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Brooke... One day at a time. Well maybe. :)

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  • I usually eat 10 bananas a day too, sometimes if I'm feeling extra bananas I'll eat 20-30. They're just good, and I never tire of them. Surprisingly good nutrient profile too. And, yeah, real cheap. I like to fry them in butter or coconut oil sometimes and take them to work as banana chips.

    Oh, and dunk them in some chocolate!
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    • Y'all are banana crazy!!

      Bananas are good with everything. I've even eaten them fried up with ground beef and cayenne pepper... Or bananas, water chestnuts, lime juice, tuna and spices. Sounds so weird but it's good.

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      • Bananas sauteed in coconut oil + cinnamon + cocoa powder turned into an issue for me for a while.
        Is it weird in here, or is it just me?

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        • I could eat fried bananas all day, every day. If, I could find low-fat butter and someone to cook them for me

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          • I was looking over my labs again. OCD. I realized I posted the lab ranges for the CRP wrong. My CRP was <0.5 with ranges <1.0. SO that's good news. Looks like inflammation isn't a factor.

            btw... I had shrimp and bananas sautéed in butter, with garlic, lime, cilantro and cayenne pepper. nom nom nom

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            • Originally posted by max219 View Post
              Thanks for asking . I've been doing well, increasing my strength through lifting, still putting on some fat (and muscle) though. I've been trying not to talk or think about nutrition much anymore since it kinda consumes me. I still love learning about it though.
              I understand. That's great that you're still getting stronger. Have you had any stalls yet? Stronglifts eventually got to hard for me. That could have been partly due the low cortisol I started experiencing around that time too.

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              • I have stalled but usually got it the next time around. I haven't been doing the squats and deadlifts unfortunately cause my hamstring is still weak. I've been trying to rehab that back, so been doing RDLs and split squats instead. Hopefully soon I can get back on the leg lifts properly, since those are the best ones to do.

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                • I was just reading on adrenalsweb.org about cortisol supplements. I found this about holy basil-

                  Holy Basil (or Tulsi) is used to lower high cortisol it is regarded as an 'adaptogen' or anti-stress agent. Recent studies have shown that the leaves afford significant protection against stress. It purifies blood and helps prevent several common ailments. Holy Basil is not the same kind of basil that you grow in your back yard.

                  That's interesting cos' a few weeks ago when I was having blood sugar spikes and felt very depressed, I was taking the Holy Basil supplement. I had been rotating it with Eleuthero and Rhodiola. Since I'm most likely low cortisol in the mornings right now, no wonder this spiked my blood sugar, it spiked my adrenalin even more by lowering my cortisol.

                  For as long as I can remember, around 9:00am my body starts requiring more insulin. If I'm not careful, I get a high blood sugar shortly after 9. I always thought it was a cortisol spike. Now I'm thinking it's been adrenalin all along. Back when I did the 24 hour salvia test, it showed borderline low cortisol in the morning and through midday. Around 4-5pm, it showed a spike in cortisol. Looking back on that... for as long as I can remember, my blood sugar usually drops anywhere from 3:30-5:00. Then, if I'm not careful it spikes again by the time it's 7:00pm.

                  The main problem is that I was untreated hypothyroid way too long. Once I was treated, it was with T4 only meds that I couldn't convert very well. This caused so much stress on the my adrenals. That caused blood hormonal blood sugar fluctuations. I always wondered my it seemed so hard to keep my blood sugar steady. The only way I'm able to do that is by checking my blood sugar about 15x a day. That may look a little OCD but, it's what I've had to do.

                  If you have read this far, Thank you for caring! I'm just so glad that I'm starting to make sense of all of this. The more I find out, the closer I get to a solution.

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                  • Originally posted by brooke.S. View Post
                    That's interesting cos' a few weeks ago when I was having blood sugar spikes and felt very depressed, I was taking the Holy Basil supplement. I had been rotating it with Eleuthero and Rhodiola. Since I'm most likely low cortisol in the mornings right now, no wonder this spiked my blood sugar, it spiked my adrenalin even more by lowering my cortisol.
                    Tut tut - you neglected to mention these when I asked you about your pill intake

                    That's brilliant you're starting to figure things out! Where will you go from here? Have you tweaked your diet at all / looked into Ray Peat's views on T1 Diabtes? might be helpful to post on that forum too.
                    "I think the basic anti-aging diet is also the best diet for prevention and treatment of diabetes, scleroderma, and the various "connective tissue diseases." This would emphasize high protein, low unsaturated fats, low iron, and high antioxidant consumption, with a moderate or low starch consumption.

