Bennett JL, Lam C, Kalluri SR, Saikali P, Bautista K, Dupree C, Glogowska M, Case D, Antel JP, Owens GP, Gilden D, Nessler S, Stadelmann C, Hemmer B.
Ann Neurol. 2009 Nov;66(5):617-29.
One of the specialists in the last discussion mentioned that they had looked up whether periodontal disease is linked to stroke and found that there does seem to be a correlation between the two. While reading this short article that showed data from 1,137 men I thought…. “Where is the data for women?”
So I decided to look up scholarly articles on gender differences between both sexes, and periodontal disease. I was not very lucky. I had my eye on an article called…
“Stroke. 2004 Sep;35(9):2029-35. Epub 2004 Jul 15.
Gender differences in the relationship between periodontal disease, tooth loss, and atherosclerosis.
Desvarieux M, Schwahn C, Völzke H, Demmer RT, Lüdemann J, Kessler C, Jacobs DR Jr, John U, Kocher T.
Source
Division of Epidemiology, School of Public Health, University of Minnesota, USA.”
But I was unable to find a pdf version I didn’t have to pay for, if anyone can find it please post a link on the site:)
Anyway I did come across something that I found interesting on this site (http://www.astdd.org/docs/Xiong2006periopregnancy.pdf) that relates to periodontal disease therefore inflammation in women. This review article States that there may be I link between periodontal disease and premature birth in pregnant women as well as preeclampsia and miscarriage. The periodontal pathogens seem to cause persistent inflammation, which is present throughout the disease. The study reviewed 25 studies and showed that 18 of those suggested an association. The studies where from all over the world the places ranged from USA, Chile, Turkey, Austria, Brazil, Canada, Hungary, Iceland, Saudi Arabia, and some others.
Nilsson OB, Adedoyin J, Rhyner C, Neimert-Andersson T, Grundström J, Berndt KD, Crameri R, Grönlund H.
PLoS One. 2011;6(9):e24558. Epub 2011 Sep 13.
Stroke (cerebral ischemia) is the third most common cause of death in the United States. Cerebral ischemia is caused by the lack of blood and oxygen to areas of the brain due to thrombosis (blockage) or bursting of blood vessels. Consequently, brain cells can die leading to irreversible brain damage. This damage can be severe or minor, depending on the blockage and the area damaged. Although loss of brain function is a major concern, other complications succeeding cerebral ischemia can be deadly. In fact, patients who experience a stroke are more likely to die from infection after day one than any other stroke related complications. Infections are very common due to a physiological suppression of the immune system. So why not administer immunotherapy with IFNγ to increase an immune response? This option does seem like the best strategy, but what if there is a proactive reason for immunodepression after a stroke.
If the immune system is being inhibited after a stroke, logically you could guess that the body is preemptively getting ready for an auto-immune response. Interestingly, a study was set up to test this theory. With a mouse model, this study detected increased numbers of myelin oligodendrocyte glycoprotein (MOG) specific T-cells after cerebrial ischemia. This means that T cells had an antigenic determinant for cells that partake in the myelinization of nerves. Three experiments tested the effects of this autoimmune phenotype.
1. Transgenic mice for these autoimmune T-cells developed autoimmune encephalitis, which is multiple sclerosis for mice.
2. Transferred MOG specific T-cells into naïve mice, which also developed autoimmune encephalitis.
3. Transferred splenocytes from mice (post cerebrial ischemia) into healthy mice. After inducing cerebrial ischemia, the mice experienced a worse outcome. To test this, naïve splenocytes were transferred into healthy mice without any difference in the outcome of the subsequent stroke.
This could explain immunodepression as a result of an auto-pathogenic expression in our immune system following a stroke. If this is so, how could we use these findings to decrease infection? An antibiotic therapy would most likely prove to be better than an administration of IFNγ to prevent infection, but wouldn’t prevent against viral infections. Thoughts?
Source:
One of the most popular diets on the market right now is the hCG diet. In fact one of my friends recently asked me if I know what hCG actually is and if it will work to loose weight, immediately I answered the best way is through lifestyle changes of eating right and exercising regularly of course, but then I got curious… so with that in mind I decided to find out.
The way the HCG “system” works is you take an oral or injected hormone and follow a diet plan, but lets start from the beginning with a series of questions that I would like answered if I was my friend.
