My Lucy
In Loving Memory my Lucy December 2016
February 28, 2013
Categories of holistic anti cancer supplements
Categories of holistic anti cancer supplements
1) Holistic supplements which enhance cellular immunity
Astragalus, Echinacea, Aloe mucopolysaccharides, Omega3, carotenoids,
mushroom and yeast extracts, Green tea polyphenols, reduced glutathione,
vitamin C
2) Holistic supplements which minimize oxidative stress and destroy free radicals
Resveratrol, reduced glutathione, green tea, quercitin , curcumin, Selenium, vitamin C and E, Alpha Lipoic acid
3) Holistic supplements which support the liver and detoxification process .
Reduced glutathione, N acetylcysteine, Curcumin, Resveratrol, SAM-E, E, milk thistle,
4) Holistic supplements that normalize the clock of the cell cycle
Resveratrol, , tocotrienols, curcumin, green tea polyphenols, vitamin D,
CoQ10, reduced glutathione, Quercitin
5) Holistic supplements that enhance cancer cell differentiation
Vit D3, caratenoids, Ganoderma mushrooms, Quercitin
6) Holistic supplements that encourage apoptosis
Green tea polyphenols, quercitin, CoQ10, Ganoderma, Curcumin
7) Holistic supplements that are anti angiogenic ( inhibit new blood vessel proliferation) supplements
Omega3, Green tea polyphenols, Aloe Vera
8) Holistic supplements that kill malignant cells by stimulating intercellular production Of hydrogen peroxide
Vitamin C, Artemesinin
9) Holistic supplements that create an inhospitable biologic terrain for cancer cells to
live in. They increase alkalinity & oxygenation,
honey
10) Holistic supplements blocking different stages of cancer developement: initiation, promotion and progression
Resveratrol, Selenium, garlic, catechins and polyphenols from green tea,
Cruciferous vegetables (Brassica), quercitin, Ascorbic acid, omega 3 fatty
Acids, vitamin E, proanthocyanidins
11) Miscellaneous holistic supplements
Glucosinolates from cruciferous veggies, sprouts, cabbage
Types of Dog Cancers
Squamous Cell Carcinoma: Cancer that occurs in the mouth, underneath the tongue or along the gums of the middle-aged and older cats. Common signs of squamous cell carcinoma in cats includes difficulty eating, interest in food but not wanting to eat, drooling and odor from the mouth.
Osteosarcoma: Osteosarcoma is the most common type of bone tumor in dogs. Osteosarcoma begins in the bone but can spread throughout the bloodstream very early in the course of the disease (metastasis). The most common areas of the body for this cancer to appear are the wrist, shoulder, knee and hip. The first sign of bone cancer is lameness due to pain from the cancer. Swelling often occurs at the tumor site.
Transitional Cell Carcinoma – Tumors usually form at the bladder opening and can cause blockage and painful urinartion. Pets frequently strain while trying to urinate. Transitional Cell Carcinoma can be difficult to diagnose because many of the symptoms such as straining to urinate, blood in the urine or frequent urination are also a symptom of a urinary tract infection. This can delay the discovery of the cancer, especially since antibiotics can often result in some improvement of symptoms. Thus, at the time of diagnosis, bladder cancer can be fairly far advanced and may have spread to other parts of the body.
Adenocarcinoma: Anal sac adenocarcinomas are tumors arising from the apocrine glands present on either side of the rectum. These tumors can range greatly in size from a very small mass that can be found only after a rectal examination or a large mass protruding from the rectum. While the tumor appears locally, it is quite common for them to metastasize, often to the lymph nodes in between the spine and colon. Symptoms vary depending upon the gender of the pet and can include increased thirst, weakness, persistent licking at the site, difficulty defecating, decreased appetite.
Hemangiosarcoma - Most commonly found in the spleen, liver and heart and the prognosis is determined by the location of the disease. The cancer arises from the blood vessels and results in the production of abnormal blood vessels that can be weak and prone to leaking. As the cancer progresses, the cancerous vessels can rupture and results in blood loss. As the spleen is the organ most commonly affected by this type of cancer, rupture can lead to blood loss into the abdomen. This is an emergency situation and can result in weakness and collapse. Many pets with hemangiosarcoma often require a splenectomy.
Mast Cell Tumors - Mast cell tumors are among the most common tumors in dogs and are the most common type of skin cancer found in dogs. The most common location to find mast cell tumors is, by far, the skin, followed by the spleen, liver, and bone marrow. Both normal and cancerous mast cells contain chemicals that can be released into surrounding tissues. When these chemicals (particularly histamine) are released into the normal surrounding body tissues, side effects can include digestive problems (for ex: bleeding ulcers), skin rashes, shortness of breath and other symptoms. Mast cell tumors vary greatly in their size, shape, appearance and texture. The only way to definitely identify them is with a biopsy and pathology report.
Lymphoma - is cancer of the lymphatic tissue. The lymph system is a core part of the body’s immune system. The lymphatic system is an extensive drainage network that defends the body against infections. It is comprised of a network of lymphatic vessels that carry lymph (a clear, watery fluid that contains protein, salts, glucose and other substances) throughout the body. The lymphatic system also serves as a low pressure drainage system that collects interstitial fluid throughout the body and returns it to the bloodstream. The most common sign of lymphoma is a painless enlargement of the lymph nodes.
February 25, 2013
Hemangiosarcoma in Dogs Herbal and Holistic Treatments
Dog Hemangiosarcoma
Canine hemangiosarcoma is an incurable tumor of cells that line blood vessels (endothelial cells). Based on current estimates of the lifetime risk of cancer in dogs and the prevalence of hemangiosarcoma, we predict that of 65 million pet dogs living in the United States today, as many as two million may get this cancer and die from it. Although dogs of any age and breed are susceptible to hemangiosarcoma, it occurs more commonly in dogs beyond middle age, and in breeds such as Golden Retrievers, German Shepherd Dogs, Portuguese Water Dogs, and Skye Terriers, among others.Hemangiosarcoma develops slowly and is essentially painless – so clinical signs are usually not evident until the advanced stages when the tumors are resistant to most treatments. Less than 50% of dogs treated with standard-of-care for this tumor (surgery and intensive chemotherapy) survive more than six months. Many dogs die from severe internal bleeding before there is an opportunity to institute treatment.
DIAGNOSIS/INITIAL EVALUATION
Because these tumors arise in internal organs there is often little
warning that they are present prior to time they cause severe clinical
signs of disease. A common estimate of the average time from discovery
of the tumor until death occurs in affected dogs is six to eight weeks
but death occurs more rapidly than this in a number of cases.
Visible bleeding, usually in the form of nosebleeds, and signs
associated with blood loss, such as tiring easily, episodes of
unexplained weakness, pale color to the mucous membranes of the mouth
and eyes, increased respiratory rates, abdominal swelling and
depression are the most common presenting signs for patients with
hemangiosarcoma. A few dogs just suddenly die with no clinical signs
having been noted by their families prior to death. Bleeding disorders
associated with hemangiosarcoma are sometimes confused with immune
mediated hemolytic anemia (IMHA) because the type of anemia caused by
the two conditions is very similar and early clinical signs are often
very similar, as well. Hemangiosarcomas can cause very large tumors,
sometimes as large as ten or more pounds, when they affect the spleen.
In most instances tumors of this size in this location are found on
physical exam. In other cases the tumor affects the heart and is hard
to find on a physical exam and even easy to miss or X-rays. Sometimes
there are hundreds of small tumors spread throughout the body and
surgical exploration or an autopsy are the only ways to identify the
problem.The blood disorder that most commonly accompanies the presence of hemangiosarcoma tumors is disseminated intravascular coagulation (DIC). This is blood clotting that is occurring inappropriately inside the blood vessels. It uses up all of the blood clotting elements rapidly and dogs with this condition usually have platelet deficiencies, increased blood clotting times, decrease in fibrin content in the blood and an increase in fibrin degradation products (FDPs). This is probably the cause of death in most dogs affected with hemangiosarcoma.
