Sunday, September 24, 2017

Low Brain Cholesterol—Separating Fact from Fiction



Where do you find the highest concentration of cholesterol in your whole body? In your BRAIN. The brain is cholesterol-rich on purpose—because it needs large amounts of cholesterol to function properly. So, what does that mean for the growing number of people choosing naturally cholesterol-free plant-based diets? And what about the 15 million Americans who take statin medications like Lipitor to lower their cholesterol levels? People who are trying to lower their cholesterol levels are worried about heart health. But how does lowering cholesterol affect mental health?
What is cholesterol?
Poor cholesterol—so misunderstood. Cholesterol is a waxy substance naturally embedded in our membranes, the flexible packaging surrounding every cell in our bodies. Cholesterol contributes structural firmness to membranes and keeps them from falling apart. Membranes are not simply protective cell wrappers; they are dynamic, highly intelligent structures that participate in cellular signaling and the transport of substances into and out of cells. Cholesterol is also an essential ingredient in vitamin D and many other hormones in the body, including estrogen and testosterone. All animal foods (meat, seafood, poultry, dairy, and eggs) contain cholesterol because all animal cells need cholesterol. 

Why does the brain need cholesterol?

Although the brain represents only 2% of total body weight, it contains 20% of the body’s cholesterol. What is all that cholesterol doing up there? Synapses— the magical areas where communication between brain cells takes place—are lined by cholesterol-rich membranes responsible for passing neurotransmitters like serotonin, GABA, and dopamine back and forth. Myelin, the white matter that insulates brain circuits, is made from tightly-wound membranes containing 75% of the brain’s cholesterol. Cholesterol also helps guide developing nerve endings to their destinations on “lipid rafts”. If the brain is too low in cholesterol, its membranes, synapses, myelin and lipid rafts can’t form or function properly, bringing all brain activity—including mood regulation, learning, and memory— to a screeching halt.

Do people who take statin drugs need to worry about low brain cholesterol? 

YES. “Statins” are drugs designed to lower your level of LDL cholesterol—the so-called “bad cholesterol.” They work by turning down the activity of HMG-CoA reductase, the enzyme our cells use to build new cholesterol molecules. Unfortunately, statins do cross the blood-brain barrier and enter brain cells, where they reduce the brain’s natural ability to make the beautiful cholesterol molecules the brain needs to do its important work.
We used to think that only certain statin drugs could cross into the brain, but it turns out that they ALL do; it’s just that some reach higher levels inside the brain than others. But don’t let that lull you into a sense of false security—even Pravastatin (Pravachol), which has the hardest time making the journey, penetrates the brain enough to interfere with its cholesterol factory. 
There haven’t been many human experiments testing the effects of statins on brain function, but the few that have been done suggest there is a real risk of cognitiveproblems in some people:
“RCTs [randomized controlled trials] on effect of statins and cognitive function have shown debatable and controversial results with three RCTs reporting poorer performance scores in a minority of cognitive tests among statin users. Hence, we conclude that there is a need for more randomized control trials and until then benefits of statins must be weighed against the risks of cognitive decline on an individual basis.” [Chatterjee S et al 2015 Curr Cardiol Rep 17:4]
All statin manufacturer package inserts include the same warning:
“There have been rare postmarketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These cognitive issues have been reported for all statins. The reports are generally nonserious, and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks).” 
Nonserious? Seriously? I don’t know about you, but I wouldn’t want any of those side effects. They say they are rare, but “post-marketing” reports tend to be rare, because most people don’t report side effects directly to the manufacturer. If you feel fuzzy-headed on a statin, trust your experience over the fine print. Stop the statin and see for yourself if the fog lifts. 

Statins and Heart Disease

Stop the statin?! What about high cholesterol and heart disease? Won’t millions of arteries across the country slam shut?
Statins are a bad idea —not just because they can gum up your brain, slow your hormone production, reduce your coenzyme Q10 levels, cause muscle pain, and put you at risk for other potential side effects, but also because they may not even reduce your risk for heart attacks. Prominent cardiologist Dr. Aseem Malhotra agrees: heart disease is NOT about cholesterol or saturated fat.
Heart disease is about insulin resistance (aka pre-diabetes) and inflammation within your blood vessels. Diets high in refined carbohydrates (like sugar, flour, cereals and fruit juice) can lead to abnormally high insulin levels. It just so happens that insulin boosts the activity of your cholesterol-building enzyme, HMG-CoA-reductase—the very same enzyme that statin drugs suppress! [Nelson DL, Cox MM. Lehninger Principles of Biochemistry. 5th ed. New York, NY: W.H. Freeman; 2008:842.]

