Vaccine Magic Explained: Even When it’s the Wrong Strain, it Still Kinda Works by “Vaccine Magic”
What's the best way to consume it: If you want to avoid the life span-shortening symptoms of aging, you need to maintain optimal AMPK activity. After initial stabilization management requires consideration of the size of defect, prematurity and associated anomalies. The Rothschilds plan was to cause the United States to build up such a debt in fighting this war that they would have to surrender to the Rothschilds and allow the charter for the Rothschild owned First Bank of the United States to be renewed. Here this loop of bowel undergoes a degree counterclockwise twist at its neck.
This study mirrored another one last year which showed that rats fed the compound developed fewer tumors and a delay in tumor establishment. The study's co-author, Salman Hyder gave a sad commentary on today's horrible Pharma paradigm. He pointed out that since this is a compound that you can extract from plants not patentable we won't see industry putting a dime into research. And since its effects are not specific on any one cancer process, it's not likely that government funding agencies will help either.
I've written extensively about the wonders of bioflavonoids. The late Tom Lahey, who told me about luteolin in Advanced Memory Formula , also provided me with a wealth of information on bioflavonoid actions against cancer. Curcumin belongs to this family as does green tea, Seanol and resveratrol. I am observing innovative combinations of bioflavonoids having remarkable effects in a combined approach to cancer. In addition to the foods I've already mentioned, you'll find apigenin in apples, leeks, onions, broccoli, cherries, grapes, tomatoes, and tea.
Note that these plant foods reduce your risk of getting cancer in the first place. Other foods include basil, oregano, cilantro, tarragon, beans, and barley. You'll do very well to include such produce in your daily diet! Yours for better health and medical freedom, Robert J.
Epub May 9. If you'd like to receive your own Second Opinion Health Alert, please sign up on our website: It's vital these substances heal cancer cells and leave normal cells untouched.
I've told you about some of my discoveries in the past. They include resveratrol, green tea, Alginol, and others. But today I'm going to tell you about another plant that safely starves cancer cells as efficiently as a powerful chemo drug.
In fact, it even works on pancreatic cancer cells, which are particularly difficult to kill. This plant is a common vegetable from Asia called "bitter melon. And it did so after just 72 hours of treatment! In the past, I've told you about apoptosis. That's nature's way of dealing with wayward or old cells. They simply kill themselves. Bitter melon juice induced this programmed cell death along several different pathways. And even better, it also activated a pathway which knocks out the cancer cells' metabolism of glucose.
In other words, it literally starved them of the sugar they need to survive. Do these lab-dish studies apply to living animals? University of Colorado researchers gave mice bitter melon at doses easily achievable in humans.
This level of effectiveness beat the most commonly used chemo drugs for this lethal cancer. The dose used in mice translates to 6 grams of powder for an average-sized adult 75 kg.
Big Pharma is rushing to find patentable petrochemicals to achieve what God put into the bitter melon fruit. You don't need any fancy chemicals to treat cancer.
What's more, the actions of bitter melon may help diabetics as well. Researchers recently found that bitter melon ameliorates metabolic syndrome by its beneficial effects on glucose metabolism.
Healing cancer must be multifocal. Eliminate dental infections and toxic dental materials, alkalinize your body, avoid chemical and heavy metal exposure, detoxify, forgive, oxidize the body with oxidation therapy, and give specific nutrients to throw a monkey wrench into cancer's peculiar metabolic pathways.
You can find bitter melon extract at most health food stores and online. Better yet find a grocery store many Asian markets that sells it, buy a lot and freeze it. Pregnant or lactating women probably shouldn't overdo this veggie. Science News, March 12, Box , Norcross, GA , or Readers are advised to consult with their own physician before implementing any health idea they read about, whether here or in any other publication. For Cancer, along with Bitter Melon www. Avoid all sweeteners except a small amount of either steam-distilled stevia www.
The reason you have to use even these safe sweeteners judiciously is that when your tongue tastes something sweet, it tells your pancreas to churn out insulin in preparation for sugar, and when comes, you get hypoglycemia low blood sugar, dizziness, weakness, etc.
And, surprisingly, I am in agreement with the mainstream. Cancer is a systemic disease, though currently treated conventionally as a local problem you carve out. Cells that degenerate into cancer have to make many genetic switches to "make it". Even after a cell turns to cancer, the abnormal cell must evade your immune system, the last line of defense. A functioning immune system will pick off cancer cells before they pick you off.
But cancer cells have learned to confuse your immune cells. Cancer cells express a protein called CD47 in large amounts in their membranes. This protein tells your macrophages immune cells , "Do not eat me. Researchers in the lab of Irving Weissman at Stanford have treated mice with an antibody that blocks and hides the CD47 marker. It effectively hides the CD47 and calls on the immune system to kill the cancer.
Now, the lab has recently tested this in cultured human cancer cells. They found that by blocking the CD47 "do not eat me signal," the macrophages did, indeed, attack and eat the cancer cells.
But without the antibody, the macrophages ignored the cancer cells completely. In the living mice so treated, implanted human cancers all had shrinkage of the tumors, no spread to lymph nodes, and remained cancer-free for four months that's a long time for a rodent after the treatment was stopped. From an editorial in Science, "In mice given human bladder cancer tumors, for example, 10 of 10 untreated mice had cancer that spread to their lymph nodes.
Only one of 10 mice treated with anti-CD47 had a lymph node with signs of cancer. I've maintained for 30 years that cancer is a failure of the immune system. That failure is due in part to the cancer blinding itself to your immune cells. Kelley and Gonzales successfully treat treated cancer with proteolysis pancreatic enzymes.
These enzymes may eat away the immune "cloaking" of cancer, enabling your immune cells to go and eat them up. It fits my observations of some cancers, even in late stage, disappearing with immuneenhancing oxidation and nutritional therapies. Conventional medicine is likely to move to a single antibody to "cloak" the cloaking protein.
This may work, but as a single protein, it also may have significant toxicity as does other single antibody immune treatments. Also, cancer may simply outwit a single antibody by making other cloaking proteins, much like insects outwit pesticides. Nevertheless, I really like this line of research and will keep you posted.
I don't think that there will ever be a "one size fits all" approach to cancer. We have seen some stunning successes, but have our "failures" as well. If you have cancer, please see an integrative physician who can work with your immune system with a variety of approaches, including nutritional and oxidation. Cancer cells secrete an enzyme called nagalase, which pulls a sugar molecule off a key protein called Gc.
This process inactivates the cancer-hunting macrophages so that they cannot see the tumor cells just like CD A discovery found that GcMAF inactivates nagalase. The Gc protein is no longer inactivated, enabling immune cells to see and attack cancer cells right in your body. It now is in Japan at www. You also can find it at www. Patients, with the assistance of their integrative doctors, can order the product and have their doctor administer it. This will be an exciting addition to our therapies, most of which are designed to enhance immune function.
Proceedings National Academy of Sciences, vol. Also in this issue: Six agricultural pesticides are suspected. These include maneb, mancozeb, methyl parathion, and carbaryl If you find this information useful, please subscribe to Dr. This diet is made up primarily of raw fruits and vegetables. While many have said this diet won't work, the proof that it does continues to come out.
In fact, each passing year brings new proof of my long-term observations and conclusions. Now there's yet more proof that the heat you use on your foods does, indeed, cause you much greater risk for diabetes and vascular disease.
This new proof comes from a new randomized, cross-over diet study on 62 volunteers. Cross-over studies are great in that they allow the studied groups to switch roles. That adds a lot of significance to the findings. The researchers in this study evaluated the effects of Maillard reaction products MRP on the volunteers. MRP is a name for a chemical process by which heat generates literally hundreds or more of a complex mixture of compounds responsible for a huge range of odors and flavors.
Heating starches to high temperatures creates acrylamide. I've told you in the past about how this compound can increase your risk of cancer.
Flavor scientists have used heat over years to create artificial flavors, which you'll find in processed foods. The diets of the two groups differed only in the type and amount of heat inflicted on the foods they ate. One group steamed their food and the other used high temperature cooking. After one month, those consuming high-heat treated diets compared to steaming saw significantly lower insulin sensitivity.
