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Saturday, July 18, 2015

Treat the Inflammation not the Cholesterol




   Dr. Dwight Lundell, former Chief of Staff and Chief of Surgery at Banner Heart Hospital in Arizona told the world not to take statin drugs.  “We physicians with all our training, knowledge and authority often acquire a rather large ego that tends to make it difficult to admit we are wrong. So, here it is. I freely admit to being wrong. As a heart surgeon with 25 years experience, having performed over 5,000 open-heart surgeries, today is my day to right the wrong with medical and scientific fact.
His frontal attack on the field of cardiology tears apart the practice of prescribing medications to lower cholesterol and a diet that severely restricted fat intake. Doctors in this field have been continually bombarded with scientific literature, continually attending education seminars, all of which insisted heart disease resulted from the simple fact of elevated blood cholesterol. They were wrong. Unfortunately for too many people—dead wrong.

Dr. David Brownstein has debated publically about this issue and many people do recognize how off base the world of cardiology actually is. I have gone as far as writing an essay telling people to run from their statin prescribing cardiologist. And I have written an essay about The Statin Disaster and the recent increasing recommendation and prescription of this quite useless drug.
We know that inflammation in the artery wall is the real cause of heart disease. Simply stated, without inflammation being present in the body, there is no way that cholesterol can accumulate in the wall of the blood vessel and cause heart disease and strokes. Without sufficient magnesium in the body inflammation results and it is the inflammation that causes cholesterol to become trapped.
Magnesium, not statin drugs should be the foundation drug of for the prevention and treatment of heart disease, diabetes, and arteriosclerosis; it serves as a natural calcium antagonist, normalizes blood pressure and irregular heartbeat. Magnesium is The Ultimate Heart Medicine!

What are the biggest culprits of chronic inflammation? 
Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, flour and all the products made from them) and the excess consumption of omega-6 vegetable oils like soybean, corn and sunflower that are found in many processed foods. Low magnesium though is the most basic culprit as is excessive irregular breathing, which reduces both CO2 and O2 levels in the body, both of which cause systemic inflammation.

Magnesium is the perfect medicine for cardiologists. It is the nutritional medicinal with pharmaceutical properties that no allopathic drug can hope to equal, yet doctors routinely ignore it. Worse, they use calcium channel blockers, statin drugs and other questionable substances with nightmarish side effects, which include suppressing already low magnesium levels.

Though magnesium is safe and easy to use and is available for immediate use in emergency departments, rarely is its full potential appreciated or harnessed.[1] The two forms of magnesium I recommend are magnesium chloride and magnesium bicarbonate. The magnesium bicarbonate is for oral use with all of one’s water, and the magnesium chloride (oil) can be used both orally and topically.

Low Magnesium Hardens Arteries

Dr. Russell Blaylock says, “There is evidence that magnesium deficiency may play a role in atherosclerosis, also called hardening of the arteries. In one study that used experimental animals, magnesium supplementation inhibited the deposit of lipids in the walls of the aorta ­ that is, it inhibited plaque formation, a major factor in atherosclerosis.

“To see if there was a relation between ionized magnesium and blood lipids (such as cholesterol), researchers examined 29 men with an average age of 72.5 years, who had impaired insulin sensitivity, a common condition in the elderly. They found that the level of blood-ionized magnesium ­ but not total blood magnesium ­ correlated closely with levels of LDL (potentially harmful) cholesterol and total cholesterol. Because magnesium is a powerful anti-inflammatory element, it would be expected to help prevent cholesterol from oxidizing; this may explain why it reduces atherosclerotic plaque in experimental animals.”