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Monday, September 18, 2017

Surgical Castration Instead of Drugs in Prostate Cancer

For some men with metastatic prostate cancer, surgical castration to remove the testicles (orchiectomy) could be a better option than "chemical castration" achieved by long-term use of prostate gonadotropin-releasing hormone (GnRH) agonist products, as it may carry less risk for adverse events, suggests a new study published online December 23 in JAMA Oncology.
"The paradigms of treatment for advanced prostate cancer are ever changing, but there remains a group of men who require permanent castration. For those men, orchiectomy is a reasonable alternative that is associated, according to our study, with lower risks of fractures, peripheral arterial disease, and cardiac-related complications than GnRH agonists," commented lead author Quoc-Dien Trinh, MD, from Harvard Medical School in Boston, Massachusetts.
"Unfortunately, for a multitude of reasons, most of which are unjustified, urologists and medical oncologists no longer offer the option of orchiectomy," he continued. "This is in spite of guidelines continuing to recommend orchiectomy as a first-line treatment for men presenting with metastatic prostate cancer."

For the last 50 years, androgen-deprivation therapy has been the cornerstone of treatment of metastatic prostate cancer, the authors write.
However, achieving androgen deprivation by bilateral orchiectomy has basically been eliminated from clinical practice, mainly because of aesthetic and psychological issues, but also because medical therapy is reversible and easy to administer, the authors write.
The current standard of care is long-term use of GnRH agonist products such as goserelin (Zoladex, AstraZeneca) and leuprolide (Lupron, AbbVie).
However, there is mounting evidence that androgen-deprivation therapy is linked to significant adverse effects, such as cardiovascular events, diabetes, acute kidney injury, and bone loss, the authors write. The US Food and Drug Administration requires that GnRH agonist product labeling include a warning about the increased risk for diabetes and cardiovascular disease.
Past research looking at adverse cardiac events associated with GnRH agonist products has suggested there is a lower cardiac risk in patients with orchiectomies. That led to the hypothesis that cardiac adverse effects may be related to GnRH agonist products, rather than androgen deprivation per se.
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Saturday, September 9, 2017

Muscle Growth and Estrogen

Estrogen is often called a “female hormone,” which is a misnomer, as this steroid hormone is also produced in the male body. It’s also true that women produce far greater amounts of estrogen than men, just as men produce about 10 times more testosterone than women.
Men’s greater testosterone levels are often cited as the reason that they are able to build more muscle than women. Recent studies, however, show that despite the negligible amounts of testosterone they produce while weight training, women are able to make similar muscle gains to men’s. That relates more to the fact that anabolic hormones produced during exercise don’t have as great an effect on muscle growth as was previously realized. Think about that the next time you read an article about the best ways to boost anabolic hormones during training.
If men’s bodies produce estrogen, what is the purpose? After all, nature is not known to be profligate in its actions; everything it does, it does for a reason. Although the precise functions of estrogen in men aren’t entirely clear, it appears to play a role in the maturation and development of sperm, which means that estrogen may effect male fertility.
Estrogen is vital to bone development in women, and a lack of it in older women often results in osteoporosis, a bone-thinning disease. Some scientists suggest that estrogen may play a similar role in men. Men deficient in testosterone are also subject to osteoporosis, although it’s not as common in men as in women, and when it does occur, it usually strikes in the spine.
Men are often advised not to take supplements or drugs that lower estrogen for extended times because of possible adverse affects on the cardiovascular system. That’s based on the established cardiovascular protection offered by estrogen to women. Younger women rarely suffer from heart attacks or strokes, and the reason is attributed to their higher estrogen levels. Estrogen offers cardiovascular protection in several ways. For one thing, it aides the synthesis and release of nitric oxide.

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Sunday, July 2, 2017

Secrets to Alzheimer's, ALS and Parkinson's Disease: Dr. Paul Alan Cox at TEDxJacksonHole

Published on Oct 31, 2012
Paul Alan Cox is a Harvard Ph.D. who has searched for new medicines from plants used by traditional healers in the Pacific and Southeast Asia. For these efforts TIME magazine named him one of 11 "Heroes of Medicine." His efforts in preserving island rain forests were recognized with the Goldman Environmental Prize.

In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x=independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations)

Unconventional But Effective Therapy for Alzheimer's Treatment: Dr. Mary T. Newport at TEDxUSF

When Dr. Newport's husband Steven was diagnosed with early onset Alzheimer's, as a Doctor herself, she explored routine treatment options. But when his symptoms became so severe that he was not able to participate in clinical trials, her scientific deductions led to coconut oil, which has led to amazing results.