They also had much lower plasma concentrations of long-chain omega-3 fatty acids, vitamin C, and vitamin E. These findings were highly significant. The authors concluded that consuming high heat-treated foods increases your risk of type-2 diabetes and vascular disease.
What an international stir that would make! But you can do it right in your own kitchen! How to flush metals from your body and make yourself healthier and more youthful at the same time! No painful or uncomfortable treatments involved I'm a maverick who looks outside the box. I've been to India where I've seen hard-working vegetarian peasants losing limbs to diabetes in their 30s. And no, they were not obese. They cook their foods to oblivion in oil.
We've known for years that heat destroys crucial vitamins like C, B6, and now E. It also destroys fatty acids, denatures proteins, and limits mineral availability. But we are now getting an inkling of how heated foods causes yet deeper and subtler damage. Heat creates compounds not found in nature. These compounds could be highly immune activating, carcinogenic, toxic oxidants, oxidized lipids the underlying cause of vascular disease dangerous amines, and more.
I urge you to move toward the Living Foods Diet. Science is proving me right month after month. It's no wonder that I see miracle after miracle in my practice. But they're not "miracles. Use only water to cook with.
That upper limit of heat may be below the threshold for the most toxic chemical reactions. Never cook with oil. There's just no control for how hot it gets. Am J Clin Nutr. Epub Mar As a token of our appreciation for being our valuable customer, we'd like to give you two special reports that show you how to make your supplements work even better and how to stop cancer, memory loss, and diabetes for just pennies a day absolutely free.
All you have to do right now is click the "Like Us On Facebook" button below to become a fan of our Facebook page and get instant access to these two special reports. Click the "Like Us On Facebook" button below. If you would like to contact us with a question or comment, please send us a message to feedback secondopinionnewsletter. The compound capsaicin — that causes this pungent heat — is also found to kill cancer cells.
In fact, in the last few years, the research on chili peppers has focused on many organs including, the pancreas, brain, prostate, colon and breast. Do chili peppers harm healthy cells? Among them, the study on prostate cancer cells drew more interest from researchers. Experiments, on the compound capsacisin reveal that this compound specifically targeted the tumors and cancerous cells without affecting the healthy cells. It was found that capsaicin was able to do this by interfering with protein synthesis of the cancer cells, degradation of the cell DNA and interfering with cell transcription mechanisms of cancerous cells.
While capsaicin affected the mitochondrial pathway of the cancer cells, there was no interference in the activity of healthy cells. This was observed in cancer-induced albino rats in lab studies. A study published in Cancer Research revealed that capsaicin was effective in inhibiting prostate cancer cells.
The study found that capsaicin promoted automated cell death in primary types of prostate cancer cell lines — as well as in cancer cells caused by hormones. Furthermore, capsaicin decreased the expression of prostate-specific antigen PSA and inhibited the ability of the dihydrotestosterone to activate PSA. When lab animals received four weeks of treatment with capsaicin, it was observed that prostate cancer growth and size significantly decreased.
Chili peppers do more than just prevent cancer Compounds in chili peppers have been associated with multiple benefits like positive immune health, weight loss, lower risk of diabetes, and heart-healthy effects. A randomized, cross-over study among 27 healthy subjects revealed that consuming freshly chopped chili prevented the oxidation free radical damage to the fat cells — which was a crucial factor in decreasing heart problems.
Capsaicin is also anti-inflammatory in nature. It inhibits substance P, a neuropeptide associated with inflammation that results in pain, heart diseases and other conditions. Because of this property, it has been used in a variety of chemotherapy studies for pain relief and also in many treatments involving nerve fiber disorders, conditions like psoriasis, arthritis plus many more. Researchers say, the hotter the pepper, the higher is its capsaicin content, good examples include habanero and scotch bonnet peppers followed by jalapeno.
Ways to use chili peppers in your next recipe Chili peppers can give any bland recipe an interesting taste. So, the next time you sauté vegetables in a stir fry try adding some chili peppers to accentuate its health benefits as well as spice up a bit. Other ways to super-charge your recipes include, adding minced chili peppers to plain yoghurt as a salad dressing; in salsa for extra hot taste; pureeing a small amount with tomatoes or olives to give a surprising twist to your recipes.
Just be very careful when you are handling fresh chili peppers, direct contact with skin, lips and eyes can cause a severe burning sensation. Be sure to use cooking gloves instead of bare hands when using them for cooking.
Consuming chili peppers, in moderation, is considered safe, however if you are allergic to peppers or night shade family, it is a good idea to keep away from this spice. Another important point to keep in mind is to buy organic hot peppers instead of conventionally grown ones.
Looking for natural health solutions? Sign up now — for our free, weekly show featuring the greatest minds in natural health and science plus a free gift! International Imuunopharmacology, vol 17 2 Cancer Res Mar 15;66 6: Clinical applications of capsaicinoids. Clin J Pain Jun;16 2 Suppl: Laetrile cures cancer — naturally http: You can also download the free iPhone application that is available in the iTunes store.
Shopper's Guide to Pesticides in Produce http: Cosmetic Safety Database http: This article lists the "dirty dozen" as well as which foods have the least pesticide residue: The Curse of Convenience http: From as far back as first having a fire to warm us, we learned to contain it in stones that radiated the heat leading to what most of us love and still Produced with Free Range Studios and hosted by Annie Leonard, the seven-minute film by The Story of Stuff Project reveals the implications for consumer and worker health and the environment, and outlines ways we can move the industry away from hazardous chemicals and towards safer alternatives.
The film concludes with a call for viewers to support legislation aimed at ensuring the safety of cosmetics and personal care products. And, for all you fact checkers out there, http: The amount of lead found in of the lipstick products tested was greater than the maximum 0. NaturalNews issues boycott of Kashi, Silk, Larabar and more http: Russia bans GMOs in the wake of the cancer tumor rat study. France is seeking a European-wide ban on GMOs. Is the end of Monsanto's evil reign near?
Boycott of "Organic Cheater" Brands PDF printable version of the above press release can be found here. Your list states Nature's Gate does not make a natural or organic claim.
Communicating the verifiable benefits of organic farming and products to society. Shopper's Guide to Personal Care Products List of over businesses who have signed on to endorse this campaign http: Bronner's Lawsuit with Ecocert read the cross complaint http: Shopper's Guide to Personal Care Products Read and print the shopper's guide to 1,4-dioxane-free personal care products http: The guide is now also available as an iPhone application.
The Best and Worst Vegetables to Eat http: One person's food may be another person's poison. Jack Thrasher on the Health Dangers of Molds http: Vitamin D and Tuberculosis] http: See articles about GMO and other topics: It does include generic tips designed to help consumers identify and avoid genetically modified GM foods, including the hidden GM ingredients labeled ingredients on foods that read more like a chemical periodic table on grocers shelves.
Here's a list of relative mercury contamination in wild fish: The types of fish that are higher in omega-3 are healthier for you smaller Salmon, Sardines and Anchovies , and wild-caught or line-caught are much healthier choices than farmed fish usually fed corn meal, which is high in omega-6 pro-inflammatory oil, even if its "organic", ground up smaller fish, hogs, etc.
Wild fish eat krill, plankton and algae, which is why they are high in healthy astaxanthin and omega-3 oils. The following are ingredients that may be made from GM soy, corn, cotton, or canola You can learn more about the Non-GMO project by visiting: High levels of EMF exposure are generated by common household devices such as hair dryers, can openers, heating pads and even some computer monitors.
EMF exposures destroy health and well-being, claims panel of top international scientists http: There is no end to the tricks that endocrine disruptors can play on our bodies: The list also includes common contaminants that many people don't realize can be hormone disruptors, not only those familiar toxins - arsenic, mercury and lead - but other, less familiar chemicals such as glycol ethers and perfluorinated chemicals. The guide is intended for consumers of all ages, particularly young people who are most at risk from these dangerous substances.
