations could be at play. However, the major concern for these disorders is related to clinical presentation during endocrine emergencies. Besides taking care of clinical pathology, nutritional status optimization is essential in such patients to avoid unwanted avoidable complications. 
| Is It Just A Matter Of Habit?|| |
Nowadays, obesity can easily be called the mother of all endocrine diseases as it is a cause and manifestation in almost all important endocrine disorders such as diabetes, insulin resistance, metabolic syndrome, and thyroid problems.  It is also a well-known risk factor for cardiovascular diseases. Countries world over are trying to fight this pandemic. Malnutrition in the form of over-nutrition coupled with lack of physical activity has led to an alarming increase in the prevalence of obesity. This epidemic has greatly influenced how we practice our daily clinical work and has mandated a radical change in our approach toward handling such patients during medical, surgical, and anesthetic care. , However, the matter cannot be simplified in terms of eating habits and preferences and a lot is desired to stop the progress of this ever-increasing epidemic of modern times.
Lack of time in today's urbanized society has led to an increased adoption of pre-packaged processed foods that usually have a high content of sugar, salt and trans fats, decreased roughage, and fiber content. Typical western diet has canned food, refined flour, sugar, frozen or preserved meats, and sweetened carbonated drinks. Ample evidence exists to prove that diets rich in these substances are inclined to make individuals gain unhealthy non-muscle mass weight and encourage atherosclerosis and are associated with an increased risk of diabetes, metabolic syndrome, and cardiovascular diseases.  On the contrary, paleolithic diet comprising of raw vegetables and fruits, seeds, moderate grains, and minimally refined and cooked foods has been found to help reduce adiposity, blood glucose levels, hyperlipidemia, and insulin resistance. ,
However, inter-individual differences do exist in the endocrine disease frequency and body mass composition among people having same cultural diet. Therefore, there must be some factors at the genetic level that control aspects such as appetite, metabolic rate, and insulin sensitivity. Recent genome wide association studies have identified transcription factor TCF7L2 variants to have highest risk of type 2 diabetes. Such genome wide associations have been identified in individuals that make them susceptible to develop type 2 diabetes and are further regulated by nutritional factors like high-fat feeding and ambient glucose levels in islet cells. ,
| Nutritional Risk Factors and Endocrine Diseases In Adults|| |
Malnutrition refers to a deviation from what can be considered an optimum nutrition intake according to the gender, age, and weight. All components of diet such as carbohydrates, fats, proteins, and vitamins impact upon the functioning of endocrine system of the body. In simple terms, it is understood that excess nutrition leads to obesity. Excess nutrition in this context translates to excess calories. However, there are aspects of diet other than calories that may very well put an individual at an increased risk of being obese, insulin resistant, or diabetic.
Correlation of body weight to risk of endocrine diseases can be seen across all age groups. While, on one hand, macrosomic infants have a higher risk of developing type 2 diabetes mellitus in later life, aging is again associated with a decreased β cell function and insulin sensitivity and increased glucagon production from pancreatic α cells. ,, Weight loss achieved with a combined approach of calorie restriction and physical activity was shown to improve both α and β cell function of the pancreas in older obese adults within 6 months, possibly by decreased β cell glucotoxic and lipotoxic effects of ambient blood glucose, and free fatty acids, respectively.  Also, presence of nutritional risk factors, over as well as under-nutrition, was found to pose an increased risk for metabolic syndrome in the elderly. 
As with other chronic or critical illnesses, nutritional status also correlates with prognosis in complications of endocrine diseases such as diabetic foot ulcers. In fact, nutritional management in such patients becomes very complex as blood glucose targets are aimed to aid in ulcer healing, while maintaining protein intake at the same time.  Similarly, complications of diabetic ketoacidosis, mainly hypokalemia and hypoglycemia, were more severe in malnourished children. 
