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Ayurvedic Terminology and Its Corresponding Modern Terminology WSR to ARISTA VIDNYANA


Ayurvedic and Modern Terminology with special reference to arista vidnyan

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Manovaha srotas – A Clinical Approach


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The prevalence of psychiatric disorder in the community is of such magnitude that every doctor must be able to carryout psychiatric assessment. The range of presenting problems in patients with psychiatric disorders is wide. Many patients with emotional disturbance may present, not with overt psychiatric symptoms, but with more respectable physical symptoms. In some patients physical and psychiatric illness may co-exist. There may be a direct causal relationship between the two, as in the Unmada rogi who have Arochaka getting Panduroga. On the other hand, physical & psychiatric illness may be unrelated, as in the patient of Apasmara in whom Madhumeha may also co-exist. In addition, every patient’s reaction to his illness will be influenced by his emotional state and this will itself affect the cause of the illness. Therefore the necessity to know the psychosomatic condition increases when we start to understand the underlying pathogenesis of all psychosomatic diseases which are the individual reaction and variable perception depending upon the Satva bala and that also give and the special attention to understand psychic constitution which are sixteen in number, seven of satvika, six of Rajas and three of tamasa prakriti.

For the understanding of the somatic diseases as the knowledge of sharira is essential, the Mano-vichaya is required to know the manasaroga.

However, Manas is Atindriya and it’s action is either observable or inferable. Manas which is a non-material component of the body is composed of three substance specific mixture which are Satva, Rajas and Tamas. They are triguna or parama padarthas. They have the characteristic of being promotive for knowledge and thinking, rational thinking and permission for allowing the existance of opposite qualities. The dominance of Satva makes one of intelligently active and not ruling over others by any means. The dominance of Rajas is notable when one has tendency to supercede others by all means and more maneuvering for achieving desired. The dominance of Tamas causes least efforts and curiosity but prefers to be in stage of unawareness and effortlessness. Not to bother of ignorance and not to make any efforts is the characteristic of Tamas.

Curiosity, efforts to satisfy the curiosity and-detachment are three features or every living being. This is due to qualities of Satva, Rajas and Tamas, herited by that individual. There should be efforts to understand the dominance of one triguna. The expression of disease will be modified according to dominance, i.e. Guru Vyadhita and Laghuvyadhita of Pravara and Avara Satva respectively. Therefore, the recognition of existance and dominance of anyone of omni-substance is essential and it is possible to note the behavioural and psychological manifestations for the evaluation of manas-roga and dominance of specific guna/dosha.

BEHAVIOURAL AND PSYCHOLOGICAL MANIFESTATION OF TRIGUNA:

SATVAEnlightening,

Efforts for more

knowledge,

Cleanliness,

Theism, Appreciates

existence of Almighty,

Straight forward dealing

Gratitudeous, Polite,

Prompt to learn, Serious,

Of good memory, intellect,

Welfare wisher.

 

RAJASPropulsive &

dynamic,

Over expression

of pain & pleasure,

Effort-some

Industrious, Egoistic,

Angry, Reacting,

Pretender

Jealous, Brave

Tense, Cruel,

Greedy.

 

TAMASInhibitive

Ignorant

Excessive

fatigue

of sense organs,

Atheism, more sleep

Inactive, Poor,

worrying, Commits

Mistakes, unhygienic.

 

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manovaha srotas

A Comprehensive Guide to Ayurvedic Case Recording


A Comprehensive Guide to Ayurvedic Case Recording – Is a detailed case paper format dealing with wide aspects of ayurvedic diagnosis. Collection of references and parameters to guide clinician and students to reach at there conclusion about the underlying pathology.

As an Ayurveda physician, an authentic and reliable algorithm in management of disease condition is built upon the detail patients history obtained through a standard procedure.

Ayurvedic case recording.PDF

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Prof. Dr. S. N. Ojha

An Experimental study of Macroangiopathy, a common complication of Diabetes Mellitus, with Ayurveda perspective


An Experimental study of Macroangiopathy, a common complication of Diabetes Mellitus, with Ayurveda perspective

Prof. Ojha S. N.

M.D.(Ayu.) Ph.D.
Principal
Dr. D.Y Patil college of ayurved and research centre Pimpri pune 18
.

►  The prevalence of macroangiopathy is increased in Diabetes Mellitus.

►  Endothelial cell injury is thought to be an early event leading to atherosclerosis which may be initiated by several factors including molecular, receptorial and cellular factors provide a continuous mechanism of vascular damage.

►  Dhamanipratichaya (Atherosclerosis), Kaphaja nanatmaja vikar, is responsible for diabetic angiopathy and in turn cardiovascular complications like IHD or vatika hridroga

RISK FACTORS

Madhumeha (Diabetes Mellitus)

Atimedaswita (Obesity)

Grathita rakta (Thrombosis)

Atibhaya Shokadi (Stress)

Samameda (Dyslipidaemia)

Vyan vata (Receptorial factor)

Insulin resistance

Physical inactivity

Dhumpan (Smoking)

Hypertension

Dhamani or srotodushti (Endothelial wall injury)

Samanavrita apan

INTRODUCTION

►The study of a simple experimental model of  myocardial injury in animals was considered of value.