EWG researchers compiled the new Dirty Dozen list by scouring scientific literature and identifying the most hazardous and widely-used hormone-disrupting chemicals that pollute the environment and ultimately our bodies. These substances are frequently found in food, water and consumer products. Studies have linked them to a wide array of health problems, including cancer, birth defects, lowered sperm count, lowered IQ, obesity and thyroid disease.
This is a must-see list of chemicals to avoid - check it out today! Click here to see 12 of the worst hormone disruptors, how they do their dirty deeds, and some tips on how to avoid them. See this brand-new list of the dirtiest and most common endocrine disruptors. We hope you learn something new from the endocrine disruptor Dirty Dozen. Take a look at the label on your jar of skin cream.
Do you see any of these ingredients? Now, this is a big deal - because The medical world already knows this. The same way your skin soaks up the medicine in those patches, it absorbs all of the ingredients in your skin cream - including the toxic ones. And that can cause health problems for you down the road.
These harsh skin care chemicals can also destroy your complexion - and make you look years older. Claim a FREE Special Report that reveals how breakthrough plant stem cell technology - combined with 36 other "all-natural" skin-restoring nutrients - can help you smooth away the appearance of lines and wrinkles Your complexion is still too dull Your anti-aging cream is letting you down — and it may be worse than you think Hidden inside most skincare products are dangerous chemicals and synthetic ingredients.
Take a good look at the label on your anti-aging cream. You may be shocked to find: The trouble is… they also mimic estrogen, which can throw your hormonal balance out of whack and trigger potentially serious problems with your reproductive system. It can cause allergic reactions, skin irritations, and even liver abnormalities and kidney damage. Sodium Laurel Sulfate has also been found to cause urinary tract, bladder and kidney infections Especially DEA, which has been linked to kidney, liver and other organ damage They can also destroy your complexion — and make you look years older than you actually are Think that the label that says "organically grown" has anything to do with the packaging, storage, and transport of that product to stores?
What if I told you that cow, pig, and chicken collagen is now used in place of wax on your fruits and vegetables, among many other things much worse than you can probably imagine? And what if then I told you, as with most atrocities that happen now-a-days, that this is all approved by the FDA Since the early 12th century, there has been a tradition of applying wax onto the skins of fruits and vegetables for longer storage life. Today, that tradition is being carried on with a whole new generation of chemicals and compounds that are genetically designed to accomplish the same goal.
But in these modern times, the health and well-being of the consumer of that apple is not necessarily the goal of this unnatural, inorganic process. Prepare yourself to be shocked and amazed that our Federal agency that is designed to protect us, the Food and Drug Administration, is allowing these dangerous and unhealthy practices to be perpetrated on an unwitting public, all in the name of profits.
This video was recently posted to Youtube, showing a woman peeling off of her freshly bought supermarket romaine lettuce what appears to be a plastic coating, similar to the type one would peal off of the screen of a new electronic gadget.
She has no idea what she has discovered Shopper's Guide to Pesticides in Produce It's also important to remember that not all organic compounds are good for us either. For instance, lead is a naturally-occuring compound and completely organic and it's deadly to humans.
The same goes for the leaves of rhubarb plants, arsenic found in many fruit pits, and mistletoe to name a few. Download our free Guide or get it for your iPhone or Android!
This is probably the most urgent question the public has about these novel foods. Opinion polls show that up to 90 percent of the American public wants GE foods labeled. But despite this overwhelming demand, almost no foods on U.
And the biotech industry does not voluntarily identify them, fearing, probably correctly, that the majority of Americans would avoid GE foods if given a choice. As a result, the U. However, this is not the case with most of our major trading partners around the globe who have instituted mandatory labeling of all GE foods and ingredients. The Guide is designed to help you reclaim your right to know about the foods you are buying, and help you find and avoid GE foods.
In addition to a list of brands that produce non-GE foods, the mobile app also offers contact information for the companies that DO use GE ingredients. This feature enables you to personally voice your opposition on the use of GE foods directly to these companies, right from the app.
Our Shoppers Guide gives you valuable information on common GE ingredients, brands to look for, and look out for, and common sense tips to keep you in the know. Stop shopping in the dark and get your Shoppers Guide today! PC PDF file http: The New Dirty Dozen http: The medical establishment usually chalks up those deaths to cancer.
But the media and The missing link - How to beat cancer with garlic http: This arsenal of cancer cell killers relies on certain nutrients to have the fuel to do its Turmeric and curcumin prevent formation of new blood vessels induced by arsenic, cancer http: Most of turmeric's health benefits are attributed to the trio of yellow-orange chemicals Alcohol consumption is directly related to breast cancer: How I took it, and how much I took. Bear in mind, this is what I did. You will have to decide for yourself what is Best for You!
As promised, we've just published detailed new heavy metals composition charts on vegan proteins and rice proteins. These charts also include data on the exciting new SunWarrior "Warrior Blend" formulas, which turn out to be remarkably low in the heavy metals we've tested for: How avoiding conventional dentistry can literally save your life If you see a dentist, make sure she's a holistic dentist.
It turns out that conventional dentistry is incredibly toxic and can quite literally cause your death: The American Dental Association continues to maintain that mercury fillings and root canals are safe dental procedures, in spite of the overwhelming evidence against High Intensity Short Duration exercise -- not aerobic which generates lots of free radicals; search www.
Just exercise more, scientists discover A more active lifestyle doesn't just reduce your risk of cancer and improve survival rates among cancer patients: Medical mutilations have been performed lately on women told they are genetically Obamacare to punish healthy eaters as insurance rates double or triple for those who choose to take care of their health According to an analysis just published by the Wall Street Journal, healthy people will pay double or triple their current A detailed analysis of Obamacare health insurance rates reveals something very disturbing: Healthy people will be paying double or triple the rates they are currently paying, while premiums will go down for those who live on junk foods and develop chronic disease.
The economic incentives are all backwards: Obamacare will punish healthy people while subsidizing those who refuse to take care of their health. Here are the numbers: There has been some decline in cigarette smoking in the USA, but with all the known health issues associated with smoking cigarettes, it seemed there should be almost no new domestic smokers at all.
But the power of advertising has prevailed, even more so in third world countries with less restrictions on cigarette advertising. Is it the Tobacco Plant, or Something Else? Avoid enclosed areas where people smoke. The Department of Health and Human Services had approved chemical additives to cigarettes by Among them are ammonia compounds to create a nicotine freebase effect. Then there are the toxic additives to the paper to make it burn evenly. Cadmium is a heavy metal with a half-life of 10 to 30 years residence in human tissue, and it easily surpasses toxic levels.
Few mention chemtrails or aerosol geoengineering exposure because most deny their existence. Deny them all you want, but the heavy metal nanoparticles have been trapped in ground level water or air traps after heavy chemtrailing include, among others, barium, aluminum, and cadmium. Retired neurosurgeon and author Dr. Russell Blaylock has voiced concerns over chemtrail aluminum nanoparticles that are breathed in and make their way into the central nervous system and brain.
Access a study on that here. Then begin watching your sky objectively. You can protect yourself from those toxic nanoparticles by detoxing heavy metals often. My favorites are lots of chlorella, fresh organic cilantro, and cliniptilolite zeolite powder not capsules or liquids. Here are 6 foods for natural heavy metal chelation. A five day detox with 1.
Shallenberger - Real Cures newsletter July , Vol. But which ones are the most important? Almost all of my diabetic patients have seen tremendous results using these. Chromium piccolinate— Chromium is an important element in your glucose tolerance factor GTF. GTF is made up of chromium, niacin, and the amino acids cysteine, glutamic acid, and glycine, and worksin tandem with insulin to regulate blood sugar levels.
I suggest a dose of 1, mcg to 3, mcg daily. Alpha lipoic acid— Serves a central role in fat metabolism. It is critical for the production of acetyl-coenzyme A from fat. Acetyl-coenzyme A is the substance that kick starts the energy production cycle.
In the event of a deficiency of this enzyme, lactic acid levels rise in the body and can lead to lactic acidosis — a potentially life-threatening condition.