Diagnosis of hemangiosarcoma can be accomplished in a number of ways. Identification of a tumor in the spleen or heart raises a high degree of suspicion for this tumor. Abdominal swelling is also highly suggestive in an older large breed dog. If fluid is aspirated from the abdomen and it looks like blood it is even more suggestive of hemangiosarcoma. If blood is drawn and will not clot when left in the syringe it is another sign that a dog may have this tumor. In some cases careful evaluation of the type of bleeding disorder present is necessary to raise the suspicion of hemangiosarcoma.
Canine hemangiosarcoma is among the most challenging and mysterious diseases encountered in veterinary practice. It is an incurable tumor of cells that line blood vessels, called vascular endothelial cells. Hemangiosarcoma is relatively common in dogs; it is estimated that this type of cancer accounts for 5-7% of all tumors seen in dogs. Considering the lifetime risk of cancer for dogs is between 1 in 2 and 1 in 3, we can calculate that 1.5 to 2.5 million of the ~72 million pet dogs in the United States today will get hemangiosarcoma and succumb from it. (WHAT!?)
Although dogs of any age and breed are susceptible to hemangiosarcoma, it occurs more commonly in dogs beyond middle age (older than 6 years), and in breeds such as Golden Retrievers, German Shepherd Dogs, Portuguese Water Dogs, Bernese Mountain Dogs, Flat Coated Retrievers, Boxers and Skye Terriers, among others. According to the Golden Retriever Health Study published in 2000, the estimated lifetime risk of hemangiosarcoma in this breed is 1 in 5, illustrating the magnitude of this problem.
Unlike other cancers, hemangiosarcoma is almost an exclusive disease of dogs. In dogs, the common primary sites for hemangiosarcoma are the spleen, the right atrium of the heart, and the subcutis, which is the tissue beneath the skin. The pattern of growth for these tumors involves infiltration into normal tissues surrounding the tumor as well as distant spread (metastasis). The disease is indolent; in other words, it does not cause pain and the rate of growth in the early stages is relatively slow. Dogs harboring even large hemangiosarcomas may show no clinical signs or evidence that they have a life threatening disease. Generally, the tumor cells retain some normal aspects of behavior, so they try to make blood vessels. But these vessels are tortuous and malformed, and blood cells tend to pool in them and clot. The clots then prevent blood and nutrients from reaching tumor cells, in turn causing them to die. This creates small ruptures in the tumor through which blood may escape into the abdomen, heart sac, chest, or subcutaneous space. Depending on the amount of blood lost, affected dogs may show non-specific (constitutional) signs such as lethargy and weakness, but these are transient and resolve as dogs reabsorb the blood components and make new blood cells. The clinical signs are recurrent, but they also are subtle enough to go unnoticed for some time. Since hemangiosarcoma tends to metastasize aggressively to lungs, liver, intestines, and the membranous connective tissue that supports the intestines), distant spread (either microscopic or macroscopic) has inevitably occurred once the disease is finally diagnosed. The eventual outcome for patients with this disease often follows the rupture of a large or rapidly growing tumor, which results in acute, severe hemorrhage, collapse, shock, and death.
What Causes Hemangiosarcoma
We do not precisely know what causes canine hemangiosarcoma. The observations that the disease occurs more commonly in dogs than in other animals, and that some breeds are at higher risk than others tell us that heritable factors must contribute to risk. Tumors arise when cells accumulate mutations that eliminate normal constraints of growth and genetic integrity. These mutations provide cells a selective growth advantage within their environment, essentially the same evolutionary phenomenon that we call natural selection, albeit on a microscopic scale. Most mutations arise because the enzymes that control cell division are not foolproof.
Fortunately, most of these mutations are silent (they neither help nor hurt the cell or the organism), and the body has mechanisms to eliminate most cells that acquire deleterious mutations.
We have identified some of the fundamental properties of canine hemangiosarcoma, and it is possible one or more of these may prove to be an “Achilles heel” for the tumor. For example, most of these tumors make growth factors that they need to survive, or they “coerce” cells in their environment to do this for them. One of these growth factors is vascular endothelial growth factor-A or VEGF, which acts by binding specific receptors on the hemangiosarcoma cells. New drugs under development by various pharmaceutical companies are designed specifically to interfere with the signals transmitted by these receptors. The reliance of hemangiosarcoma cells on VEGF signals to survive should make them more sensitive than normal cells to these drugs. Several groups are working to bring these drugs into the clinic, but the process is slow because testing must be done in a careful, deliberate way to ensure the compounds are safe and effective.
Standard Treatment for Canine Hemangiosarcoma
Standard Treatment and prognosis for Hemangiosarcoma vary by location. Cutaneous Hemangiosarcoma is often curable with surgery alone, provided the lesion is small and confined to the dermis. Cutaneous Hemangiosarcoma often occur in areas of glabrous skin on lightly pigmented dogs and arise as a result of sunlight exposure.Lesions that are larger or deeper may be either primary or metastatic lesions and warrant more aggressive treatment. Treatment of splenic, atrial, or subcutaneous Hemangiosarcoma consists of surgical excision of the primary tumor and adjuvant chemotherapy. Recommended chemotherapy for Hemangiosarcoma is single-agent doxorubicin, intravenously given every 3 weeks. Use of an indwelling catheter is important because of the catastrophic tissue slough that occurs after doxorubicin extravasation. Owners should be warned of the potential of cardiotoxicity. A total of 4-6 doses of doxorubicin are recommended. Median survival time after surgery alone is reported to be 2-3 months, with the addition of chemotherapy increasing the median survival time to 4-6 months. The VAC protocol may be useful; however it has a higher morbidity rate with no increase in survival time. Dogs with splenic Hemangiosarcoma that have ruptured may have a poorer prognosis than those not ruptured. Currently several drugs are being investigated for their antiangiogenic properties, and may be useful for treatment of Hemangiosarcoma in the future. Follow-up for Hemangiosarcoma should include monthly thoracic radiographs and physical examinations.
Regrettably, the standard-of-care for this disease has not seen significant advancement over the past 20 or 30 years. There is presently no readily available, effective test for early diagnosis of hemangiosarcoma. Careful analysis of blood samples by experienced pathologists may hint at the presence of chronic hemorrhage and blood vessel abnormalities that are suggestive of hemangiosarcoma. However, this method is neither sensitive nor specific to confirm the diagnosis. Non-invasive imaging methods are useful aids to diagnose the disease. In particular, ultrasound is moderately specific, but it is not sensitive, and the tumor must be large enough to be grossly visible. In addition, biopsies are required for confirmation of imaging results. Repeated biopsies of tissues where the tumors may arise (without other evidence for the presence of a tumor) are of little use to provide early diagnosis, and considering the fact that there is some risk to these procedures, such an approach is practically and ethically unacceptable.
The options for therapy of canine hemangiosarcoma are limited, largely because the disease is not diagnosed until the late stages. The conventional standard treatment consists of surgery to shrink or remove the primary tumor, when possible, followed by intensive chemotherapy. In some cases, surgery is not feasible, or it can be impractical or inappropriate (for example, if there is evidence of extensive metastatic spread to sites beyond the primary tumor). Median survival for dogs treated with surgery alone is approximately 90 days, and that is extended to approximately 180 days by the addition of chemotherapy using one of several protocols available. Because the goal for chemotherapy in pet dogs is to extend life with good quality, toxicity is generally not a major issue of concern(WHAT?!), and when it occurs it is most often managed without much difficulty.
