Chronic Hypoxia of Islet cell results in Diabetes Mellitus

Discussion in 'Optometry Archives' started by taopanacea@hotmail.com, Feb 19, 2006.

  1. Guest

    Chronic Hypoxia of Islet cell results in Diabetes Mellitus
    The terms of Insulin Resistance/Sensibility should be stopped in use

    C. T. Zhu/

    Abstract: DM, as a typical modern disease, its root lies in unhealthy
    habit of dieting and living style. Taking of high calorie food, such as
    beef and mutton, keeping intemperance, and/or smoking deteriorate blood
    quality, demonstrated by viscosity of blood, i.e. hemorheology. When
    the hemorheology of one's blood gets worse the blood stream would be
    hard to deliver sufficient oxygen to tissue cells around body. When
    tissues fall in oxygen debt the cells couldn't generate enough energy
    to meet their biological demand for energy. Body is surly to take
    reactions to challenge the situation. It has 3 options to take: 1) do
    its best to supply more oxygen to tissues; 2) supply more of those,
    such as glucagons, helpful to increase of blood sugar, the primary
    fuel; 3) increase the secretion of insulin to help cells absorb more
    fuel in. At the beginning phase of progression to DM, both glucagons
    and insulin are in the high altitude. However, since hemorheology keeps
    beyond the body's capability the situation of oxygen debt of tissues
    have to be on. When the power of both glucagons and insulin keep in
    balance the sugar level of blood will be in normal at the expense of
    high level of insulin, so-called insulin resistance. Sugar glycates red
    blood cell (RBC) to make it loose electrical polarity, as a result RBC
    aggregates. Meanwhile, high sugar level activates fibrinogen to worsen
    the hemorheology. In other words, hypoxia elicits high level of blood
    sugar, and high sugar level in turn promotes hypoxia of tissues. When
    this relation keeps on glucagons are to override insulin and push the
    sugar level higher and higher, totally out of control.
    However, not all worsened hemorheology results in DM, demonstrated by
    those suffering hypertension or/and thrombus. This could be explained
    by the mechanism of secretion of insulin and glucagons. Insulin
    secretion is dictated by the rate of lactate effluent from ß cell
    islet (Take a look at the thesis made by guys in Manchester U. later at
    insulin secretion section) The secretion of glucagons is dictated by
    the stock of ATP and AMP in a islet cell, other than other tissue
    cells.
    As a remark, hypoxia here is about tissue cells in oxygen debt other
    than blood lacking of oxygen. When blood gets less oxygen during
    pulmonary cycle body is to compensate by increasing pulse, breathing
    rate, and more of RBC generation.
    Background: The research to DM now is so deeply sophisticated that
    ordinary one has no courage to get in it. Ironically though, the
    current research could do no more than admitting that DM is incurable.
    Should we suspect that current research is somewhat deviated from the
    proper path? Modern medical about DM is unexceptionally based on the
    two concepts: Insulin Resistance (IR) and Insulin Sensibility (IS).
    When anything is good to lowering of sugar level it is read as
    "increase of IS" while otherwise as "increase of IR". As IR and
    IS could explain everything that results in increase or decrease of
    glucose level people are complacent enough not to get into anything
    behind IR and IS. This me reminds of "ghost" which was used for
    quite a long time to explain any natural phenomenon which people
    couldn't comprehend long time ago.
    Encouraged by my experience of healing DM patients I dare to explain DM
    without IR and IS.
    Recall at the historical observations
    Let's take a look at observations shared commonly by all DM patients.