Dr. Blaylock continues saying, “In my research, I came across a study from 1959 that demonstrated some remarkable findings concerning the interrelationship between calcium and magnesium and atherosclerosis. Researchers knew from previous studies that feeding animals large doses of magnesium markedly reduced the amounts of lipids deposited in the heart valves of the left side of the heart and in the aorta. This study looked not only at lipid deposits in the wall and valves of the heart, but also calcium deposits in the kidneys, which are common in people with kidney disease associated with atherosclerosis.”
More on Nutrition

Dr. Lundell also points out that by consuming excessive omega-6, the cell membrane produces chemicals called cytokines that directly cause inflammation. Today’s mainstream American diet has produced an extreme imbalance of omega-6 vs. omega-3s. The ratio of imbalance ranges from 15:1 to as high as 30:1 in favor of omega-6. That’s a tremendous amount of cytokines causing inflammation. In today’s food environment, a 3:1 ratio would be optimal and healthy.
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There is no escaping the fact that the more we consume prepared and processed foods, the more we cause inflammation in the body. The human body cannot process, nor was it designed to consume, foods packed with sugars and soaked in omega-6 oils. One tablespoon of corn oil contains 7,280 mg of omega-6; soybean contains 6,940 mg. Instead, use olive oil or butter from grass-fed beef.


Thursday, July 16, 2015

Severe depression linked with inflammation in the brain







Severe depression linked with inflammation in the brain


Depression Neurology / Neuroscience Immune System / Vaccines Mental Health add your opinionemailMNT featured
MNT Knowledge Center
Clinical depression is associated with a 30% increase of inflammation in the brain, according to a new study published in JAMA Psychiatry.
illustration depicting brain of depressed person

The new study is the first to find definitive evidence of inflammation in the brain of depressed patients.
Inflammation is the immune system's natural response to infection or disease. The body often uses inflammation to protect itself, such as when an ankle is sprained and becomes inflamed, and the same principle also applies to the brain. However, too much inflammation is unhelpful and can be damaging.

Increasingly, evidence is suggesting that inflammation may drive some depressive symptoms, such as low mood, loss of appetite and reduced ability to sleep.

What the new study set out to investigate was whether inflammation is a driver of clinical depression independent of other physical illness.

Researchers from the Centre for Addiction and Mental Health's (CAMH) Campbell Family Mental Health Research Institute in Toronto, Canada, used positron emission tomography (PET) to scan the brains of 20 patients with depression and 20 healthy control participants.

In particular, the team closely measured the activation of microglia - immune cells that play a key role in the brain's inflammatory response

The PET scans showed significant inflammation in the brains of the people with depression, and the inflammation was most severe among the participants with the most severe depression. The brains of people who were experiencing clinical depression exhibited an inflammatory increase of 30%.

Previous studies have examined markers of inflammation in the blood of depressed people, in an attempt to solve the "chicken or egg" debate of whether inflammation is a consequence of or contributor to major depression.

For instance, in 2012, a study conducted by Duke University Medical Center researchers and published in Biological Psychiatry found an association between the number of cumulative depressive episodes experienced by study participants and increased levels of an inflammation marker in their blood called C-reactive protein (CRP).

"Our results support a pathway from childhood depression to increased levels of CRP, even after accounting for other health-related behaviors that are known to influence inflammation. We found no support for the pathway from CRP to increased risk for depression," said Duke study leader Dr. William Copeland.

The Duke team concluded that depression, therefore, is more likely to contribute to inflammation in the body as opposed to arising as a consequence of inflammation.

Medical News Today did not have access to data on whether the patients in the CAMH study exhibited brain inflammation prior to developing depression or after symptom onset. However, the CAMH researchers claim that their study is the first to find definitive evidence of inflammation in the brains of depressed patients.

Should future depression therapies target inflammation?
"This finding provides the most compelling evidence to date of brain inflammation during a major depressive episode," says senior author Dr. Jeffrey Meyer, who holds a Canada Research Chair in the neurochemistry of major depression. He adds:

"This discovery has important implications for developing new treatments for a significant group of people who suffer from depression. It provides a potential new target to either reverse the brain inflammation or shift to a more positive repair role, with the idea that it would alleviate symptoms."