Mary T. Newport, M.D. grew up in Cincinnati, Ohio, and was educated at Xavier University and University of Cincinnati College of Medicine. She is board certified in pediatrics and neonatology, training at Children's Hospital Medical Center in Cincinnati, and Medical University Hospital in Charleston, SC. She is founding director of the newborn intensive care unit at Spring Hill Regional Hospital, practicing full-time through All Children's Specialty Physicians and volunteer clinical faculty at University of South Florida. She was also founding director of the neonatal intensive Care unit at Mease Hospital Dunedin.

In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x = independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations)

CLICK TO SEE THE VIDEO

Thursday, June 22, 2017

Extra virgin olive oil staves off Alzheimer's, preserves memory

Temple University research shows extra-virgin olive oil protects against memory loss, preserves the ability to learn and reduces conditions associated with Alzheimer's disease.

Researchers at the college's Lewis Katz School of Medicine found mice with EVOO-enriched diets had better memories and learning abilities compared to the rodents who didn't eat the oil.

The real effect of EVOO appeared in the inner-workings of the mice's brains. Neuron connections in the brain were better preserved in those on an EVOO diet.

Also, olive oil reduces brain inflammation and activates the autophagy process, whereby intracellular debris and toxins are removed. Such debris and toxins are firm markers of Alzheimer's disease. A reduction in autophagy, researchers claim, is suspected to be the beginning of Alzheimer's disease.

Olive oil is the cornerstone of the Mediterranean diet, which is praised for its various health benefits. This study, which was published Wednesday in the Annals of Clinical and Translational Neurology, adds to that previous research.

"The thinking is that extra-virgin olive oil is better than fruits and vegetables alone," said senior investigator Domenico Pratico, a professor at the Lewis Klein School of Medicine. "As a monounsaturated vegetable fat, it is healthier than saturated animal fats."

The two groups of mice didn't differ in appearance after months on their respective diets. The mice were tested at 9 and 12 months with those on an EVOO diet testing better on working and spatial memory and learning abilities.

Alzheimer's disease is the most common form of dementia in the United States and affects a person's thought, memory and language. The U.S. Centers for Disease Control and Prevention said the disease typically starts after age 60 with mild memory loss. There is no cure.

Alzheimer's cases are on the rise. In 2013, 5 million Americans had the disease. That number is expected to triple to 14 million by 2050.

Pratico said the "exciting" finding sets researchers up for another experiment. The next step is to introduce EVOO later in the aging process.

"Thanks to the autophagy activation, memory and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer's disease were significantly reduced," Pratico said. "We want to know whether olive oil added at a later time point in the diet can stop or reverse the disease."
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Wednesday, June 14, 2017

Aspirin 'major bleed' warning for over-75s

People over 75 taking daily aspirin after a stroke or heart attack are at higher risk of major - and sometimes fatal - stomach bleeds than previously thought, research in the Lancet shows. Scientists say that, to reduce these risks, older people should also take stomach-protecting PPI pills.
But they insist aspirin has important benefits - such as preventing heart attacks - that outweigh the risks. And they warn that stopping aspirin suddenly can be harmful. Anyone with concerns should speak to a doctor before considering changing medication, they say.

'Lifelong pills'

Doctors in the UK generally prescribe daily aspirin (75mg) for life after a person has a stroke or heart attack to help prevent more attacks. But researchers have known for some time that aspirin can increase the risk of stomach bleeds.
Until now, most research involved people under 75, showing that the risk of serious bleeds was low in this group. But with around half the people on lifelong aspirin in the UK now over 75, researchers at Oxford University decided to find out whether the benefits still outweigh the risks in this group.
Their study followed 3,166 patients who had previously had a stroke or heart attack and were prescribed aspirin or similar blood-thinning drugs. They found that, for patients aged under 65, the annual rate of disabling or fatal bleeds was less than 0.5% (around one person in every 200 people taking the medication). Meanwhile, for people aged 75 to 84, this rose to three people having major bleeds in every 200.
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Wednesday, December 7, 2016

DES causes birth defects & transgender development

 Diethylstilbestrol (DES) was the first synthetic estrogen to be created. Never patented, it was cheap and easy to produce, so DES was made by hundreds of drug companies in the U.S. and around the world. DES was prescribed to millions of pregnant women in the mistaken belief that it could prevent miscarriage. It did not work but instead, DES harmed the mothers, the children born of those pregnancies and possibly the grandchildren and beyond.
DES Action USA for more information


DES was prescribed to millions of pregnant women, primarily from 1938 – 1971, but certainly not limited to those years. In some cases DES prescriptions were written into the 1980s in the U.S., as well as other countries, in the mistaken belief the drug prevented miscarriage and ensured a healthy baby. But it didn’t work and instead DES harmed the mothers who were prescribed it, the children born of those pregnancies and now possibly their grandchildren and beyond.
Never patented, DES was cheap and easy to produce, so hundreds of drug companies made it in the U.S. and around the world. DES was marketed under numerous brand names.
DES was prescribed if a woman had a previous miscarriage, diabetes, or a problem pregnancy with bleeding, threatened miscarriage or premature labor.
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Gynecologist's Guide for treating DES Daughters  

Saturday, November 26, 2016

USA CAUSES OF DEATH - INTERACTIVE CHART



Compare with other nations, etc...