Surgery and chemotherapy have limited success in prolonging survival times and increasing quality of life in dogs with HSA. Splenectomy alone gives an average survival time of 1–3 months. Advances in medical oncology are resulting in increased survival rates and a better quality of life for veterinary cancer patients. An understanding of mechanisms of metastasis has led to the development of new treatments designed to delay or inhibit tumor spread. Promising new treatment options include novel delivery systems (inhalation or intracavitary chemotherapy); use of immunomodulators such as liposome-encapsulated muramyl tripeptide-phosphatidylethanolamine; antimetastatic agents such as inhibitors of angiogenesis (interferons, thalidomide), matrix metalloproteinase inhibitors, and minocycline; dietary modifications; and gene therapy. Inhibitors of angiogenesis (meaning anti-angiogenesis) seem to be safe and, unlike conventional chemotherapy, do not induce drug resistance. Although many of the newer approaches are still under development and review, the use of multimodality therapy incorporating innovative treatment modalities may offer the best therapeutic option for dogs affected with HSA.
The nature of hemangiosarcoma itself draws attention to the prolific formation of blood vessels through the tumors. These vessels typically rupture causing loss of blood internally. Yun Nan Bai Yao herbs really helps slow the bleeding. As another integral part of natural healing for hemangiosarcoma is to help prevent the formation of new blood vessels with anti-angiogenesis supplements. Powerful medicinal mushrooms have been shown to discourage the rapid growth of these blood vessels and support the immune system.
A basic start I have seen people using is:
Mushrooms have been used in traditional Chinese medicine for more than 2,000 years. The compound in the mushroom that is believed to have immune-boosting properties is polysaccharopeptide, or PSP. In the last two decades, some studies have suggested that PSP Beta glucans also has a tumor-fighting effect. Read about medicinal Mushrooms and Beta Glucans below.
Many dose dogs at 800-1600mg twice a day.
More then any other cancer I work with I think this is the most important one to make sure you have a good holistic vet on board. I know, I know I have said that a few times already.
"I saw this thread and just joined the boards so I could give you a little information. Our lab was diagnosed with this disease on March 8. He was given 1 month to live (large spleen tumor and spread to the liver) but has been doing okay. No additional bleeding, no weight loss, pink gums etc. The oncologist said we could have the spleen removed (but the cancer would remain since it had spread) and do chemo (they would not do chemo without the surgery); this might extend his life by a few months but we felt the pain and stress with little extension of live was not worth it for him. The vet oncologist put him on a Chinese herb called Yunnan payio/baiyo that inhibits bleeding (2 capsules 2 times a day for an 80 lb dog). We can get this from the vet or order online (cheaper). We also give many other supplements and feed a high protein, no grain diet with supplements of omega 3 fatty acids. Other supplements include milk thistle (for the liver), immune support, anemia meds, medicinal mushrooms, and others. "
Mushroom Derived Compound Lengthens Survival in Dogs With Cancer
Mushroom-Derived Compound Lengthens Survival in Dogs With Cancer, Study Suggests
Dogs with hemangiosarcoma that were treated with a compound of Beta glucans derived from the Coriolus versicolor mushroom had the longest survival times ever reported for dogs with the disease. These promising findings offer hope that the compound may one day offer cancer patients -- human and canine alike -- a viable alternative or complementary treatment to traditional chemotherapies.
The study was conducted by two University of Pennsylvania School of Veterinary Medicine faculty. They published their findings in an open-access article in the journal Evidence-Based Complementary and Alternative Medicine.
The Coriolus versicolor mushroom, known commonly as the Yunzhi or Turkey Tail mushroom, has been used in traditional Chinese medicine for more than 2,000 years. The compound in the mushroom that is believed to have immune-boosting properties is polysaccharopeptide, or PSP. In the last two decades, some studies have suggested that PSP Beta glucans also has a tumor-fighting effect.
"There have been a series of studies looking at groups of people with cancer," "The issue with those studies is that they weren't necessarily measuring what most people would think is the most clinically important result, which is, do people taking PSP Beta glucans live longer?"
To address this critical question,University of Pennsylvania School of Veterinary Medicine pursued a study in dogs with naturally occurring hemangiosarcoma, an aggressive, invasive cancer that arises from the blood cells and typically affects the spleen. It commonly strikes golden retrievers and German shepherds.
Fifteen dogs that had been diagnosed with hemangiosarcoma participated in the trial. Divided into three groups of five, each group received a different dose -- 25, 50 or 100 mg/kg/day -- of (Beta glucans), a formulation of PSP.
The owners were instructed to give their dog capsules of (Beta glucans), compounded by Penn pharmacists, daily. Each month, the owners brought their dogs to Penn's Ryan Veterinary Hospital for follow-up visits. There, the researchers took blood samples and conducted ultrasounds to determine the extent that tumors developed or grew and spread in the dogs' bodies.
Based on the ultimate endpoints -- how quickly the tumors progressed and how long the dogs actually lived -- the results of the researchers' trial suggest that the Beta glucans was effectively fighting the tumors.
"We were shocked," University of Pennsylvania School of Veterinary Medicine said. "Prior to this, the longest reported median survival time of dogs with hemangiosarcoma of the spleen that underwent no further treatment was 86 days. We had dogs that lived beyond a year with nothing other than this mushroom as treatment."
There were not statistically significant differences in survival between the three dosage groups, though the median survival time was highest in the 100 mg group, at 199 days, eclipsing the previously reported median survival time.
The results were so surprising, in fact, that the researchers asked Penn Vet pathologists to recheck the dogs' tissue biopsies to make sure that the dogs really had the disease.
"They reread the samples and said, yes, it's really hemangiosarcoma," University of Pennsylvania School of Veterinary Medicine said.
Chemotherapy is available for treating hemangiosarcoma, but many owners opt not to pursue that treatment once their dog is diagnosed. "It doesn't hugely increase survival, it's expensive and it means a lot of back and forth to the vet for the dog," Cimino Brown said. "So you have to figure in quality of life."
As an added benefit, University of Pennsylvania School of Veterinary Medicine have found no evidence of adverse effects from the Beta glucans treatment.
"Although hemangiosarcoma is a very sad and devastating disease, in the long term, if we prove that this works, this treatment can be a really nice alternative for owners to have increased quality time with their pet at the end of its life."
Evid Based Complement Alternat Med. 2012;2012:384301. doi: 10.1155/2012/384301. Epub 2012 Sep 5.
Single agent polysaccharopeptide delays metastases and improves survival in naturally occurring hemangiosarcoma.Brown DC, Reetz J.
Source
Veterinary Clinical Investigations Center, Department of Clinical Studies, School of Veterinary Medicine and University of Pennsylvania, 3900 Delancey Street, Philadelphia, PA 19104-6010, USA.Abstract
The
2008 World Health Organization World Cancer Report describes global
cancer incidence soaring with many patients living in countries that
lack resources for cancer control. Alternative treatment strategies that
can reduce the global disease burden at manageable costs must be
developed. Polysaccharopeptide (PSP) is the bioactive agent from the
mushroom Coriolus versicolor. Studies indicate PSP has in vitro
antitumor activities and inhibits the growth of induced tumors in animal
models. The investment of resources required to
complete large-scale, randomized controlled trials of PSP in cancer
patients is more easily justified if antitumor and survival benefits are
documented in a complex animal model of a naturally occurring cancer
that parallels human disease. Because of its high metastatic rate and
vascular origin, canine hemangiosarcoma
is used for investigations in antimetastatic and antiangiogenic
therapies. In this double-blind randomized multidose pilot study,
high-dose PSP Beta Glucans significantly delayed the progression of metastases and
afforded the longest survival times reported in canine hemangiosarcoma.
These data suggest that, for those cancer patients for whom advanced
treatments are not accessible, PSP as a single agent might offer
significant improvements in morbidity and mortality.
- [Study on effects of Astragalus, Angelica and their combination on vascular endothelial cell proliferation in vitro].
Lei Y, Gao Q, Li YS.
Source
Xiyuan Hospital, China Academy of TCM, Beijing 100091.