►Myocardial necrosis can be induced in experimental animals by various means.

►As the rabbits have a coronary arterial pattern akin to human, it was felt worthwhile to test the feasibility of producing myocardial ischaemia in them by slow iv administration of isoprenaline and simultaneously recording ECG events.

OBJECTIVE

►To evaluate the curative effect of Parawata-Shakrit in induced myocardial ischaemia in rabbits before the use of drug in man.

MATERIAL & METHODS

Test article          – Fecal matter of Pigeon

Characteristic      – Yellowish brown  powder

Test system         – Rabbit

Strain                   – Albino

Body weight range                – 1 to 1.5 kg.

Number of animals                – Per group – 6

Total number of group         – 3

STUDY DESIGN

►Albino rabbits of either sex weighing 1 to 1.5 kg. were divided into 3 groups

►Each group consists of six rabbits

►All 18 rabbits sedated by diazepam, I.V.

2 mg/Kg.

Group  I :- Control group

Rabbits of this group were infused by isoprenaline (2mg/kg) dissolved in 25ml of normal saline through marginal ear vein at rate of 4 drops per minute for a period of 2 hrs. for two consecutive days under diazepam (I.V. 2mg/kg) sedation.

Group II :- Treatment group

Animals of this group were treated with Parawata – Shakrit powder suspension (1gm/kg P.O.) at 3 hrs. and 12 hrs. after the completion of second dose of isoprenaline infusion on second day.

Group III :- Treatment group

Animals were treated with Parawata-Shakrit powder suspension (1gm/kg P.O.) at 24 hrs. and 36 hrs. after the completion of second dose of isoprenaline infusion on second day

Parameter

►The blood was collected from each animal for testing of AST, Sugar, Cholesterol and Clotting time.

►The twelve leads ECG was recorded in each animals on day-0, day-1, day-2, day-3, day-4 and day-5, ECG of day-0 was taken as normal ECG, on day-1 & day-2 ECG was taken immediate after completion of isoprenaline infusion.

►Animals were observed for clinical features related to overstimulation of sympathetic nervous system, viz heart rate, breathlessness, discomfort, foaming, lacrimation urination and defecation.

►On fifth day of isoprenaline infusion the animals belonging to each group were sacrified. Heart was dissected and preserved in 10% formal dehyde solution. The biopsy of heart was carried out to study gross and microscopic pathological changes.

Day-0 ECG

Gr-I Day-2  ECG

Gr – I  Day – 4  ECG

Gr – I  Day – 5 ECG

Gr – II  Day – 2 ECG

Gr – II  Day – 3 ECG

Gr – II  Day – 4 ECG


Gr – II  Day – 5 ECG

Gr – III  Day – 2 ECG

Gr – III  Day – 3 ECG

Gr – III  Day – 4 ECG

Gr – III  Day – 5 ECG

Discussion and Conclusion

►The characteristic features of distress and shock following the isoprenaline infusion was observed in rabbits in this study, were similar to clinical features seen in AMI in human.

►Dwivedi et al (1987) have also reported a quick onset of such reactions due to iv administration of isoprenaline in rabbits.

►Trolese Mongheal et al (1977) have also reported marked cardioaccelaration within 30 seconds of the infusion of isoprenaline in dogs.

►In this study iv infusion of isoprenaline at dose of 2mg/kg to rabbits resulted in progressive and pronounced abnormalities in ECG recording.

►The presence of deep and widened Q-wave, ST segment elevation or depression & T-wave inversion were present in ECG of rabbits following the isoprenaline infusion.

►Tachycardia was also noted in all ECG

►Increase in SGOT level which reflects the severity of myocardial damage.

 

►In group II, treated with Parawata Shakrit (1gm/kg orally) following the second dose of isoprenaline infusion at 3 hrs. & 12 hrs., significant beneficials effects were observed on ECG findings

►ECG of day 3, 4 & 5 revealed small Q wave, normal ST segment and T-wave.

►In one animal T-wave inversion was persisting up to day 5, but ST segment was normal.

►Microscopic study also revealed the less severity of myocardial ischaemia in comparison with control group.

►In groups-III, the animals were treated with Parawata-Shakrita (1gm/kg P.O.), following the second dose of isoprenaline infusion at 24 hrs. and 36 hrs. showed good response in reduction of induced myocardial ischaemia.

►ECG finding of day 4 & day 5 revealed almost normal findings.

►There was normal ST segment & microscopic study, indicates the reduction in myocardial ischaemia as compared to control group

 

►The effects of drug in reducing the Myocardial ischaemia is less in group III than group II, but reduction was significant.

►As per comparative study with other available thrombolytic drugs, as mentioned in text, this drug was observed effective even after 24 hrs. of onset of myocardial ischaemia.

►Ischaemia occurs due to increased demand of oxygen & decreased supply, it is observed (Haft J I 1972) that catecholamine may produce the intravascular platelet aggregation & subsequently thrombus formation Parawata Shakrita by inducing fibrinolytic or thrombolytic mechanism may reperfuse the area.