Chart ranks total deaths for the top 50 causes by age and gender. Rank is determined by official CDC final death total and certain causes such as types of heart disease and cancer are split out for age adjusted death rate rankings to give you an expanded view of what actually takes place. For this reason they will not always match rankings for top 15 causes for age adjusted death rates which use a different combination of ICD-10 Codes.

You can click on any cause to highlight it to make it easy to follow as you change ages or select a different gender. To remove highlight click the cause again. Use buttons in center to select gender and Use Green Links to sort by age range. Note how the cause of death column rankings change. Scroll to the bottom of the page to see population by age range selected. Use Drop Down at top left of Page to see this chart and other data for individual states. Citation is at the bottom of page.

SEE INTERACTIVE CHART

Friday, September 16, 2016

Recovery from Tendonosis and Tendonitis

My tendon damage was caused by a disagreement with Keflex, but many have tendon and muscle damage from Statins, Cipro or other drugs. I am nearly recovered after several years and I see no reason my experience wouldn't help others. I am still a work in progress, but I am increasingly optimistic.

Nearly five years ago I had surgery in Bangkok from an excellent doctor. However, I got a rare bacterial infection that became evident when I returned home.  Normally, Ciprofloxacin would have been prescribed. However, in my case a previous medical provider thought I had reacted adversely to Cipro and so Keflex on a PICC line was prescribed. The PICC line was inserted into my right arm and threaded into a main artery. I was given Keflex in syringes to be injected into the PICC line. Keflex couldn't kill the infection.

Keflex is in the Cephalosporin family and I am now allergic to this as well. Later my urologist told me I needed to use Cipro and after 28 days at 250 mg the infection was gone. I avoided the 500 mg strength to mitigate possible additional damage to my tendons.  It seems that I was not allergic to Cipro and have used it since. If only that earlier error could have been avoided.  Everyone is different and some react to Cipro. But, Keflex damaged my tendons and it seems to have affected the cardiac pacemaker function causing arrhythmia which fortunately is not too serious.  A cardiac treadmill nuclear medicine study of my heart showed it worked well under load so I was able to avoid a pacemaker after consulting an Electro Kinesiologist, an advanced specially for cardiologists. Some arrhythmia patients may show progress with time and exercise and this seems to be my case.   

Tendonitis and Tendonosis are common physical conditions that cause discomfort and can be crippling. Both involve the tendons, and can be caused by physical exertion and modern medicines. Tendonitis can often be cured more easily, but tendonosis is less well understood and its effects can last a lifetime. First, let's address the structure of tendons which is necessary to understanding the difference and treatment of these two conditions.

Tendons consist of a tough central cord surrounded by a sheath. There is little blood circulation so healing time can be lengthy as blood is central to transporting nutrition needed for healing. The cord is composed of chains of cells aligned end to end to support stress of movement and exercise. One might envision this is like a cable suspending a bridge with many threads of wire held together to support great weight.

On one hand, we may have tendonitis which is caused by overuse. This can be remedied by not using that area as much.  Tendonitis is an irritation between the central cord and the sheath. With lessened use that area will often cure itself. Otherwise a doctor may be needed.

When the tendon is damaged by statin drugs or antibiotics it can cause crippling injury which can confine the victim to a wheelchair. Often this is mislabeled as tendonitis and this obscures understanding and rehabilitation. Tendonosis is a much more serious malady.  Statins and powerful antibiotics can damage cells including tendons and muscles. Tendons connect muscles to bones and when they are damaged one can be crippled or at least in pain. I've had tendonitis in my right ankle from statins and no longer take them.

The first symptom of my tendonosis was pain in the tendons behind each knee. We didn't understand and treated it as though it was tendonitis and walked less although there was mild pain. I stopped Keflex, but the damage was done and through Dr. Google, I discovered it was tendonosis, not tendonitis. I saw several doctors who didn't mention tendonosis and I later read that this is often misdiagnosed as tendonitis. My hands also had tendon issues which fortunately are nearly resolved.