Severe depression affects 4% of the general population. However, more than half of people with major depression do not respond to antidepressants. Dr. Meyer suggests that future studies should investigate the possible impact of anti-inflammatory drugs on depression symptoms.

"Depression is a complex illness and we know that it takes more than one biological change to tip someone into an episode," says Dr. Meyer. "But we now believe that inflammation in the brain is one of these changes and that's an important step forward."

C. Gilman Jones











Designer protein 'blocks all known strains of HIV'





Designer protein 'blocks all known strains of HIV'

HIV / AIDS Immune System / Vaccines Infectious Diseases / Bacteria / Viruses Sexual Health / STDs add your opinionemailMNT featuredAcademic journal

MNT Knowledge Center

A novel drug candidate against HIV has been created by a joint team led by researchers at The Scripps Research Institute in Jupiter, FL. The scientists consider it to be so potent and effective that it could form the basis of a vaccine alternative.
drugs and syringe

The scientists designed a protein that simultaneously binds to two sites on the surface of the virus, which blocks it from entering a host cell.
"Our compound is the broadest and most potent entry inhibitor described so far," says Michael Farzan, a Scripps Research Institute professor who led the effort.

"Unlike antibodies, which fail to neutralize a large fraction of HIV-1 strains," continues Farzan, "our protein has been effective against all strains tested, raising the possibility it could offer an effective HIV vaccine alternative."

Farzan claims that the project is the culmination of more than a decade's work on the biochemistry of how HIV enters cells.

The results of the study, which are published in the journal Nature, demonstrate how the new drug candidate blocked every strain of HIV-1, HIV-2 and SIV (simian immunodeficiency virus), including the variants that are most difficult to block.

The new drug was also found to protect against doses of the virus higher than those that normally occur in human transmission for at least 8 months after injection.

New protein was engineered following previous research on the CCR5 co-receptor
When a cell is infected by HIV, it inserts its own single-stranded RNA into the host cell. This insert of genetic code allows the virus to transform the cell into a "manufacturing site" for HIV.

However, the Scripps researchers had previously investigated a co-receptor - CCR5 - that could be used to prevent infection by manipulating related proteins. CCR5 is the first "anchor point" on the surface of a cell that HIV binds to before it can penetrate the cell.

"When we did our original work on CCR5, people thought it was interesting, but no one saw the therapeutic potential," says Farzan. "That potential is starting to be realized."

Using the CCR5 work as a point of departure, the scientists designed a protein that mimics the receptor and simultaneously binds to two sites on the surface of the virus, which prevents it from entering a host cell.

Study first author Matthew Gardner explains how the protein prevents the virus from penetrating cells:

"When antibodies try to mimic the receptor, they touch a lot of other parts of the viral envelope that HIV can change with ease. We've developed a direct mimic of the receptors without providing many avenues that the virus can use to escape, so we catch every virus thus far."

A delivery mechanism for the drug candidate was designed using an engineered adeno-associated virus. This is a small, relatively harmless virus that does not cause disease. The adeno-associated virus turns cells into manufacturing sites that churn out enough of the new protective protein to potentially last for decades.

The data published by the team shows that the new drug candidate binds more strongly to the HIV-1 envelope than the best neutralizing antibodies currently known to work against the virus. Although it will be years before the protein can be tested in humans, it has been successful against SIV in a macaque model.

Recently, we looked at news that a recombinant strain of HIV exhibiting unprecedented aggression has been identified in Cuba.

Scientists researching this new HIV strain found that, after binding to CCR5, the virus moves to the next co-receptor - CXCR4 - much more quickly than other HIV strains. The move of the virus to CXCR4 is typically associated with onset of AIDS symptoms.

While this transition from CCR5 to CXCR4 is normally very difficult, the recombinant HIV variant was found to contain a protease that makes this transition easier to occur and also enables the virus to replicate in greater numbers than usual.