Linda’s comment:…..Heavy-metals are a food for Lyme critters….I started on my journey of removing the heavy metals from my body almost 2 years ago….I had 14 amalgams removed….I went on the FIGHT protocol and I’m slowly removing these metals….having that many amalgams, we know that I have mercury deep in my bones….get with it and begin the journey of removing the heavy metals from your bodies…it is a slow process, but you must start somewhere…..Having Lyme disease, the mercury serves as heavy armor for the critters….We are getting slammed daily from our dirty environment with heavy metals….we are in a fight for our lives…..The FIGHT program will make your journey much easier…

Dr. Gordon’s comments:

Mercury is seriously increasing in our environment from coal burning power plants, dentistry etc. How could you prove that mercury is not a contributor to anyone’s health problems, whether mental or physical?

Read this and realize that if treatment was free, and safe, probably everyone on the planet deserves mercury detoxification.

What is the dental component vs. the coal burning component? The answer to that will depend on the individual, as that is where the mercury in fish is largely coming from.

Here is an excerpt from this great well reference article by Mark Hyman MD:

“Whether your fillings are new or old, the mercury in them is constantly absorbed into your body. And even if you stop being exposed to that mercury, it sticks around. It takes up to 18 years for the body to clear half of the dose of mercury from the body. Once mercury is in the body it comes out only VERY slowly.

In fact, people with amalgam fillings have significantly elevated blood mercury levels, three to five times more mercury in the urine, and two to twelve times more mercury in their tissues than those without amalgam fillings.

However blood and urine mercury levels don’t necessarily relate to the mercury load in your body tissues or severity of clinical symptoms.

Research on sheep and monkeys with dental amalgams has shown that blood mercury levels remained low – even though their tissue mercury levels were raised.

Urine mercury levels aren’t much better as an indicator of your total mercury load. They mainly reflect the cumulative dose of inorganic mercury in the kidneys and there exists only a very weak correlation with levels in other target tissues”

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://drhyman.com/mercury-get-this-poison-out-of-your-body-85/

Excerpt:

10 Truths and Tips about Mercury Toxicity
1.Industrial exposure to mercury is significant and mostly comes from coal burning (220 million pounds a year) and chlor-alkali plants. 
2.The main ways that humans are exposed to mercury are from contaminated fish and dental amalgams or silver fillings. 
3.Mercury can affect nearly all your organs, especially the brain, heart, kidneys, and gut. 
4.Many chronic diseases may be caused or worsened by mercury, including neurologic disease, ADHD, autism, heart disease, autoimmune diseases, and more. 
5.Some of us are genetically better adapted to detoxify mercury than others, leading to variable effects within the population. 
6.You should reduce your exposure by avoiding large ocean fish (like tuna, swordfish, shark, and tilefish) and river fish. Eat only small wild fish. If it fits in your pan, it is probably okay. 
7.Blood tests are relatively worthless for analyzing mercury toxicity, unless you have had a significant recent exposure or eat a lot of sushi or tuna. 
8.Hair tests only check for mercury from fish, not from fillings so they only give you a partial picture. 
9.The only way to find out your total body load of mercury is to take a medication with sulfur molecules that binds to the mercury like fly paper. This is called DMSA or DMPS. This test should ONLY be done by a trained physician and involves taking one dose of this medicine, followed by a 6- or 24-hour urine collection to see how much comes out. (In my opinion, the most reliable testing is done by Doctorsdata.com). 
10.If you are toxic and sick, you may consider addressing your dental health by seeing a biological dentist who can safely help you deal with mercury in your mouth. 

ILADS Video – Mitochondria Function Presentation

 Part I

Part II

View more FPInterviews information

Excerpt:

Cat-scratch disease resulting from Bartonella henselae infection
is usually a benign, self-limited process in immunocompetent
children. Even the rare cases associated with neurologic
manifestations are not generally fatal. We report a case of a
previously healthy 6-year-old boy with cat-scratch disease,
systemic dissemination, and encephalitis that led to his death.
Autopsy revealed perivascular lymphocytic infiltrates and
microglial nodules in the brain. To our knowledge, this finding
has not been previously reported in B. henselae infection,
possibly because of the paucity of material available for
complete neuropathologic evaluation. This case illustrates the
extreme severity of the spectrum with which cat-scratch disease
can present and provides evidence of brain histopathology that
may be representative of the disease.

Blood clots kill and they make today’s focus on cholesterol looks badly misguided. Many natural approaches help and add Carnitine to that list. I recently attended the Nevada Homeopathic and Integrative Medicine conference in Reno.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://www.nhiondemand.com/HSJArticle.aspx?id=912&utm_source=NHI+OnDemand+Newsletter+List&utm_campaign=a61eed16f7-HSJ_Sep30_2010&utm_medium=email

Excerpt:

NHIondemand.com
Date: 9/27/2010

L-Carnitine Plays a Role in Preventing Cardiovascular Disease.