    1. No DM patient has proper hemorheology.
    --This is result of enjoying modern life. No one oppose this
    proposition though no one sticks it out with it. There may be some one
    claiming cholesterol indicators are more important than hemorheology.
    The fact is that there we can see occasionally DM patients with proper
    cholesterol indicators. This implicates that hemorheology is closely
    related with DM. When hemorheology is not in order tissues wouldn't
    get enough oxygen. It implicates oxygen may have its part in formation
    of DM.
    2. Blood lactate level of DM is about 3 times that of normal people. As
    lactate is only metabolite of glycolysis tissues of DM patients undergo
    severe oxygen debt.
    3. Debility is shared by all DM patients. This symptom is observed even
    after sugar level is normalized, which implicates DM is about more than
    so called insulin resitance. This also implicates DM patients
    couldn't generate lasting amount of energy. When oxygen is in debt
    cells are no way to generate lasting amount of energy.
    4. When drinking alcohols DM patients can enjoy short time of normal
    life, perfectly normal like a healthy man. Alcohols boost hemorheology.
    This implicates proper hemorheology is perfectly helpful for DM
    patients. Proper hemorheology can surly deliver rich oxygen to tissues.
    Can delivery of rich oxygen make sugar level normal?
    5. Glucagon level of DM patients is all in high altitude. When
    glucagons climb up sugar level is definitely going up as glucagons are
    for mobilization of fuels, right contrary to insulin. It is rationale
    to say that when glucagons are stronger than insulin sugar level goes
    up and up.
    (-look at this link, http://www.TaoPanacea.com/Archives/DataE.htm,
    which is clinically observed data of lactate ,insulin and glucagons.)
    Items of 1, 2, 3, and 4 above all finger at issue of oxygen debt. Could
    DM be direct result of hypoxia of tissues?
    It should be noted that hypoxia here is about tissues in debt other
    than air lacking oxygen. When blood gets oxygen less than enough during
    pulmonary cycle, like instances in plateau or anemia, body will call up
    compensation mechanism to makeup the shortage, like increasing rate of
    pulse and breathing, and/or generating more of RBC. What would the body
    take when tissues falls in hypoxia?
    Glucose is metabolized in two forms in body: Glycolysis to result in 2
    molecules of lactate while oxygen is in short; Oxidation to result in 6
    molecules of water and carbon dioxide while oxygen is sufficient. It is
    worth to note that there is great gap between glycolysis and oxidation
    in terms of energy generation. Glycolysis contributes only 2 ATPs while
    oxidation 38. Let's think about this scenario.
    In a moment, a cell needs 380 ATPs to meet its biological demand. If
    all these energy is derived by oxidation it needs 10 molecules of
    glucose and 60 molecules of oxygen to generate 380 ATPs exactly. What
    if oxygen available is 5% less than enough? As a matter of fact,
    glycolysis could be the only option to makeup the difference. Let's
    make a simple calculation. As oxygen available is 57(60x95%) only 9.5
    molecules of glucose could be oxidized. As a result 361 ATPs are
    generated. To generate another 19 ATPs by glycolysis another 9.5
    molecules of glucose has to be put into consumption since one molecule
    of glucose contributes only 2 ATPs by way of glycolysis. As a result 5%
    shortage in oxygen results in 19 molecules of glucose in total to
    generate 380 ATPs which could be delivered merely 10 molecules of
    glucose when oxygen supply is sufficient. Translated, it is 90%
    increase in glucose consumption. Would the body meet this big demand?
    In philosophical view, body will do its best to assist tissues generate
    enough energy. Body has 3 options to do so.
    a)Adjust blood and vessel to make more oxygen permeate through
    membrane of cells, which is surly impractical at all. So, body has
    another 2 options to take.
    b)Put more fuel, primarily glucose, into blood stream, which could be
    realized by increasing secretion of glucagons and adrenaline.
    c)Assist cells increase efficiency in acquiring glucose, which must
    be realized by secreting more insulin.
    --a, b, and c of above are termed DanTai Effect in whole.
    DanTai effect is definitely have the effect of high level of insulin
    and high level of glucagons with possibly normal level of glucose,
    which is obviously the reality with people in the beginning phase of
    progression to DM. In other words, when tissues fall in oxygen debt
    body calls up DanTai effect. At the beginning phase of progression to
    DM, the strength of glucagons and insulin is in balance. When this
    balance doesn't stand sugar level either goes down or up. We discuss
    the latter case as it is exactly what we call DM. Why the balance
    between insulin and glucagons loose their ground at last? This is due
    to mechanism of glucagons secretion.
    On the other hand high blood sugar works negatively to oxygen delivery
    mechanism. High sugar level promotes RBC aggregation by glycating RBC
    and activates fibrinogen to worsen the hemorheology. Translated, higher
    blood sugar level boosts more severe hypoxia, as worsened hemorheology
    curtails oxygen transportation, which in turn results in higher blood
    sugar level. As a result, when this fashion lasts long DM is definitely
    going to be formed.
    The analysis above is plausible in philosophical view, but as observed
    clinically not all people, such as hypertension patients or thrombus
    patients, with improper hemorheology gets DM. The reason lies in the
    mechanisms of insulin secretion and glucagons secretion.
    Sure, we expounded etiology of DM without reference to IR or IS. Should
    we say DM is irrelevant with IS or IR, both of which are descriptive
    and inclusive terms other than scientific terms.
    Mechanisms of insulin and glucagons
    Hypertension patients and thrombus patients suffer from worsened
    hemorheology. However they could escape from claw of DM. Therefore we
    can conclude worsening of hemorheology not necessarily results in DM.
    But DM is most likely result of chronic hypoxia of tissues. Answer to
    this phenomenon could be found in mechanisms of insulin and glucagons.
    Cohort in Manchester U. made a great experiment back in 1989, the
    thesis of which was published in Biochem. J. (1989) 259, 507-511. The
    thesis could be referenced by this link:
    http://www.TaoPanacea.com/Archives/InsulinSecretion.Pdf. The statement
    below is quoted from the thesis:


    The secretion of insulin from perfused rat pancreatic islets was
    stimulated by raising the glucose concentration from 5.6 to 20 mm or by
    exposure to tolbutamide. The addition of sodium lactate (40 mM) to
    islets perfused in the presence of glucose (5.6 mM) resulted in a
    small, transient, rise in the rate of secretion. The subsequent removal
    of lactate, but not glucose or tolbutamide, from the perfusate produced
    a dramatic potentiation of insulin release. The rate of efflux of
    45Ca2" was also increased when islets were exposed to a high
    concentration of glucose or lactate or to tolbutamide, and again
    subsequently upon withdrawal of lactate. Efflux of 86Rb+ was modestly
    inhibited upon addition of lactate and markedly enhanced by the
    subsequent withdrawal of lactate from islets. The output of ["4C]
    lactate from islets incubated in the presence of [U-'4C] glucose
    increased linearly with increasing concentrations of glucose (1-25 mM).
    It is proposed that the activation of islets by the addition or
    withdrawal of lactate is not due to increased oxidative flux, but
    occurs as a result of the electrogenic passage of lactate ions across
    the plasma membrane, resulting in islet celldepolarization, Ca2" entry
    and insulin secretion. The production of lactate via the glycolytic
    pathway, and the subsequent efflux of lactate from the islet cells with
    concomitant exchange of H+ for Na+, could be a major determinant of
    depolarization and hence insulin secretion, in response to glucose.


    Their conclusion is "The efflux of lactate from the islet cells could
    be a major determinant of depolarization and hence insulin secretion,
    in response to glucose". The more fast the lactate is discharged from
    islet cell the more secretion of insulin is resulted. I term their
    observation as Lactate Theory of Insulin Secretion (LTIS). LTIS could
    explain neatly about the insulin curves extracted from DM patients,
    which is still confuses professionals in the field though. DM
    patient's basal insulin level is about 10% higher than normal people
    while their insulin level trails far behind that of normal people
    postprandial (Take a look at
    http://www.TaoPanacea.com/Archives/DataE.htm).
    1) DM patients produce far more lactate than normal people in basal
    condition, about 3 times that of normal people, so it is likely that
    their islet cells discharge lactate in higher rate, resulting in higher
    secretion of insulin in basal situation;
    2) After meal, normal people undergo steep elevation of glucose level.
    High level of sugar curtails significantly the delivery of oxygen to
    islet cells. As a result, big volume of lactate production in islet
    cells is made, resulting in secretion of insulin 5~6 times their basal
    insulin level. Since DM patient's sugar level is positioned high even
    before the meal, therefore glucose elevation is less steep than normal
    people postprandial, hence the milder change in oxygen delivery,
    resulting in less steep elevation in lactate production in islet cells.