I bought a walker so I could ambulate about the house, but the pain got worse so I became dependent on a wheelchair for a few months.  I became discouraged that I would ever recover. I dearly missed my 5-mile daily walks and began to research on power-chairs. My wife wouldn't give up and strongly discouraged me from buying  one so I continued using the manual chair and in time began to use the walker again. Over time, I gradually recovered my tendons so they no longer hurt. My favorite topical for pain was menthol gel 2.5% that I got at our local 99 cent store. I had other things, but this was the best for me. I often lived with pain preferring to avoid possible additional drug reactions.

As my tendons hurt less I became more mobile and began to go to our gym. I live in a 55+ community and we have a variety of equipment. The medical provider referred me to a physical therapist who said the pain was due to a need to stretch. Well stretch, I did, and perhaps that helped, but it certainly didn't improve my condition. They really didn't understand my condition. My tendons were damaged and needed to heal and be rehabilitated so they would regain their tensile strength.

I needed to gradually exercise without straining tendons or my now flaccid muscles. It was a process of try and fail, sometimes overdoing and causing myself a relapse of a couple weeks. I gradually figured it out and tried doing less than what I thought I could. Because of the damage to the tendon cord, the cells evidently did not align and link into a chain as they heal according to one article. They need mild stress, but excessive tension initially caused some strain. I assume muscle cells link in a similar manner. When strain is excessive, the tendon may part and require surgical intervention. Some materials may yield under stress, but tendons are built for strength and do not seem to demonstrate significant plasticity. When I over-exercised, I assumed the pain was from damaged cells and rested until the pain stopped. I gradually learned and recovery has been gradual.

I needed to pick the equipment I would use. I chose the rowing machine as it can provide a gentle workout without requiring me to carry my body, thus avoiding damaging strain on the knee tendons. Rowing also helped my heart, arms and back which hadn't been used much. As time went on, the pain in my tendons gradually subsided and I gradually walked more. First with the walker and then without. We still use the walker to more groceries from the garage to the kitchen, but I hope I never again to need it to walk.

The rowing machine also helped rebuild my legs and I continually discovered "new" muscles I didn't know I had. Gradually, this subsided and I began to use other machines. Gradually, gradually, careful to not cause strain, but encourage rehabilitation. Once, I walked two miles, a major victory, but my leg muscles complained, but in time, I should be back to my 5-mile daily walks and begin to lose the extra 20 pounds I gained.

It has often been discouraging, but I am recovering and I have more confidence to diet more effectively. I hope all of this is helpful. If you have tendon or muscle damage from statin drugs, keep the faith. You too, very likely, with patience and care can improve your tendon and muscle condition. Patience, patience... gradual, gradual is the pace I learned.

Now, I have learned that finasteride can slow healing. It is often prescribed for men to slow or stop growth of the prostate which grows around the arithera and compresses it causing difficulty passing urine. It converts testosterone into products which will not encourage prostate growth thus it is not recommended for women. Since my surgery eliminated my testosterone production it is no longer appropriate for me. Recently I noticed a psychological effect and researched the drug. I no longer take it.  I notice my tendons seem to be healing faster now although tendons heal very slowly due to poor blood circulation within tendons.

Wednesday, July 6, 2016

Good fats can cut risk of death by 27%, study says


"Bad" fats include trans fats and saturated fats. Saturated fats are common in the American diet, in red meats and full-fat dairy. Research in this area has been mixed, with some studies finding that whole-milk dairy products could be linked to less body fat and obesity, possibly because they promote feelings of fullness and therefore less is consumed. A recent study associated dairy and butter with lower rates of diabetes, although it still found a 1% higher risk of death per tablespoon of butter.
Trans fats are the major culprit when it comes to health problems. Though they can be found naturally in small amounts in meat and dairy products, the major sources are from artificial trans fats used in processed foods.
The Food and Drug Administration banned trans fatsfrom products in 2013, but they can still be found in many foods like crackers, cookies, doughnuts, muffins, pies and cakes, often in trace amounts that quickly add up. Research from the Harvard School of Public Health has showed that the risk of heart disease rises by 23% for every 2% of calories obtained from trans fats.

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Friday, June 10, 2016

Understanding The Liver and Cholesterol

And come to the liver, one of my favorite organs. Certainly the heart, the brain, and the immune system get more play in the popular imagination than the liver, but that's only because the liver is so misunderstood. Next to the skin, the liver is the largest organ in the body. In many ways, it is the most important organ, and the last to be considered when it comes to health. In addition to being large, the liver is also a complicated organ involved in at least 200 separate functions. Generally speaking, the liver performs a vital role in regulating, synthesizing, storing, secreting, transforming, and breaking down many different substances in the body. In this issue, we explore the anatomy and physiology of the liver in detail from a natural health perspective, and conclude with a discussion of how the body regulates cholesterol and why statin drugs may not be all that doctors promote.

