LadyIvy

Oh and class of 97 here

Oh, I hadnt even thought about that. I have 6 years to go and didnt think I would before I decided on surgery. You just made my night!

Just noticed that the thirties forum isn't used very often. I would love to get to know more people here. I am a 31 year old female that is preparing for surgery. I don't have a date yet, but just finished my last step so it should be soon. I have a 7 year old son and am concerned as to how he is going to react to the surgery. Do any of you have young children? How did they handle it?

I am fairly new to my job and should be getting my date soon. I was worried about this as well. I am not taking paid leave, nor am I using vacation time, or trying to use the FMLA. So I am glad someone posted this. I don't want everyone I work with to know (and they will). I would just like to leave it at "I have been scheduled for surgery and I will supply you with any documentation you may need". Luckily, I only work weekends so if I take almost a full 3 weeks off that is only 6 missed days of work. Good luck to you!

Also, the patient can have a BMI of 35.5-39.9 as long as it is paired with a co-morbidity such as diabetes mellitus, hypertension or hypercholesterolemia.

Hi everyone, Just wanted to say hello since I am new to this particular forum. I have not yet been sleeved, but have decided to go through with the procedure and have been preparing for a couple of months now. I finally finished the last of my requirements so am just waiting on a phone call to set a date. I'm excited and scared to death at the same time for numerous reasons. I can't wait to explore the forum more and understand the sleeve "for better or for worse" so that I can be as prepared as possible come surgery day! I look forward to chatting with you all

Regarding neuron growth and Ghrelin: Here is what I see in this primary article. (I found a few others that mirror the same results I just figured I would include the one). Ghrelin does seem to positively correlate with the growth of some neurons. However, these neurons control appetite and hunger along with other dietary regulatory functions. So, by this research, yes wikipedia is right in saying that Ghrelin seems to support neuron growth. Although, based on the other studies I have looked at, there are other places in your body that contain Gherlin. Removal of the stomach does not remove Gherlin from your body. If it is true that Ghrelin stimulates neuron growth in the areas of the brain that dictate appetite, then the neurons do not stop growing, they just slow down. The body has many specialized neurons that only respond to certain chemical ques. Not all neurons are related to memory function. There are not enough studies done on this to predict other roles that Gherlin might play. In this, we are all a bunch of lab rats. It is very clear the detrimental effects of chronic obesity. I will continue researching this and let you guys know if I find anything new. Does anyone read this differently? I am a biologist, not a neurologist or biochemist so I could be missing something. Thank you for the original posting. I really needed to look more into the biochemical function of this hormone anyway Memory loss can be attributed to so many things in the case of a surgery like the sleeve. As was mentioned above, we also have to look at the chance that it could be post-op healing, dehydration, change in metabolism, lack of nutrition, psychological and physical stress etc. http://journal.9med.net/qikan/article.php?id=196709 1. Hypothalamic appetite regulation Feeding is a basic behavior that is necessary for life. Long-term lack of food results in death. It is well accepted that appetite is controlled by the brain and that feeding behavior is regulated by complex mechanisms in the central nervous system, in particular the hypothalamus (70, 207, 256). Removal of the lateral hypothalamus causes hypophagia (decreased feeding), leading to death due to severe weight loss. On the other hand, removal of the ventromedial hypothalamus causes hyperphagia (increased feeding); treated animals increase both feeding amount and frequency, leading to weight gain and severe obesity. Thus feeding is regulated by a balance of stimulating and inhibiting forces in the hypothalamus. Recent identification of appetite-regulating humoral factors reveals regulatory mechanisms not only in the central nervous system, but also mediated by factors secreted from peripheral tissues (174, 216, 250, 267). Leptin, produced in adipose tissues, is an appetite-suppressing factor that transmits satiety signals to the brain (79). Hunger signals from peripheral tissues, however, had remained unidentified until the recent discovery of ghrelin. 2. Ghrelin neurons in the hypothalamic appetite regulatory region Immunohistochemical analyses indicate that ghrelin-containing neurons are found in the arcuate nucleus of the hypothalamus, a region involved in appetite regulation (133, 148). This localization suggests a role of ghrelin in controlling food intake. Moreover, a recent report has indicated that ghrelin is also expressed in previously uncharacterized hypothalamic neurons that are adjacent to the third ventricle between the dorsal, ventral, paraventricular (PVN), and arcuate (ARC) hypothalamic nuclei (48). In the ARC, these ghrelin-containing neurons send efferent fibers onto NPY- and AgRP-expressing neurons to stimulate the release of these orexigenic peptides and onto POMC neurons to suppress the release of this anorexigenic peptide (Fig. 10). Neural network of ghrelin in the PVN is more complex. In the PVN, ghrelin neurons also send efferent fibers onto NPY neurons, which in turn suppress GABA release, resulting in the stimulation of corticotrophin-releasing hormone (CRH)-expressing neurons, leading to ACTH and cortisol release (Fig. 10). 3. Ghrelin is a potent appetite stimulant When ghrelin is injected into the cerebral ventricles of rats, their food intake is potently stimulated (122, 173, 211, 246, 266). Among all discovered orexigenic peptide, ghrelin has been found to be the most powerful. Chronic intracerebroventricular injection of ghrelin increases cumulative food intake and decreases energy expenditure, resulting in body weight gain. Ghrelin-treated mice also increase their fat mass, both absolutely and as a percentage of total body weight. Not only intracerebroventricular injection, but also intravenous and subcutaneous injection of ghrelin have been shown to increase food intake (173, 246, 265). Ghrelin is produced primarily in gastrointestinal organs in response to hunger and starvation, and circulates in the blood, serving as a peripheral signal telling the central nervous system to stimulate feeding. 4. Mechanism of appetite stimulation by ghrelin The hypothalamic ARC is the main site of ghrelin's activity in the central nervous system. The ARC is also a target of leptin, an appetite-suppressing hormone produced in adipose tissues, and NPY and AgRP, which are both appetite-stimulating peptides (76, 163). NPY and AgRP are produced in the same population of neurons in the ARC, and their appetite-stimulating effects are inhibited directly by leptin. At least part of the orexigenic effect of ghrelin is mediated by upregulating the genes encoding these potent appetite stimulants (Fig. 10). As suggested by the distribution of ghrelin-containing neurons in the hypothalamus (Fig. 10), intracerebroventricular injection of ghrelin induces Fos expression in NPY-expressing neurons and increases the amount of NPY mRNA in the ARC (122, 173, 211). Moreover, intracerebroventricular ghrelin injection increases the AgRP mRNA level in the hypothalamus. The appetite-stimulating effects of ghrelin are blocked by an antagonist of NPY receptor 1. Intracerebroventricular injection of an AgRP inhibitor, anti-NPY IgG, or anti-AgRP IgG inhibits the appetite-stimulating effects of ghrelin. Intravenous injection of ghrelin also stimulates NPY/AgRP neurons in the hypothalamus. Immunohistochemical analysis indicated that ghrelin neuron fibers directly contact NPY/AgRP neurons (48). These results indicate that ghrelin exerts its feeding activity by stimulating NPY/AgRP