New Blog!

I'm restarting!  http://dsconfess.com

I'll delete this blog tomorrow.

Not Giving Up

I weigh 243.  DS FAIL.  The argument will be I failed it, and I won't disagree.

I lost my best window of weight loss.  With the almost dying and caloric tube feedings for several months after surgery, I didn't even start to lose until after the window closed.  After the first year, my body recovered and the weight gain has been continuous and inexorable. 

I don't feel as if I've been overeating, but I haven't been restricting what I eat, or dieting, either.

I'd been avoiding the scale and was shocked when I got on it.  I knew I'd gained weight, but didn't know it was that bad. 

I'm back with a renewed determination. 

Funny, it wasn't being fat that did it.  I think I've become resigned to that.  It was hot flashes and menopausal symptoms. Good Lord.  It's 100 degrees outside and there's an 500 degree oven on in my body too?  The sweating, the panting, the flushes, the sweating some more.  I can barely describe the discomfort.  My daughter says I sleep in Antarctica with AC blasting and multiple fans blowing gales on me.  It's the only way I can sleep at all. 

My last period was Dec '08, a little over two months before my surgery.  I think I've had no menopausal symptoms since now because of the weight loss and estrogen release.

I think I want to keep on releasing estrogen for another year and steel myself for this menopause with at least a normal sized body.  Hopefully, my fat still has enough estrogen it to forestall these symptoms. I'm fifty and on schedule and all, but I just don't want to deal with this over this gawdawful summer. 

I probably have some sort of mental block against being normal sized, because the menopause reason makes finally approaching weight loss so much easier.  I will put "Get Therapy" on my stat to do list too.  It probably should have been on there long ago. 


 My decision as to how to go about this is to cut carbs to the bone.  My goal is to low carb 75 pounds away. 

Holidays have settled out

215

I'm not dieting either.  I'm chilling as far as my weight.  I'm going to work on my head as far as diet--because what I tried for years before definitely never worked for me.  More to come as this gels.

Holiday Fall Out

218.5 pounds.  The weight gain was astonishing and easy.  Just like old days.

I'm back on the diet train, but I'm really struggling to make it something more livable and less like a diet.  I  want to lose fifty pounds.  I have that old feeling of looking up to this fifty pounds as an unsurmountable, unclimbable mountain of pain.

Back to the diet trenches.  Was the DS worth it?  Because of my complications and lack of satisfactory weight loss, I have to say "just barely."  I lived through it and lost 65-70 pounds.  The weight loss did increase my health immeasurably, but I might have to fight to keep it off.  Bottom line, I'm still fat.

Yes, it was only barely worth it--but if I had died, and I came close, it would have been tragically unworth it.  As it is, I have to live with the decision for the rest of my life.  Even if I do regain, I can't let my labs and supplements slip or I could suffer dire consequences.

For those people who blithely tell you to travel, to do this, to do that in regards to the DS--well, they might have the means to do whatever and you might not.  I didn't.  I had little close family, no friends, no husband, no support system, a fixed income, a child still in school, and a chronic illness along with fat that was  killing me.

I listened to all the input and weighed it, but I simply could not do what some others could--travel to this doctor or that.  I did what I could do, and tried to make the best decisions I could.

That's all we can do--our best.  

Consider the decision to have the DS well, very well.  If you live, it might be worth it, but maybe not.  I'm on the border of not-worth-it.  But if you die, it definitely won't be worth it, but you won't know it.  I almost died and I can tell you this--I wasn't worried.  I would have simply slipped away.

Weight and Eating Report

I've been 213.5 the last couple of days.  Day before yesterday, that was depressing, because I'd done well.  Yesterday, not so good.

My body is stabilizing from the rapid weight loss, I guess.

I'm starving now, going to cook some beef.

Weight and Eating Report

I'm holding steady at 213.5.  Yesterday wasn't stellar.  I ran around and thus was unorganized with my food.  I ate out at Burger King--yep, the bun.  What else?  Just a few slips, a bite here, a bite there.  Hopefully, today will be better.

Why curcumin works for my RA

I was diagnosed with RA after an awful flare that hospitalized me back in April after my DS Feb 4 (and those hospitalizations for complications through March).  I take Curcumin (needs to have piperine in too to work) and Coramega.  It makes a noticeable difference and I have NO other flares close to the first one after nine months and my pain is under control without Motrin.


