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  • DrDeanStMart

    Member
    November 10, 2018 at 8:32 am in reply to: Pitting edema – Post show Blood work

    I would consult a kidney specialist.

    LDH is still high although it did come down a bit and ALT is still high even with resting.

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  • DrDeanStMart

    Member
    November 9, 2018 at 7:03 pm in reply to: T3 dosing frequency ?

    Roughly 24 hour half life

    https://wvrtaal.files.wordpress.com/2016/12/saravanan-24-h-eced_699.pdf

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  • DrDeanStMart

    Member
    November 9, 2018 at 4:10 pm in reply to: Evening Primrose oil

    6 x 300mg = 1.8g.

    Can go mad and have a 7th to really push over the edge to 2.1g

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  • DrDeanStMart

    Member
    November 9, 2018 at 4:01 pm in reply to: Dr. Dean St. Mart – Training Journal

    Sounds like nervous system is over reached if resting HR is elevated.

    Deload CNS for 4-5 days to allow it to calm down

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  • DrDeanStMart

    Member
    November 9, 2018 at 3:59 pm in reply to: Dr. Dean St. Mart – Training Journal

    Its quite possible that the HGH is triggering an immune response, in response to the stress insult of flying

    EFFECT OF GROWTH HORMONE (GH) ON THE IMMUNE SYSTEM
    https://www.ncbi.nlm.nih.gov/pubmed/16444180

    A growing body of evidence indicates a bi-directional relationship between the neuroendocrine system and immune functions.

    It is well known that lymphoid organs such the thymus, the spleen and peripheral blood produce growth hormone (GH) and GH receptor is expressed on different subpopulations of lymphocytes.

    Many in vitro and in animal studies demonstrate an important role of GH in immunoregulation.

    GH stimulates T and B cells proliferation and immunoglobulin synthesis, enhances the maturation of myeloid progenitor cells and is also able to modulate cytokine response.

    However, in humans GH deficiency (GHD) is not usually associated with immunodeficiency and only minor abnormalities of immune function have been reported, as compared to those observed in GHD animals.

    It is possible that in humans the GH produced locally in the immune system compensates for the lack of endocrine GH.

    In this review the main actions of GH on immune system in vitro, in animal models and in humans are summarized.

    Today we know that growth hormone (GH) and insulin like-growth-factor type I (IGF-I) are virtually synthesized in every tissue in the body, not only in the pituitary gland and liver.

    What has become more fascinating is the finding of receptors for these hormones on immunological cells, suggesting a communication between the immune and endocrine systems.

    Mainly the role of the growth hormone/insulin-like growth factor-I (GH/IGF-I) axis on the immune function has been discussed.

    A compelling body of observations indicates that GH is necessary for the development of the immune system and for the maintenance of immunocompetence. The immunostimulatory effect of GH appears to be generally postulated on both cell mediated and humoral reactions.

    The evidence that immune and neuroendocrine mechanisms can affect each other has been classified as follows:

    A) Immune, endocrine, or neural cells can express receptors for cytokines, hormones, neurotransmitters and neuropeptides;

    B) Immune and neuroendocrine products coexist in lymphoid, endocrine and neural tissue;

    C) Endocrine and neural mediators can affect the immune system;

    D) Immune mediators can affect endocrine and neural structures (1).

    A role for prolactin (PRL), GH, IGF-I and thyroid hormones in the regulation of the immune system is often not acknowledged in major immunology texts.

    Nevertheless, the use of one or more of these hormones as immunostimulants in humans is being considered, making it of critical importance to resolve the precise role of PRL, GH, IGF-I and thyroid hormones in immunity (2).

    It is well known that lymphoid organs such the thymus, the spleen and peripheral blood produce GH and respond to GH by synthesizing and releasing IGF-I (5). The presence of cell surface receptors for GH and IGF-I on different subpopulations of lymphocytes suggests that there is a local mechanism of action of these hormones in addition to the traditional endocrine mode of action (6, 7). It is now well established that GH-receptor (GH-R) is ubiquitously expressed on peripheral blood mononuclear cells (PBMC), and a higher expression was found on CD20+ cells (B cells), corresponding approximately to that found on IM-9 cell line, whereas CD2+ cells (T cells and natural killer cells) expressed much lower amounts (8).