►Vasodilation may be another mechanism through which drug may exert its action.

 

 

Ayurvedic Approach to IMMUNOLOGY


 

 

 

Prof. Dr. S. N. Ohja

Prof. S. N. Ojha M.D. Ph.D

Principal, 

Padmashree Dr. D.Y. Patil College Of Ayurved & Research centre.

Pimpri, PUNE

 

————————————————————————————————————————————————————–

AYURVEDIC APPROACH TO IMMUNOLOGY 

 

Vyadhikshamatwa is defined as the capability of sharir to prevent the utpatti of the disease and also to resist almost all types of organism, toxins  nija & agantuj hetu that tend to damage the body constitution.

 

The ability of the body to defend itself against specific unwanted invading agents depends upon the biological defenses (Bala) of the sharir.

Bala is of 3 types

The natural, inherited body defence of sharir & mana is known as sahaja bala or innate  inmunity

Defence obtained with respect to ritu; (bala is increased in hemanta & shishira ritu) and bala obtained depending on development of dhatus considering the age

 

Neonates are in a state of physiological immunodeficiency during adolescence human body undergoes several immunological changes

—Specific foods like fresh fruits, vegetables and food rich in certain fatty acids may foster a healthy immune systems. Fruits like amalaki are rich source of Vit .C

IMMUNITY

Immunity is a biological term that describes a state of having sufficient biological defenses to avoid infection, disease, or other unwanted biological invasion.

Immunity involves both specific and non-specific components.

The non-specific components act either as barriers or as eliminators of wide range of pathogens irrespective of antigenic specificity.

Other components of the immune system adapt themselves to each new disease encountered and are able to generate pathogen-specific immunity.

TERMINOLOGY

 

  •  Adaptive immune system
  •  Antibody
  •  Antigens
  •  Antimicrobial peptides
  •  Apoptosis
  •  B lymphocytes
  •  B cell receptor of antigen
  •  Complement
  •  Co stimulatory molecules
  •  Cytokines
  • Dendritic cells
  •  Innate Immune System
  •  Large granular lymphocytes
  •  Natural Killer Cells
  •  Pathogen associated molecular patterns

(PAMP)

  •  Pattern recognition receptors (PRRs)
  •  T Cells
  •  T Cell receptor for antigen
  •  Tolerance
  •  CD  classification of human lymphocyte

differentiation antigens

INNATE IMMUNE SYSTEM

Innate immune defenses are non specific, meaning these systems respond to pathogens in a generic way.

MAJOR COMPONENTS OF INNATE IMMUNE SYSTEM

  •  Pattern recognition receptors (PRR)
  •  Antimicrobial peptides
  •  Complement components        
  •  Cytokines
  •  Cells

Macrophages,             Plasmacytoid dendritic cells

Myeloid dendritic cells,                 NK-T cells

Natural Killer cells (NK) Neutrophils

Eosinophils                                         Mast cells

Basophills                                            Epithelial cells.

COMPONENTS

Cellular – T Cell precursors in thymus

– Naïve mature T lymphocytes before antigen

exposure

– Memory T lymphocytes after antigen

exposure

– Helper T lymphocytes

– Cytotoxic T lymphocytes

Humoral – Bone marrow derived (B) lymphocyte

– Naïve B cells prior to antigen recognition

– Memory B cell after the antigen recognition

– Plasma cells that recreate specific antibody.

Cytokines            –

A further subdivision of adaptive immunity is characterized by the cells involved.

  •  Humoral immunity is the aspect of immunity that is mediated by secreted antibodies,

Humoral immunity is active when the organism generates its own antibodies.

passive when antibodies are transferred between individuals.

  •  Cell mediated immunity involves T-lymphocytes alone.

Cell mediated immunity is active when the organisms’ own T-cells are stimulated.

Passive when T cells come from another organism.

Passive immunity

  •  Passive immunity is the transfer of active immunity, in the form of readymade antibodies, from one individual to another.
  •  Passive immunity can occur naturally, when maternal antibodies are transferred to the fetus through the placenta, and can also be induced artificially, when high levels of human (or horse) antibodies specific for a pathogen or toxin are transferred to non-immune individuals.

 

  • Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, to reduce the symptoms of ongoing or immunosuppressive diseases.
  •  Passive immunity provides immediate protection, but the body does not develop memory, therefore the patient is at risk of being infected by the same pathogen later.
  • Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, to reduce the symptoms of ongoing or immunosuppressive diseases.
  •  Passive immunity provides immediate protection, but the body does not develop memory, therefore the patient is at risk of being infected by the same pathogen later.
  • Naturally acquired passive immunity
  • Maternal passive immunity is a type of naturally acquired passive immunity, and refers to antibody-mediated immunity conveyed to a fetus by its mother during pregnancy.
  • Maternal antibodies (MatAb) are passed through the placenta to the fetus by an FcRn receptor on placental cells. This occurs around the third month of gestation.
  •  IgG is the only antibody isotype that can pass through the placenta.
  • Passive immunity is also provided through the transfer of IgA antibodies found in breast milk that are transferred to the gut of the infant, protecting against bacterial infections, until the newborn can synthesize its own antibodies.
  • Artificially acquired passive immunity
  • It is a short-term immunization induced by the transfer of antibodies, which can be administered in several forms; as human or animal blood plasma, as pooled human immunoglobulin for intravenous (IVIG) or intramuscular (IG) use, and in the form of monoclonal antibodies (MAb).
  • Passive transfer is used prophylactically in the case of immunodeficiency diseases, such as hypogammaglobulinemia.
  •  It is also used in the treatment of several types of acute infection, and to treat poisoning.
  •  Immunity derived from passive immunization lasts for only a short period of time,
  • there is also a potential risk for hypersensitivity reactions,
  • serum sickness, especially from gamma globulin of non-human origin.
  • Passive transfer of cell-mediated immunity
  • Passive or “adoptive transfer” of cell-mediated immunity, is conferred by the transfer of “sensitized” or activated T-cells from one individual into another.
  •  It is rarely used in humans because it requires histocompatible (matched) donors, which are often difficult to find.
  • In unmatched donors this type of transfer carries severe risks of graft versus host disease.
  • It has, however, been used to treat certain diseases including some types of cancer and immunodeficiency.
  • This type of transfer differs from a bone marrow transplant, in which (undifferentiated) hematopoietic stem cells are transferred.

 

Naturally acquired active immunity

.Naturally acquired active immunity occurs when a person is exposed to a live pathogen, and develops a primary immune response, which leads to immunological memory.

This type of immunity is “natural” because it is not induced by deliberate exposure.

Many disorders of immune system function can affect the formation of active immunity such as immunodeficiency (both acquired and congenital forms) and immunosuppression.

Artificially acquired active immunity

Artificially acquired active immunity can be induced by a vaccine, a substance that contains antigen.

A vaccine stimulates a primary response against the antigen without causing symptoms of the disease.

There are four types of traditional vaccines:

  •  Inactivated vaccines are composed of micro-organisms that have been killed with chemicals and/or heat and are no longer infectious. Examples are vaccines against flu, cholera, bubonic plague, and hepatitis A. Most vaccines of this type are likely to require booster shots.
  •  Live, attenuated vaccines are composed of micro-organisms that have been cultivated under conditions which disable their ability to induce disease. These responses are more durable and do not generally require booster shots. Examples include yellow fever, measles, rubella, and mumps.
  •  Toxoids are inactivated toxic compounds from micro-organisms in cases where these (rather than the micro-organism itself) cause illness, used prior to an encounter with the toxin of the micro-organism. Examples of toxoid-based vaccines include tetanus and diphtheria.
  •  Subunit -vaccines are composed of small fragments of disease causing organisms. A characteristic example is the subunit vaccine against Hepatitis B virus.

Most vaccines are given by hypodermic injection as they are not absorbed reliably through the gut.

Live attenuated Polio and some Typhoid and Cholera vaccines are given orally in order to produce immunity based in the bowel.

Lymphocytes

  •  The cells of the adaptive immune system are special types of leukocytes, called lymphocytes.
  •  B cells and T cells are the major types of lymphocytes and are derived from hematopoietic stem cells in the bone marrow.
  •   B cells are involved in the humoral immune response,  whereas T cells are involved in cell-mediated immune response.
  • T cells recognize a “non-self” target, such as a pathogen, only after antigens (small fragments of the pathogen) have been processed and presented in combination with a “self” receptor called a major histocompatibility complex (MHC) molecule.
  • Subtypes of T cells: the killer T cell and the helper T cell.
  •  Killer T cells only recognize antigens coupled to Class I MHC molecules,
  • Helper T cells only recognize antigens coupled to Class II MHC molecules.
  • A third, minor subtype are the γδ T cells that recognize intact antigens that are not bound to MHC receptors.
  • the B cell antigen-specific receptor is an antibody molecule on the B cell surface, and recognizes whole pathogens without any need for antigen processing.
  • Each lineage of B cell expresses a different antibody, so the complete set of B cell antigen receptors represent all the antibodies that the body can manufacture.
  • Histological examination of the immune system

    The key primary lymphoid organs of the immune system are like thymus and bone marrow, and secondary lymphatic tissues such as spleen, tonsils, lymph vessels, lymph nodes, adenoids, and skin.

    Many components of the immune system are actually cellular in nature and not associated with any specific organ but rather are embedded or circulating in various tissues located throughout the body.

    Developmental immunology :

    The body’s capability to react to antigen depends on a

    •   person’s age,
    •   Antigen type,
    •   Maternal factors
    •   The area where the antigen is presented.

    Neonates are said to be in a state of physiological immunodeficiency, because both their innate and adaptive immunological responses are greatly suppressed. In neonates, opsonic activity and the ability to activate the complement cascade is very limited.

    Phagocytic activity is also greatly impaired in newborns.

    Maternal factors also play a role in the body’s immune response.

    At birth most of the immunoglobulin is present is maternal IgG.

    Because IgM, IgD, IgE and IgA don’t cross the placenta

    Although some IgA is provided in breast milk. These passively acquired antibodies can protect the newborn up to 18 months, but their response is usually short-live and of low affinity.