| Impact of Endocrine Disrupting Chemicals on Hormonal Homeostasis|| |
Surplus calories causing endocrine diseases are just one part of the story. An increasingly identified group of chemicals can very well be the hidden culprit in this game. Getting an exposure to endocrine disrupting chemicals (EDCs) is inevitable so far as current average diet is concerned. EDCs encompass a wide range of chemicals ranging from pesticides and related compounds, synthetic solvents, and plastics.  Even if all ingredients in a diet are "organic," EDCs cannot be ruled out from it with certainty. Also, the materials in which food and water are packaged, stored, and dispensed are likely to contain these chemicals.  Grossly, these disrupt our endocrine system by mimicking the natural hormones. At molecular level, how these EDCs then affect our endocrine system and metabolism is a subject being actively pursued.  It is by now clear that exposure to these chemicals during early development stages can cause reproductive endocrine and metabolic disorders by interfering with and disturbing the hormonal milieu of the body. 
Most important mode of exposure seems to be ingestion through food. Importantly, in utero exposure to these chemicals disrupts endocrine regulation and increases the risk of obesity. Proven EDCs implicated in this mechanism are diethylstilbestrol, tributyltin, polychlorinated biphenyls, perfluoro octanoic acid, and hexachlorobenzene. Compounds being researched as potential obesogens are dioxin and non-dioxin like compounds, organochloride pesticides, brominated flame retardants, phthalates, and perflourinated alkyl acids.  Apart from obesity and diabetes, these endocrine disrupters can disturb actions of all hormones, namely, sex hormones, glucocorticoids, and thyroid hormones. EDCs cause endocrine disruption in hypothalamic-pituitary axis, pancreas, thyroid, and reproductive organs. They either act through hormone receptors or may act via other numerous mechanisms. Most important and widespread of these chemicals is bisphenol A (BPA).  Studies have generated so much interest in the public health impact of this compound that most manufacturers of baby products now market their products as "BPA free." It is manufactured in large amounts and utilized for making plastic containers. It is detectable in urine of majority of people and researchers have found an association between urinary BPA levels and obesity as well as diabetes mellitus independent of other confounding risk factors for diabetes.  There needs to be a reduced exposure to such chemicals for which spreading awareness and legal measures are required.
| Nutritional Programming|| |
Imbalance between physical activity and excess calorie intake in adults causes obesity. However, different individuals respond differently to diet and its modification so far as endocrine diseases are concerned. Human and animal model studies have revealed that changes in the early environment, that is, pregnancy and/or lactation can bring about permanent changes in the cellular and metabolic functions. Then again, animal models have repeatedly revealed an association between maternal over as well as underfeeding to insulin resistance, diabetes, and cardiovascular diseases in the later life.  The concept of nutritional programming wherein variations in maternal nutrition bring about permanent changes in the fetus seems to implicate nutritional risk factors in the development of endocrine diseases. Animal subjects such as rodents and sheep have been introduced to under or overfeeding in utero in various studies. , Nonetheless, the results have been contradictory and controversial and are still being investigated further so far as application to human subjects is concerned.
To be more precise, it is worth knowing and understanding how this nutrition intake affects only some people and not all. Also, how environmental factors such as type and amount of nutrition and epigenetics modify the expression of genes implicated in causation of obesity and related endocrine diseases. ,,, Once these mechanisms are elucidated, the next step is development of novel strategies and therapeutic interventions to target such markers.
| Role of Adipokines|| |
Adinopectin and leptin are two prototypical adipocyte-derived hormones whose expression is linked to and regulates the nutritional standing and, in turn, the endocrine machinery.  Over-nutrition as a consequence of overfeeding as well as decreased energy outflow resulting from decreased physical activity combines to produce increased adipocyte tissue content. A level of adiponectin that is primarily expressed in adipocytes is inversely related to hepatic glucose production, insulin resistance, serum fatty acid, and triglyceride levels. 
Leptin is currently the focus of many studies that are trying to elucidate its neuroendocrine, immunomodulator, and proinflammatory function.  Rodrigues et al., were able to show that early over-nutrition in rats can affect hypothalamo-pituitary-thyroid axis through leptin signaling pathway.  This over-nutrition in the postnatal phase can have important implications on the development of endocrine diseases in later life. Also, high levels of leptin are present in obese individuals.  Through a myriad of central and peripheral effects, it determines our feeding behavior and energy balance.  Apart from adiponectin and leptin, other hormones and hormone-like substances are being identified that act in consonance with the external environmental and dietary factors and regulate functioning of the endocrine system.
| Conclusion|| |
No matter what the future research may discover at the molecular and genetic level, presently, the biggest threat to the endocrine health of humans is obesity. In majority of cases, obesity is nutritionally linked to over-nutrition. Such challenges have to be faced daily in routine clinical practice and are expected to grow only in future.