    In the immune system, GH is required for growth of the thymus gland and the spleen, for lymphocyte proliferation and differentiation and bone marrow function.
    In vitro and in animal studies

    It is well established that GH enhances thymic epithelial cell proliferation in vitro (9).

    GH also stimulates thymulin secretion, one of the most important thymic hormone, in primary cultures of human thymic epithelial cells and in a rat thymic epithelium cell line (9).

    The effect of GH is abrogated by antibodies against either IGF-I or IGF-I-R, indicating that GH acts through the production of IGF-I.

    With regard to T cell function, GH can stimulate DNA synthesis in human T-lymphocytes as well as the in vitro proliferation of both phytohaemoagglutinin-activated normal and leukemic human T-lymphocytes, and this latter effect seems to be mediated by IGF-I (13).

    Moreover, GH may have stimulatory effects on the production of the cytokine such as interleukin-2 (IL-2) and IL-6 and enhances the cytotoxic activity of human natural killer (NK) cells (14, 15), that are lymphoid cells that mediate MHC unrestricted killing of tumors and virally-infected cells.

    GH and IGF-I enhances the in vitro proliferation of human myeloid progenitor cells and their maturation towards mature granulocytes (22).

    GH has been shown to induce priming of superoxide anion production of macrophages and neutrophils, which is necessary for phagocytosis (23, 24), and to prime monocytes to release increased amounts of H2O2 (25).

    Both in vitro and in vivo priming with GH demonstrate an activation of human monocyte chemotaxis and migration (26, 27).

    The process of haemopoiesis, occurring primarily within the bone marrow, involves the proliferation and differentiation of pluripotent haemopoietic stem cells into committed or pathway-restricted progenitors.

    Human studies have shown no significant alteration in haematopoiesis in children and adults with GH/IGF-I deficiency or excess. GH/IGF-I treatment leads to either no effect or an increase in markers of haematopoiesis.

    Furthermore, several studies have demonstrated that GH is able to modulate cytokine responses.

    Cytokines are a large family of protein mediators including interleukins (ILs), colony stimulating factors (CSFs), interferons (IFNs), tumor necrosis factor (TNF) and growth factors, with a wide range of functions and target cells; they do, however, share a number of general properties.

    Cytokine production is usually transient; their expression is initiated by activation of gene transcription and the subsequent cytokine mRNA transcripts are unstable, so cytokines are rapidly secreted, resulting in a ‘burst’ of cytokine release. These proteins initiate their action by binding to specific cell surface receptors on target cells; they have also been shown to have redundant functions, i.e. several cytokines can mediate a common event due to the use of receptors with common signal transduction subunit. Cytokines play a major role in the initiation, propagation and regulation of immune and inflammatory responses.

    The pituitary gland is needed for the synthesis of TNF- by macrophages.

    Hypophysectomized rats have markedly depressed macrophage synthesis of TNF- and exogenous GH partially reverses the effect of hypophysectomy (30).

    Injection of GH in aging animals induces an up-regulation of IL-6 production by thymocytes (31). Foetal calf thymocytes treated ex vivo with GH exhibit increased transcript levels of IL-1, IL-1, IL-6 and GM-CSF (32).

    Furthermore, incubation of human PBMC with different concentrations of hGH significantly increases the number of IFN--secreting cells as well as the concentration of IFN- (33).

    Both GH and IGF-I may act to protect the host from lethal bacterial infection by promoting the maturation of myeloid cells, stimulating phagocyte migration, priming phagocytes for production of superoxide anions and cytokines, and enhancing opsonic activity.

    GH has been shown to interact directly with lymphocytes, increasing the expression of GH surface receptors on the lymphocyte cell surface (37, 38, 39) and enhancing the secretion of IFN- and immunoglobulin by lymphocytes in vitro (19).