    During adolescence the human body undergoes several physical, physiological and immunological changes. These changes are started and mediated by different hormones.

     

    Depending on the sex either testosterone or 17-β-oestradiol, act on male and female bodies accordingly, start acting at ages of 12 and 10 years

    There is evidence that these steroids act directly not only on the primary and secondary sexual characteristics, but also have an effect on the development and regulation of the immune system.[7]

    The female sex hormone 17-β-oestradiol has been shown to regulate the level of immunological response.[10]

    Similarly, some male androgens, like testosterone, seem to suppress the stress response to infection; but other androgens like DHEA have the opposite effect, as it increases the immune response instead of down playing it.

    As in females, the male sex hormones seem to have more control of the immune system during puberty and the time right after than in fully developed adults.

    Other than hormonal changes physical changes like the involution of the Thymus during puberty will also affect the immunological response of the subject or patient.

    Clinical immunology :

    Clinical immunology is the study of diseases caused by disorders of the immune system (failure, aberrant action, and malignant growth of the cellular elements of the system).

    It also involves diseases of other systems, where immune reactions play a part in the pathology and clinical features.

    The diseases caused by disorders of the immune system fall into two broad categories:

    1) Immunodeficiency, in which parts of the immune system fail to provide an adequate response (examples include chronic granulomatous disease).

    2) autoimmunity, in which the immune system attacks its own host’s body (examples include systemic lupus erythematosus, rheumatoid arthritis, Hashimoto’s disease and myasthenia gravis).

    Other immune system disorders include different hypersensitivities, in which the system responds inappropriately to harmless compounds (asthma and other allergies) or responds too intensely.

    Disorders of human immunity

    The immune system is a remarkably effective structure that incorporates specificity, inducibility and adaptation.

    Failures of host defense do occur, however, and fall into three broad categories:

    1) Immunodeficiencies,

    2) Autoimmunity,

    3) Hypersensitivities.

    Immunodeficiencies :

    Immunodeficiencies occur when one or more of the components of the immune system are inactive.

    The ability of the immune system to respond to pathogens is diminished in both the young and the elderly, with immune responses beginning to decline at around 50 years of age due to immunosenescence.[68][69]

    In developed countries, obesity, alcoholism, and drug use are common causes of poor immune function.[69]

    However, malnutrition is the most common cause of immunodeficiency in developing countries.[69]

    Diets lacking sufficient protein are associated with impaired cell-mediated immunity, complement activity, phagocyte function, IgA antibody concentrations, and cytokine production.

    Deficiency of single nutrients such as iron; copper; zinc; selenium; vitamins A, C, E, and B6; and folic acid (vitamin B9) also reduces immune responses.[

    Additionally, the loss of the thymus at an early age through genetic mutation or surgical removal results in severe immunodeficiency and a high susceptibility to infection.

    Immunodeficiencies can also be inherited  Chronic granulomatous disease, where phagocytes have a reduced ability to destroy pathogens, is an example of an inherited,

    ‘acquired’.

    congenital, immunodeficiency. AIDS and some types of cancer cause acquired immunodeficiency.

    Autoimmunity :

    Overactive immune responses comprise the other end of immune dysfunction, particularly the autoimmune disorders.

    the immune system fails to properly distinguish between self and non-self, and attacks part of the body.

    Hypersensitivity :

    Hypersensitivity is an immune response that damages the body’s own tissues.

    They are divided into four classes (Type I – IV) based on the mechanisms involved and the time course of the hypersensitive reaction.

    Type I hypersensitivity is an immediate or anaphylactic reaction, often associated with allergy.

    Symptoms can range from mild discomfort to death.

    Type I hypersensitivity is mediated by IgE, which triggers degranulation of mast cells and basophils when cross-linked by antigen.

    Type II hypersensitivity occurs when antibodies bind to antigens on the patient’s own cells, marking them for destruction.

    This is also called antibody-dependent (or cytotoxic) hypersensitivity, and is mediated by IgG and IgM antibodies.[74]

    Immune complexes (aggregations of antigens, complement proteins, and IgG and IgM antibodies) deposited in various tissues trigger Type III hypersensitivity reactions

    Type IV hypersensitivity (also known as cell-mediated or delayed type hypersensitivity) usually takes between two and three days to develop.

    Type IV reactions are involved in many autoimmune and infectious diseases, but may also involve contact dermatitis (poison ivy).

    These reactions are mediated by T cells, monocytes, and macrophages.

    Physiological regulation :

    Hormones can act as immunomodulators, altering the sensitivity of the immune system.

    female sex hormones are known immunostimulators of both adaptive and innate immune responses.

    Some autoimmune diseases such as lupus erythematosus strike women preferentially, and their onset often coincides with puberty.

    By contrast, male sex hormones such as testosterone seem to be immunosuppressive.

    Other hormones appear to regulate the immune system as well, most notably prolactin, growth hormone and vitamin D. Conversely, some hormones are regulated by the immune system, notably thyroid hormone activity

    The age-related decline in immune function is also related to dropping vitamin D levels in the elderly.