1. Question 1: what is hCG?
a. hCG (Human chorionic Gonadotropin) is a hormone that regulates pituitary gland secretions in both men(very small amounts) and women. The placenta also releases it during pregnancy and is used as fertility treatments for women.
2. Question 2: Ok so if it’s a hormone that is released during pregnancy, how is it thought to help people lose weight? How was this even discovered?
a. I took this quote from http://www.hcgobesity.org/
i. While working in India, he (Dr. ATW Simeons, a British Physician) noticed that the so-called "fat boys," who showed Adiposogenital dystrophy improved their undescended testis when they were treated with hCG. But he also observed that body fat distribution modified during the treatment course. Therefore he hypothesized that if those children were concomitantly submitted to a very Hypocaloric diet they could reduce their body weight, consuming the "fat on the move".
b. This is kind of a cool idea, but after some experiments many researchers found that hCG was “of no use in the management of obesity” (the link above has more detail if you interested, and also a link to the scientific paper)
3. Question 3: If it obviously doesn’t work, then why are people saying its working?
a. The diet. The diet consists of 500 calories for a majority of days your on it! As we all know this is not enough to sustain anybody.
| Phases | Dosage | Calories | Days |
| Loading | 10-15 Drops 3 Times Daily | 1500 – 2000 Calories | 2 |
| Maintenance | 10-15 Drops 3 Times Daily | 500 Calories | 21-40* |
| Stabilization | No Drops Needed | Calorie intake should be gradually increased upto 800 (Women) – 1000 (Men). Avoid Sugar & Starch. | 21 |
| Total | | 44 | |
| *Maintenance Phase is not restricted to mere 21 protocol days but can be stretched till 40 days. | |||
“There are 3 phases of HCG diet plan. They are known as Loading, Maintenance and Stabilization Phase. Dieters should follow 2 days of loading phase, 21 – 40 days of Maintenance & 21 days of Stabilization phase.
Maintenance & Stabilization Phases are accompanied by VLCD (Very Low Calorie Diet) & are instrumental in burning Abnormal Fat.” http://www.hcg-diet.info/
4. Lets say people decide to ignorer the fact that it does not work and still do the hCG program, what are the risks?
a. Starvation (that’s my personal one lol)
i. Although http://www.hcg-diet.info/hcg-diet-info/faq/ disagrees with me… “Although you can expect to feel hungry during the first few days, your body will soon adjust to the HCG diet and once the HCG hormone begins to adjust your body’s metabolic rate, the hunger pangs will soon fade. In fact, because large amounts of calories are released from fat stores, it is not uncommon for HCG dieters to struggle to reach the 500-calorie threshold because they feel permanently full!
1. I don’t believe that!!!!!
b. I took the following from http://factoidz.com/the-health-risks-of-the-hcg-diet/
• Potentially life-threatening ovarian hyperstimulation syndrome (OHSS), call your doctor immediately if you have severe pelvic pain, stomach pain, swelling of the hands and feet, stomach swelling, weight gain, shortness of breath, vomiting, diarrhea and urinating less than normal.
• Mood swings
• Headaches
• Swelling breasts and water retention
• Increased risk of blood clots
• Restelessness
• Depression
• Hypoglycemia
• Gout
• Do not use HCG if you are pregnant, it can cause birth defects.
• Call your doctor if you have the symptoms of pain, warmth, tingling in your arms or legs, redness, severe headache, extreme dizziness and confusion.
• And remember, HCG is a fertility drug, if you do get pregnant, HCG can increase your chances of having twins, triplets or even quadruplets.
These are just a few, some sites even mention weight gain as a side effect!
4. The last Question is…Is this ultimately a good method for weight loss?
a. NO! The hormone does not work, as mentioned in a double blind study the placebo group lost as much weight as the actual hCG program patients (found under first web link given) and the risks are to great to ignore. So I would not advise anyone to follow this program… exercise and eating right are the key!
Now, the big question is how we are going to do that?
One way is by understanding the structural characteristic of human immune system. That is, at least now I understand why it is important to understand the very detail of anatomy and function of antibodies. So, let me step into the detail of it by put what we have learned so far from our class into the context of influenza case.
So far, we have learn that antibody have hypervariable region called Vl (for the light chain) and Vh (for the heavy chain). There are also CDR (Complementary Determining Region) which determine the specificity of each antibody to antigen. We believe also that the antibody have million preexisting “types” to anticipate whatever kind of pathogen molecular structures. But perhaps that won’t works for influenza viruses?