Lipoic acid is important for preventing the onset of diabetes, improving blood sugar control, reducing the incidence of cataracts in diabetics, preventing kidney damage which is a common diabetes complication , and it also helps prevent peripheral neuropathy which is common in diabetics. Many cases of diabetic neuropathy can be improved and even cured using mg, three times a day. In the absence of neuropathy, I recommend doses of mg two times a day. I consider lipoic acid an absolutely essential part of any treatment or prevention strategy for diabetes.
Niacinamide— This is a specific form of niacin. Niacin is a nutrient all of us should get more of. For diabetics, it's one of the most important nutrients for maintaining proper fat metabolism and correct triglyceride levels. I have my patients take a minimum of mg of niacinamide a day. Preferably , mg daily. L-Carnitine— L-Carnitine works incombination with fat molecules, lipoic acid, and acetyl-coenzyme A to penetrate the membrane of the mitochondria. I recommend 1, mg to 3, mg of carnitine daily.
Glycyrrhiza glabra— You probably know this one as licorice. Licorice is one of my favorite herbs for my diabetic patients because of its amazing effect on exhausted adrenal glands. It contains natural precursors for the production of adrenal hormones. It works in a similar way to the adrenal hormone aldosterone, which is often deficient in adrenal insufficiency. In rare cases, supplementing with licorice can slightly elevate blood pressure levels.
If you have hypertension, it's important to keep a check on blood pressure levels when taking licorice. In addition, licorice can also lead to a decline in potassium levels.
Vanadium— Like chromium, vanadium is another trace mineral that plays an enormous role in the activity of insulin. In the form of vanadyl sulfate, it not only improves insulin resistance, but has its own insulin effect, making it especially important for people with low insulin levels. It does this by increasing the number of islet cells in the pancreas and actually regenerates and repairs islet cells previously destroyed by free radicals.
Other herbs— I also recommend a number of herbal supplements to help improve insulin sensitivity. One is Galega officinalis, which contains an ingredient called guanidine from which the diabetes drug metformin is produced.
And the second is Mormodica Charantia, or bitter lemon. I recommend mg of a 4: Together, these two herbs alone can have a modest effect on insulin sensitivity, but when combined with the other supplements mentioned here, they can make quite a difference.
Clots, Strokes -- but not for bleeding strokes] Dr. The smaller the window the better. Legs one day; upper body next. Too much exercise is not good and prematurely wears the body out. Intense in and out. The more stressed you are the more acidic you are and the more cortisol death hormone and toxic hydrogen peroxide is being released leading to more and more and more problems.
You want to bring down the stress, cortisol and hydrogen peroxide levels while simultaneously raising ph. MATCHA tsp daily lowers cortisol, activates ampk and autophagy, inhibits mtor, energy, appetite suppression. Zero cream sweeteners, fats or calories these all halt the positive effects of the fast, create insulin resistance and insulin secretion. Aspirin or willow before bed ampk activator, lowers morning cortisol. The fat around your organs goes first and the fat around your belly last.
Stay the course; slow and steady wins the race!!!! Or keep it simple and get Interstellar Spice and Peel. Diabetes is a byproduct of free radical damage. Flavonoids are the most powerful free radical scavengers on the planet. No wonder diabetes and insulin resistance is rampant! Our findings confirm a fundamental role of RLIP76 in regulating the function of obesity-promoting pro-inflammatory cytokines, and provide a novel mechanism for targeted therapy of obesity and metabolic syndrome.
Thus, in the absence of RLIP76, increases in these lipid-peroxidation products are insufficient by themselves to turn on any signaling pathway that can increase BG or lipids. Resveratrol, commonly used anti-oxidant, is known to activate AMPK which could contribute to its protective effects from high fat diet induced insulin-resistance  , .
HMG-CoA limits the rate of cholesterol synthesis in liver tissue. Loss of RLIP76 significantly affects the activation of stress and apoptosis pathway proteins  ,  , .
These medications generally function to increase the effectiveness of insulin-mediated postprandial inhibition of hepatic gluconeogenesis. RLIP76 knock-out mice survive well and are active. In our extensive and previously published studies, RLIP76 inhibition specifically leads to targeting signaling of importance in diabetes mellitus and other oxidative stress related conditions like cancers where targeting RLIP76 leads to selective cancer cell death without affecting the survival of normal cells and tissues  ,  — .
Hence, both global and selectively targeted approaches can be reasonably pursued as required while targeting RLIP In conclusion, our results suggest that RLIP76 is a key effector controlled by multiple proteins known to regulate the metabolic abnormalities of diabetes and metabolic syndrome, and that in its absence drugs that target these proteins will fail to function.
A novel strategy for targeting breast cancer. Intake of citrus fruits is known to reduce the risk for incidence of breast cancer. Western blot and histopathological analyses of resected tumors showed a decline in the levels of survival and proliferation markers Ki67, pAkt, survivin, and cell cycle proteins CDK4 and cyclin B1.
Collectively, the ability of 2HF to decrease RLIP76, VEGF and regulate critical proliferative, apoptotic and differentiation proteins together provides strong rationale to further develop 2HF based interventions for targeting breast cancer. Nootkatone, a characteristic constituent of grapefruit peel, stimulates energy metabolism and prevents diet-induced obesity by activating AMPK.
Here, we identified and characterized nootkatone, a constituent of grapefruit, as a naturally occurring AMPK activator. Whole body energy expenditure evaluated by indirect calorimetry was also increased by nootkatone administration.
Long-term intake of diets containing 0. These findings indicate that long-term intake of nootkatone is beneficial toward preventing obesity and improving physical performance and that these effects are due, at least in part, to enhanced energy metabolism through AMPK activation in skeletal muscle and liver. While it is generally accepted that the primary cause of obesity is energy imbalance, i.
Hence, molecular processes and pathways more proximal to the origins of obesity—those that directly regulate energy metabolism or caloric intake—appear to be more feasible targets for therapy. In particular, nitric oxide NO is emerging as a central regulator of energy metabolism and body composition. NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin resistant patients, and increasing NO output has remarkable effects on obesity and insulin resistance.
This review discusses the role of NO in regulating adiposity and insulin sensitivity and places its modes of action into context with the known causes and consequences of metabolic disease. Catalase neutralizes the toxic effects of hydrogen peroxide. You WANT a lean agile muscular physique like Bruce Lee —NOT the freak of nature, totally unhealthy hulk a n a b o l i c s t e r o i d artificially induced body building fake muscle mass. Abnormal, artificial muscle and mass comes at the expense of longevity by hyperactivating mTOR.
All time stupid idea. Do you know any hulk sized super centenarians? Green and black teas have been extracted by serial chloroform, ethyl acetate and n-butanol, and divided into four subfractions designated as GT for green tea and BT for black tea, respectively. The total extracts from green and black teas exhibited a potent scavenging capacity of exogenous H2O2 in a dose-dependent manner.
It appeared that the total extracts from black tea scavenged H2O2 more potently than those from green tea. When tested individually, the potency of scavenging H2O2 by green tea subfractions was: In addition, we demonstrated that total fractions of green and black teas substantially inhibited the induction of 8-OHdG in calf thymus by all three portions of UV spectrum UVA, B and C.
Consistent with the capacity of scavenging H2O2, the subfractions from black tea showed a greater inhibition of UV-induced 8-OHdG than those from green tea. At low concentrations, the order of potency of quenching of 8-OHdG by green tea subfractions was: Addition of - -epigallocatechin gallate EGCG , an ingredient of green tea extract, to low concentration of green and black tea extracts substantially enhanced the scavenging of H2O2 and quenching of 8-OHdG, suggesting the important role of EGCG in the antioxidant activities of tea extracts.
These results suggest that aging-associated reductions in AMPK activity may be an important contributing factor in the reduced mitochondrial function and dysregulated intracellular lipid metabolism associated with aging. Specific signaling through AMPK and p38 MAPK to PGC-1 may therefore explain in part the metabolic remodeling in- duced by intense interval exercise training, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.
Background— Intermittent fasting IF , a dietary regimen in which food is available only every other day, increases the life span and reduces the incidence of age-associated diseases in rodents. We have reported neuroprotective effects of IF against ischemic injury of the brain. In this study, we examined the effects of IF on ischemic injury of the heart in rats.
