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 

Weight and Eating Report

I lost another pound and a half!  My morning weight is 213.5.  My morning weight before my weight gain was 212.5 so I'm only a pound away from baseline.

This low carb eating is working as far as losing weight.  The protein drinks (I really only like it in hot beverages, usually coffee, caf or decaf, but low cal spiced apple cider packets will work too) make it easier to stick to lower carb eating.

I am eating some carbs in the evening without it stalling my weight loss.  I had chicken, green beans, dressing,  and cranberry sauce for dinner last night.  Got the cravings and dug out a protein bar.  Later realized that it wasn't a low carb one, but one of those Snickers Marathon bars.  Need to buy some Atkins bars.

I woke up starving.  I'm sipping my coffee with whey protein and have a low carb omelet in the oven (2 eggs with 1/2 c half and half and a T of French onion dip, 4 slices of bacon cut up and fried with 1/2 a small onion, and topped with grated sharp cheddar).  Have finally kicked my potato jones to the curb (none in the house except some potato flakes in the pantry).

Why did I have SUCH a hard time doing this--controlling my eating enough to take off the rest of the weight I want to lose?  I don't want to speak too soon, I've only been doing this for a few days--but if I could control my eating reliably, I'd not have needed the surgery.

My immediate goal is to make Onederland.  That would be wonderful.  It would be more wonderful if I could make by my year surgery date.

Weight and Eating Report

I lost a pound. 215 morning weight.

I'm doing good at avoiding sugar...but need tightening up on the carbs.  Slipped in a bit of bread.

I'm revising the eating plan.  I'm going to include protein drinks and allow a serving of carb (such as one piece of bread or a bit of potato) with dinner.

Coffee with whey protein (20 g)  Take calcium, my extra D and anti inflammatories for RA (curcumin, Cormega) 

No carb sit down meal with protein--usually eggs Take the rest of my supplements and iron.  I'm taking KCl too.

Drink with whey protein   Take calcium

No cab sit down meal 

Drink with whey protein  Take calcium

One serving of carbs with a sit down meal 2nd omeprazole

So far, so good.  I made the best eggs, yum!  I fried bacon and onion then added frozen spinach. I mixed up eggs with heavy cream and French onion dip and poured the mixture into the cast iron skillet with the spinach and bacon and added this brie cheese that I found at the back of the fridge.  Diced it.  Then I baked it in the oven until the eggs were firm.  Almost better than sex!

Went to church this morning.  They had a pot luck afterwards, and I slipped up a bit on the carbs, but not badly.  Have gotten my protein drinks in, just have one more to go.  

Weight and Diet Report

Other than taking my supplements and trying to mind my health, I've been ignoring the weight.  It bothers me that I haven't lost the weight I wanted to lose as easily as I wanted to lose it.

I've been going hog wild on sweets over the holidays.  I got on the scale earlier this week and saw a five point weight gain.  Up to 217.5 from 212.5 early am weight.  That shook me.

I thought of an eating plan I believed I could stick to and so far, so good.   I'm down to 216  after one day.

Stop the sweets and sugar!  Just stop.  Eat meals.  Mandatory food.  Once I eat the mandatory food, the plan is that I'm satisfied and won't eat more crap.  NO sugared beverages.

Breakfast
Eggs...I like them baked.  I mix three with heavy cream and sourcream onion dip with a little Lawry's season salt and smokehouse pepper and bake in a small cast iron skillet with unlimited bacon
Coffee and half and half

Lunch
Lettuce and raw veggie salad with a cup of meat salad.  I love the chicken salad from Aldis.

Dinner
Meat
Veggies I like

Snacks
Cheese or peanut butter and Wasa Fiber Rye crackers (low carb)
Olives, nuts, cream cheese

More labs: Vits A&D

My D was up to 28 from 18 in just a few weeks with just a few thousand IUs supplemented.  A was 35 mcg, within normal limits.

In Western nations apparently toxicity from too much A is far more of a danger than deficiency.  From wikipedia...

Since vitamin A is fat-soluble, disposing of any excesses taken in through diet is much harder than with water-soluble vitamins B and C, thus vitamin A toxicity may result. This can lead to nausea, jaundice, irritability, anorexia (not to be confused with anorexia nervosa, the eating disorder), vomiting, blurry vision, headaches, hairloss, muscle and abdominal pain and weakness, drowsiness and altered mental status.

Acute toxicity generally occurs at doses of 25,000 IU/kg of body weight, with chronic toxicity occurring at 4,000 IU/kg of body weight daily for 6–15 months.^[25] However, liver toxicities can occur at levels as low as 15,000 IU per day to 1.4 million IU per day, with an average daily toxic dose of 120,000 IU per day. In people with renal failure 4000 IU can cause substantial damage. Additionally excessive alcohol intake can increase toxicity. Children can reach toxic levels at 1500IU/kg of body weight.^[26]

In chronic cases, hair loss, dry skin, drying of the mucous membranes, fever, insomnia, fatigue, weight loss, bone fractures, anemia, and diarrhea can all be evident on top of the symptoms associated with less serious toxicity.^[27]

It has been estimated that 75% of people may be ingesting more than the RDA for vitamin A on a regular basis in developed nations. Intake of twice the RDA of preformed vitamin A chronically may be associated with osteoporosis and hip fractures. This may be due to the fact that an excess of vitamin A can block the expression of certain proteins that are dependent on vitamin K. This could hypothetically reduce the efficacy of vitamin D, which has a proven role in the prevention of osteoporosis and also depends on vitamin K for proper utilization^[28].

High vitamin A intake has been associated with spontaneous bone fractures in animals. Cell culture studies have linked increased bone resorption and decreased bone formation with high vitamin A intakes. This interaction may occur because vitamins A and D may compete for the same receptor and then interact with parathyroid hormone which regulates calcium.^[26]Indeed, a study by Forsmo et al. shows a correlation between low bone mineral density and too high intake of vitamin A.^[29]

Toxic effects of vitamin A have been shown to significantly affect developing fetuses. Therapeutic doses used for acne treatment have been shown to disrupt cephalic neural cell activity. The fetus is particularly sensitive to vitamin A toxicity during the period of organogenesis.^[14]

These toxicities only occur with preformed (retinoid) vitamin A (such as from liver). The carotenoid forms (such as beta-carotene as found in carrots), give no such symptoms, but excessive dietary intake of beta-carotene can lead to carotenodermia, which causes orange-yellow discoloration of the skin.^[30][31][32]

Researchers have succeeded in creating water-soluble forms of vitamin A, which they believed could reduce the potential for toxicity.^[33] However, a 2003 study found that water-soluble vitamin A was approximately 10 times as toxic as fat-soluble vitamin.^[34] A 2006 study found that children given water-soluble vitamin A and D, which are typically fat-soluble, suffer from asthma twice as much as a control group supplemented with the fat-soluble vitamins.^[35]

Chronically high doses of Vitamin A can produce the syndrome of "pseudotumor cerebri".^[36] This syndrome includes headache, blurring of vision and confusion. It is associated with increased intracerebral pressure.^[37]

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