The second threat could be endocrine disrupter chemicals to which we are exposed daily and which we ingest daily with sources of nutrition. To what extent and how they affect on the normal endocrine functioning is not yet known. When their effects and mechanisms of action are better characterized, this knowledge could be utilized so far as pharmacotherapy and preventative medicine for the endocrine system is concerned. Till then, the mantra or the recommendation is to watch what we eat or, in other words, practice mindful eating and eat to live, and not the other way around.
| References|| |
|1.||Bajwa SS, Kulshrestha A. Critical nutritional aspects in intensive care patients. J Med Nutr Nutraceut 2012;1:9-16. |
|2.||Tarry-Adkins JL, Ozanne SE. Mechanisms of early life programming: Current knowledge and future directions. Am J Clin Nutr 2011;94 (6 Suppl):1765-71S. |
|3.||Fall CH. Evidence for the intra-uterine programming of adiposity in later life. Ann Hum Biol 2011;38:410-28. |
|4.||de Moura EG, Passos MC. Neonatal programming of body weight regulation and energetic metabolism. Biosci Rep 2005;25:251-69. |
|5.||Legler J, Hamers T, van Eck van der Sluijs-van de Bor M, Schoeters G, van der Ven L, Eggesbo M, et al. The OBELIX project: Early life exposure to endocrine disruptors and obesity. Am J Clin Nutr 2011;94 (6 Suppl):1933-8S. |
|6.||Bajwa SS, Sehgal V. Anesthesia and thyroid surgery: The never ending challenges. Indian J Endocr Metab 2013;17:228-34. |
|7.||Bajwa SS, Sehgal V. Anesthetic management of primary hyperparathyroidism: A role rarely noticed and appreciated so far. Indian J Endocr Metab 2013;17:235-9. |
|8.||Bajwa SJ, Sehgal V, Bajwa SK. Clinical and critical care concerns in severely ill obese patient. Indian J Endocrinol Metab 2012;16:740-8. |
|9.||Bajwa SJ, Kalra S. Diabeto-anaesthesia: A subspecialty needing endocrine introspection. Indian J Anaesth 2012;56:513-7. |
|10.||Hari Kumar K, Baruah MM. Nutritional endocrine disorders. J Med Nutraceut 2012;1:5-8. |
|11.||Virtanen SM, Knip M. Nutritional risk predictors of beta cell autoimmunity and type 1 diabetes at a young age. Am J Clin Nutr 2003;78:1053-67. |
|12.||Schug TT, Janesick A, Blumberg B, Heindel JJ. Endocrine disrupting chemicals and disease susceptibility. J Steroid Biochem Mol Biol 2011;127:204-15. |
|13.||Bajwa SJ, Jindal R. Endocrine emergencies in critically ill patients: Challenges in diagnosis and management. Indian J Endocrinol Metab 2012;16:722-7. |
|14.||Fung TT, Schulze M, Manson JE, Willett WC, Hu FB. Dietary patterns, meat intake, and the risk of type 2 diabetes in women. Arch Intern Med 2004;164:2235-40. |
|15.||Qi L, Cornelis MC, Zhang C, van Dam RM, Hu FB. Genetic predisposition, Western dietary pattern, and the risk of type 2 diabetes in men. Am J Clin Nutr 2009;89:1453-8. |
|16.||Jönsson T, Olsson S, Ahrén B, Bøg-Hansen TC, Dole A, Lindeberg S. Agrarian diet and diseases of affluence-do evolutionary novel dietary lectins cause leptin resistance? BMC Endocr Disord 2005;5:10. |
|17.||Ho MM, Yoganathan P, Chu KY, Karunakaran S, Johnson JD, Clee SM. Diabetes genes identified by genome-wide association studies are regulated in mice by nutritional factors in metabolically relevant tissues and glucose concentrations in islets. BMC Genet 2013;14:10. |