Cardiovascular disease or heart disease is a class of diseases that involve the heart or blood vessels (arteries and veins). There are several risk factors for cardiovascular disease that are essentially immutable. These are older age, male gender, and a family history of CVD. Additionally, three major risk factors identified include cigarette smoking, dyslipidemia (high cholesterol), and hypertension. Other identified factors associated with increased risk for cardiovascular disease include physical inactivity, sleep problems, diabetes mellitus, rheumatoid arthritis, obesity, excessive intake of alcohol, thrombotic and fibrinolytic factors, elevated homocysteine levels, certain infections and inflammation, exogenously administered estrogens and androgens, certain psychosocial factors, increased fasting glucose. and frequency of migraines. The synergism of the presence of multiple risk factors must also be considered.

L-carnitine is an amino acid that is synthesized from the amino acids lysine and methionine. Because it can be synthesized in the body, L-carnitine is usually not considered to be an essential nutrient. However, it could be classified as an essential nutrient for premature infants and other individuals who are not able to synthesize it in sufficient amounts. In addition to its use in clinical conditions, L-carnitine is used with exercise programs to reduce muscle soreness.

A study published in the journal Renal Failure investigated the effects of L-carnitine on plasma coagulation and anticoagulation. The researchers enrolled thirty-six hemodialysis patients and the patients randomly received either 1000 mg a day L-carnitine or a placebo for 12 weeks. Blood was collected at the beginning of the trial and at the end to compare changes in plasma activity. The results were the L-carnitine group experienced significant reductions in serum C-reactive protein (marker for systemic inflammation) and plasma fibrinogen (an inflammation-related coagulator) in comparison to the placebo group. The authors stated “Therefore, l-carnitine may play an effective role in preventing cardiovascular diseases in these patients.”1

1 Hakeshzadeh F, Tabibi H, Ahmadinejad M, et al. Effects of L-Carnitine supplement on plasma coagulation and anticoagulation factors in hemodialysis patients. Ren Fail. 2010;32(9):1109-14.

Dr. Gordon’s Comments:

This article can be helpful if you understand how I would use PSA information and what I believe active surveillance should entail. I want to keep my patients away from needless, often repeated, biopsies and other far too aggressive prostate treatments.

We know that Dr Black at Dartmouth years ago proved that by age 60, autopsies find cancer of the prostate in 60% of all subjects tested. So with elevated PSA test, I like to do other tests such as caprofile.net for $371, as that picks up many cancers and tells you who has elevated anaerobic metabolism going on (Warburg Nobel prize, cancer is anaerobic). Also I like to consider the concept we learn from the Kobayashi Cancer Panel of tests, where he proved that ALL early cancers suggested by tumor tests would normalize with adequate life style based programs. So our goal is to put a program together that will in time invariably lead to normalization of those tests.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://www.nhiondemand.com/HSJArticle.aspx?id=913&utm_source=NHI+OnDemand+Newsletter+List&utm_campaign=a61eed16f7-HSJ_Sep30_2010&utm_medium=email

Excerpt:

Date: 9/28/2010
Over Diagnosis and Overtreatment for Prostate Cancer.
Source: Archives of Internal Medicine

Prostate cancer is a form of cancer that develops in the prostate, a gland in the male reproductive system. Most prostate cancers are slow growing; however, there are cases of aggressive prostate cancers. The cancer cells may metastasize (spread) from the prostate to other parts of the body, particularly the bones and lymph nodes. Prostate cancer may cause difficulty urinating, urinary retention, problems during sexual intercourse, or erectile dysfunction. Other symptoms can potentially develop during later stages of the disease such as fatigue, nausea, weakness, back pain, swollen lymph nodes, discomfort in the perineum, hip pain, or weight loss. Blood may be present in the urine. Most prostatic cancers are detected in asymptomatic men who have an elevated PSA (Prostate Specific Antigen) level or a nodular or enlarged prostate at the time of examination.

Prostate cancer screening is utilized to detect the tumor while it is localized in the prostate and is most easily and successfully treated. Biopsy of the prostate is essential for establishing the diagnosis and is indicated when an abnormality is detected by palpation or elevated PSA. 

Recent data suggests that prostate cancer screening may lead to over treatment in men who do not actually need any cancer treatment. The study reviewed information from 123,934 men with newly diagnosed prostate cancer. Researchers found that 14 percent had PSA values below 4 ng/mL, 73.5 percent were between 4.1 and 20 ng/mL and 12.5 percent had levels above 20 ng/mL. Men with screen-detected prostate cancer and PSA values less than 4 ng/mL were 1.49 and 1.39 times more likely to receive radical prostatectomy and radiation therapy, respectively, and were less likely to have high-grade disease than men who had non-screen-detected prostate cancer. This means that many men with low-risk prostate cancer are receiving aggressive cancer treatment even though active surveillance may be a safer and acceptable alternative for some men with PSA levels below 10 ng/mL.1

1 Shao YH, Albertsen PC, Roberts CB, et al. Risk profiles and treatment patterns among men diagnosed as having prostate cancer and a prostate-specific antigen level below 4.0 ng/ml. Arch Intern Med. 2010;170(14);1256-61.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20929776&retmode=ref&cmd=prlinks