    As people age, two things happen that negatively affect their vitamin D levels. First, they stay indoors more due to decreased activity levels.

    This means that they get less sun and therefore produce less cholecalciferol via UVB radiation.

    Second, as a person ages the skin becomes less adept at producing vitamin D.

    Sleep and rest.

    Complex feedback loops involving cytokines, such as interleukin-1 and tumor necrosis factor-α produced in response to infection, appear to also play a role in the regulation of non-rapid eye movement (REM) sleep.

    Nutrition and diet :

    The functioning of the immune system, like most systems in the body, is dependent on proper nutrition.

    It has been long known that severe malnutrition leads to immunodeficiency.

    Overnutrition is also associated with diseases such as diabetes and obesity, which are known to affect immune function.

    More moderate malnutrition, as well as certain specific trace mineral and nutrient deficiencies, can also compromise the immune response.[108]

    Specific foods may also affect the immune system; for example, fresh fruits, vegetables, and foods rich in certain fatty acids may foster a healthy immune system.

    Likewise, fetal undernourishment can cause a lifelong impairment of the immune system.

    In traditional medicine, some herbs are believed to stimulate the immune system,such as echinacea, licorice, ginseng, astragalus, sage, garlic, elderberry, and hyssop, as well as honey although further research is needed to understand their mode of action.

    Medicinal mushrooms like Shiitake, Lingzhi mushrooms, the Turkey tail mushroom, Agaricusblazei, and Maitake have shown some evidence of immune system up-regulation in in vitro and in vivo studies, as well as in a limited number of clinical studies.

    Manipulation in medicine

    The immune response can be manipulated to suppress unwanted responses resulting from autoimmunity, allergy, and transplant rejection, and to stimulate protective responses against pathogens that largely elude the immune system

    Immunosuppressive drugs are used to control autoimmune disorders or inflammation when excessive tissue damage occurs, and to prevent transplant rejection after an organ transplant.

    Anti-inflammatory drugs are often used to control the effects of inflammation.

    The glucocorticoids are the most powerful of these drugs; however, these drugs can have many undesirable side effects (e.g., central obesity, hyperglycemia, osteoporosis) and their use must be tightly controlled.

    Therefore, lower doses of anti-inflammatory drugs are often used in conjunction with cytotoxic or immunosuppressive drugs such as methotrexate or azathioprine.

    Cytotoxic drugs inhibit the immune response by killing dividing cells such as activated T cells. However, the killing is indiscriminate and other constantly dividing cells and their organs are affected, which causes toxic side effects.

    Immunosuppressive drugs such as ciclosporin prevent T cells from responding to signals correctly by inhibiting signal transduction pathways.

     

    In some cases, the drug itself is not immunogenic, but may be co-administered with an immunogenic compound, as is sometimes the case for Taxol.

    Manipulation by pathogens :

    The success of any pathogen is dependent on its ability to elude host immune responses.

    Therefore, pathogens have evolved several methods that allow them to successfully infect a host, while evading detection or destruction by the immune system.[

    An evasion strategy used by several pathogens to avoid the innate immune system is to hide within the cells of their host (also called intracellular pathogenesis).

    Here, a pathogen spends most of its life-cycle inside host cells, where it is shielded from direct contact with immune cells, antibodies and complement.

    Some examples of intracellular pathogens include viruses, the food poisoning bacterium Salmonella and the eukaryotic parasites that cause malaria (Plasmodium falciparum) and leishmaniasis (Leishmania spp.).

    Other bacteria, such as Mycobacterium tuberculosis, live inside a protective capsule that prevents lysis by complement.

    Many pathogens secrete compounds that diminish or misdirect the host’s immune response.

    Some bacteria form biofilms to protect themselves from the cells and proteins of the immune system.

    Such biofilms are present in many successful infections, e.g., the chronic Pseudomonas aeruginosa and Burkholderiacenocepacia infections characteristic of cystic fibrosis.

    Other bacteria generate surface proteins that bind to antibodies, rendering them ineffective; examples include Streptococcus (protein G), Staphylococcus aureus (protein A), and Peptostreptococcusmagnus (protein L).

    The simplest approach is to rapidly change non-essential epitopes (amino acids and/or sugars) on the surface of the pathogen, while keeping essential epitopes concealed.This is called antigenic variation. An example is HIV, which mutates rapidly, so the proteins on its viral envelope that are essential for entry into its host target cell are constantly changing. These frequent changes in antigens may explain the failures of vaccines directed at this virus.  In HIV, the envelope that covers the viron is formed from the outermost membrane of the host cell; such “self-cloaked” viruses make it difficult for the immune system to identify them as “non-self” structures.

 

Charakokta Gramyadosh Related Diseases – Hridrog (CVD) And Hypertension


By.

Prof. Dr. S. N. Ojha M.D Ph.D

Principal

Padmashree Dr. D.Y. Patil College of Ayurved and Research Centre Pune

Understanding Of Charakokta Gramyadosh And Related Diseases With Special Reference To Hridrog (CVD) And Hypertension

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Introduction

The term ‘Lifestyle’ is a rather diffused concept often used to denote “the way people live”, reflecting a whole range of social values; attitudes and activities.