    On the basis of all these findings, it is reasonable to hypothesize that if the pituitary gland can influence the immune system, then its absence or removal should result in detectable alterations in immunity.

    Indeed there are a number of reports using different approaches which support this contention.

    The majority of these studies but not all (44, 45), show that hypophysectomized animals exhibited impaired humoral (46) and cell-mediated immunity (47).

    If on one hand it is demonstrated that GH is able to influence cytokine responses, on the other hand a vast body of evidence show that cytokines, and particularly the proinflammatory cytokines IL-1, IL-6 and TNF-affect the GH/IGF-I axis.

    These effects are relevant in human pathological conditions for the understanding of the stunted growth associated with chronic inflammatory diseases or diseases with recurrent infections in childhood.

    IL-1, IL-6 and TNF-appears to have different effects on the GH/IGF-I axis: some data suggest that TNF- may directly inhibit GH pituitary production while IL-1 has been shown to induce GH production by pituitary cells in vitro (48).

    The unifying concept that emerges from reconsidering these studies is that immune system defects in dw/dw mice, and the positive effects of hormones on restoring thymopoiesis or antigen-responsiveness to normal, have been observed primarily when animals were stressed because of suboptimal environmental conditions. Thus a hypothesis that will be developed is that positive hormonal effects on immunity occur primarily as an adaptation to stress (2).

    Recently it has been described ghrelin, a polypeptide that seems to be implicated in GH release, energy balance and food intake in rodents and humans
    Ghrelin is secreted predominantly from X/A-like enteroendocrine cells of the stomach (53; 54) and its effects are mediated through a G protein-coupled receptor called growth hormone secretagogue receptor (GHS-R) (55). The wide tissue distribution of GHS-R in the lymphoid system suggests that ghrelin may function as signal modulator among the endocrine, nervous and immune systems.

    In a recent study (56) it is shown that GHS-R and ghrelin are expressed in human T-lymphocytes and monocytes and ghrelin acts via GHS-R to specifically inhibit the expression of proinflammatory cytokines such as IL-1, IL-6 and TNF-.

    Ghrelin is also useful in prolonged critical illness, a syndrome with protein wasting and paradoxical fat storage in which there is insufficient GH secretion and decreased IGF-I concentrations. It is shown that ghrelin can reverse this pathophysiological state (57).

    Moreover, it has been suggested that GH may influence cytotoxic activity mediated by Natural Killer (NK) cells which are lymphocytes involved in the immune surveillance for viral infections and neoplastic diseases.

    A vast body of evidence confirms the existence of a bidirectional relationship between the endocrine system and immune function.

    Specifically concerning the growth hormone (GH)/insulin-like growth factor-I (IGF-I) system, the presence of such a bidirectional influence with cytokines, the soluble factors released by immune cells, has been shown by several studies.

    The proinflammatory cytokines TNF, IL-1 and IL-6 have been shown to affect the GH/IGF-I system at several levels with relevant in vivo consequences in human diseases.

    Conversely, GH not only regulates growth but can also control the immune function.

    In particular, the release of IL-1 and TNF- is increased in response to an acute GH administration in GHD children, in spite of no differences in these cytokine levels between controls and GHD patients (70).

    Cytokine release could also be affected by short-term hGH administration in short non-GHD children, indicating a direct effect of GH on the immune function (70).

    Moreover, long-term hGH treatment has been demonstrated to increase both serum IL-6 and TNF- and LPS-induced lymphocyte production of the same cytokines in GHD children (Pagani, 2004 unpublished data).

    In GHD humans, it is possible that the GH produced locally in the immune system compensates for the lack of endocrine GH. This may explain why a deficiency in pituitary GH or endocrine IGF-I appears to have minor effects on immune function in humans, as compared to the effects of such deficiency in rats.
    In contrast, in GHD adults basal TNF- levels are high and fall after prolonged GH administration (71).