 As I mentioned above, the liver is the heaviest and largest gland inside the body, weighing in at about 3 pounds. Only your skin (also a single functioning organ) is larger. Your liver occupies almost the entire right upper quadrant of the abdominal cavity. (Remember that in virtually all medical diagrams, right and left are reversed.) It nestles up against the diaphragm on the top and against the ribs on the right -- stretching across the body, almost touching ribs on the left. Thus, barring extreme trauma such as bullet wounds and automobile accidents (or if it is not enlarged), it is fully protected -- a testament to how important the body considers the organ.

 Physically, it is divided into four lobes, a large right and a small left lobe. Nestled between those two lobes are two less easily visible lobes, the quadrate lobe sitting on top and the caudate lobe sitting just underneath and extending to the bottom of the liver.

 Obviously, a three pound organ cannot just "hang" in the abdominal cavity. It needs to be secured.  And in fact, it is suspended from the back of the diaphragm by two ligaments, the falciform and the suspensory ligaments. The falciform ligament in particular runs up through the entire liver, dividing the left and right lobes before attaching to the diaphragm. There is one other interesting note about the falciform ligament. The umbilical vein, when you are inside the womb, runs from the umbilical cord up between the left and right lobes of the liver. Within a week of birth, that vein is completely obliterated and replaced by the fibrous cord known as the falciform ligament.

 The liver has a reserve capacity of some 50-80%. That means you can destroy up to 80 percent (and in some cases possibly even more) of the liver's function and have no demonstrable negative symptoms. And as amazing as that is, it's not the most amazing part. As I have mentioned frequently over the years when talking about detoxing the liver, the liver is one of the few human organs that can regenerate itself. It can actually regenerate (in a matter of weeks) up to an 80% loss of tissue. Once regenerated, it will fill the same space it occupied before, and will take roughly the same shape as before. And when it's done regenerating, it stops! Though it grows faster than any cancer known to man, its regeneration does not become malignant, and the liver will stop growth at approximately its normal size. This is particularly useful after trauma such as an automobile accident that has damaged part of the liver. The damaged or diseased tissue can be removed by the surgeon with no loss of liver function, and in a matter of a few weeks, the liver will have regenerated all of its lost tissue. You've gotta love this stuff!
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Familial Hypercholesterolemia: How to Lower Your Elevated LDL Cholesterol

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Cholesterol is naturally produced by your body and is essential to its function throughout your everyday life. However, excessively high levels of cholesterol—in particular, LDL cholesterol— are bad and can lead to serious health problems such as clogged arteries, heart disease, and stroke.
What is LDL Cholesterol?
LDL stands for Low-Density Lipoproteins. This type of cholesterol is produced by the liver and is instrumental in the creation of cell walls, hormones, and digestive juices. However, when your LDL level is high, it can start to form a plaque-like substance on the walls of your cardiovascular system, blocking the natural flow of blood and leaving you at severe risk for heart attack and stroke. Put simply, LDL is the bad kind of cholesterol. But fear not – there are several ways in which you can lower your LDL cholesterol and encourage the development of High-Density Lipoproteins (good cholesterol), which actually function to limit the level of LDL cholesterol in your system.
Diet
Altering your diet is the easiest way to lower your elevated LDL cholesterol, and should be your first course of action, as every cholesterol-lowering strategy starts with your dietary habits. A balanced diet consisting of fruits, vegetables, whole grains, fish, and various plants will significantly help you lower your LDL cholesterol level. It’s best to limit the amount of red meat, eggs, and dairy you consume. Plant-based diets not only help lower your LDL, but they can also help clear plaque buildup from your arteries.
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New Blood Test Better Predicts Heart Attack Risk