                    In practice, this means that a major part of the diet should be milk, cheese, eggs, shellfish, fruits and coconut oil, with vitamin E and salt as the safest supplements."

                    - Ray Peat

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                    • Originally posted by YogaBare View Post
                      Tut tut - you neglected to mention these when I asked you about your pill intake

                      That's brilliant you're starting to figure things out! Where will you go from here? Have you tweaked your diet at all / looked into Ray Peat's views on T1 Diabtes? might be helpful to post on that forum too.
                      I stopped taking them 2 weeks ago, after I had the blood sugar spikes. I'm looking into taking an adrenal cortex. A moderator from the yahoo adrenals group recommended over the adaptogens for raising cortisol.

                      I bought some cantaloupe and have been eating it today... so good. I just found this in one of Peat's articles-

                      I think the basic anti-aging diet is also the best diet for prevention and treatment of diabetes, scleroderma, and the various "connective tissue diseases." This would emphasize high protein, low unsaturated fats, low iron, and high antioxidant consumption, with a moderate or low starch consumption. In practice, this means that a major part of the diet should be milk, cheese, eggs, shellfish, fruits and coconut oil, with vitamin E and salt as the safest supplements. It should be remembered that amino acids, especially in eggs, stimulate insulin secretion, and that this can cause hypoglycemia, which in turn causes cortisol secretion. Eating fruit (or other carbohydrate), coconut oil, and salt at the same meal will decrease this effect of the protein. Magnesium carbonate and epsom salts can also be useful and safe supplements, except when the synthetic material causes an allergic bowel reaction..

                      He confirmed what happens to me after a low blood sugar. If you remember, I said my blood sugar always drops from 3:30-5:00, that's when the salvia test showed a cortisol spike. Anywho, it's all interesting but I'm not sure if I'm going to do many tweaks other than what I'm doing with thyroid meds and cortisol a the moment.

                      I've looked around on the forum.. . I might try to find out if any T1's are there eating a Peat inspired diet.

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                      • I had read about the T3 Circadian Method about 6 months ago. At the time I didn't realize I had low cortisol in the morning-midday. The premise is that the body needs T3 during the wee hours of the morning for the adrenals to start working properly. The problem is, most that are on thyroid meds usually take their last dose in the evening. This probably isn't too much of a problem if the person is a great T4 converter but from the looks of it, most are not.

                        I wake up around 6:00am during the week. I already wake up at 5:00am and take T3. So now, I've started waking up at 4:30 and taking it. Each week, I'll move it back another 30 minutes up until I'm at 4 hours before wake up time. At some point, I'll start to notice more energy in the mornings and that means I'm at or close to the proper time for my first T3 dose.

                        This method can be done with and T3 containing thyroid med except for slow release. I'm using Cynomel because I'm also doing the rT3 protocol. The point T3 Circadian Method is to raise cortisol in the morning, so it's only meant for those with low morning cortisol.

                        Circadian T3 Method (CT3M or T3CM) for Adrenals--a great way to treat your low cortisol! | Stop The Thyroid Madness


                        I've gone a little crazy with taking my temps! To check adrenal function, one would check at 3,6 and 9 hours after waking. I check at waking, after exercise, 3,4,5,6,7,8,9.... lol

                        Ok, maybe not that much! It's does freak me out to see my temperature drop from 97.6 to 97.2! It's recommended to not exercise if you have adrenal fatigue. BUT... I have to, for T1 diabetes. I am cutting back a little on coffee though as it can be worse for adrenal fatigue. Friday instead of 1.5 cups of the strongest coffee ever, I had only 3/4 cup of strong coffee. My temp still dropped during my workout but I was able to do more with out my heart rate getting as high.

                        I'm on a journey to get to the bottom of all this!