Abstract
OBJECTIVE:
To study the effects of Astragalus membranaceus (AM), Angelica sinensis (AS) and their combination on human umbilical vein endothelial cell (HUVEC) proliferation and cells cycle.METHODS:
The effects were observed and studied by means of taking the cultured HUVECs as model to determine the cell proliferation with MTT method, cell cycle was analyzed with cytometry, and vascular endothelial growth factor (VEGF) expression with SABC method. The regulatory effects of AM, AS and their combination on the HUVEC proliferation promoting were observed and studied.RESULTS:
AM and AS, used singly or in combination, could promote the growth of endothelial cells, increase the cell population in S phase, the effects showed more significant when used in combination (P < 0.05 or P < 0.001). Meanwhile, VEGF expression in all the medicated group was up-regulated, but in the PBS control group, it showed only weak expression (P < 0.05 or P < 0.01).CONCLUSION:
AM and AS have effect in promoting vascular endothelial cell proliferation and DNA synthesis, and showed synergistic effect when they were used in combination, suggesting that these two Chinese herbs could have certain effect on the genesis and development of neogenetic vascularization in ischemic myocardium..
February 22, 2013
Treating weight loss in dogs with cancer
Treating weight loss in dogs and cats with cancer
It is very common for cats and dogs who have cancer to loss weight even when they are eating well. This is because the cancer is stealing their nutrients and not allowing the body to have what it needs. Weight loss in the face of a healthy appetite and proper nutrition is called cachexia.
There is a simple protocol I use to address this issue if it isn’t just an issue of appetite.
- Add in Fish Oil at 2-3X recommended dosage. Cancer can not use fat and Omega 3 oils help to reverse cachexia.
- Feed 1-2 tablespoons of canned sweet potato or pumpkin at every meal for the average sized dog. Use a teaspoon for cats. This helps with digestion and helps them use the nutrients in their food better.
- Add in 1-2 eggs a day for the average sized dog or part of an egg for cats. Eggs are a very good source of 100% digestible protein. Cooked is best. You can hard boil a dozen at a time and keep them in the refrigerator to make it easier.
- Consider feeding multiple meals a day or increase the amount of food. Feed grain free food to your carnivore. This can really help and probably seems obvious.
- There are some other herbal formulas that can help but they differ from animal to animal, so consider seeing a veterinary herbalist if the above doesn’t work.
Eating is very important. The Chinese say that eating and sleeping are the two most important things to getting better.
Animals on 20 different supplements occasionally get poor appetites. Wouldn't you? The first thing I would do is take away most, if not all of the supplements and get them eating for a few days and then slowly add stuff back in.Be careful to not over do it with western medications as well and remember that if your animal is on certain herbals or getting acupuncture you can sometimes get by with a smaller dose of drugs like prednisone.Get help from your holistic or western vet if your animal is not eating. There are many ways to stimulate appetite in both modalities.
If appetite is an issue then I recommend working with a holistic vet with acupuncture and herbs or consulting with your animal’s regular veterinarian about appetite stimulants and anti-nausea medications.
From The April 1998 issue of Nutrition Science News
Fish Oil Slows Cancer Cachexia By Richard N. Podell, M.D.
For cancer patients with a poor prognosis, good news, no matter how slim, is still good news. The American Cancer Society (ACS), nationally headquartered in Atlanta, estimates that 29,000 Americans will be diagnosed with pancreatic cancer in 1998. Of those patients, the ACS predicts 18 percent will survive at least one year after the diagnosis and only 4 percent will survive more than five years. The slim bit of good news comes from research that shows fish oil helps slow or reverse cachexia, a condition of physical wasting and malnutrition often developed by cancer patients.1 Cachexia is especially common to pancreatic cancer, where rapid weight loss is often the dominant symptom. Weight and muscle mass drop off rapidly and out of proportion to the accompanying loss of appetite. Neither more food nor intravenous nutrition reverses the problem. Cachexia directly accounts for an estimated 10 to 22 percent of all cancer deaths. Many experts believe cachexia reflects an increased metabolic rate caused by inflammatory biochemicals that cancer triggers. The best way to reverse cachexia is to treat the cancer.
However, pancreatic cancer does not have a safe, effective treatment. In test-tube experiments, fish oils and their omega-3 fatty acids inhibit the growth of several types of human cancer, including pancreatic. Fish oil also inhibits certain cancers in mice and, through a separate effect, can reverse their cachexia. This month's featured study is from the University of Edinburgh, Department of Surgery, Royal Infirmary in Scotland.4 Eighteen patients with inoperable pancreatic cancer received a daily dose of 12 1 g capsules of a fish-oil dietary supplement that contained 18 percent eicosapentaenoic acid (EPA) and 12 percent docosahexaenoic acid (DHA). All of the patients had been losing 3 pounds per month on average before taking fish oil. In the first three months of supplementation their average weight increased by about two-thirds of a pound per month. Eleven of the 18 patients gained weight, three remained stable and four continued to lose weight, but more slowly. Tests showed that the weight gain was not caused by fluid retention. Both patients and doctors in the study were aware of the treatment. However, there are several reasons to believe the weight gain was not a placebo effect. First, the weight loss in previous months had been large and progressive with no reversal. Second, the fish-oil patients did much better than another group who were treated with intravenous gamma linolenic acid (GLA), a different type of oil. The intravenous treatments with GLA, given by the same doctors, were ineffective in reversing weight loss. Therefore, there was no significant placebo effect.
The authors concluded: "Oral fish-oil supplementation significantly altered the progression of cachexia in a group of pancreatic cancer patients. Before supplementation, all of the study group experienced progressive weight loss; however, following administration of fish oil, three-quarters of the group were either weight-stable or actually gained a small amount of weight. It is unlikely that the observed changes in weight were caused by a placebo effect since administration of GLA to a matched group of weight-losing pancreatic cancer patients had no significant influence on the overall pattern of weight loss."
Animal studies using fish oil are encouraging. One study showed reduced cachexia in mice with cancer.5 Other studies showed fish oil decreased the subject's tendency to break down fat6 and increased the ability to preserve muscle mass.7
"Fish oil supplements help thwart the loss of muscle mass in dogs suffering from heart disease, according to a study at Tufts Univ. School of Veterinary Medicine. "We are very excited about these results," said Dr. Lisa M. Freeman, a veterinary nutritionist at Tufts. "My hunch is that a higher dose of fish oil might have even more of an effect, but we need to do more studies in this area."Dogs with heart disease, like people, experience a phenomenon called cachexia, or loss of muscle mass, that decreases strength and immune function. When ill, the body produces elevated levels of hormone-like substances called cytokines, the major one being tumor necrosis factor, tohelp fight the offending pathoge. But at high levels and for prolonged periods, cytokines can suppress appetite and cause a loss of muscle mass. "People with heart disease have increased levels of cytokines, probably as a compensatory response to the disease, but this eventually can have detrimental effects for the patient," Freeman said. "We wanted to study this mechanism to determine if it could be managed nutritionally, and it turns out that fish oil does indeed reduce cytokine levels." Although veterinarians have observed cachexia clinically in their patients for years, the precise mechanism of the condition had not been studied in dogs before. Freeman, who also is a researcher at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts, conducted the fish oil study in collaboation with colleagues from the veterinary school and the HNRCA. In the eight-week study, 28 dogs with congestive heart failure caused by dilated cardiomyopathy, a naturally occurring disease that weakens the heart muscle in some middle-age dogs and is generally fatal within four to six months, were divided into two groups. One group was given fish oil, and the other received a placebo. Both groups were also given appropriate medical treatments for their condition. Fish oil is not a magic bullet for treating canine heart disease, Freeman cautions, but the Tufts researchers found a reduction in cytokine levels and an improvement in muscle mass in these animals. "But even more exciting was the finding that reductions in cytokine levels were associated with a longer survival time," Freeman said. "We'll need to study this further, certainly, but it looks promising." The study was funded by the National Institutes of Health, Hills Pet Products, the Mark Morris Institute and the American Society for Parenteral and Enteral Nutrition.