LDL Particle Number

The Quebec Cardiovascular Study was the first large study demonstrating that heart attack can occur when a person’s LDL particle number is high and LDL level is low.8 This has been repeatedly confirmed in other studies, most recently in the AMORIS study, which enrolled a remarkable 175,000 participants and demonstrated the superiority of LDL particle number (measured as apoprotein B) in predicting heart attack risk.9 This measure can be thought of as actually counting the number of LDL particles in one cubic centimeter, or one milliliter of blood.
LDL particle number is among the most powerful tools we have to predict the risk of heart attack. It can be measured directly as LDL particle number by the nuclear magnetic resonance spectroscopy method or indirectly as apoprotein B, which is a more widely available method. Apoprotein B is the major protein particle of LDL, with a single protein per LDL particle. Apoprotein B thus provides a “count” of LDL particles.
How can LDL level be low when the particle number is high? Because the amount of cholesterol contained per particle can vary widely. If you have many LDL particles that contain less cholesterol in each particle, the conventionally measured LDL level will be low, but your heart disease risk will be high. Greater numbers of cholesterol-containing particles in the blood means more cholesterol deposition in plaque. The combination of low LDL level and high LDL particle number is very common, creating a situation whereby many people are mistakenly told that they are not at risk for heart attack.
High LDL particle number responds to the same treatments as high LDL level, but this method of assessment provides greater confidence in determining who to treat and how intensively to do so. Statin prescription drugs lower LDL particle number, as does the non-statin prescription drug ezetimibe, though it is less potent. Niacin (vitamin B3) lowers LDL particle number less potently than the statins, but will achieve a 10-20% reduction. In addition to prescription medicines, many nutritional strategies can lower LDL particle number.
High LDL particle number can be a source of danger even when LDL level has been reduced by treatments such as cholesterol-lowering statin drugs. This is why people who take a cholesterol-lowering medication can still suffer a heart attack. LDL particle number provides much more powerful feedback on the adequacy of treatment and is therefore a tool for further reduction of risk.10,11

Small LDL

LDL particles vary in size—big, medium, and small. The size difference is crucial. Small LDL particles are a far more destructive force than their larger counterparts. Like finely tuned weapons designed to wreak maximum damage, smaller particles more effectively penetrate the cellular barrier and enter arterial walls, contributing to atherosclerotic plaque. They also persist longer in the circulation, which allows more opportunity to cling like little magnets to tissues within the walls.
Once in the arterial wall, small LDL particles are more prone to oxidation, which stimulates the release of inflammatory and adhesive proteins. Small, dense LDL promotes endothelial dysfunction and enhanced production of pro-coagulants by endothelial cells. Small, dense LDL thus appears to be more atherogenic—that is, more likely to contribute to the build-up of plaque within arteries—than normal LDL.12,13
Small LDL can be an inherited predisposition that is activated by unhealthy lifestyles and weight gain. When the genetic factors are strong, it can occur in healthy people who are not overweight. It frequently causes heart disease and is found in more than half of all people who suffer heart attacks. Small LDL particles triple the likelihood of developing coronary plaque and suffering a heart attack.
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A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef

There is considerable support among the nutritional communities for the diet-heart (lipid) hypothesis, the idea that an imbalance of dietary cholesterol and fats are the primary cause of atherosclerosis and cardiovascular disease (CVD) []. Health professionals world-wide recommend a reduction in the overall consumption of SFAs, trans-fatty acids (TAs) and cholesterol, while emphasizing the need to increase intake of n-3 polyunsaturated fats [,].
Such broad sweeping nutritional recommendations with regard to fat consumption are largely due to epidemiologic studies showing strong positive correlations between intake of SFA and the incidence of CVD, a condition believed to result from the concomitant rise in serum low-density-lipoprotein (LDL) cholesterol as SFA intake increases [
,]. For example, it is generally accepted that for every 1% increase in energy from SFA, LDL cholesterol levels reportedly increase by 1.3 to 1.7 mg/dL (0.034 to 0.044 mmol/L) [-].

Beyond changes in genetics, some producers have also altered their feeding practices whereby reducing or eliminating grain from the ruminant diet, producing a product referred to as "grass-fed" or "grass-finished".
Historically, most of the beef produced until the 1940's was from cattle finished on grass. During the 1950's, considerable research was done to improve the efficiency of beef production, giving birth to the feedlot industry where high energy grains are fed to cattle as means to decrease days on feed and improve marbling (intramuscular fat: IMF).
In addition, U.S. consumers have grown accustomed to the taste of grain-fed beef, generally preferring the flavor and overall palatability afforded by the higher energy grain ration[
]. However, changes in consumer demand, coupled with new research on the effect of feed on nutrient content, have a number of producers returning to the pastoral approach to beef production despite the inherent inefficiencies.
Research spanning three decades suggests that grass-only diets can significantly alter the fatty acid composition and improve the overall antioxidant content of beef. It is the intent of this review, to synthesize and summarize the information currently available to substantiate an enhanced nutrient claim for grass-fed beef products as well as to discuss the effects these specific nutrients have on human health.
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Does Fish Oil Raise Cholesterol?


  • Several studies have, indeed, confirmed that fish oil raises LDL cholesterol, usually by 5-10 mg/dl. Occasionally, it may be as much as 20 or more milligrams, as in Katie's case, enough for some people to be scared away from continuing this supplement. 

    Unfortunately, many physicians often assume that it's the (minor) cholesterol content of fish oil capsules, or some vague, undesirable effect of fish oil. It's nothing of the kind. And, if you were to rely on basic cholesterol values, it does indeed appear to be the case.