    3) Blood lactate level of DM patients is close to 3 times that of
    normal people; therefore lactate from islet cells of DM patients is
    more difficult to come out.
    Above 3 reasons explain why DM patient have their insulin level curve
    far different from that of normal people. We could infer that the
    longer islet cells suffer from hypoxia the less reactive to sugar
    level. When this situation goes on, the secretion of insulin could be
    impaired and glucagons might be in better position.
    Let's sit upon the mechanism of glucagons now.
    The conventional wisdom tells us ATP/AMP value in tissue dictates
    secretion of glucagons. As glucagons are secreted by a-islet cells the
    proper proposition should be "ATP/AMP value in a-islet cells
    dictates secretion of glucagons". When ATP/AMP value goes down, like
    in the case of a-islet cells falling in oxygen debt, the secretion of
    glucagons is promoted. When severity of hypoxia, like in the case of
    DM, overrides the gain of ATP due to elevation of sugar level the
    secretion of glucagons becomes rampant. As a result glucagons get upper
    hand than insulin at last. That's DM.

    It should be noted here that in case worsened hemorheology of blood
    stream is not expressed in vessel web of islet cells both insulin
    secretion and glucagons should be in order while other parts of body
    suffer from hypoxia. This is why thrombus or hypertension patients
    could escape from DM. But it is sure when hemorheology gets worse to a
    point where islet cells are choked of hypoxia meaningfully DM would be
    guaranteed. .
    There seems other reason as well. We have to note that DanTai effect
    mobilizes high volume of insulin secretion and glucagons secretion,
    which is pathological in fact. Can DanTai Effect stay in use without
    damaging islet cells? The reality is ß islet cell is susceptible to
    damage as clinically demonstrated by many DM patients. When damage is
    suffered more than 85% DM type 1 is realized. When ß islet cell get
    damaged the secretion of insulin is very likely negatively effected.
    When this damage helps glucagons get upper hand DM is also guaranteed.

    The treatment
    hypoxia. Accordingly treatment should be for improving delivery oxygen
    to islet cells. When islet cells get sufficient oxygen the value of
    ATP/AMP goes up and the secretion of glucagons becomes down and down
    and gives its way to insulin like in the normal fashion. Meanwhile the
    secretion of insulin would be close to normal as well and it is great
    pleasures to human kind were ß islet cell could recover bit by bit in
    this case.
    To deliver sufficient oxygen to islet cells, the only practical way is
    to improve hemorheology of the whole blood system. In fact, the
    improvement of blood hemorheology results in healing or cure of
    hypertension, thrombus, and many other cardio-vascular diseases.
    Therefore treatment of DM is most difficult thing to do. Can there be
    such magic thing that could help blood get back to its old time happy
    condition?
    Through our great amount of effort and endeavor, we come up with an
    herbal remedy, Oxygen Booster, which delivers magic result in improving
    blood hemorheology. We have a measure for efficacy for Oxygen Booster.
    One should feel fresh in brain and vigorous around the body after
    taking Oxygen Booster Capsule. As sugar curtails delivery of oxygen DM
    patients should take bigger dose of Oxygen Booster along with chemical
    medicine (Metformine the best while one has no weakest liver) or
    insulin injection. In any case to see the sign of working---fresh brain
    and vigor in body-- that Oxygen Booster works well is paramount
    prerequisite. Within 30~60 days after Oxygen Booster delivers efficacy
    one can get his/her hemorheology normalized.
    Oxygen Booster delivers magic result which couldn't be explained by
    conventional wisdom. This is the direct cause of making new theory of
    DM etiology come to birth.

    Email:
    Web Page: Http://www.TaoPanacea.com
     
    , Feb 19, 2006
    #1
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  2. CatmanX Guest

    So what dumbfuck?

    It is easy. Diabetes = receptors not responding to insulin. The cause
    is too much glucose in too high quantities.

    Solution: reduce sugar intake significantly, reduce/cease all grain
    intake.

    Not so hard is it?

    dr grant

    the diabetes god
     
    CatmanX, Feb 20, 2006
    #2
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