Methods and Results— After 3 months of IF or regular every-day feeding control diets started in 2-month-old rats, myocardial infarction MI was induced by coronary artery ligation. Twenty-four hours after MI, its size in the IF group was 2-fold smaller, the number of apoptotic myocytes in the area at risk was 4-fold less, and the inflammatory response was significantly reduced compared with the control diet group.
Serial echocardiography revealed that during 10 weeks after MI with continuation of the IF regimen , the left ventricular LV remodeling and MI expansion that were observed in the control diet group were absent in the IF group. In a subgroup of animals with similar MI size at 1 week after MI, further observation revealed less remodeling, better LV function, and no MI expansion in the IF group compared with the control group.
Conclusions— IF protects the heart from ischemic injury and attenuates post-MI cardiac remodeling, likely via antiapoptotic and antiinflammatory mechanisms. Nitric oxide repairs the damaged mitochondria which excretes toxic hydrogen peroxide in your body which grays your hair and rapidly ages you. Drink your arugula and beet juice daily and before and after dry fasts! Beets and arugula are the highest natural sources of nitrates that convert through bacteria in saliva to nitic oxide.
It has been recently found that mitochondrial biogenesis and function are enhanced by nitric oxide NO , which is a key signaling molecule in vascular homeostasis. To understand dry fasting deliberate dehydration and starvation is to understand hormesis. Even water and oxygen in excess can be deadly; as can their absence. What we are doing is deliberately stressing the body— to make it more resilient. Too much dry fasting can kill just as over eating or over drinking can kill.
Wake me up when we got a real crisis on our hands. All about hormesis here: SIRT1 stands for sirtuin silent mating type information regulation 2 homolog 1 S. SIRT1 is an enzyme that deacetylates proteins that contribute to cellular regulation reaction to stressors, longevity.
A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction CR delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 SIRT1 is induced in CR rats as well as in human cells that are treated with serum from these animals.
Insulin and insulin-like growth factor 1 IGF-1 attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death.
Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells. Immune system defects are at the center of aging and a range of diseases. Here, we show that prolonged fasting reduces circulating IGF-1 levels and PKA activity in various cell populations, leading to signal transduction changes in long-term hematopoietic stem cells LT-HSCs and niche cells that promote stress resistance, self-renewal, and lineage-balanced regeneration.
Multiple cycles of fasting abated the immunosuppression and mortality caused by chemotherapy and reversed age-dependent myeloid-bias in mice, in agreement with preliminary data on the protection of lymphocytes from chemotoxicity in fasting patients.
These findings link the reduced levels of IGF-1 caused by fasting to PKA signaling and establish their crucial role in regulating hematopoietic stem cell protection, self-renewal, and regeneration. However, thermogenic gene expression remained impaired even when the receptor was bypassed with a cell-permeable cAMP analog, revealing the existence of a second inhibitory mechanism. Ramadan fasting has not only been spiritually beneficial but it has physical, psychological, social and health benefits.
Ramadan is a month of self regulation, process of self purification, truthfulness and self trainings with the hope that this training will last beyond the end of Ramadan.
One advantage of fasting is that the poor are given attention and benefits from charity and the faithful practice of the concept of neighbourhood and hospitality. The physiological effect of fasting includes lowering of blood sugar, lowering of cholesterol and lowering of the systolic blood pressure.
In fact, Ramadan fasting would be an ideal recommendation for treatment of mild to moderate, stable, non-insulin diabetes, obesity and essential hypertension. Fasting is powerful therapeutic processes that can help people recover from mild to severe health conditions.
Our body has a self healing power, in order to activate this power, the stomach must be kept empty, if Ramadan fasting is done properly it can help to recover from most diseases. P53, also known as TP53 or tumor protein EC: It is very important for cells in multicellular organisms to suppress cancer.
Ghrelin the anti-aging hunger hormone is released about 12 hours after your last meal. This is why you want lots of Ghrelin: But what about lack of water and kidneys? Klotho, a protein counteracting aging, is a powerful inhibitor of 1,dihydroxyvitamin D3 [1,25 OH 2D3] formation and regulator of mineral metabolism. The present study reveals a novel effect of bicarbonate, i. An acidogenic Western diet results in mild metabolic acidosis in association with a state of cortisol excess, altered divalent ion metabolism, and increased bone resorptive indices.
Acidosis-induced increases in cortisol secretion and plasma concentration may play a role in mild acidosis-induced alterations in bone metabolism and possibly in osteoporosis associated with an acidogenic Western diet. Our results decipher the mechanism by which catechins such as EGCG, or green tea in general, have been successfully consumed for thousand of years for general health benefits. These polyphenolic compounds may serve as model structures for the development of novel agents to treat the metabolic syndrome and related diseases.
Acid administration causes an increase in the liver glycogen concentration and in the daily excretion of nitrogen and sulfur in the urine, while the alkalosis leads to a decrease from normal in all of these values.
It is concluded from this that the antiketogenic effect of acidosis depends upon an increase in protein catabolism and an increase in glucose formation therefrom, while alkalosis is ketogenic because it has an opposite effect upon this process. We want MORE ketosis fat burning not less!
Once your ph drops you are eating muscle. These data provide a potential therapeutic strategy against cardiomyocyte injury triggered by pH fluctuations. It usually takes place around the 18 hour mark and goes away after a few hours. This is the brain switching off glucose and now using ketones for fuel. The headache could also be symptomatic of caffeine withdrawal.
Totally normal; push through, it passes. For example, fasting protects mice against high dose chemotherapy in part by reducing serum IGF-I signalling but does not protect cancer cells, since oncogene mutations prevent the activation of the stress resistance pathways in response to the reduction in glucose, IGF-I and other growth factors caused by nutrient deprivation Over 24 weeks, a low-carbohydrate diet program led to greater weight loss, reduction in serum triglyceride level, and increase in HDL cholesterol level compared with a low-fat diet.
ADHD Adiponectin is associated with longevity and heightened insulin sensitivity and has anti cancer properties; it is a hormone excreted primarily from adipose tissue fat. Fasting is exceptional for releasing Adiponectin and preventing adhd not to mention inhibiting disease and prolonging life.
Centenarians and high Adiponectin levels https: FGF21 the starvation hormone Fibroblast growth factor FGF21 is a hormone secreted by the liver during fasting that elicits diverse aspects of the adaptive starvation response. Among its effects, FGF21 induces hepatic fatty acid oxidation and ketogenesis, increases insulin sensitivity, blocks somatic growth and causes bone loss. These findings raise the possibility that FGF21 can be used to extend lifespan in other species. While FGF21 is expressed in numerous tissues, including liver, brown adipose tissue, white adipose tissue and pancreas, circulating levels of FGF21 are derived specifically from the liver in mice.
The sacred role of glucose as source of energy now is broken into small pieces. Therefore human body build up its biomass arising from glucose, thereby carbohydrates or meals are just a source of carbon chains of different lengths, branching; combinations with other elements and so forth.
We could say that glucose C6 H12O6 is the perfect building block. Our body is able to synthesize even nucleic acids with it. But our body fulfills its energy needs by means of the unexpected and astonishing capacity of melanin to split and re-form the water molecule.
For constipation or bowel issues: You can also skip this altogether and drink this at feeding window and dry fast or fluid restrict ie. Explore both options to find best fit. You want a plan that you can stick to and that provides results.
Some of these effects became more intense in cytokine-induced cells. Most of the above processes are more pronounced in cytokine-induced cells. He Shou Wu Polygonum multiflorum. Both Rhodiola rosea extracts and salidroside have contrast molecular mechanisms on cancer and normal physiological functions.
The molecular mechanism is, however, not well understood. PPD also decreases the levels of proteins related to cell proliferation. Moreover, PPD-induced apoptosis is characterized by a dose-dependent down-regulation of Bcl-2 expression and up-regulation of Bax, and is accompanied by the activation of Caspase-3 as well. Further molecular mechanism is revealed by direct stochastic optical reconstruction microscopy dSTORM —a novel high-precision localization microscopy which enables effective resolution down to the order of 10 nm.
