Changes

===== ''Medadhatu'' =====

===== ''Medadhatu'' =====

''Meda'' vitiation is common and dominant ''dushya'' in the pathogenesis of ''madhumeha''. ''Kapha'' and ''meda'' both have close resemblance in regard to functions as well as in regard to qualitative parameters. Both get vitiated more or less by same etiological factors. In ''madhumeha'' vitiation of ''meda'' results by two ways:

''Meda'' vitiation is common and dominant ''dushya'' in the pathogenesis of ''madhumeha''. ''Kapha'' and ''meda'' both have close resemblance in regard to functions as well as in regard to qualitative parameters. Both get vitiated more or less by same etiological factors. In ''madhumeha'' vitiation of ''meda'' results by two ways:<ref> sourced from http://www.slideshare.net/ayurmitra/madhumeha-kc041-gdg </ref>

#Qualitative: ''Abaddha'' (loose): The normal function of ''meda'' is to produce unctousness in the body along with ''drudhatva'' (compactness). This ''abadhatva'' (looseness) causes derangement in the structure of ''meda'' producing ''shaithilya'' (flabbiness) in the body this can be well correlated with FFA excess.

#Qualitative: ''Abaddha'' (loose): The normal function of ''meda'' is to produce unctousness in the body along with ''drudhatva'' (compactness). This ''abadhatva'' (looseness) causes derangement in the structure of ''meda'' producing ''shaithilya'' (flabbiness) in the body this can be well correlated with FFA excess.<ref> sourced from http://www.slideshare.net/ayurmitra/madhumeha-kc041-gdg </ref>

#Quantitative: ''Bahu''(excess): Here in the pathogenesis, ''meda'' is in excess quantity. This ''medadhatu'' is ''aparipakva'' (immature). It obstructs the path of ''vayu'' along with ''kapha''. This provoked ''vata'' increases the ''agni'', so patient eats more and more food causing excessive deposition of ''aparipakva meda''. This in turns causes severe depletion of the other ''dhatus'' and produces various sign and symptoms.  

#Quantitative: ''Bahu''(excess): Here in the pathogenesis, ''meda'' is in excess quantity. This ''medadhatu'' is ''aparipakva'' (immature). It obstructs the path of ''vayu'' along with ''kapha''. This provoked ''vata'' increases the ''agni'', so patient eats more and more food causing excessive deposition of ''aparipakva meda''. This in turns causes severe depletion of the other ''dhatus'' and produces various sign and symptoms.  

===== ''Mamsadhatu'' =====

===== ''Mamsadhatu'' =====

It is one of the main ''dushyas'' (vitiating factors) described by Charaka in regards to ''prameha''. He narrated it especially in ''kaphaja prameha'' and ''avaranjanya madhumeha''. ''Mamsa'' and ''Kapha'' possess similar qualities and both give strength to the body. When vitiated, ''mamsa'' loses its normal consistency and develops ''shaithilya'' and provide space in between for the accumulation of morbid matter. That in turn results in ''putimamsa pidika'' (Ca.Ni. 4/8). ''Mamsa dushti'' can be compared to deranged protein metabolism which is an integral part of diabetes mellitus. Research studies have found that glucocorticoid activities and acidosis stimulates protein and amino acid catabolism . Amino acids breakdown in liver results in increased production of urea and these free amino acids can be compared with ''abaddha mamsa''. ''Putimamsa'' and ''pidaka'' are the morbid states of ''mamsa dhatu''. Two major changes take place in ''mamsa dhatu'' - protein degradation and reduction in its blood supply, both of which along with elevated blood sugar level form a favorable media for the growth and multiplication of microorganisms. The results are putrefaction and evolution of multiple septic foci in ''mamsa dhatu''. Diminished protein synthesis hampers the healing process and these complications adopt chronic course.

It is one of the main ''dushyas'' (vitiating factors) described by Charaka in regards to ''prameha''. He narrated it especially in ''kaphaja prameha'' and ''avaranjanya madhumeha''. ''Mamsa'' and ''Kapha'' possess similar qualities and both give strength to the body. When vitiated, ''mamsa'' loses its normal consistency and develops ''shaithilya'' and provide space in between for the accumulation of morbid matter. That in turn results in ''putimamsa pidika'' (Ca.Ni. 4/8). ''Mamsa dushti'' can be compared to deranged protein metabolism which is an integral part of diabetes mellitus. Research studies have found that glucocorticoid activities and acidosis stimulates protein and amino acid catabolism <ref> May, RC et al. 1996. Glucocorticoids and acidosis stimulate protein and amino acid catabolism in vivo. Kidney Int. 1996 Mar;49(3):679-83. </ref>. Amino acids breakdown in liver results in increased production of urea<ref> Vaudevan et al. 2011. Textbook of biochemistry for medical students, Sixth Edition, JP Medical Publishers </ref> and these free amino acids can be compared with ''abaddha mamsa''. ''Putimamsa'' and ''pidaka'' are the morbid states of ''mamsa dhatu''. Two major changes take place in ''mamsa dhatu'' - protein degradation and reduction in its blood supply, both of which along with elevated blood sugar level form a favorable media for the growth and multiplication of microorganisms. The results are putrefaction and evolution of multiple septic foci in ''mamsa dhatu''. Diminished protein synthesis hampers the healing process and these complications adopt chronic course.