I give Lucy Fish Oil, Pepcid sometimes and a break from all her pills about once a week at random days. Glutamine may help http://dognasalcancertreatmentforlucy.blogspot.com/2012/06/glutamine-and-cancer.html
February 16, 2013
Holistic Treatments not just for humans video
Holistic Treatments not just for humans!
As shown on CBS News.
February 15, 2013
February 11, 2013
Bloodroot Neoplasene Berberine Oregon Grape Root Cancer Uses
One of the main health benefits of the Bloodroot herb determined from recent studies is that Bloodroot herbal extract has certain anti-cancer agent properties that are useful in the treatment of skin cancer. It has also been established that Bloodroot contains a chemical substance called berberine which helps fight tumors in the brain and several other types of cancers. Bloodroot extracts are used in minimal doses to treat bronchial infections and sore throats. Bloodroot tinctures have been used over several centuries in treating bleeding lungs, pneumonia, the common cold, whooping cough, croup, laryngitis, emphysema and sinus congestions. The root of Bloodroot has the ability to work well as an anesthetic, carthartic, emetic, expectorant, diuretic, sedative and stimulant. Bloodroot also helps in effective peripheral blood circulation. It has been used in treating liver conditions like jaundice.
Bloodroot contains berberine, a substance that may fight cancer and brain tumors. Berberine is an alkaloid found in Bloodroot and it exhibits tumoricidal and anti-carcinogenic properties. One study, published in April 2002 edition of Biochemical Pharmocology, found that these sanguinarine alkaloids caused cell death in multi-drug-resistant human cervical cells. . Sanguinarine, a plant-based compound with very similar chemical classification as berberine. Often used as a home remedy for skin cancers in humans and animals, Bloodroot provides the main ingredient for homemade black salves, which can cause dangerous side effects when used incorrectly.
Neoplasene is a relatively new drug now available for veterinary use (Rx from vet only) that is derived from the perennial herb bloodroot (Sanguinaria canadensis), so named because of the reddish sap of the root. It has historically been used as a dye, an emetic (induces vomiting) and a wart and tumor treatment, esp. by Native Americans. In external cancers it has been used as a caustic escharotic paste called Black Salve, which "burns" any flesh it comes into contact with, whether it is healthy or not. This is indiscriminate necrosis. Neoplasene is really not Black Salve it is not whole bloodroot. It is, only in part, an isolate of the active ingredients of bloodroot called benzylisoquinoline alkaloids, with the primary one being sanguinarine.
Neoplasene® process stimulates the immune system by killing cancer cells. It causes cancer cells to die by a process known as apoptosis. This is a self termination process. The immune system of the patient is then stimulated to handle them as it would any other dying cells, by way of inflammation. It does all this while sparing healthy, normal cells. This makes it extremely unique and valuable. So, unlike most conventional “chemo” treatments it is not toxic at recommended doses (except to cancer cells). Furthermore, according to the most current information, unlike most conventional chemo treatments, Neoplasene works on any type of cancer cell.
Contraindications: Large oral internal doses of Bloodroot are poisonous. Too much can be fatal. In toxic oral doses, it causes burning in the stomach, intense thirst, vomiting, faintness, and vertigo. Self-medications should not be attempted with Bloodroot as unwanted visual distortions can occur even in small doses. Large doses of Bloodroot can irritate your mucous membranes. It makes you really nauseous if not very careful . Neoplasene is fine for external use.
( THESE ARE THE REASONS WHY WE DO NOT USE BLOODROOT. WE JUST NEED THE ACTIVE PART CALLED BERBERINE WHICH IS EXTREMELY SIMILAR TO Sanguinarine. WHICH YOU CAN GET FROM OREGON GRAPE ROOT AND NOT HAVE THESE SIDE EFFECTS AT ALL. SEE BELOW)
Berberine has drawn extensive attention towards its antineoplastic effects.[63][64] It seems to suppress the growth of a wide variety of tumor cells, including breast cancer,[65] leukemia, melanoma,[66] epidermoid carcinoma, hepatoma, pancreatic cancer,[67] oral carcinoma, tongue carcinoma,[68] glioblastoma, prostate carcinoma and gastric carcinoma.[69][70] Animal studies have shown that berberine can suppress chemical-induced carcinogenesis, clastogenesis,[71] tumor promotion, tumor invasion,[72][73][74][75][76] prostate cancer,[77][78][79][80] neuroblastoma,[81][82] and leukemia.[48][83]
Berberine is a plant alkaloid with a long history of medicinal use in both Ayurvedic and Chinese medicine. It is present in Hydrastis canadensis (goldenseal), Coptis chinensis (Coptis or goldenthread), Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), and Berberis aristata (tree turmeric). The berberine benzylisoquinoline alkaloids can be found in the roots, rhizomes, and stem bark of the plants.
From modern biomedical studies, anticancer effects have been demonstrated in berberine. The underlying molecular mechanisms involve cell-cycle arrest, apoptosis induction and anti-inflammation. Berberine is an essential anticancer compound. Berberine also demonstrates effects of antiangiogenesis, anti-invasion and anti-metastasis in some cancer cell lines, however, more investigations are required to unravel the underlying mechanisms involved.
It is also a radiosensitizer of tumor cells, but not of normal cells. How berberine mediates these effects is not fully understood, but its ability to inhibit angiogenesis and to modulate Mcl-1, Bcl-xL, cyclooxygenase (COX)-2, MDR, tumor necrosis factor (TNF)- and IL-6, iNOS, IL-12, intercellular adhesion molecule-1 and ELAM-1 expression, MCP-1 and CINC-1, cyclin D1,[84] activator protein (AP-1), HIF-1, PPAR-, and topoisomerase II has been shown. By using yeast mutants, berberine was found to bind and inhibit stress-induced mitogen-activated protein kinase kinase activation. Because apoptotic, carcinogenic, and inflammatory effects and various gene products (such as TNF-α, IL-6, COX-2, adhesion molecules, cyclin D1, and MDR) modulated by berberine are regulated by the transcription factor nuclear factor- B (NF- B), it is postulated this pathway plays a major role in the action of berberine.[85] Berberine suppressed NF-κB activation induced by various inflammatory agents and carcinogens. This alkaloid also suppressed constitutive NF-κB activation found in certain tumor cells. It seems to protect against side effects of radiation therapy in lung cancer.[86]
Berberine extracts and decoctions have also demonstrated significant antimicrobial activity against a variety of organisms including bacteria, viruses, fungi, protozoans, helminths, and chlamydia. Currently, the predominant clinical uses of berberine include bacterial diarrhea, intestinal parasite infections, and ocular trachoma infections.
A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs.
Sun Y, Xun K, Wang Y, Chen X.
Source
School of Pharmacy, Chengdu Medical College, Chengdu, China.
Abstract
Natural products represent a rich reservoir of potential small chemical molecules exhibiting antiproliferation and anticancer properties. An example is berberine, a protoberberine alkaloid widely distributed in medical plants used in traditional Chinese prescriptions. Recent advances have shown that berberine exerts anticancer activities both in vitro and in vivo through different mechanisms. Berberine shows inhibitory effects on the proliferation and reproduction of certain tumorigenic microorganisms and viruses, such as Heliobacter pylori and hepatitis B virus. Transcriptional regulation of some oncogene and carcinogenesis-related gene expression and interaction with both DNA and RNA are also well documented. Besides, berberine is a broad spectrum enzyme inhibitor, which affects N-acetyltransferase, cyclooxygenase-2, and topoisomerase activities and gene/protein expression. These actions, together with the regulation of reactive oxygen species production, mitochondrial transmembrane potential, and nuclear factor-kappaB activation might underlie its antiproliferative and proapoptotic effects. More importantly, the suppression of tumor growth and metastasis, the beneficial application in combined medication, and the improvement of multidrug resistance both in vivo and in vitro clearly show its potential as an alternative medicine for tumor chemotherapy.