    But it's not.
    What has happened is that triglycerides have been reduced. Triglycerides occur in particles called very low-density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL). Given Katie's high triglyceride level of 201 mg/dl before fish oil, we can safely assume that VLDL and perhaps IDL (a less common pattern) were also elevated in Katie's blood. Fish oil effectively reduces triglycerides, as it did in Katie, and VLDL and IDL are also reduced. Since LDL particles start out as VLDL particles (the first particle that emerges from the liver), fish oil can cause a "shift" of particles from VLDL to LDL. Thus, the apparent rise in LDL.

    Another factor: Conventional LDL cholesterol is a calculated value, not measured. (Many people are surprised when they first hear this.) The calculation for LDL is thrown off-sometimes considerably-by any reduction in HDL or rise in triglycerides from average values. In Katie's case, the rise in HDL from 48 to 54 mg/dl along with the reduction in triglycerides from 201 to 92 mg/dl mean that calculated LDL has become more accurate and rises towards the true measured value. The actual rise in true LDL cholesterol may be small to none.

    Omega-3 fatty acids from fish oil therefore provide the appearance of raising LDL cholesterol, but the actual-measured-rise is usually small to none.

    Omega-3 fatty acids have been convincingly shown to reduce risk of heart attackstroke, heart rhythm disorders, and are powerful tools to reduce triglycerides. It's a shame to avoid this wonderfully effective and healthy tool because of the appearance of rising cholesterol.
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Small LDL Cholesterol: Epidemic of the New Century


There's a new risk factor for heart disease-and it's not high cholesterol. It's rapidly skyrocketed into first place as the number one most common trigger for heart disease.

Ask your family physician what the number one cause for heart disease is, and he/she will likely reply "high cholesterol" without hesitating. Most Americans would answer the same. After all, the media overflows with discussions about cholesterol and how drugs can reduce it.

Just 30 years ago, small LDL was far less common because lifestyles were different and the technology for identifying small LDL was unavailable. Why the surge in the small LDL pattern? Two reasons: 1) The explosion of excess weight and obesity in the U.S., which triggers formation of small LDL particles, and 2)over-reliance on processed carbohydrates, especially wheat-based convenience foods, that increase expression of the small LDL pattern enormously. 

Small LDL has climbed into first place as the number one cause of heart disease. (Number two: low HDL cholesterol.) Given current trends, as many as 80-90% of those with heart disease, 40-50% of the overall adult population may harbor this pattern.

Official agencies like the American Heart Association and the USDA have lost touch with the emergence of small LDL as a trigger for heart disease. The USDA Food Pyramid, for instance, advises American adults to eat 6-8 servings of grains per day. This advice is a sure-fire method to ignite expression of the small LDL pattern. The American Heart Association's Heart Check Mark program endorses products like Cocoa Puffs, Berry Kix and Cookie Crisp cereals and hundreds of other similar products as "heart healthy" that likewise act as potent triggers of the small LDL pattern.
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Why “Average” Cholesterol Values Can Be So Bad


With all the fuss about cholesterol, how can such a thing happen? Does it mean that cholesterol, LDL in particular, should be even lower to provide protection against heart attack and heart disease?

Not necessarily. What it does mean is that the causes for heart disease should be sought beyond cholesterol.

With Jack, we performed a blood test called lipoprotein analysis using a technique called nuclear magnetic resonance, or NMR. Despite the seemingly complicated name, it is a simple blood test that, in my experience, uncovers hidden causes for heart disease even when standard cholesterol numbers look fine. Jack's lipoprotein panel told an entirely different story. 

In this technique, there is an actual count of the number of LDL particles present in Jack's blood, rather than the calculation usually used to obtain standard LDL cholesterol. Jack's LDL particle number was 1880 nmol/l, a very high value among the worst 10% of men and women. LDL particle number of 1880 nmol/l is approximately the same as LDL cholesterol of 188 mg/dl (simply drop the last digit to generate an approximate "true" LDL), almost 70 mg higher than the estimated value of 119 mg. (This degree of inaccuracy, in fact, is not at all uncommon.)

Lipoprotein analysis also examines the size of LDL particles-large, small, or in-between. 95% of all Jack's LDL particles were small, a very severe pattern. The Quebec Cardiovascular Study is among the clinical studies demonstrating that the combination of high LDL particle number and small LDL raises heart disease risk by 600%. 

Jack also showed a severe excess of intermediate-density lipoprotein (218 nmol/l). This is an important pattern that suggests that dietary fats are not cleared for 24 hours or so after a meal, a phenomenon that heightens risk forcarotid disease and strokeaneurysms, as well as heart disease.
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