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                        • I think a lot of posters on this thread:

                          Ray Peat Eating Guidelines : Semi Low-Carb Plans Forum : Active Low-Carber Forums

                          have diabetes. Here are some things I found a while ago:

                          Clin Exp Allergy. 1999 May;29(5):673-80.
                          Isolation and characterization of major banana allergens: identification as fruit class I chitinases.
                          Sanchez-Monge R, Blanco C, Díaz-Perales A, Collada C, Carrillo T, Aragoncillo C, Salcedo G.

                          Sugar lowers free fatty acids, allowing for the conversion (or "streaming") of alpha cells into insulin-producing beta cells. Free "essential" fatty acids destroy beta cells.

                          Stem Cells. 2010 Sep;28(9):1630-8.
                          Pancreatic β-cell neogenesis by direct conversion from mature α-cells.
                          Chung CH, Hao E, Piran R, Keinan E, Levine F.
                          Because type 1 and type 2 diabetes are characterized by loss of β-cells, β-cell regeneration has garnered great interest as an approach to diabetes therapy. Here, we developed a new model of β-cell regeneration, combining pancreatic duct ligation (PDL) with elimination of pre-existing β-cells with alloxan. In this model, in which virtually all β-cells observed are neogenic, large numbers of β-cells were generated within 2 weeks. Strikingly, the neogenic β-cells arose primarily from α-cells. α-cell proliferation was prominent following PDL plus alloxan, providing a large pool of precursors, but we found that β-cells could form from α-cells by direct conversion with or without intervening cell division. Thus, classical asymmetric division was not a required feature of the process of α- to β-cell conversion. Intermediate cells coexpressing α-cell- and β-cell-specific markers appeared within the first week following PDL plus alloxan, declining gradually in number by 2 weeks as β-cells with a mature phenotype, as defined by lack of glucagon and expression of MafA, became predominant. In summary, these data revealed a novel function of α-cells as β-cell progenitors. The high efficiency and rapidity of this process make it attractive for performing the studies required to gain the mechanistic understanding of the process of α- to β-cell conversion that will be required for eventual clinical translation as a therapy for diabetes.

                          Trends Endocrinol Metab. 2011 Jan;22(1):34-43. Epub 2010 Nov 8.
                          β-cell regeneration: the pancreatic intrinsic faculty.
                          Desgraz R, Bonal C, Herrera PL.
                          Type I diabetes (T1D) patients rely on cumbersome chronic injections of insulin, making the development of alternate durable treatments a priority. The ability of the pancreas to generate new β-cells has been described in experimental diabetes models and, importantly, in infants with T1D. Here we discuss recent advances in identifying the origin of new β-cells after pancreatic injury, with and without inflammation, revealing a surprising degree of cell plasticity in the mature pancreas. In particular, the inducible selective near-total destruction of β-cells in healthy adult mice uncovers the intrinsic capacity of differentiated pancreatic cells to spontaneously reprogram to produce insulin. This opens new therapeutic possibilities because it implies that β-cells can differentiate endogenously, in depleted adults, from heterologous origins.

                          Bioessays. 2010 Oct;32(10):881-4. doi: 10.1002/bies.201000074. Epub 2010 Aug 27.
                          A new paradigm in cell therapy for diabetes: turning pancreatic α-cells into β-cells.
                          Sangan CB, Tosh D.
                          Cell therapy means treating diseases with the body’s own cells. One of the cell types most in demand for therapeutic purposes is the pancreatic β-cell. This is because diabetes is one of the major healthcare problems in the world. Diabetes can be treated by islet transplantation but the major limitation is the shortage of organ donors. To overcome the shortfall in donors, alternative sources of pancreatic β-cells must be found. Potential sources include embryonic or adult stem cells or, from existing β-cells. There is now a startling new addition to this list of therapies: the pancreatic α-cell. Thorel and colleagues recently showed that under circumstances of extreme pancreatic β-cell loss, α-cells may serve to replenish the insulin-producing compartment. This conversion of α-cells to β-cells represents an example of transdifferentiation. Understanding the molecular basis for transdifferentiation may help to enhance the generation of β-cells for the treatment of diabetes.