There are 16 antigenically different HA subtypes and 9 antigenically different NA subtypes of influenza viruses. The combination of these two components define all known existing subtypes of Influenza A viruses.
Now, the problem is how our antibody system could provide a rather broad strain protection, than only targeting the HA surface antigen of the viruses, which capable for changing rapidly to avoid and escape from our immune system.
One way to study how our immune system can protect us is to study the how antibody that the survivor of a novel influenza infected person works on preventing from fatal condition.
There is a clue that the antibody of the survivor have a broad protection of flu viruses which might involve a specific region HA2 which is located at the stem or stalk of the HA protein, not at the head!. The HA1 region at the head is believe as a decoy for influenza viruses to escape from neutralization. So, it is suggested that vaccine developer should re-focus on Broad Neutralizing Antibodies (BnAb) that targeting hydrophobic stem region of HA2 and inhibit fusion process, which showed to be cross reactive for multiple viruses, rather then focus on antibody that works on HA1 epitopes. Do you believe that?
Reference:
Han, T. and W. A. Marasco "Structural basis of influenza virus neutralization." Ann N Y Acad Sci. 2011 Jan, 1217: 178-90.
View here.
The most interesting topic that I found in our review articles was in “Young adult obese subjects with and without insulin resistance: what is the role of chronic inflammation and how to weigh it non-invasively” in The Journal of Inflammation. The method they used in answering the question of their paper, whether insulin resistance can be independent of metabolic syndrome, was by looking at the C-reactive protein and Fibrinogen levels associated with chronic inflammation in patients with metabolic syndrome. One of their ways to measure this was longitudinal spleen size. The paper found that the spleen becomes enlarged in young obese children with insulin resistance as opposed to young obese children without insulin resistance, spleen size is associated with insulin resistance and steatosis, and concluded that spleen size is a good way to diagnose insulin resistance. When do you usually hear about the spleen, a lymph organ with the main function of filtering red blood cells, playing any kind of role in diabetes? I tried looking up other articles that also showed any links between the Spleen and diabetes. Some articles tried to prove a causation pattern where a swollen spleen was because of diabetes. Others are finding new ways to use the cells of the spleen to find ways to treat diabetes by transferring spleen stem cells from a “diabetes resistant” rat to a “diabetes prone” rat. Here are some of the articles that I found interesting about this.
http://www.journal-inflammation.com/content/6/1/6
http://diabetes.diabetesjournals.org/content/38/1/24.abstract
http://diabetes.diabetesjournals.org/content/41/4/527.short
http://sageke.sciencemag.org/cgi/content/abstract/2005/3/pe2
We’ve all heard of things that can be harmful to the human body. Things like viruses, bacterium and parasites. But in the recent scientific world, many scientists are beginning looking into prions. What are prions? Prions are misfolded cellular proteins that are infectious and harmful to the body. Unlike the other infectious agents such as viruses, fungus, bacteria and such, prions does not have DNA,s RNAs, or both. They are abnormal proteins that have the ability to convert healthy proteins to diseased ones. And since these misfolded proteins is just an isoform of our healthy proteins. It makes it nearly impossible for the antibodies our system to detect them as ‘foreign’. The first prion is believed to have come from cows that ate feeders with infectious sheep scrapie and crushed up sheep bones back in the 1980s in Great Britian. Once an infectious prion gets into the body it begins to convert good proteins and replicates without being caught by patrolling lymphocytes! Once replication is done, the prions migrate to the nervous system and lymphoid organs. Prion causes deadly diseases such as Bovine Spongiform Encephalopathy (BSE) aka “Mad Cow Disease” and variant Creutzfeldt-Jakob disease (vCJD). Both diseases are brain degenerative diseases. BSE are found in cattle and vCJD are brain damage in humans. Holes are formed in the tissues of the brain that makes it look like a “sponge” and causes loss of emotions, memory, movement, speech, and sight.