===== ''Majjadhatu'' =====

===== ''Majjadhatu'' =====

===== Exclusion of ''asthi'' as a ''dushya'' =====

===== Exclusion of ''asthi'' as a ''dushya'' =====

Among the ten ''dushyas'' of ''prameha, asthi'' (bone) is not included. According to modern physiology, bone is a tissue that undergoes frequent remodeling and has a large capacity for regeneration. In the adult remodeling occurs so that the skeleton is replaced approximately every 10–11 yr. This physiological remodeling is initiated by osteoclasts that re-absorb bone and is followed by the formation of an equivalent amount of new bone by osteoblasts, bone loss is noted when the amount of bone resorption exceeds the amount of new bone formation.  

Among the ten ''dushyas'' of ''prameha, asthi'' (bone) is not included. According to modern physiology, bone is a tissue that undergoes frequent remodeling and has a large capacity for regeneration. In the adult remodeling occurs so that the skeleton is replaced approximately every 10–11 yr. This physiological remodeling is initiated by osteoclasts that re-absorb bone and is followed by the formation of an equivalent amount of new bone by osteoblasts,<ref> Parfitt A. 1982 The coupling of bone formation to bone resorption: a critical analysis of the concept and of its relevance to the pathogenesis of osteoporosis. Metab Bone Dis Relat Res 4:1–6. </ref>  <ref> Mundy G 1989 Local factors in bone remodeling. Rec Prog Horm Res 45:507–531. </ref> bone loss is noted when the amount of bone resorption exceeds the amount of new bone formation.  

Diabetes has also been associated with a net loss of bone. A number of studies have reported that type 1 diabetes alters bone remodeling by reducing the formation of new bone, leading to osteopenia. This has been shown by a decrease in bone mineral density in humans and alterations in the formation of new bone in animal studies. In contrast, the presence of bone loss in type 2 diabetes is less clear, and current understanding suggests that this form of diabetes is not typically associated with osteopenia. The reasons for the lower bone mineral density in type 1 diabetes are not known.

Diabetes has also been associated with a net loss of bone. A number of studies have reported that type 1 diabetes alters bone remodeling by reducing the formation of new bone, leading to osteopenia. This has been shown by a decrease in bone mineral density in humans and alterations in the formation of new bone in animal studies<ref> Hayward M, Fiedler-Nagy C 1987 Mechanisms of bone loss: rheumatoid arthritis, periodontal disease and osteoporosis. 22:251–254. </ref>  <ref> Tuominen J, Impivaara O, Puukka P, Ronnenmaa T 1999 Bone mineral density in patients with type 1 and type 2 diabetes. Diabetes Care 22:1196–1200. </ref>  <ref> Krakauer J, McKenna M, Burderer N, Rao D, Whitehouse F, Parfitt A 1995 Bone loss and bone turnover in diabetes. Diabetes 44:775–782. </ref>  <ref> Macey L, Kana SM, Jingushi S, Terek RM, Borretos J, Bolander ME 1989 Defects of early fracture-healing in experimental diabetes. J Bone Joint Surg Am 71:722–733. </ref>. In contrast, the presence of bone loss in type 2 diabetes is less clear, and current understanding suggests that this form of diabetes is not typically associated with osteopenia<ref> Gebauer G, Lin S, Beam H, Vieira P, Parsons J 2002 Low-intensity pulsed ultrasound increases the fracture callus strength in diabetic BB Wistar rats but does not affect cellular proliferation. J Orthop Res 20:587–592. </ref>  <ref> Barrett-Conner E, Holbrook T 1992 Sex differences in osteoporosis in older adults with non-insulin-dependent diabetes mellitus. JAMA 268:3333–3337. </ref>  <ref> Loe H 1993 Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care 16:329–334. </ref>  <ref> Nelson R, Shlossman M, Budding L, Pettitt DJ, Saad MF, Genco RJ, Knowler WC1990 Periodontal disease and NIDDM in Pima Indians. Diabetes Care 13:836–840. </ref>. The reasons for the lower bone mineral density in type 1 diabetes are not known.

==== ''Vataja prameha'' as type 1 diabetes mellitus ====

==== ''Vataja prameha'' as type 1 diabetes mellitus ====