It is composed of cultural and behavioural patterns and lifelong personal habits that have developed through process of socialization. Health requires the promotion of healthy lifestyle.

Our acharyas had accumulated a considerable body of evidence which indicate association between health and lifestyle of individuals.

Charak in Rasayan Adhyaya Ayurved-samuthaniya pada has elaborated that gramya aahar chosen by the society was not successful in making inroads in community health.

Sedentary lifestyle was responsible for less physical activity which became the cause of preventable diseases.

          A sedentary lifestyle and lack of physical  activity can contribute to or be a risk factor for

1) Anxiety

2) Cardiovascular disease

3) Deep Vein thrombosis

4) Depression

5) Diabetes

6) Hypertension

7) Obesity

8 ) Osteoporosis

9) Lipid disorders

10) Kidney stone

11) Mortality in elderly men by 30% and double risk in elderly woman.

What does gramya aahar include?

Charak in Rasayan adhyaya has describe gramya aahar to be consist of –

–         Amla, lavana, katu, kshar pradhan aahar

–         Shuska shaka, shuska mansa, teel-tail & kalka and ruksha content which have a very low nutritional value

–         Klinna, guru, pishtanna, adhyasana, avyayam and abhisyandi aahar which are source of extra calories.

–         Virudha, asatmya, visham aahar, and paryushit anna which have an impact on our immune system.

–         Day sleeping, Indulging in excessive exercise and sex, Alcohol intake, which increases oxidation process and release oxidants and free radicals.

–         Pshycological factors such as bhaya, krodha, lobha, shoka, moha which are cause for the neuro-hormonal imbalance, for example excess adrenaline secretion and inturn over sympathetic activity.

 

Pathophysiology due to gramya aahar

Due to intake of gramya aahar following changes occur in the sharir.

A)              Mansani shithilibhavanti – Lack of exercise causes muscle atrophy ( abhadha, anibhida mansa)

Shrinking and weakening of the muscles causes increasing susceptibility to physical injury.

B)               Vimuchyante sandhaya – Joints are vitiated so does the physic reducing the body activity.

C)               Vidahyate raktam – Due to nutritional deficiency shudha rakta utpatti does not takes place. One can easily compare the hetus explain in vidhishonitiya adhyaya, pandu roga and gramya aahar.

Formed rakta dhatu is unable to carryout proper jeevan karma, poshan karma and unable to increase bala.

D)              Vishyandate cha-analpam meda – Due to samanya between klinna, guru, pishtamay aahar with meda dhatu, drava guna vridhi takes place and that is the reason why syandan word has been used to explain vridha medha dhatu.

The hetus are similar to sthaulya and prameha hetu as explained in sutrasthan 17th chapter.

E)               Na – Sandhiyate ashtishu – Majja – Majja dhatu is unable to reside in ashtidhatu. Due to nutritional deficiency bone marrow does not get properly stimulated and is unable to form normal erythrocytes, leucocytes and platelets leading to pancytopenia.

F)                Shukram na pravartate – Due to nutritional deficiency sarvottam dhatu is unable to be formed completely does leading to shukra apravartan.

In context of sthaulya too Charak has explained shukra bahutwat and due to aavaran by meda dhatu person feels impairment in ejaculation of semen.

G)              Oja kshaya – Essential nutrients are not made available in required quantity does leading to symptoms of oja kshaya or depressed immune system.

Physical fitness is correlated with immune system function, a reduction in physical fitness is generally accompanied by a weakening of the immune system.

Lakshana produced by gramya dosha:

–         Glayati

–         Sidati (depression)

–         Nidra

–         Tandra (Drowsiness)

–         Aalasya (Lassitude)

–         Nirutsaha (Loss of interest)

–         Swashiti (Dyspnoea on simple exertion)

–         Asamartha chesta sharir manasinam – Reduced physical & mental activity.

–         Nasta smriti, budhi – loss of memory & reduced intellect

–         Nasta chaya – Loss of lusture

–         Roganam adhistanabhutam – Cause for various preventable diseases.

Contribution in pathogenesis of Heart diseases

Epidemology

–         1.5 million people die of CVD every year.

–         2.4 million people suffer from IHD

–        Indiasuffers the highest loss in potentially productive years of life [ 35-64 years ]

–         By 2030, the loss is expected to rise to 17.9 million / year.

–         Prevalence of CVD is reported 2-3 times higher in urban area than rural population.

Aetiology

A] Beej swabhavat ‘sthula matapitrujanya bhavat’. Atherosclerotic vascular disease often runs in families. This may be due to a combination of shared genetic, environmental and lifestyle factors. This has been explained by Charak in astoninditiya adhyaya by using the words ‘tasya hi ittyadi’

Chakrapani coments as ‘Samprati sthulasya sadarana api aaharat medojan aaha’ ie in a person with family history a normal diet also has a tendency for increasing meda dhatu.

The most common inherited risk chracteristics (hypertension, hyperlipidaemia, diabetes) are polygenic.