PMID: 19704371 [PubMed - indexed for MEDLINE]
^ Sun Y, Xun K, Wang Y, Chen X (20 August 2009). "A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs". Anticancer Drugs 20 (9): 757–69. doi:10.1097/CAD.0b013e328330d95b. PMID 19704371.
^ Tang J, Feng Y, Tsao S et al. (August 2009). "Berberine and Coptidis Rhizoma as novel antineoplastic agents: a review of traditional use and biomedical investigations". Journal of Ethnopharmacology 126 (1): 5–17. doi:10.1016/j.jep.2009.08.009. PMID 19686830.
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^ Ho YT, Lu CC, Yang JS et al. (October 2009). "Berberine induced apoptosis via promoting the expression of caspase-8, -9 and -3, apoptosis-inducing factor and endonuclease G in SCC-4 human tongue squamous carcinoma cancer cells". Anticancer Research 29 (10): 4063–70. PMID 19846952.
^ Auyeung KK, Ko JK (October 2009). "Coptis chinensis inhibits hepatocellular carcinoma cell growth through nonsteroidal anti-inflammatory drug-activated gene activation". International journal of molecular medicine 24 (4): 571–7. PMID 19724899.
^ Tang F, Wang D, Duan C et al. (October 2009). "Berberine inhibits metastasis of nasopharyngeal carcinoma 5-8F cells by targeting Rho kinase-mediated Ezrin phosphorylation at threonine 567". The Journal of Biological Chemistry 284 (40): 27456–66. doi:10.1074/jbc.M109.033795. PMC 2785675. PMID 19651779.
^ Sindhu G, Manoharan S (April 2010). "Anti-Clastogenic Effect of Berberine against DMBA-Induced Clastogenesis". Basic Clin Pharmacol Toxicol. 107 (4): 818–24. doi:10.1111/j.1742-7843.2010.00579.x. PMID 20406204.
^ Pandey MK, Sung B, Kunnumakkara AB, Sethi G, Chaturvedi MM, Aggarwal BB (July 2008). "Berberine modifies cysteine 179 of IκBα kinase, suppresses nuclear factor-κB-regulated antiapoptotic gene products, and potentiates apoptosis". Cancer Research 68 (13): 5370–9. doi:10.1158/0008-5472.CAN-08-0511. PMID 18593939.
^ Kim JB, Ko E, Han W, Shin I, Park SY, Noh DY (November 2008). "Berberine diminishes the side population and ABCG2 transporter expression in MCF-7 breast cancer cells". Planta Medica 74 (14): 1693–700. doi:10.1055/s-0028-1088313. PMID 18951337.
^ Kim S, Choi JH, Kim JB et al. (2008). "Berberine suppresses TNF-α-induced MMP-9 and cell invasion through inhibition of AP-1 activity in MDA-MB-231 human breast cancer cells". Molecules 13 (12): 2975–85. doi:10.3390/molecules13122975. PMID 19052522.
^ Liu J, He C, Zhou K, Wang J, Kang JX (January 2009). "Coptis extracts enhance the anticancer effect of estrogen receptor antagonists on human breast cancer cells". Biochemical and Biophysical Research Communications 378 (2): 174–8. doi:10.1016/j.bbrc.2008.10.169. PMID 19000652.
^ Thirupurasundari CJ, Padmini R, Devaraj SN (February 2009). "Effect of berberine on the antioxidant status, ultrastructural modifications and protein bound carbohydrates in azoxymethane-induced colon cancer in rats". Chemico-biological Interactions 177 (3): 190–5. doi:10.1016/j.cbi.2008.09.027. PMID 18951886.
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^ Lin CC, Ng LT, Hsu FF, Shieh DE, Chiang LC (January 2004). "Cytotoxic effects of Coptis chinensis and Epimedium sagittatum extracts and their major constituents (berberine, coptisine and icariin) on hepatoma and leukaemia cell growth". Clin. Exp. Pharmacol. Physiol. 31 (1–2): 65–9. doi:10.1111/j.1440-1681.2004.03951.x. PMID 14756686.
^ Lin CC, Lin SY, Chung JG, Lin JP, Chen GW, Kao ST (March 2006). "Down-regulation of cyclin B1 and up-regulation of Wee1 by berberine promotes entry of leukemia cells into the G2/M-phase of the cell cycle". Anticancer Research 26 (2A): 1097–104. PMID 16619512.
^ Khan M, Giessrigl B, Vonach C et al. (January 2010). "Berberine and a Berberis lycium extract inactivate Cdc25A and induce α-tubulin acetylation that correlate with HL-60 cell cycle inhibition and apoptosis". Mutation Research 683 (1–2): 123–30. doi:10.1016/j.mrfmmm.2009.11.001. PMID 19909759.
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^ Li GH, Wang DL, Hu YD et al. (September 2009). "Berberine inhibits acute radiation intestinal syndrome in human with abdomen radiotherapy". Medical Oncology (Northwood, London, England) 27 (3): 919–25. doi:10.1007/s12032-009-9307-8. PMID 19757213.
Swanson Premium Full Spectrum Oregon-Grape Root - LUCY GETS 1 Capsule at PM meal
Oregon-Grape Root CONTAINS BERBERINE – VERY SIMILAR TO BLOODROOT(THE COMPOUNDS IN BLACK SALVE and NEOPLASENE). IT HAS ANTI-ANGIOGENIC, IMMUNE MODULATION, APOPTOSIS, AND COX-2 properties, TNF, TIP cells and more. Also antibiotic, anti-inflammatory, antiparasitic. But the Oregon Grape Root's Berberine won't make them sick to their stomach like bloodroot or Neoplasene. Stimulates white blood production from the bone marrow, anti-cancer properties, supports liver function.
HERE IS AN EXCERPT FROM A USER OF NEOPLASENE:
"I would be willing to try neoplasene on a tumor on the outside of the body or a tumor that was not internal but could fall off after it died . But I would not try it on nasal cancer or a cancer deep inside the body.
Neoplasene causes inflammation in the cancer cells and that causes apoptosis to occur ( cellular suicide) so you get alot of swelling and in the nasal passages there is not a lot of room so he would get very stuffed up. He was also on the anti-angiogenesis protocol from his oncologist which cuts off the blood supply to a tumor and his oncologist was a bit hesitant to doing both as neither he nor the holistic vet had done both at the same time but after they talked they thought maybe just maybe hitting a tumor at the blood supply and then from the surface with a drug that might cause apoptosis might just work. It may have been working but we will never know for sure or maybe it was working too fast or maybe it was not working and this was just the natural progression of the cancer but eventually Dash did develop swelling on his muzzle and for several months it did not grow but suddenly it got huge, swelled his eye shut and then it ruptured. All the other dogs I got to know on here or via another site that had nasal cancer treated with neoplasene also died and one thing we all seemed to have in common was the difficult act of even getting it down the nose as many of us used it via nose drops and it was a battle. Some gave it orally but I know it can then cause GI issues such as bleeds so Dash's doctor did nose drops instead."
February 6, 2013
Coconut oil has antibacterial, antiviral, and anti-fungal properties
Although supplements can be a confusing topic for many pet owners, most dog owners have heard of the benefits of feeding fish oils. There are however, a variety of oils that you can also use to your dog’s benefit, each with different actions and benefits.
Coconut oil consists of more than 90% saturated fats, with traces of few unsaturated fatty acids, such as monounsaturated fatty acids and polyunsaturated fatty acids. Most of the saturated fats in coconut oil are Medium Chain Triglycerides (MCTs). The main component (more than 40%) of coconuts oil's MCTs is lauric acid, followed by capric acid, caprylic acid, myristic acid and palmitic. Coconut oil also contains about 2% linoleic acid (polyunsaturated fatty acids) and about 6% oleic acid (monounsaturated fatty acids).