                          Diabetes. 2012 Mar;61(3):632-41. Epub 2012 Feb 14.
                          Free fatty acids block glucose-induced β-cell proliferation in mice by inducing cell cycle inhibitors p16 and p18.
                          Pascoe J, Hollern D, Stamateris R, Abbasi M, Romano LC, Zou B, O’Donnell CP, Garcia-Ocana A, Alonso LC.
                          Pancreatic β-cell proliferation is infrequent in adult humans and is not increased in type 2 diabetes despite obesity and insulin resistance, suggesting the existence of inhibitory factors. Free fatty acids (FFAs) may influence proliferation. In order to test whether FFAs restrict β-cell proliferation in vivo, mice were intravenously infused with saline, Liposyn II, glucose, or both, continuously for 4 days. Lipid infusion did not alter basal β-cell proliferation, but blocked glucose-stimulated proliferation, without inducing excess β-cell death. In vitro exposure to FFAs inhibited proliferation in both primary mouse β-cells and in rat insulinoma (INS-1) cells, indicating a direct effect on β-cells. Two of the fatty acids present in Liposyn II, linoleic acid and palmitic acid, both reduced proliferation. FFAs did not interfere with cyclin D2 induction or nuclear localization by glucose, but increased expression of inhibitor of cyclin dependent kinase 4 (INK4) family cell cycle inhibitors p16 and p18. Knockdown of either p16 or p18 rescued the antiproliferative effect of FFAs. These data provide evidence for a novel antiproliferative form of β-cell glucolipotoxicity: FFAs restrain glucose-stimulated β-cell proliferation in vivo and in vitro through cell cycle inhibitors p16 and p18. If FFAs reduce proliferation induced by obesity and insulin resistance, targeting this pathway may lead to new treatment approaches to prevent diabetes.

                          Endocrine. 2011 Apr;39(2):128-38. Epub 2010 Dec 15.
                          Long-term exposure of INS-1 rat insulinoma cells to linoleic acid and glucose in vitro affects cell viability and function through mitochondrial-mediated pathways.
                          Tuo Y, Wang D, Li S, Chen C.
                          Obesity with excessive levels of circulating free fatty acids (FFAs) is tightly linked to the incidence of type 2 diabetes. Insulin resistance of peripheral tissues and pancreatic β-cell dysfunction are two major pathological changes in diabetes and both are facilitated by excessive levels of FFAs and/or glucose. To gain insight into the mitochondrial-mediated mechanisms by which long-term exposure of INS-1 cells to excess FFAs causes β-cell dysfunction, the effects of the unsaturated FFA linoleic acid (C 18:2, n-6) on rat insulinoma INS-1 β cells was investigated. INS-1 cells were incubated with 0, 50, 250 or 500 μM linoleic acid/0.5% (w/v) BSA for 48 h under culture conditions of normal (11.1 mM) or high (25 mM) glucose in serum-free RPMI-1640 medium. Cell viability, apoptosis, glucose-stimulated insulin secretion, Bcl-2, and Bax gene expression levels, mitochondrial membrane potential and cytochrome c release were examined. Linoleic acid 500 μM significantly suppressed cell viability and induced apoptosis when administered in 11.1 and 25 mM glucose culture medium. Compared with control, linoleic acid 500 μM significantly increased Bax expression in 25 mM glucose culture medium but not in 11.1 mM glucose culture medium. Linoleic acid also dose-dependently reduced mitochondrial membrane potential (ΔΨm) and significantly promoted cytochrome c release from mitochondria in both 11.1 mM glucose and 25 mM glucose culture medium, further reducing glucose-stimulated insulin secretion, which is dependent on normal mitochondrial function. With the increase in glucose levels in culture medium, INS-1 β-cell insulin secretion function was deteriorated further. The results of this study indicate that chronic exposure to linoleic acid-induced β-cell dysfunction and apoptosis, which involved a mitochondrial-mediated signal pathway, and increased glucose levels enhanced linoleic acid-induced β-cell dysfunction.
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                          • Hey, I mentioned the T3 thing in here!
                            Make America Great Again

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                            • Originally posted by Derpamix View Post
                              Hey, I mentioned the T3 thing in here!
                              I'm confused Derp... the T3 Circadian?

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                              • Wait, maybe it was somewhere else I did...
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