It shows the expression and spatial arrangement of mTOR and its downstream effectors, demonstrating that this ginsenoside exerts its excellent anticancer effects via down-regulation of mTOR signaling pathway in Hep-2 cells. Taken together, our findings elucidate that the antitumor effect of PPD is associated with its regulation of mTOR expression and distribution, which encourages further studies of PPD as a promising therapeutic agent against laryngeal carcinoma.
Total extracts or saponins from this plant have been shown to exert a wide range of beneficial effects such as reducing cholesterol and blood glucose levels, strengthening immunity, and inhibiting cancer growth [ ]. These activities likely overlap with diverse downstream effects on AMPK activation [ 9 ].
In vitro studies revealed that damulin A and B, two dammarane-type saponins purified from the leaves of G. We recently reported that, the ability of a G. In both cultured HepG2 and L6 myotube cells, this heat-processed G. Although the antiobesity activities of G. Parents should know the objectives, indications and limitations of an orchiopexy: To improve spermatogenesis producing an adequate number of spermatozoids surgery should be done before the age of two.
Electron microscopy has confirmed an arrest in spermatogenesis reduced number of spermatogonias and tubular diameter in undescended testis after the first two years of life. Other reasons to pex are: The management is surgical; hormonal Human Chorionic Gonadotropin treatment has brought conflicting results except bilateral cases.
Surgery is limited by the length of the testicular artery. Palpable testes have a better prognosis than non-palpable. Laparoscopy can be of help in non-palpable testis avoiding exploration of the absent testis. Viens, MS University of Toronto. An umbilical hernia is a small defect in the abdominal fascial wall in which fluid or abdominal contents protrude through the umbilical ring.
The presence of a bulge within the umbilicus is readily palpable and becomes more apparent when the infant cries or during defecation. The actual size of the umbilical hernia is measured by physical examination of the defect in the rectus abdominis muscle, and not by the size of the umbilical bulge. The size of the fascial defect can vary from the width of a fingertip to several centimetres. Embryologically, the cause of an umbilical hernia is related to the incomplete contraction of the umbilical ring.
The herniation of the umbilicus is a result of the growing alimentary tract that is unable to fit within the abdominal cavity. Umbilical hernias are more prevalent in females than in males and are more often seen in patients with African heritage. The increased frequency of umbilical hernias has also been attributed to premature babies, twins and infants with long umbilical cords.
There is also a frequent association with disorders of mucopolysaccharide metabolism, especially Hurler's Syndrome gargoylism. Most umbilical hernias are asymptomatic; the decision to repair the umbilical hernia in the first years of life is largely cosmetic and is often performed because of parental request, not because of pain or dysfunction.
In the past, some parents use to tape a coin over the umbilical bulge, however, manual compression does not have an effect on the fascial defect. Treatment of umbilical hernia is observation. However, surgical repair is recommended if the hernia has not closed by the age of five. The incidence of incarceration trapped intestinal loop is rare, even in larger defects. Females should especially have their umbilical hernia corrected before pregnancy because of the associated increased intra-abdominal pressure that could lead to complications.
The procedure is simple and incidence of complication such as infection is extremely rare. The repair is usually done as outpatient surgery under general anesthetic. Inguinal and umbilical hernia repair in infants and children. Surg Clinics of North Am 73 3: Swenson's Pediatric Surgery - 5th edition.
The developing human - 4th edition. Philadelphia, WB Saunders, pp. Some observations on umbilical hernias in infants. The comparative incidence of umbilical hernias in colored and white infants. J Natl Med Assoc The three most common abdominal wall defect in newborns are umbilical hernia, gastroschisis and omphalocele. Omphalocele is a milder form of primary abdominoschisis since during the embryonic folding process the outgrowth at the umbilical ring is insufficient shortage in apoptotic cell death.
Defect may have liver, spleen, stomach, and bowel in the sac while the abdominal cavity remains underdeveloped in size. The sac is composed of chorium, Wharton's jelly and peritoneum. The defect is centrally localized and measures cm in diameter. A small defect of less than 2 cm with bowel inside is referred as a hernia of the umbilical cord.
Epigastric localized omphalocele are associated with sternal and intracardiac defects i. Cardiac, neurogenic, genitourinary, skeletal and chromosomal changes and syndromes are the cornerstones of mortality. Cesarean section is warranted in large omphaloceles to avoid liver damage and dystocia. After initial stabilization management requires consideration of the size of defect, prematurity and associated anomalies.
Primary closure with correction of the malrotation should be attempted whenever possible. Antibiotics and nutritional support are mandatory. Manage control centers around sepsis, respiratory status, liver and bowel dysfunction from increased intraabdominal pressure. The protruding gut is foreshortened, matted, thickened and covered with a peel.
The IA might be the result of pressure on the bowel from the edge of the defect pinching effect or an intrauterine vascular accident. Rarely, the orifice may be extremely narrow leading to gangrene or complete midgut atresia. In either case the morbidity and mortality of the child is duplicated with the presence of an IA. Alternatives depend on the type of closure of the abdominal defect and the severity of the affected bowel.
With primary fascial closure and good-looking bowel primary anastomosis is justified. Angry looking dilated bowel prompts for proximal diversion, but the higher the enterostomy the greater the problems of fluid losses, electrolyte imbalances, skin excoriation, sepsis and malnutrition. Closure of the defect and resection with anastomosis two to four weeks later brings good results. Success or failure is related to the length of remaining bowel more than the specific method used. Initially do an Apt test to determine if blood comes from fetal origin or maternal origin blood swallowed by the fetus.
If this coagulation profile is normal the possibilities are either stress gastritis or ulcer disease. If the coagulation profile is abnormal then consider hematologic disease of the newborn and manage with vitamin K.
The apt test is performed by mixing 1 part of vomitus with 5 part H2O, centrifuge the mixture and remove 5 ml pink. If the coagulation profile is abnormal give Vit K for hematologic disorder of newborn. If it's normal do a rectal exam.
A fissure could be the cause, if negative then consider either malrotation or Necrotizing enterocolitis. The stress includes prematurity, sepsis, hypoxia, hypothermia, and jaundice. These babies frequently have umbilical artery, vein catheters, have received exchange transfusions or early feeds with hyperosmolar formulas.
The intestinal mucosal cells are highly sensitive to ischemia and mucosal damage leads to bacterial invasion of the intestinal wall. Gas-forming organisms produce pneumatosis intestinalis air in the bowel wall readily seen on abdominal films. Full-thickness necrosis leads to perforation, free air and abscess formation. These usually premature infants develop increased gastric residuals, abdominal distension, bloody stools, acidosis and dropping platelet count.
The abdominal wall becomes reddened and edematous. There may be persistent masses and signs of peritonitis. Perforation leads to further hypoxia, acidosis and temperature instability.
The acid-base status is monitored for worsening acidosis and hypoxia. The white blood cell count may be high, low or normal and is not generally of help. Serial abdominal films are obtained to look for evidence of free abdominal air, a worsening picture of pneumatosis intestinalis, or free portal air.
Therapy consist initially of stopping feeds, instituting nasogastric suctioning and beginning broad-spectrum antibiotics ampicillin and gentamycin.
Persistent or worsening clinical condition and sepsis or free air on abdominal films require urgent surgical intervention. Attempts to preserve as much viable bowel as possible are mandatory to prevent resultant short gut syndrome. Complicated NEC is the most common neonatal surgical emergency of modern times, has diverse etiologies, significant mortality and affects mostly premature babies.
Consist of a right lower quadrant incision and placement of a drainage penrose or catheter under local anesthesia with subsequent irrigation performed bedside at the NICU.
Initially used as a temporizing measure before formal laparotomy, some patient went to improvement without the need for further surgery almost one-third. They either had an immature fetal type healing process or a focal perforation not associated to NEC? Some suggestion made are: PPD should be an adjunct to preop stabilization, before placing drain be sure pt has NEC by X-rays, persistent metabolic acidosis means uncontrolled peritoneal sepsis, do not place drain in pts with inflammatory mass or rapid development of intraperitoneal fluid, the longer the drainage the higher the need for laparotomy.