Most of the coconut oil benefits come from these MCTs. For example, the lauric acid in coconut oil has antibacterial, antiviral, and anti-fungal properties. Capric and caprylic acid have similar properties and are best known for their anti-fungal effects.
Besides caprylic acid, two other medium chain fatty acids found in coconut oil have been found to kill yeasts. A study done at the University of Iceland showed “capric acid, a 10-carbon saturated fatty acid, causes the fastest and most effective killing of all three strains of yeasts tested, leaving the cytoplasm disorganized and shrunken because of a disrupted or disintegrated plasma membrane. Lauric acid, a 12-carbon saturated fatty acid, was the most active at lower concentrations and after a longer incubation time.” This study shows great promise that all the medium chain fatty acids in coconut oil work together to kill yeasts, funguses, viruses, and bacteria.
In addition, MCTs are efficiently metabolized to provide an immediate source of fuel and energy, enhancing athletic performance and aiding weight loss. In dogs, the MCTs in coconut oil balance the thyroid, helping overweight dogs lose weight and helping sedentary dogs feel energetic.
As a bonus, coconut oil improves any dog’s skin and coat, improves digestion, and reduces allergic reactions.
Fed regularly to pets, coconut oil may have multiple benefits:
Skin Conditions
Clears up skin conditions such as eczema, flea allergies, contact dermatitis,and itchy skin
Reduces allergic reactions and improves skin health
Makes coats become sleek and glossy, and deodorizes doggy odor
Prevents and treats yeast and fungal infections, including candida
Disinfects cuts and promotes wound healing
Applied topically, promotes the healing of cuts, wounds, hot spots, dry skin and hair, bites and stings
Digestion
Improves digestion and nutrient absorption
Aids healing of digestive disorders like inflammatory bowel syndrome and colitis
Reduces or eliminates bad breath in dogs
Aids in elimination of hairballs and coughing
Immune System, Metabolic Function, Bone Health
Coconut oil contains powerful antibacterial, antiviral, and anti-fungal agents that prevent infection and disease
Regulates and balance insulin and promotes normal thyroid function
Helps prevent or control diabetes
Helps reduce weight, increases energy
Aids in arthritis or ligament problems
Giving coconut to your pet is an excellent health decision and can improve your pet's quality of life, but there is a right way and wrong way to start supplementing your dog or cat's diet with coconut oil.
Start slow and increase gradually.
When beginning to supplement your pet's diet with coconut oil, start slow and increase gradually. Giving too much coconut oil too soon can cause digestive and detox issues.
Because coconut oil kills bacteria, viruses, parasites, yeasts, and fungi, your pet may respond negatively to the detox aspect of taking coconut oil. Signs of detoxing too rapidly may include lethargy, headaches, flu-like symptoms, fatigue, and diarrhea.
Large amounts of coconut oil given to a dog can cause diarrhea or greasy stools while his body adjusts to the change in diet. Start with small amounts, such as ¼ teaspoon per day for small dogs or puppies and 1 teaspoon for large dogs, or even just a dab if your dog's constitution is sensitive. If your dog seems tired or uncomfortable or has diarrhea, just cut back the amount temporarily. Gradually increase the amount every few days. If your dog seems tired or uncomfortable or has diarrhea, reduce the amount temporarily. It may also be helpful to give the small amounts of coconut oil in divided doses throughout the day.
Coconut oil is best given with food. Solid or liquid coconut oil can be added to food at any meal. Solid coconut oil can easily be melted quickly in hot water.
Feeding Guidelines
A general guideline on many sites have said the optimal dose for dogs is about 1 teaspoon per 10 pounds of body weight daily or about 1 tablespoon per 30 pounds, but don't start with these amounts in the beginning!
If you cook your own pet food, coconut oil would be an excellent addition to the recipe.
Most dogs like the taste of coconut oil so you won't have trouble feeding it to them.
Coconut Oil for Pet Skin Problems
If you wish to apply topically to use coconut oil to treat a rash, wound or dry skin, but they try to lick it off, try wrapping the skin in a rag or towel for a few minutes to let the oil soak in before they get a chance to lick it off.
Different brands of coconut oil will have different tastes ranging from a bland taste, to a strong coconut taste, to a more buttery taste. You can experiment with the oil your pet finds most pleasing. I just get the Swansonvitamins.com brand. Tastes great and cheap.
I fry 2 eggs in a tablespoon of coconut oil for Lucy per day to be added to some kibble. She loves it. Oddly, she was more active and seemed in a better mood within 2 days of starting using the coconut oil to fry the eggs instead of olive oil I normally use. It really smells good with a touch of garlic. Covers up the pills odors too. I still use olive oil to fry the ground chicken or turkey chubs that I add some kibble. I might start also add half coconut oil and half olive oil for frying meat. Or go all coconut. Did I say it smells great! I got it cheap at swansonvitamins but I have seen it in stores.
Read this detailed research data PDF on Coconut oil compounds that have antibacterial, antiviral, and anti-fungal properties
Despite the unanswered question regarding whether substantial amounts of lauric acid are metabolized into monolaurin, it is important to note that lauric acid is also effective against same microorganisms. Lauric acid produces greater activity against microorganisms than caprylic acid, capric acid, or myristic acid, all of which are present in coconut oil. Given that coconut oil provides approximately 50 percent lauric acid, a substantial amount of this bactericidal and virucidal fatty acid can be obtained from consuming coconut fat in pure coconut oil, and in many foods and products.
In addition, it is important to note that lauric acid appears to have immune-boosting properties as evidenced by feeding coconut oil to laboratory animals in whom the expected immune-factor responses (inhibition of interleukin-1) to endotoxin were induced via corn-oil feeding.56-57 Ingesting this on a daily basis may be an inexpensive way to both treat and prevent infection from microorganisms.58
CLINICAL BOTTOM LINE
The antiviral, antibacterial, and antifungal properties of lauric acid and monolaurin have been recognized for nearly three decades by only a small number of researchers: their work, however, has resulted in 100 or more research papers and numerous U.S. and foreign patents. Prof. Dr. Jon J. Kabara performed the original seminal research in this area of fat research. Kabara in1968 first patented certain fatty acids (FAs) and their derivatives (e.g., monoglycerides (MGs) that can have adverse effects on various microorganisms. While nontoxic and approved as a direct food additive by the FDA, monolaurin adversely affects bacteria, yeast, fungi, protozoa, and envelope viruses.
Kabara1-24 found that the properties that determine the anti-infective action of lipids are related to their structure: e.g., free fatty acids & monoglycerides. While the monoglycerides are active; diglycerides and triglycerides (fats) are inactive. Of the saturated fatty acids, lauric acid has greater antiviral activity than caprylic acid (C-8), capric acid (C-10), or myristic acid (C-14).
Fatty acids and monoglycerides produce their killing/inactivating effects by several mechanisms. An early postulated mechanism was the perturbing of the plasma membrane lipid bilayer. The antiviral action attributed to monolaurin is that of fluidizing the structure in the envelope of the virus, causing the disintegration of the microbial membrane. More recent studies indicate that one antimicrobial effect in bacteria is related to monolaurin's interference with signal transduction/toxin formation (Projan et al 1994)46.
Another antimicrobial effect in viruses is due to lauric acid's interference with virus assembly and viral maturation (Homung et al 1994)31. The third mode of action may be on the immune system itself (Witcher et al, 1993)35.
Antiviral Effects
Hierholzer and Kabara (1982)37 first reported the antiviral activity of the monoglyceride of lauric acid
(monolaurin) on viruses that affect humans. They showed virucidal effects of monolaurin on enveloped RNA and DNA viruses. This work was done at the Center for Disease Control of the U.S. Public Health Service. This study was carried out using selected virus prototypes or recognized representative strains of enveloped human viruses. All these viruses have a lipid membrane. The presence of a lipid membrane on viruses makes them especially vulnerable to lauric acid and its derivative monolaurin. These initial findings from the Center of Disease Control (CDC) have been confirmed by many other investigators.
