Human is exposed to a huge number of environmental influences that have effects on epigenetic mechanisms. Epigenetics is a field in biology that focuses on inherited changes in the gene expression caused by mechanisms other than changes in the DNA sequence. Environmental epigenetics describes how environmental factors affect cellular epigenetics and, hence, the human health. A foundational goal for the people is to improve their health, which typically includes positive changes in lifestyle and especially diet. The aim of this work is to explain the fundamentals of epigenetics, the relationship the environmental factor and the medical care aspects of epigenetics with a focus on human systems, environmental epigenetics and explains the effects of diet and environmental epigenetics on human health and disease. Epigenetics explains how environmental exposures can modify gene expression and influence cell properties. Epigenetic change is a regular and natural occurrence but can be influenced by several factors such as human age, parenting, the environment, diseases and disorders, drugs and addiction, lifestyle, diet (Here, it focus on the possible epigenetic connections between improving health and consuming foods) and sport exercise. How the same genotype can give rise to different phenotypes under different environmental conditions. The initiation in a research project in the field of epigenetics explains the influence of environmental factors on the properties of cells and gene expression. Identification of the fundamental epigenetic modifications and markers help to recognize the health disorders at earlier stages of the diseases, improving treatment outcomes and quality of life for many people. Extensive research in this field would do a great deal to protect public health, both now and in future generations. More researches are required from scientific and medical community to view human health and the pathogenesis of disease, inspiring a new generation of technologies and innovations with the potential to revolutionize diagnostics and therapeutics.

X-linked adrenoleukodystrophy (X-ALD) is a devastating genetic disease with three main phenotypes (childhood cerebral forms, adrenomyeloneuropathy(AMN) and Addison disease(AD). Tuberculosis is the commonest cause of AD in underdeveloped countries whereas autoimmune destruction accounts for 75-80% cases in developed countries. This is the first case report of X-AMN/ALD in two brothers in Bangladesh confirmed by raised very long chain fatty acid (VLCFA). Our index patient of 19 years presented with anorexia, weakness, vomiting, weight loss for three years with increased pigmentation in perioral skin, lips, tongue, mucus membrane, palmar creases, knuckles, reduced scalp hair(figure-1a-d), postural hypotension, low BMI, was found to have low basal Cortisol (9.00 am),  ACTH >1250  pg/ml (normal<46), was diagnosed with AD. After three months he developed progressive spastic paraparesis along with cognitive declination and behavioral abnormality. His only brother was normotensive, clinically asymptomatic at presentation had only increased pigmentation on tongue, palmar crease, scanty scalp hair(figure-1,2a-d) and extensor planter reflexes. He had high ACTH(>1250 pg/ml) with normal basal cortisol (9.00am). Plasma VLCFA analysis revealed significantly high C26:0 with abnormal ratio of C24:0/C22:0 and C26:0/C22:0 in both brothers, with normal level in mother(table-1). MRI (T2 & FLAIR) showed bilateral hyperintense basal ganglia in index patient(Figure2:3a-c). Electrophysiological studies of nerve (SEPs, VEPs, BAEPs, NCS, EMG) were normal in both. Both were given steroid replacement. After three years, index patient became bed bound with slurred speech, urinary urge incontinence and his asymptomatic brother developed spastic paraparesis with cognitive impairment. None had gonadal impairment. Follow up MRI revealed lesion in brainstem in both along with atrophy of thoracic segment of spinal cord in index patient(Figure2:4a-f) and cerebellum, internal capsule involvement in his brother(Figure3:5a-d). Both were of pure AMN variety but due to presence of cognitive impairment and behavioral abnormality they can be categorized as rare cerebral variety of AMN