B] Previous exposure to behavioural risk  factors such as

i) Avyayam (Insufficient physical activity)

Physical inactivity roughly doubles the risk of coronary heart disease. Regular exercise (brisk walking, cycling, swimming for 20 minutes) appears to have a protective effect which may be related to increase HDL cholesterol, lower blood pressure, reduced blood clotting and collateral vessel development.

Sedentary activities include sitting, reading watching television and computer use for much of the day with little or no vigorous exercise.

Nature reviews Cardiology suggest that enforced rest during illness or injury has physiologically become linked to life preserving metabolic and stress related responses such as inflammation that aid recovery during illness and injury but which due to being NON-ADAPTIVE during health now lead to chronic disease.

ii) Inappropriate nutrition

Diet deficient in fresh fruit, vegetables and polyunsaturated fatty acids are associated with an increased risk of vascular disease.

Charak has explained the role of shuska shaka, shuska phala, teel, teelpalala, kshar katu anna to be cause of gramya dosha and so hridroga.

Low levels of vitamin C, vitamin E and other antioxidants may enhance the production of oxidized LDL.

Charak explains intake of nitya pathya in which he includes aamalaki, rich source of vitamin C and wheat a good source of vitamin E.

Vrukshamla, dadima, matulunga are good source of vitamin C and are so classified under Hrudya gana.

Homocysteine is derived from methionine and is metabolized through pathways associated with folic acid, with vitamin B and vitamin B12 as cofactors.

Elevated Homocysteine level confers an independent and incremented risk for vascular disease.

Direct endothelial toxicity, failure of nitric oxide release, smooth muscle cell proliferation, LDL proliferation, platelet abnormalities, abnormal factor V, VII, vWF have been implicated.

Folate supplementation helps to reduce homocysteine levels. Over cooking [vidagda aahar] destroys folic acid from leafy vegetables a good source of folic acid.

Leafy vegetables, liver, meat, milk fruit cereals are good source of folic acid but overcooking destroys it. Vidagda aahar causes rakta dusti has been referred by our acharyas.

Alcohol (Madhya sevan) is antagonist to folic acid. It is the cause explained in Raktapitta, Pandu, Medodustikarak and a gramyadoshkar bhava.

Heavy drinking is associated with hypertension and excess cardiac events. Alcohol beverages are rich in calories and so included under santarpanottha aahar by Charak (C.Su. 23/3)

Essential fatty acids are those that cannot be synthesized by humans they can be derived by food only. Research has shown that diet rich in EFA reduces serum cholesterol and LDL. Coconut oil, Palm oil are low source of EFA while Safflower oil, Sunflower Oil, Soyabean Oil, Sesame Oil are relatively very good source of linoleic acid, a important EFA.

Atisampurna aahar, guru, madhur snighda, pichchhil, paistik, anup mansa, varija mansa are all high calori diet. They are the rich source of fats. Fat consumption induces very little energy expenditure as most is stored. ‘Meda eva upacheyate  na tathe tare dhatawa.’

The above hetu are responsible for dyslipidaemia.

Cholesterol is found in all foods of animal origin.

LDL has been shown to function in delivery of cholesterol to body cells. Excessive level of LDL thus leads to the accumulation of cholesterol particularly smooth muscles cell of the vascular system (Vishyandate cha analpam meda)

Butter, Coconut oil, Palm oil are rich source of saturated fatty acids which increase plasma cholesterol.

Trans fatty acids render the plasma lipid profile even more atherogenic than saturated fatty acids, by not only elevating LDL cholesterol but also by decreasing HDL cholesterol.

Secondly it takes years for trans fatty acids to be flushed oil from the body-

Trans fatty acids are high is concentration in

–         Deep fried fast food

–         Cake mixes

–         Cereal and Energy bars

–         Chips, Crackers and Whipped toppings

–         Packed Cookies and Candy

–         Packed doughnuts

–         Pies and Cakes.

Excessive Salt intake increase the incidence of hypertension.

Upakledan, dosha sanchyanubanda, and its action to bring shaithilyata to mansa and shonita forms an important cause for Hridroga.

Diabetes Mellitus is an important cause for atherosclerosis and hence cardiovascular disease. Angiopathy is a common complication of diabetes mellitus. Insulin resistance is associated with obesity and physical inactivity as potent risk factor for CAD.

Hetus explained in concept of prameha in sutrasthan 17th chapter hold the concept of meda vridhi in madhumeha leading to hridroga.

Haemostatic factors : Platelet activation and high levels of fibrinogen and factor VII are associated with an increased risk of myocardial infarction (coronary thrombosis)

Animal fat (anup varija mansa) are low source of Essential fatty acids. EFA decreases platelet adhesiveness thus due to low source of EFA platelet aggregation helps in coronary thrombosis.

Antioxidant theory:-

Faulty dietary habits, exposure to carcinogen, sunlight, certain toxic drugs, cigarette smoking over exercise all increase free radicals. These free radicals are short of electron while in circulation through blood. These free radicals snatch electron from other tissue molecules and cause damage. This is one of the cause of I.H.D.

Antioxidant like vitamin A,C,E, neutralize free radicals by donating their electron. Hence diet low in vit. A,C,E and other antioxidant are the cause of CVD.