Research has shown that enveloped viruses are inactivated by added fatty acids and monoglycerides in both human and bovine milk (Isaacs et al 1991)33. Others (Isaacs et al 198632, 199053, 199133, 199463; Thormar et al 198762) have confirmed Kabara's original statements concerning the effectiveness of monolaurin.
Some of the viruses inactivated by these lipids are the measles virus, herpes simplex virus (HSV-1 and -2), herpes family members (HIV, hepatitis C, vesicular, stomatitis virus (VSV), visna virus, and cytomegalovirus (CMV). Many of the pathogenic organisms reported to be inactivated by these antimicrobial lipids are those known to be responsible for opportunistic infections in HIV -positive individuals. For example, concurrent infection with cytomegalovirus is recognized as a serious complication for HIV positive individuals (Macallan et al 199364).
Until now few nutritionists in mainstream nutrition community seem to have recognized the added benefit of antimicrobial lipids in the support of infected patients. These antimicrobial fatty acids and their derivatives are essentially nontoxic to man. According to the published research, lauric acid is one of the best "inactivating" fatty acids, and its monoglyceride is even more effective than the fatty acid alone (Kabara 19788, Sands et al 197940, Fletcher et al 198519, Kabara 198521).
Antibacterial Effects
The potentially pathogenic bacteria inactivated by monolaurin include Listeria monocytogenes, Staphylococcus aureus, Streptococcus agalactiae, groups A, F and G streptococci, gram-positive organisms, and some gram- negative organisms if pretreated with a chelator (Boddie and Nickerson, 199236; Kabara, 19788, 198418; Isaacs et al., 199053, 199133, 199463; Isaacs and Schneidman, 199165; Isaacs and Thormar, 198632, 199152; Thormar et al., 198762; Wang and Johnson, 199234).
Decreased growth of Staphylococcus aureus and decreased production of toxic shock syndrome toxin-1 was shown with 150 mg monolaurin per litre (Holland et al., 199430). Monolaurin was shown to be 5,000 times more inhibitory against Listeria monocytogenes than is ethanol (Oh and Marshall, 199369). Helicobacter pylori was rapidly inactivated by medium-chain monoglycerides and lauric acid, and there appeared to be very little development of resistance of the organism to the bactericidal effects of these natural antimicrobials (Petschow et al., 199670).
A number of fungi, yeast, and protozoa are also inactivated or killed by monolaurin. The fungi include several species of ringworm (Isaacs et al 199133). The yeast reported to be affected is Candida albicans (Isaacs et al 199133). The protozoan parasite Giardia lamblia is killed by monoglycerides from hydrolyzed human milk (Hemell et al 198667, Reiner et al 198666, Crouch et al 199168, Isaacs et al 199133).
Chlamydia trachomatis is inactivated by monolaurin (Bergsson et al 199825). Hydrogels containing monocaprin/monolaurin are potent in vitro inactivators of sexually transmitted viruses such as HSV-2 and HIV- 1 and bacteria such as Neisserian gonorrhea (Thormar102-103).
Monolaurin does not appear to have an adverse effect on desirable gut bacteria, but rather on only potentially pathogenic microorganisms. For example, Isaacs et al (199133) reported no inactivation of the common Esherichiacoli or Salmonella enteritidis by monolaurin, but major inactivation of Hemophilus influenza,
Staphylococcus epidermis and Group B gram positive streptococcus.
The phenomenal rate of prescriptions dispensed for antibiotic use, and to a lesser extent, antiviral has grown exponentially in the past several decades. Antibiotic has limited specificity and generally does not recognize “good” bacteria (often referred to as probiotics or forlife) from “bad” bacteria (meaning those bacteria that may cause disease.) Antibiotics try to destroy all bacteria and are usually unsuccessful.
More antibiotic therapy may start perpetuating a chronic illness. The cycle of antibiotic therapy may go on for months and months, and repetitious indiscriminate use of antibiotics destroys weak bacteria and sets up the stage for the more virulent bacteria to survive (as in survival of the fittest). The new, stronger, pathogenic bacteria are now “resistant” to the established antibiotic and another antibiotic must be found to fight the new pathogen. We are rapidly approaching that point in history of having super bacteria: disease causing bacteria that are unaffected by any antibiotic. In its failure, antibiotic therapy has taken with it the health of those same individuals it strives to help.
The great advantage of lauric acid is that it does not produce resistant microorganisms during use. Not only does auric acid not produce resistance but also it is known to help resistant organisms from forming.
A group of researchers from the University of Minnesota led by P.M. Schlievert reported in the March 199294 issue of Antimicrobial Agents and Chemotherapy that monolaurin inhibited strains of strep and staph bacteria that cause toxic shock syndrome. Other researchers also studied effectiveness of monolaurin in this area.71-100 In similar research published in October 2007101, Filipino research wrote in the Journal of Drugs in Dermatology that "sensitivity rates of Gram-positive Staphylococcus aureus, Streptococcus spp., and coagulase negative Staphylococcus, Gram-negative E. vulneris, Enterobacter spp., and Enterococcus spp. to 20 mg/mL monolaurin was 100 percent."
Most recently, Schlievert and his Minnesota colleagues demonstrated that monolaurin prevented acute simian immunodeficiency virus infection in female rhesus monkeys. The monolaurin worked by decreasing the expression of SIV toxins and reducing inflammation of vaginal walls. As the researchers wrote in Nature on April 23, 2009, their findings linking "interfering with innate host responses that recruit the target cells necessary to establish systemic infection, opens a promising new avenue for the development of effective interventions to block HIV-1 mucosal transmission."
Research continues104-124 in measuring the effects of the monoglycerin, monoglyceride derivative of capric acid, monocaprin, as well as the effects of lauric acid. Chlamydia trachomatis is inactivated by lauric acid, capric acid and monocaprin (Bergsson et al., 199825). Hydrogels containing monocaprin are potent in vitro inactivators of sexually transmitted viruses such as HSV-2 and HIV-1 and bacteria such as Neisseria gonorrhoeae (Thormar102- 103).
Research suggests that monolaurin offers some degree of immune support for the influenza virus and also for the following viruses, including, cytomegalovirus, according to the article and description of studies on using monolaurin to destroy viruses at: Monolaurin – A Natural Immune Boosting Powerhouse, Friday, October 31, 2008 - Byron J. Richards, CCN:
In studies performed at the Respiratory Virology Branch, Centers for Disease Control, Monolaurin was shown to remove all measurable infectivity against the following RNA and DNA viruses:
Viruses
HIV or HIV-1, -6 Visna virus
Herpes simplex virus-i (HSV-1 &2) Vesicular stomatitis virus (VSV)
Measles virus Rubella virus
Epstein-Barr virus (EBV) Respiratory syncytial virus Influenza virus Dengue virus (Type 1-4) Leukemia virus Cytomegalovirus (CMV)
Semliki forest virus Lymphocytic choriomeningitis
Human papilloma virus (HPV) Pneumovirus
Monolaurin has also been proven to deactivate the following in laboratory tests:
Bacteria
Gram-positive organisms Gram-negative organisms Bacillas anthracis (Anthrax) Chlamydia pneumonia Listeria monocytogenes Neisseria gonorrhoeae Staphylococcus aureus Helicobacter pylorus
Groups A, B, F & G streptococci Mycoplasma pneumonia Streptococcus agalactiae Vibrio parahaemolyticus Mycobacteria Clostridium perfringens
Yeasts, Fungi, and Molds Aspergillus Niger Malassezia, species Saccharomyces cerevisiae Penicillium citrinum Ringworm or tinea (Trichophyton) Candida utilis A number of protozoa like Giardia lamblia are also inactivated or killed by Lauric Acid.
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