In the initial evaluation a history should be obtained for bleeding disorders, skin lesions, and aspirin or steroid ingestion. The physical exam for presence of enlarged liver, spleen, masses, ascites, or evidence of trauma or portal hypertension. Labs such as bleeding studies and endoscopy, contrast studies if bleeding stops. Common causes of Upper GI bleeding are: Esophagus a Varices- usually presents as severe upper gastrointestinal bleeding in a year old who has previously been healthy except for problems in the neonatal period.
This is a result of extrahepatic portal obstruction portal vein thrombosis most commonly , with resulting varices. The bleeding may occur after a period of upper respiratory symptoms and coughing.
Management is initially conservative with sedation and bedrest; surgery ir rarely needed. Treatment consist of antacids, frequent small feeds, occasionally medications and if not rapidly improved, then surgical intervention with a fundoplication of the stomach. This was thought to be uncommon in children because it was not looked for by endoscopy. It probably occurs more often than previously thought.
Treatment initially is conservative and, if persistent, oversewing of the tear through an incision in the stomach will be successful. They bleed when there is ectopic gastric mucosa present. Total excision is curative. Occasionally requires surgical intervention with local repair or ligation of hepatic vessels.
Anal fissure is the most common cause of rectal bleeding in the first two years of life. Outstretching of the anal mucocutaneous junction caused by passage of large hard stools during defecation produces a superficial tear of the mucosa in the posterior midline. Pain with the next bowel movement leads to constipation, hardened stools that continue to produce cyclic problems. Large fissures with surrounding bruising should warn against child abuse.
Crohn's disease and leukemic infiltration are other conditions to rule-out. The diagnosis is made after inspection of the anal canal. Chronic fissures are associated with hypertrophy of the anal papilla or a distal skin tag. Management is directed toward the associated constipation with stool softeners and anal dilatations, warm perineal baths to relax the internal muscle spasm, and topical analgesics for pain control.
If medical therapy fails excision of the fissure with lateral sphincterotomy is performed. Meckel's diverticulum MD , the pathologic structure resulting from persistence of the embryonic vitelline duct yolk stalk , is the most prevalent congenital anomaly of the GI tract. MD can be the cause of: Diagnosis depends on clinical presentation. Rectal bleeding from MD is painless, minimal, recurrent, and can be identified using 99mTc- pertechnetate scan; contrasts studies are unreliable.
Persistent bleeding requires arteriography or laparotomy if the scan is negative. Obstruction secondary to intussusception, herniation or volvulus presents with findings of fulminant, acute small bowel obstruction, is diagnosed by clinical findings and contrast enema studies.
The MD is seldom diagnosed preop. Diverticulitis or perforation is clinically indistinguishable from appendicitis. Mucosal polyps or fecal umbilical discharge can be caused by MD. Overall, complications of Meckel's are managed by simple diverticulectomy or resection with anastomosis.
Laparoscopy can confirm the diagnosis and allow resection of symptomatic cases. Removal of asymptomatic Meckel's identified incidentally should be considered if upon palpation there is questionable heterotopic gastric or pancreatic mucosa thick and firm consistency present. Histology features a cluster of mucoid lobes surrounded by flattened mucussecreting glandular cells mucous retention polyp , no malignant potential. Commonly seen in children age with a peak at age As a rule only one polyp is present, but occasionally there are two or three almost always confined to the rectal area within the reach of the finger.
Most common complaint is bright painless rectal bleeding. Occasionally the polyp may prolapse through the rectum. Diagnosis is by barium enema, rectal exam, or endoscopy. Removal by endoscopy is the treatment of choice. Rarely colotomy and excision are required. Wilms tumor WT is the most common intra-abdominal malignant tumor in children affecting more than children annually in the USA. It has a peak incidence at 3.
WT present as a large abdominal or flank mass with abdominal pain, asymptomatic hematuria, and occasionally fever. Other presentations include malaise, weight loss, anemia, left varicocele obstructed left renal vein , and hypertension. Initial evaluation consists of: The presence of a solid, intrarenal mass causing intrinsic distortion of the calyceal collecting system is virtually diagnostic of Wilms tumor.
Doppler sonography of the renal vein and inferior vena cava can exclude venous tumor involvement. Metastasis occurs most commonly to lungs and occasionally to liver. Operation is both for treatment and staging to determine further therapy. Following NWTSG recommendation's primary nephrectomy is done for all but the largest unilateral tumors and further adjuvant therapy is based on the surgical and pathological findings.
Important surgical caveats consist of using a generous transverse incision, performing a radical nephrectomy, exploring the contralateral kidney, avoiding tumor spillage, and sampling suspicious lymph nodes. Nodes are biopsied to determine extent of disease. Stage I- tumor limited to kidney and completely resected.
Stage II- tumor extends beyond the kidney but is completely excised. Stage III- residual non-hematogenous tumor confined to the abdomen. Stage IV- hematogenous metastasis. Stage V- bilateral tumors. Further treatment with chemotherapy or radiotherapy depends on staging and histology favorable vs. Non-favorable histologic characteristics are: Prognosis is poor for those children with lymph nodes, lung and liver metastasis. They tend to occur in younger patients.
Routine abdominal ultrasound screening every six months up to the age of eight years is recommended for children at high risk for developing WT such as the above-mentioned syndromes. It was originally thought that WT developed after the two-hit mutational model developed for retinoblastoma: When the first mutation occurs before the union the sperm and egg constitutional or germline mutation the tumor is heritable and individuals are at risk for multiple tumors.
Nonhereditary WT develops as the result of two-postzygotic mutations somatic in a single cell. The two-event hypothesis predicts that susceptible individuals such as familial cases, those with multifocal disease and those with a congenital anomaly have a lower median age at diagnosis than sporadic cases. It is now believed that several genes' mutations are involved in the overall WT pathogenesis. Loss of whole portions of a chromosome is called loss of heterozygosity LOH , a mechanism believed to inactivate a tumor-suppressor gene.
Children with the WAGR association shows a deletion in the short arm of chromosome 11 band 13 11p13 but a normal 11p15 region. Up to a third of sporadic WT have changes in the distal part of chromosome 11, a region that includes band p The region of the deletion has been named the WT1 gene, a tumor suppressor gene that also forms a complex with another known tumor-suppressor, p WT1 gene express a regulated transcription factor of the zinc-finger family proteins restricted to the genitourinary system, spleen, dorsal mesentery of the intestines, muscles, central nervous system CNS and mesothelium.
The important association of WT1 mutation and WAGR syndrome with intralobar nephrogenic rests immediately suggest that WT1 expression be necessary for the normal differentiation of nephroblasts.
Inactivation of WT1 only affects organs that express this gene such as the kidney and specific cells of the gonads Sertoli cells of the testis and granulosa cells of the ovary. WT1 has been shown to cause the Denys-Drash syndrome. Most of the mutations described in DDS patients are dominant missense mutations. A small subset of BWS has a 11p15 duplication or deletion. The region 11p15 has been designated WT2 gene and is telomeric of WT1. This might prove that two independent loci may be involved in tumor formation.
A gene for a familial form FWT1 of the tumor has also been identified in chromosome 17q. There also might be a gene predisposing to Wilms tumor at chromosome 7p, where constitutional translocations have been described. Mutation in p53 is associated with tumor progression, anaplasia and poor prognosis. Most WT are probably caused by somatic mutations in one or more of the increasing number of WT genes identified. A few chromosomal regions have seen identified for its role in tumor progression.
LOH at chromosome 16q and chromosome 1p has been implicated in progression to a more malignant or aggressive type Wilms' tumor with adverse outcome. These children have a relapse rate three times higher and a mortality rate twelve times higher than WT without LOH at chromosome 1p. Patients with WT and a diploid DNA content indicating low proliferation have been found to have an excellent prognosis. Hyperdiploidy high mitotic activity is a poor prognostic feature of Wilms tumor, rhabdomyosarcoma and Osteosarcoma.