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  • DrDeanStMart

    Member
    November 9, 2018 at 3:45 pm in reply to: Bloodwork looks a bit meh

    I actually prefer RicePure – single cap serving has 10mg monacolin K.

    Really depends on personal preference, lowering fats a touch wouldn’t hurt

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  • DrDeanStMart

    Member
    November 9, 2018 at 9:51 am in reply to: Medichecks male hormone check

    Sports Hormone Plus is a well rounded test

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  • DrDeanStMart

    Member
    November 8, 2018 at 6:37 pm in reply to: Dr. Dean St. Mart – Training Journal

    Rotation 2 this week

    Back Width
    T-Bar Row – The work gym has nowhere properly to anchor down a bar so I’m going to have to figure this one out; wil lprobably go and buy an attachment to bring in with me. Bar kept lifting out of the corner even with dumbells wedged on top.Aired on side of caution with 3 sets of 12 with 4 plates.
    Close Grip Pulldown in Dual Cable Station – 33.75 a side x 9, 26.25 x 12
    Low Lat Row Machine – 70 x 11, 70 x 11
    Scap Pull ups – BW x 3 sets
    Rack Chin – BW x 15
    Lat Pulldown – 23.25 a side on dual cable station x 15
    Rack Chin – BW x 15
    Lat Pulldown – 23.25 a side on dual cable station x 15
    Rope Pullovers – Triple drop
    DB Shrugs – 45kg x 9, 45kg x 9

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  • DrDeanStMart

    Member
    November 8, 2018 at 6:14 pm in reply to: Evening Primrose oil

    Its 6 of these Rotties on top of 3-4g EPA/DHA.

    https://www.amazon.com/Solgar-Super-Starflower-1300Mg-Softgels/dp/B008Q54ADO

    Those are the levels in clinical resarch.

    GLA feeds into a lot of pathways both inflammatory and anti inflammatory

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  • DrDeanStMart

    Member
    November 8, 2018 at 6:12 pm in reply to: Bloodwork looks a bit meh

    It could be an artefact of diet as TGs are 1.38 mmol

    For HDL – try 1200mg Panthetine, 1.5g FLUSH Niacin, 500mg Citrus Bergamot A.M / P.M.

    Increase CoQ10 to 200mg

    10mg Monacolin K RYR will lower LDL ontop of 5g Vit C and 5g Lysine at bedtime.

    Supplement with Liposomal Glutathione 2-3 times a week.

    Week of blood test lower fats to 30g per day or keep diet the same.

    Lowering fats will remove their bias towards hepatic lipid metabolism and TG production

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  • DrDeanStMart

    Member
    November 8, 2018 at 6:07 pm in reply to: Year round liver support

    Liposomal Glutahtione

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  • DrDeanStMart

    Member
    November 8, 2018 at 6:06 pm in reply to: Dr. Dean St. Mart – Training Journal

    Liquid Vit A and Lipo Glutathione 1 hour before you go to airport.
    Leave it in mouth for as long as possible.

    High dose Vit D too.

    Keep washing hands and use one of the nasal coating sprays like Vicks First Defense.

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  • DrDeanStMart

    Member
    November 8, 2018 at 9:29 am in reply to: Bloodwork looks a bit meh

    Whats diet like?
    Fat total content?
    Meal timings?

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  • DrDeanStMart

    Member
    November 8, 2018 at 8:15 am in reply to: Dr. Dean St. Mart – Training Journal

    Jim Bob – Of course. I just didn’t list it.

    Mushrooms, corgeutte, brocolli rice, brocolli, green beans, peas

    Any meal with animal protein above will have around 350-400g cooked veg with it.

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  • DrDeanStMart

    Member
    November 8, 2018 at 8:13 am in reply to: Dr. Dean St. Mart – Training Journal

    Jonathan – possibly a combination of HGH, BPC157 and TB500.

    Depends on how invasive the surgery is

    Liposomal Glutaitone and Curcumin post surgery to managed systemic inflammation and support body if anesthetic and painkillers were used.

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