How do we acquire these infectious prions? By consuming machine processed meat such as hamburger beef patties, hot dogs, meat on pizza toppings, taco fillings and sausages. America on average consumes 28 billion processed hamburgers a year. The entire world consumes an estimation of 200 billion hamburgers a year. That’s a lot of processed meat! In meat processing plants, the machine typically separates the spinal cord from the meat. However, the meat that gets separated is not always 100% free of nervous tissues. Occasionally, there are still some nervous tissues that tag along. Prions are resistant to chemicals and high pressure and temperature cannot denature the prions, so cooking or boiling the meat will not get rid of it. Having that said, the chance of getting a defective patty is fairly rare. According to U. S. Department of Agriculture, every 4 out of 70 beef patties contain spinal tissue residues and of the 4 patties none were infected with the deadly prion. But that doesn’t mean there won’t be any out there. So the next time you eat a burger, before you bite into that delicious, juicy, charbroiled burger, think twice before you do so.
Cited Sources:
Nuvolone M, Aguzzi A, Heikenwalder M. (2009) FEBS Volume 589, Issue 16, Pages 2674-2684, Protein Folding, Misfolding and Diseases “Cells and Prions: License to replicate”.
http://www.sciencedirect.com/science/article/pii/S0014579309004608
Hu W, Kieseier B, Frohman E, Eagar TN, Rosenberg RN, Hartung HP, Stüve O. (2008) J Neurol Sci. 2008 Jan 15;264(1-2):1-8. Epub “Prion proteins: physiological functions and role in neurological disorders”.
http://www.ncbi.nlm.nih.gov/pubmed/17707411
Hu W, Rosenberg RN, Stüve O. (2007) cta Neurol Scand. 2007 Aug;116(2):75-82. “Prion proteins: a biological role beyond prion diseases”.
http://www.ncbi.nlm.nih.gov/pubmed/17661791
David & Stephen Schmidt (2001) Nutrition Action June 2001 US Edition. “How Now, Mad Cow!”.
http://www.cspinet.org/nah/06_01/#3
As we discussed earlier in class, I mentioned the Pima Indian tribe and how obesity is related to type 2 diabetes here is some more insight on this topic that I have researched.
Type II diabetes is most prevalent among Native Americans especially the Pima of Phoenix, Arizona. Another Indian population that’s starting to be recognized for this epidemic is the Navajo Peoples, the largest tribe in the southwest. Both of these tribes are having an increased rate of diabetes among their population especially the younger generations. This increase is causing an exponential spike in health related issues from this disease. It also has put a financial strangle hold on the Indian Health Care programs and facilities. Not only has these two tribes been affected with this disease it has caused a cascading effect of assorted health care issues.
The Pima Tribe has been a part of a thirty year study relating diabetes with obesity. At the start of the study the Pimas incidence rate of having type-II diabetes was rising exponentially. Scientists have proven that obesity is a major risk factor in the development of diabetes. One-half of the adult Pima Indians have diabetes and 95% of those with diabetes are overweight (The Pima Indians). This result for this chronic disorder stems from the Pima and Navajo Indians eating high caloric foods. These foods are processed and refined. For thousands of years these Indian communities relied on hunting, farming, and fishing for food. The Pimas experienced seasonal droughts and hardship causing feast or famine. For these peoples to survive such periodic hardships of famine, scientists theorized they developed a “thrifty Gene.” This gene allowed these people to store fat when they feasted and in times of famine this fat storage would be used as fuel so they wouldn’t starve to death. This was their safety mechanism to survive as long as caloric intake was extremely low. Present day Native American tribes have assimilated to modern-day western lifestyles and diet. The “thrifty gene” began to oppose this new diet (redefined and processed high fat, sodium, and caloric foods), continuing to store calories in preparation for starvation mode. Researchers believe this opposing lifestyle has contributed to obesity. This gene once protected the Native Peoples from starvation but is now the reason behind chronic type II diabetes amongst these tribes.
Today diabetes is an epidemic in this country and is rising with no end in sight. The tribes that I have mentioned above, top the statistics of prevalence of type II diabetes. At least fifty percent of their population has this disorder and it’s starting to affect the younger generations which in turn will reach epidemic proportions among children. With this disease that cause multiple heath issues patient awareness through community education is critical. This in turn would reduce their risk for complications. By understanding the disease process and being aware, people can practice the skills necessary to better control their diets and maintain a more normal blood glucose level. These preventative measures would decrease health problems, obesity issues, and help by decreasing the economic effects on their health care system.
There is no doubt that the Pimas from Arizona were the trail blazers in diabetes studies. With the compiled research found on this tribe it has helped to pave a smoother understanding of how genetics and environmental changes cause such a crazy disease.
This is a very interesting topic and if you are interested in this kind of research I encourage you to read more about this issue with the Pima Indians and their relationship with type 2 diabetes.