I knew the Curcumin worked, but I just learned WHY it works.

Interleukin-1 (IL1) is essential for systemic inflammatory bone loss

Objectives: Chronic inflammation is a major risk factor for systemic bone loss leading to osteoporotic fracture and substantial morbidity and mortality. Inflammatory cytokines, particularly tumour necrosis factor (TNF) and interleukin-1 (IL1), are thought to play a key role in the pathogenesis of inflammation-induced bone loss, but their exact roles are yet to be determined.

Methods: To determine whether TNF directly triggers bone loss or requires IL1, human TNFα mice (hTNFtg) were crossed with mice lacking IL1α and IL1β (IL1−/−hTNFtg). Systemic bone architecture was evaluated using CT scanning, static and dynamic bone histomorphometry and serum markers of bone metabolism.

Results: hTNFtg mice developed severe bone loss accompanied by a severe distortion of bone microarchitecture. Bone trabeculae were thinner and decreased in numbers, resulting in increased trabecular separation. Histomorphometric analyses revealed strongly increased bone resorption in hTNFtg mice compared with wild-type mice. In contrast, IL1−/−hTNFtg mice were fully protected from systemic bone loss despite still developing inflammation in their joints. Lack of IL1 completely reversed increased osteoclast formation and bone resorption in hTNFtg mice and the increased levels of RANKL in these mice. Structural parameters and osteoclast and osteoblast numbers were indistinguishable from wild-type mice.

Conclusions: These data indicate that IL1 is essential for TNF-mediated bone loss. Despite TNF-mediated inflammatory arthritis, systemic bone is fully protected by the absence of IL1, which suggests that IL1 is an essential mediator of inflammatory osteopenia. -- http://ard.bmj.com/content/69/01/284.abstract?etoc

 Curcumin blocks IL1

Curcumin is a dietary compound with diverse anti-inflammatory and anticarcinogenic effects in several experimental models. A mechanism by which curcumin exerts these actions might be the direct modification of protein thiols, thereby altering the activity of the affected proteins. An early event in inflammatory signaling cascades is the recruitment of the interleukin-1 (IL-1) receptor–associated kinase (IRAK) to the IL-1 receptor (IL-1RI) upon stimulation with IL-1. IRAK recruitment was shownrecently to be inhibited by agents that modify thiols of IRAK. We asked, therefore, whether IRAK is also a target for curcumin. Curcumin indeed blocked IRAK thiols in a murine T-cell line stably overexpressing IRAK (EL-4^IRAK), which resulted in the inhibition of IRAK recruitment to the IL-1RI and phosphorylation of IRAK and IL-1RI-associated proteins. Inhibitory effects were not reversible by thiol-reducing agents. Thus, modification by curcumin did not occur by oxidation but rather by alkylation, as is typical for electrophilic compounds reacting as Michael addition acceptors. The block in one of the earliest events in the IL-1 signaling cascade can explain the often observed inhibition of IL-1-mediated signaling steps by curcumin further downstream. Hence, thiol modification might be a crucial step in the anti-inflammatory functions of curcumin. -- http://jn.nutrition.org/cgi/content/abstract/135/8/1859 

We have previously demonstrated that anti-inflammatory and antioxidant compound curcumin (diferuloyl-methane) inhibits the expression of monocyte chemoattractant protein-1 (MCP-1/JE) in bone marrow stromal cells by suppressing the transcriptional activity of the MCP-1/JE gene. Since both AP-1 (TRE) and NF-kB (kB) binding motifs are present in the promoter of MCP-1/JE gene, we examined the effect of curcumin on IL1 alpha- and TNF-alpha-induced activation of ubiquitous transcription factors AP-1 and NF-kB by electrophoretic mobility shift assay and Western blotting. IL1 alpha and TNF-alpha rapidly induced both AP-1 and NF-kB DNA binding activities in +/+(-)1.LDA11 stromal cells. However, treatment of these cells with curcumin blocked the activation of AP-1 and NF-kB by both cytokines. These data suggest that inhibition of MCP-1/JE transcription by curcumin involves blocking of AP-1 and NF-kB activation by IL1 alpha or TNF-alpha.  -- http://www.ncbi.nlm.nih.gov/pubmed/9439980