Excerpt:

Most hosts, including humans, are simultaneously or sequentially
infected with several parasites. A key question is whether
patterns of coinfection arise because infection by one parasite
species affects susceptibility to others or because of inherent
differences between hosts. We used time-series data from
individual hosts in natural populations to analyze patterns of
infection risk for a microparasite community, detecting large
positive and negative effects of other infections. Patterns
remain once variations in host susceptibility and exposure are
accounted for. Indeed, effects are typically of greater
magnitude, and explain more variation in infection risk, than the
effects associated with host and environmental factors more
commonly considered in disease studies. We highlight the danger
of mistaken inference when considering parasite species in
isolation rather than parasite communities.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21050324&retmode=ref&cmd=prlinks

Excerpt:

A previously healthy febrile patient with travel history to
Nicaragua showed rapid clinical deterioration with hemodynamic
shock and anuria. Diagnosis of severe malaria was established
based on intra-erythrocytic parasites and antimalarial treatment
was initiated. However, upon reevaluation Babesia microti
infection was suspected and molecular characterization by
polymerase chain reaction and sequence analysis was performed.
(c) 2010 International Society of Travel Medicine.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21040576&retmode=ref&cmd=prlinks

Excerpt:

RESULTS: A total of 4,664 patients were tested. The IgM and IgG
seropositivity rates were 9.2% and 3.3%, respectively.
Questionnaires from 2,643 (57%) patients were available for
analysis. Erythema migrans (EM) was suspected in 38% of patients,
Lyme arthritis/disseminated disease in 23% and early
neuroborreliosis in 13%. Age 0-15 years and suspected EM were
significant predictors of IgM seropositivity, whereas suspected
acrodermatitis was a predictor of IgG seropositivity. LB was
suspected in 646 patients with arthritis, but only 2.3% were IgG
seropositive. This is comparable to the level of seropositivity
in the background population indicating that Lyme arthritis is a
rare entity in Denmark, and *the low pretest probability should
alert general practitioners to the possibility of false positive
LB serology*. 
Significant predictors for treating the patient were a reported
tick bite and suspected EM.

CONCLUSIONS: A detailed description of the utilization of
serology for Lyme borreliosis with rates of seropositivity
according to clinical symptoms is presented. Low rates of
seropositivity in certain patient groups indicate a low pretest
probability and there is a notable risk of false positive
results. 38% of all patients tested were suspected of EM,
although this is not a recommended indication due to a low
sensitivity of serological testing.

Excerpt:

Abstract

Introduction: Bartonella henselae, the causative agent of the illness referred to as cat scratch disease, is a common infection, particularly in children, and clinicians need to be aware of its potential transmission to humans by arthropod vectors such as fleas and ticks in addition to animal bites and scratches. The absence of a vertebrate bite or scratch does not preclude infection with B. henselae.

Materials and Methods: Literature regarding arthropod transmission of B. henselae was reviewed.

Results: B. henselae appears to be transmitted among cats and dogs in vivo exclusively by arthropod vectors (excepting perinatal transmission), not by biting and scratching. In the absence of these vectors disease does not spread. On the other hand, disease can be spread to humans by bites and scratches, and it is highly likely that it is spread as well by arthropod vectors.

Discussion: Clinicians should be aware that a common illness, infection with B. henselae, can be transmitted by arthropod vectors and a history of an animal scratch or bite is not necessary for disease transmission.

Link:  http://www.biomedcentral.com/1471-2180/10/232

Excerpt:

Results

The results indicate that experimental colonisation of chicks was successful and that the birds showed no signs of disease even at the highest dose of Campylobacteradministered. The phage cocktail was able to reduce the titre of both C. coli and C. jejuniin faeces by approximately 2 log₁₀ cfu/g when administered by oral gavage and in feed. This reduction persisted throughout the experimental period and neither pathogen regained their former numbers. The reduction in Campylobacter titre was achieved earlier (2 days post-phage administration) when the phage cocktail was incorporated in the birds’ feed.Campylobacter strains resistant to phage infection were recovered from phage-treated chickens at a frequency of 13%. These resistant phenotypes did not exhibit a reduced ability to colonize the chicken guts and did not revert to sensitive types.

Conclusions

Our findings provide further evidence of the efficacy of phage therapy for the control ofCampylobacter in poultry. The broad host range of the novel phage cocktail enabled it to target both C. jejuni and C. coli strains. Moreover the reduction of Campylobacter by approximately 2 log₁₀cfu/g, as occurred in our study, could lead to a 30-fold reduction in the incidence of campylobacteriosis associated with consumption of chicken meals (according to mathematical models). To our knowledge this is the first report of phage being administered in feed to Campylobacter-infected chicks and our results show that it lead to an earlier and more sustainable reduction of Campylobacter than administration by oral gavage. Therefore the present study is of extreme importance as it has shown that administering phages to poultry via the food could be successful on a commercial scale.