Nephrogenic rests are precursor lesions of WT. Two types are recognized: Also the association between BWS and some cases of hemihypertrophy with abnormalities of more distant loci on chromosome 11p raises the possibility that the putative WT2 gene might be more closely linked to PLNR. An advantage of genetic testing is that children with sporadic aniridia, hemihypertrophy or the above discussed syndromes known to be at high risk for developing WT can undergo screening of the germline DNA.
This might identify if they harbor the mutation and need closer surveillance for tumor development. Neuroblastoma NB is the most common extracranial solid tumor in infants.
More than new cases are diagnosed annually in the United States. NB is a solid, highly vascular tumor with a friable pseudocapsule. Most children present with an abdominal mass, and one-fourth have hypertension. Horner's syndrome, Panda's eyes, anemia, dancing eyes or vaso-intestinal syndrome. Diagnosis is confirmed with the use of simple X-rays stipple calcifications , Ultrasound, and CT-Scan. Management of NB depends on the stage of disease at diagnosis.
Localized tumors are best managed with surgical therapy. The Evans classification for NB staging comprised: Stage I - tumor confined to an organ of origin. Stage II - tumor extending beyond an organ of origin, but not crossing the midline. Ipsilateral lymph nodes may be involved. Stage III - tumor extending beyond midline. Bilateral lymph nodes may be involved. Stage IV - remote disease involving skeleton, bone marrow, soft tissue or distant lymph nodes. A poor outcome is characteristic of higher stages, older patients and those with bone cortex metastasis.
Other prognostic variables are: Neuroblastoma is a malignant tumor of the postganglionic sympathetic system that develops from the neural crest: In vitro three cell types have been identified: These cells are responsible for producing cathecolamines and vasoactive substances which help in diagnosis and follow-up therapy. NB can behave seemingly benignly and undergo spontaneous regression, mature into a benign ganglioneuroma or most commonly progress to kill its host. This disparate behavior is a manifestation that we are dealing with related tumors with differently genetic and biological features associated with a spectrum of clinical behaviors.
Conclusive associations with environmental factors have not been proved in NB. Hereditary factors are important in NB since a few cases exhibit predisposition following a dominant pattern of inheritance. LOH of the short arm of chromosome 1 is also associated with an unfavorable outcome, suggesting that a tumor suppression gene may be found in this region.
The common region of deletion or LOH resides at the distal end of the short arm of chromosome 1 from 1p Loss or inactivation of a gene at this site is critical for progression of neuroblastoma. A few candidate genes from this site have been mapped. Gain of chromosome 17 is associated with more aggressive tumors. N-myc protooncogene is found on chromosome 2p and its activation results in tumor formation. The amplified N-myc sequence is found on extrachromosomal double minutes DM or on homogeneous staining regions HSR involving different chromosomes in neuroblastoma N-type cell lines.
N-myc amplification is strongly associated with advance stages of disease, rapid tumor progression and poor outcome independent of the stage of the tumor or the age of the patient. NB tumors associated with N-myc amplification needs aggressive therapy. N-myc amplification associated with deletion of 1p is correlated with a poor outcome.
Deletion of the long arm of chromosome 1 1q- is also a poor prognostic sign. Though most NB cells are diploid, a good number of them are hyperdiploid or triploid. Neuroblast cells needs nerve growth factor NGF for proper differentiation.
NB tumor cells do not respond to NGF or do not express the receptor. High TRK-A levels correlate strongly with improved survival and plays a role in the propensity for tumors to regress or differentiate into a more benign nature. Alteration in the NGF receptor function or expression promotes tumorigenesis. In conclusion, high levels of TRK expression are associated with better prognosis, earlier stage, lower patient age and lack of N-myc expression.
Neuroblastomas in newborns, cystic tumors, bilateral tumors in infants, and infants less than one year of age with neuroblastoma stage IV-S can undergo neuronal cell differentiation with spontaneous regression. It is thought that high level of TRK-A found in this cases might explain differentiation and regression as high level of this glycoprotein is associated with a favorable prognosis.
Regression might be associated with non-affected tumor cell apoptosis. Other biological markers associated with NB are the multidrug resistance-related protein MRP gene, telomerase activity and bcl-2 gene activity. MRP shows a strong correlation with an advanced clinical stages and poor prognosis. High telomerase activity is associated with poor prognosis and high N-myc amplification.
The bcl-2 gene produces a protein that prevents neuronal cell death apoptosis and promotes tumor progression. Bcl-2 expression is associated with a poor outcome. Apoptosis in NB may result in tumor progression. The RET proto-oncogene is a protein tyrosine kinase gene Ret protein expressed in the cells derived from the neural crest.
The activation of RET involves a chromosomal inversion of the long arm of chromosome 10 that juxtaposes the tyrosine kinase encoding domain of RET to the amino terminal sequences of at least three unrelated genes. Germline mutations in the RET gene have been associated with neuroblastoma, pheochromocytoma, multiple endocrine neoplasia MEN 2, familial medullary thyroid carcinoma MTC , radiation-induced thyroid papillary carcinoma, and recently Hirschsprung's disease.
RET analysis is a suitable method to detect asymptomatic children with MEN at risk to develop MTC allowing us to consider thyroidectomy at a very early stage of neoplasm development C-cell hyperplasia or prophylactically. High levels of neuron specific enolase and serum ferritin levels are associated with a poor prognosis in NB.
Nm and ganglioside GD2 are still other tumor markers associated with poor outcome, active disease and tumor progression. It has a peak incidence before the age of five years, and a second surge during early adolescence. Head, neck and pelvic malignancies are more prevalent in infancy and early childhood, while trunk, extremity and paratesticular sites are largely a disease of adolescents.
RMS arises from a primitive cell type and occurs in mesenchymal tissue at almost any body site excluding brain and bone. The predominant histologic type in infants and small children is embryonal rhabdomyosarcoma, occurring in the head and neck, genitourinary tract and retroperitoneum. Embryonal RMS is associated with a favorable prognosis. Botryoid RMS is a subtype of the embryonal variety, which ordinarily extends into body cavities such as bladder, nasopharynx, vagina, or bile duct.
The alveolar cell type, named for a superficial similarity to the pulmonary alveoli, is the most common form found on the muscle masses of the trunk and extremities, and is seen more frequently in older children and young adults.
Alveolar RMS is associated with a poor prognosis. This unfavorable prognosis is the result of early and wide dissemination, bones marrow involvement and poor response to chemotherapy. Clinical findings, diagnostic evaluation and therapy depend upon location of the primary tumor and are beyond the scope of this review. Head and neck RMS are most common and occur in the orbit, nasopharynx, paranasal sinuses, cheek, neck, middle ear, and larynx.
Most are treated by simple biopsy followed by combined therapy or preoperative chemotherapy and radiation followed by conservative resection. Operations for extremity lesions include wide local excision to remove as much of gross tumor as possible. The trend in management is more chemotherapy with conservative surgical therapy.
Survival has depended on primary site, stage of disease, and treatment given. Most RMS occurs sporadically. Other risk factors in the development of RMS include maternal use of marijuana and cocaine, exposure to radiation, and maternal history of stillbirth.
Alveolar and embryonal RMS are the most genetically studied sarcomas in children. In alveolar RMS novel fusion genes encoding chimeric fusion proteins have been identified. The t 2;13 activates the oncogenic potential of PAX3 by dysregulating or exaggerating its normal function in the myogenic lineage and affecting the cellular activities of growth, differentiation and apoptosis. PAX7-FKHR tumors tend to occur in younger patients, are more often in the extremity, are more often localized lesions and are associated with significantly longer event-free survival.
Still, a small subset of alveolar RMS does not contain either fusion mutation. Identification of fusion gene status by PCR is a useful diagnostic tool in differentiating RMS from other round cell tumors.
Embryonal RMS contains frequent allelic loss on chromosome 11 11p15 , a genetic feature specific for this type of tumor. Allelic loss is manifested by the absence of one of the two signals in the tumor cells indicating a genetic event such as a chromosome loss, deletion, or mitotic recombination that eliminates one allele and the surrounding chromosomal region.