|18.||Yamakawa-Kobayashi K, Natsume M, Aoki S, Nakano S, Inamori T, Kasezawa N, et al. The combined effect of the T2DM susceptibility genes is an important risk factor for T2DM in non-obese Japanese: A population based case-control study. BMC Med Genet 2012;13:11. |
|19.||Hermann GM, Dallas LM, Haskell SE, Roghair RD. Neonatal macrosomia is an independent risk factor for adult metabolic syndrome. Neonatology 2010;98:238-44. |
|20.||Monasta L, Batty GD, Cattaneo A, Lutje V, Ronfani L, Van Lenthe FJ, et al. Early-life determinants of overweight and obesity: A review of systematic reviews. Obes Rev 2010;11:695-708. |
|21.||Villareal DT, Banks MR, Patterson BW, Polonsky KS, Klein S. Weight loss therapy improves pancreatic endocrine function in obese older adults. Obesity (Silver Spring) 2008;16:1349-54. |
|22.||Kim HJ, Lee KS, Eom JS, Lim KY, Lee KW, Hong CH. Relation between nutritional risk and metabolic syndrome in the elderly. Arch Gerontol Geriatr 2011;52:e19-22. |
|23.||Zhang SS, Tang ZY, Fang P, Qian HJ, Xu L, Ning G. Nutritional status deteriorates as the severity of diabetic foot ulcers increases and independently associates with prognosis. Exp Ther Med 2013;5:215-22. |
|24.||Moulik NR, Jayashree M, Singhi S, Bhalla AK, Attri S. Nutritional status and complications in children with diabetic ketoacidosis. Pediatr Crit Care Med 2012;13:e227-33. |
|25.||Shankar A, Teppala S. Relationship between urinary bisphenol a levels and diabetes mellitus. J Clin Endocrinol Metab 2011;96:3822-6. |
|26.||Vom Saal FS, Nagel SC, Coe BL, Angle BM, Taylor JA. The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity. Mol Cell Endocrinol 2012;354:74-84. |
|27.||Choi J, Li C, McDonald TJ, Comuzzie A, Mattern V, Nathanielsz PW. Emergence of insulin resistance in juvenile baboon offspring of mothers exposed to moderate maternal nutrient reduction. Am J Physiol Regul Integr Comp Physiol 2011;301:R757-62. |
|28.||Poore KR, Boullin JP, Cleal JK, Newman JP, Noakes DE, Hanson MA, et al. Sex- and age-specific effects of nutrition in early gestation and early postnatal life on hypothalamo-pituitary-adrenal axis and sympathoadrenal function in adult sheep. J Physiol 2010;588:2219-37. |
|29.||Rodrigues AL, de Moura EG, Passos MC, Dutra SC, Lisboa PC. Postnatal early overnutrition changes the leptin signalling pathway in the hypothalamic-pituitary-thyroid axis of young and adult rats. J Physiol 2009;587:2647-61. |
|30.||Langley-Evans SC. Nutritional programming of disease: Unravelling the mechanism J. Anat 2009;215:36-51. |
|31.||Milagro FI, Mansego ML, De Miguel C, Martínez JA. Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives. Mol Aspects Med 2012. |
|32.||Gonzalez-Castejon M, Rodriguez-Casado A. Dietary phytochemicals and their potential effects on obesity: A review. Pharmacol Res 2011;64:438-55. |
|33.||Agostoni C, Baselli L, Mazzoni MB. Early nutrition patterns and diseases of adulthood: A plausible link? Eur J Intern Med 2013;24:5-10. |
|34.||Harwood HJ Jr. The adipocyte as an endocrine organ in the regulation of metabolic homeostasis. Neuropharmacology 2012;63:57-75. |
|35.||Otero M, Lago R, Gomez R, Dieguez C, Lago F, Gomez-Reino J, et al. Towards a pro-inflammatory and immunomodulatory emerging role of leptin. Rheumatology (Oxford) 2006;45:944-50. |
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